Ervous Ystem: Structural Classification

NERVOUS SYSTEM
The nervous system is the master controlling and communicating system of the body. Every
thought, action, and emotion reflects its activity. Its signaling device, or means of
communicating with body cells, is electrical impulses, which are rapid and specific and cause
almost immediate responses.
Functions of the Nervous System
To carry out its normal role, the nervous system has three overlapping functions.
 Monitoring changes. Much like a sentry, it uses its millions of sensory receptors to

monitor changes occurring both inside and outside the body; these changes are called
stimuli, and the gathered information is called sensory input.
 Interpretation of sensory input. It processes and interprets the sensory input and
decides what should be done at each moment, a process called integration.
 Effects responses. It then affects a response by activating muscles or glands (effectors)
via motor output.
 Mental activity. The brain is the center of mental activity, including consciousness,
thinking, and memory.
 Homeostasis. This function depends on the ability of the nervous system to detect,
interpret, and respond to changes in the internal and external conditions. It can help
stimulate or inhibit the activities of other systems to help maintain a constant internal
environment.
ANATOMY OF THE NERVOUS SYSTEM
The nervous system does not work alone to regulate and maintain body homeostasis; the
endocrine system is a second important regulating system.
Organization of the Nervous System
We only have one nervous system, but, because of its complexity, it is difficult to consider all of
its parts at the same time; so, to simplify its study, we divide it in terms of its structures
(structural classification) or in terms of its activities (functional classification).
Structural Classification
The structural classification, which includes all of the nervous system organs, has two
subdivisions- the central nervous system and the peripheral nervous system.
 Central nervous system (CNS). The CNS consists of the brain and spinal cord, which
occupy the dorsal body cavity and act as the integrating and command centers of the
nervous system
 Peripheral nervous system (PNS). The PNS, the part of the nervous system outside the
CNS, consists mainly of the nerves that extend from the brain and spinal cord.
ALTERED COGNITIVE-PERCEPTUAL PATTERNS: CLIENTS WITH NEUROLIGIC DISORDERS
Functional Classification
The functional classification scheme is concerned only with PNS structures.
 Sensory division. The sensory, or afferent division, consists of nerves (composed of

nerve fibers) that convey impulses to the central nervous system from sensory receptors
located in various parts of the body.
 Somatic sensory fibers. Sensory fibers delivering impulses from the skin, skeletal
muscles, and joints are called somatic sensory fibers.
 Visceral sensory fibers. Those that transmit impulses from the visceral organs are called
visceral sensory fibers.
 Motor division. The motor or efferent division carries impulses from the CNS to effector
organs, the muscles and glands; the motor division has two subdivisions: the somatic
nervous system and the autonomic nervous system.
 Somatic nervous system. The somatic nervous system allows us to consciously,
or voluntarily, control our skeletal muscles.
 Autonomic nervous system. The autonomic nervous system regulates events that are
automatic, or involuntary; this subdivision, commonly called involuntary nervous system,
has two parts: the sympathetic and parasympathetic, which typically bring about opposite
effects.
NERVOUS TISSUE : STRUCTURE AND FUNCTION
Even though it is complex, nervous tissue is made up of just two principal types of cells-
supporting cells and neurons.
Supporting Cells
Supporting cells in the CNS are “lumped together” as neuroglia, literally mean “nerve glue”.
 Neuroglia. Neuroglia includes many types of cells that generally support, insulate, and
protect the delicate neurons; in addition, each of the different types of neuroglia, also
simply called either glia or glial cells has special functions.
 Astrocytes. These are abundant, star-shaped cells that account for nearly half of the
neural tissue; astrocytes form a living barrier between the capillaries and neurons and
play a role in making exchanges between the two so they could help protect neurons from
harmful substances that might be in the blood.
 Microglia. These are spiderlike phagocytes that dispose of debris, including dead brain
cells and bacteria.
 Ependymal cells. Ependymal cells are glial cells that line the central cavities of the brain
and the spinal cord; the beating of their cilia helps to circulate the cerebrospinal fluid that
fills those cavities and forms a protective cushion around the CNS.
 Oligodendrocytes. These are glia that wraps their flat extensions tightly around the nerve
fibers, producing fatty insulating coverings called myelin sheaths.
 Schwann cells. Schwann cells form the myelin sheaths around nerve fibers that are found
in the PNS.
 Satellite cells. Satellite cells act as protective, cushioning cells.
Neurons
Neurons, also called nerve cells, are highly specialized to transmit messages (nerve impulses)
from one part of the body to another.
 Cell body. The cell body is the metabolic center of the neuron; it has a transparent
nucleus with a conspicuous nucleolus; the rough ER, called Nissl substance,
and neurofibrils are particularly abundant in the cell body.
 Processes. The armlike processes, or fibers, vary in length from microscopic to 3 to 4
feet; dendrons convey incoming messages toward the cell body, while axons generate
nerve impulses and typically conduct them away from the cell body.
 Axon hillock. Neurons may have hundreds of the branching dendrites, depending on the
neuron type, but each neuron has only one axon, which arises from a conelike region of
the cell body called the axon hillock.
 Axon terminals.These terminals contain hundreds of tiny vesicles, or membranous sacs
that contain neurotransmitters.
 Synaptic cleft. Each axon terminal is separated from the next neuron by a tiny gap called
synaptic cleft.
 Myelin sheaths. Most long nerve fibers are covered with a whitish, fatty material
called myelin, which has a waxy appearance; myelin protects and insulates the fibers and
increases the transmission rate of nerve impulses.
 Nodes of Ranvier. Because the myelin sheath is formed by many individual Schwann
cells, it has gaps, or indentations, called nodes of Ranvier.
Classification
Neurons may be classified either according to how they function or according to their structure.
 Functional classification. Functional classification groups neurons according to the

direction the nerve impulse is traveling relative to the CNS; on this basis, there
are sensory, motor, and association neurons.
 Sensory neurons. Neurons carrying impulses from sensory receptors to the CNS are
sensory, or afferent, neurons; sensory neurons keep us informed about what is happening
both inside and outside the body.
 Motor neurons. Neurons carrying impulses from the CNS to the viscera and/or muscles
and glands are motor, or efferent, neurons.
 Interneurons. The third category of neurons is known as the interneurons,
or association neurons; they connect the motor and sensory neurons in neural pathways.
 Structural classification. Structural classification is based on the number of processes
extending from the cell body.
 Multipolar neuron. If there are several processes, the neuron is a multipolar neuron;
because all motor and association neurons are multipolar, this is the most common
structural type.
 Bipolar neurons. Neurons with two processes- an axon and a dendrite- are called bipolar
neurons; these are rare in adults, found only in some special sense organs, where they act
in sensory processing as receptor cells.
 Unipolar neurons. Unipolar neurons have a single process emerging from the cell’s
body, however, it is very short and divides almost immediately into proximal (central)
and distal (peripheral) processes.
Central Nervous System
During embryonic development, the CNS first appears as a simple tube, the neural tube, which
extends down the dorsal median plan of the developing embryo’s body.
Brain
Because the brain is the largest and most complex mass of nervous tissue in the body, it is
commonly discussed in terms of its four major regions – cerebral hemispheres, diencephalon,
brain stem, and cerebellum.
Cerebral Hemispheres
The paired cerebral hemispheres, collectively called cerebrum, are the most superior part of the
brain, and together are a good deal larger than the other three brain regions combined.
 Gyri. The entire surface of the cerebral hemispheres exhibits elevated ridges of tissue
called gyri, separated by shallow grooves called sulci.
 Fissures. Less numerous are the deeper grooves of tissue called fissures, which separate
large regions of the brain; the cerebral hemispheres are separated by a single deep fissure,
the longitudinal fissure.
 Lobes. Other fissures or sulci divide each hemisphere into a number of lobes, named for
the cranial bones that lie over them.
 Regions of cerebral hemisphere. Each cerebral hemisphere has three basic regions: a
superficial cortex of gray matter, an internal white matter, and the basal nuclei.
 Cerebral cortex. Speech, memory, logical and emotional response, as well as
consciousness, interpretation of sensation, and voluntary movement are all functions of
neurons of the cerebral cortex.
 Parietal lobe. The primary somatic sensory area is located in the parietal lobe posterior
to the central sulcus; impulses traveling from the body’s sensory receptors are localized
and interpreted in this area.
 Occipital lobe. The visual area is located in the posterior part of the occipital lobe.
 Temporal lobe. The auditory area is in the temporal lobe bordering the lateral sulcus,
and the olfactory area is found deep inside the temporal lobe.
 Frontal lobe. The primary motor area, which allows us to consciously move our skeletal
muscles, is anterior to the central sulcus in the front lobe.
 Pyramidal tract. The axons of these motor neurons form the major voluntary motor
tract- the corticospinal or pyramidal tract, which descends to the cord.
 Broca’s area. A specialized cortical area that is very involved in our ability to speak,
Broca’s area, is found at the base of the precentral gyrus (the gyrus anterior to the central
sulcus).
 Speech area. The speech area is located at the junction of the temporal, parietal, and
occipital lobes; the speech area allows one to sound out words.
 Cerebral white matter. The deeper cerebral white matter is composed of fiber tracts
carrying impulses to, from, and within the cortex.
 Corpus callosum. One very large fiber tract, the corpus callosum, connects the cerbral
hemispheres; such fiber tracts are called commisures.
 Fiber tracts. Association fiber tracts connect areas within a hemisphere,
and projection fiber tracts connect the cerebrum with lower CNS centers.
 Basal nuclei. There are several islands of gray matter, called the basal nuclei, or basal
ganglia, buried deep within the white matter of the cerebral hemispheres; it helps regulate
the voluntary motor activities by modifying instructions sent to the skeletal muscles by
the primary motor cortex.
Diencephalon
The diencephalon, or interbrain, sits atop the brain stem and is enclosed by the cerebral
hemispheres.
 Thalamus. The thalamus, which encloses the shallow third ventricle of the brain, is a
relay station for sensory impulses passing upward to the sensory cortex.
 Hypothalamus. The hypothalamus makes up the floor of the diencephalon; it is an
important autonomic nervous system center because it plays a role in the regulation of
body temperature, water balance, and metabolism; it is also the center for many drives
and emotions, and as such, it is an important part of the so-called limbic system or
“emotional-visceral brain”; the hypothalamus also regulates the pituitary gland and
produces two hormones of its own.
 Mammillary bodies. The mammillary bodies, reflex centers involved in olfaction (the
sense of smell), bulge from the floor of the hypothalamus posterior to the pituitary gland.
 Epithalamus. The epithalamus forms the roof of the third ventricle; important parts of
the epithalamus are the pineal body (part of the endocrine system) and the choroid
plexus of the third ventricle, which forms the cerebrospinal fluid.
Brain Stem
The brain stem is about the size of a thumb in diameter and approximately 3 inches long.
 Structures. Its structures are the midbrain, pons, and the medulla oblongata.

 Midbrain. The midbrain extends from the mammillary bodies to the pons inferiorly; it is
composed of two bulging fiber tracts, the cerebral peduncles, which convey descending
and ascending impulses.
 Corpora quadrigemina. Dorsally located are four rounded protrusions called the
corpora quadrigemina because they remind some anatomist of two pairs of twins; these
bulging nuclei are reflex centers involved in vision and hearing.
 Pons. The pons is a rounded structure that protrudes just below the midbrain, and this
area of the brain stem is mostly fiber tracts; however, it does have important nuclei
involved in the control of breathing.
 Medulla oblongata. The medulla oblongata is the most inferior part of the brain stem; it
contains nuclei that regulate vital visceral activities; it contains centers that control heart
rate, blood pressure, breathing, swallowing, and vomiting among others.
 Reticular formation. Extending the entire length of the brain stem is a diffuse mass of
gray matter, the reticular formation; the neurons of the reticular formation are involved in
motor control of the visceral organs; a special group of reticular formation neurons,
the reticular activating system (RAS), plays a role in consciousness and the
awake/sleep cycles.
Cerebellum
The large, cauliflower-like cerebellum projects dorsally from under the occipital lobe of the
cerebrum.
 Structure. Like the cerebrum, the cerebellum has two hemispheres and a convoluted
surface; it also has an outer cortex made up of gray matter and an inner region of white
matter.
 Function. The cerebellum provides precise timing for skeletal muscle activity and
controls our balance and equilibrium.
 Coverage. Fibers reach the cerebellum from the equilibrium apparatus of the inner ear,
the eye, the proprioceptors of the skeletal muscles and tendons, and many other areas.
Protection of the Central Nervous System
Nervous tissue is very soft and delicate, and the irreplaceable neurons are injured by even the
slightest pressure, so nature has tried to protect the brain and the spinal cord by enclosing them
within bone (the skull and vertebral column), membranes (the meninges), and a watery cushion
(cerebrospinal fluid).
Meninges
The three connective tissue membranes covering and protecting the CNS structures are the
meninges.
 Dura mater. The outermost layer, the leathery dura mater, is a double layered membrane
where it surrounds the brain; one of its layer is attached to the inner surface of the skull,
forming the periosteum (periosteal layer); the other, called the meningeal layer, forms the
outermost covering of the brain and continues as the dura mater of the spinal cord.
 Falx cerebri. In several places, the inner dural membrane extends inward to form a fold
that attaches the brain to the cranial cavity, and one of these folds is the falx cerebri.
 Tentorium cerebelli. The tentorium cereberi separates the cerebellum from the
cerebrum.
 Arachnoid mater. The middle layer is the weblike arachnoid mater; its threadlike
extensions span the subarachnoid space to attach it to the innermost membrane.
 Pia mater. The delicate pia mater, the innermost meningeal layer, clings tightly to the
surface of the brain and spinal cord, following every fold.
Cerebrospinal Fluid
Cerebrospinal fluid (CSF) is a watery “broth” similar in its makeup to blood plasma, from which
it forms.
 Contents. The CSF contains less protein and more vitamin C, and glucose.

 Choroid plexus. CSF is continually formed from blood by the choroid plexuses; choroid
plexuses are clusters of capillaries hanging from the “roof” in each of the brain’s
ventricles.
 Function. The CSF in and around the brain and cord forms a watery cushion that protects
the fragile nervous tissue from blows and other trauma.
 Normal volume. CSF forms and drains at a constant rate so that its normal pressure and
volume (150 ml-about half a cup) are maintained.
 Lumbar tap. The CSF sample for testing is obtained by a procedure called lumbar
or spinal tap; because the withdrawal of fluid for testing decreases CSF fluid pressure, the
patient must remain in a horizontal position (lying down) for 6 to 12 hours after the
procedure to prevent an agonizingly painful “spinal headache”.
The Blood-Brain Barrier
No other body organ is so absolutely dependent on a constant internal environment as is the
brain, and so the blood-brain barrier is there to protect it.
 Function. The neurons are kept separated from bloodborne substances by the so-called
blood-brain barrier, composed of the least permeable capillaries in the whole body.
 Substances allowed. Of water-soluble substances, only water, glucose, and essential
amino acids pass easily through the walls of these capillaries.
 Prohibited substances. Metabolic wastes, such as toxins, urea, proteins, and most drugs
are prevented from entering the brain tissue.
 Fat-soluble substances. The blood-brain barrier is virtually useless against fats,
respiratory gases, and other fat-soluble molecules that diffuse easily through all plasma
membranes.
Spinal Cord
The cylindrical spinal cord is a glistening white continuation of the brain stem.
 Length. The spinal cord is approximately 17 inches (42 cm) long.

 Major function. The spinal cord provides a two-way conduction pathway to and from
the brain, and it is a major reflex center (spinal reflexes are completed at this level).
 Location. Enclosed within the vertebral column, the spinal cord extends from the
foramen magnum of the skull to the first or second lumbar vertebra, where it ends just
below the ribs.
 Meninges. Like the brain, the spinal cord is cushioned and protected by the meninges;
meningeal coverings do not end at the second lumbar vertebra but instead extend well
beyond the end of the spinal cord in the vertebral canal.
 Spinal nerves. In humans, 31 pairs of spinal nerves arise from the cord and exit from the
vertebral column to serve the body area close by.
 Cauda equina. The collection of spinal nerves at the inferior end of the vertebral canal is
called cauda equina because it looks so much like a horse’s tail.
Gray Matter of the Spinal Cord and Spinal Roots

The gray matter of the spinal cord looks like a butterfly or a letter H in cross section.
 Projections. The two posterior projections are the dorsal, or posterior, horns; the two

anterior projections are the ventral, or anterior, horns.
 Central canal. The gray matter surrounds the central canal of the cord, which contains
CSF.
 Dorsal root ganglion. The cell bodies of sensory neurons, whose fibers enter the cord by
the dorsal root, are found in an enlarged area called dorsal root ganglion; if the dorsal
root or its ganglion is damaged, sensation from the body area served will be lost.
 Dorsal horns. The dorsal horns contain interneurons.
 Ventral horns. The ventral horns of gray matter contain cell bodies of motor neurons of
the somatic nervous system, which send their axons out the ventral root of the cord.
 Spinal nerves. The dorsal and ventral roots fuse to form the spinal nerves.
White Matter of the Spinal Cord
White matter of the spinal cord is composed of myelinated fiber tracts- some running to higher
centers, some traveling from the brain to the cord, and some conducting impulses from one side
of the spinal cord to the other.
 Regions. Because of the irregular shape of the gray matter, the white matter on each side
of the cord is divided into three regions- the dorsal, lateral, and ventral columns; each
of the columns contains a number of fiber tracts made up of axon with the same
destination and function.
 Sensory tracts. Tracts conducting sensory impulses to the brain are sensory, or afferent,
tracts.
 Motor tracts. Those carrying impulses from the brain to skeletal muscles are motor,
or efferent, tracts.
Peripheral Nervous System
The peripheral nervous system consists of nerves and scattered groups of neuronal cell bodies
(ganglia) found outside the CNS.
Structure of a Nerve
A nerve is a bundle of neuron fibers found outside the CNS.
 Endoneurium. Each fiber is surrounded by a delicate connective tissue sheath, an

endoneurium.
 Perimeurium. Groups of fibers are bound by a coarser connective tissue
wrapping, the perineurium, to form fiber bundles, or fascicles.
 Epineurium. Finally, all the fascicles are bound together by a tough fibrous
sheath, the epineurium, to form the cordlike nerve.
 Mixed nerves. Nerves carrying both sensory and motor fibers are called mixed
nerves.
 Sensory nerves. Nerves that carry impulses toward the CNS only are called
sensory, or afferent, nerves.
 Motor nerves. Those that carry only motor fibers are motor, or efferent, nerves.
Cranial Nerves
The 12 pairs of cranial nerves primarily serve the head and the neck.
 Olfactory. Fibers arise from the olfactory receptors in the nasal mucosa and synapse with
the olfactory bulbs; its function is purely sensory, and it carries impulses for the sense of
smell.
 Optic. Fibers arise from the retina of the eye and form the optic nerve; its function is
purely sensory, and carries impulses for vision.
 Oculomotor. Fibers run from the midbrain to the eye; it supplies motor fibers to four of
the six muscles (superior, inferior, and medial rectus, and inferior oblique) that direct the
eyeball; to the eyelid; and to the internal eye muscles controlling lens shape and pupil
size.
 Trochlear. Fibers run from the midbrain to the eye; it supplies motor fibers for one
external eye muscle (superior oblique).
 Trigeminal. Fibers emerge from the pons and form three divisions that run to the face; it
conducts sensory impulses from the skin of the face and mucosa of the nose and mouth;
also contains motor fibers that activate the chewing muscles.
 Abducens. Fibers leave the pons and run to the eye; it supplies motor fibers to the lateral
rectus muscle, which rolls the eye laterally.
 Facial. Fibers leave the pons and run to the face; it activates the muscles of facial
expression and the lacrimal and salivary glands; carries sensory impulses from the taste
buds of the anterior tongue.
 Vestibulocochlear. Fibers run from the equilibrium and hearing receptors of the inner
ear to the brain stem; its function is purely sensory; vestibular branch transmits impulses
for the sense of balance, and cochlear branch transmits impulses for the sense of hearing.
 Glossopharyngeal. Fibers emerge from the medulla and run to the throat; it supplies
motor fibers to the pharynx (throat) that promote swallowing and saliva production; it
carries sensory impulses from the taste buds of the posterior tongue and from pressure
receptors of the carotid artery.
 Vagus. Fibers emerge from the medulla and descend into the thorax and abdominal
cavity; the fibers carry sensory impulses from and motor impulses to the pharynx, larynx,
and the abdominal and thoracic viscera; most motor fibers are parasympathetic fibers that
promote digestive activity and help regulate heart activity.
 Accessory. Fiber arise from the medulla and superior spinal cord and travel to muscles of
the neck and back; mostly motor fiber that activate the sternocleidomastoid and trapezius
muscles.
 Hypoglossal. Fibers run from the medulla to the tongue; motor fibers control tongue
movements; sensory fibers carry impulses from the tongue.
Spinal Nerves and Nerve Plexuses

The 31 pairs of human spinal nerves are formed by the combination of the ventral and dorsal
roots of the spinal cord.
 Rami. Almost immediately after being formed, each spinal nerve divides into dorsal and
ventral rami, making each spinal nerve only about 1/2 inch long; the rami contain both
sensory and motor fibers.
 Dorsal rami. The smaller dorsal rami serve the skin and muscles of the posterior body
trunk.
 Ventral rami. The ventral rami of spinal nerves T1 through T12 form the intercostal
nerves, which supply the muscles between the ribs and the skin and muscles of the
anterior and lateral trunk.
 Cervical plexus. The cervical plexus originates from the C1-C5, and phrenic nerve is an
important nerve; it serves the diaphragm, and skin and muscles of the shoulder and neck.
 Brachial plexus. The axillary nerve serve the deltoid muscles and skin of the shoulder,
muscles, and skin of superior thorax; the radial nerve serves the triceps and extensor
muscles of the forearm, and the skin of the posterior upper limb; the median
nerve serves the flexor muscles and skin of the forearm and some muscles of the hand;
the musculocutaneous nerve serves the flexor muscles of arm and the skin of the lateral
forearm; and the ulnar nerve serves some flexor muscles of forearm; wrist and many
hand muscles, and the skin of the hand.
 Lumbar plexus. The femoral nerve serves the lower abdomen, anterior and medial
thigh muscles, and the skin of the anteromedial leg and thigh; the obturator nerve serves
the adductor muscles of the medial thigh and small hip muscles, and the skin of the
medial thigh and hip joint.
 Sacral plexus. The sciatic nerve (largest nerve in the body) serves the lower trunk and
posterior surface of the thigh, and it splits into the common fibular and tibial nerves;
the common fibular nerve serves the lateral aspect of the leg and foot, while the tibial
nerve serves the posterior aspect of leg and foot; the superior and inferior gluteal
nerves serve the gluteal muscles of the hip.
Autonomic Nervous System
The autonomic nervous system (ANS) is the motor subdivision of the PNS that controls body
activities automatically.
 Composition. It is composed of a specialized group of neurons that regulate cardiac

muscle, smooth muscles, and glands.
 Function. At every moment, signals flood from the visceral organs into the CNS, and the
automatic nerves make adjustments as necessary to best support body activities.
 Divisions. The ANS has two arms: the sympathetic division and the parasympathetic
division.
Anatomy of the Parasympathetic Division
The parasympathetic division allows us to “unwind” and conserve energy.
 Preganglionic neurons. The preganglionic neurons of the parasympathetic division are

located in brain nuclei of several cranial nerves- III, VII, IX, and X (the vagus being the
most important of these) and in the S2 through S4 levels of the spinal cord.
 Craniosacral division. The parasympathetic division is also called the craniosacral
division; the neurons of the cranial region send their axons out in cranial nerves to serve
the head and neck organs.
 Pelvic splanchnic nerves. In the sacral region, the preganglionic axons leave the spinal
cord and form the pelvic splanchnic nerves, also called the pelvic nerves, which travel to
the pelvic cavity.
Anatomy of the Sympathetic Division
The sympathetic division mobilizes the body during extreme situations, and is also called the
thoracolumbar division because its preganglionic neurons are in the gray matter of the spinal
cord from T1 through L2.
 Ramus communicans. The preganglionic axons leave the cord in the ventral root, enter
the spinal nerve, and then pass through a ramus communicans, or small communicating
branch, to enter a sympathetic chain ganglion.
 Sympathetic chain. The sympathetic trunk, or chain, lies along the vertebral column on
each side.
 Splanchnic nerves. After it reaches the ganglion, the axon may synapse with the second
neuron in the sympathetic chain at the same or a different level, or the axon may through
the ganglion without synapsing and form part of the splanchnic nerves.
 Collateral ganglion. The splanchnic nerves travel to the viscera to synapse with the
ganglionic neuron, found in a collateral ganglion anterior to the vertebral column.
PHYSIOLOGY OF THE NERVOUS SYSTEM
The physiology of the nervous system involves a complex journey of impulses.
Nerve Impulse
Neurons have two major functional properties: irritability, the ability to respond to a stimulus
and convert it into a nerve impulse, and conductivity, the ability to transmit the impulse to other
neurons, muscles, or glands.
 Electrical conditions of a resting neuron’s membrane. The plasma membrane of a

resting, or inactive, neuron is polarized, which means that there are fewer positive ions
sitting on the inner face of the neuron’s plasma membrane than there are on its outer
surface; as long as the inside remains more negative than the outside, the neuron will stay
inactive.
 Action potential initiation and generation. Most neuron in the body are excited by
neurotransmitters released by other neurons; regardless what the stimulus is, the result is
always the same- the permeability properties of the cell’s plasma membrane change for a
very brief period.
 Depolarization. The inward rush of sodium ions changes the polarity of the neuron’s
membrane at that site, an event called depolarization.
 Graded potential. Locally, the inside is now more positive, and the outside is less
positive, a situation called graded potential.
 Nerve impulse. If the stimulus is strong enough, the local depolarization activates the
neuron to initiate and transmit a long-distance signal called action potential, also called a
nerve impulse; the nerve impulse is an all-or-none response; it is either propagated over
the entire axon, or it doesn’t happen at all; it never goes partway along an axon’s length,
nor does it die out with distance as do graded potential.
 Repolarization. The outflow of positive ions from the cell restores the electrical
conditions at the membrane to the polarized or resting, state, an event called
repolarization; until a repolarization occurs, a neuron cannot conduct another impulse.
 Saltatory conduction. Fibers that have myelin sheaths conduct impulses much faster
because the nerve impulse literally jumps, or leaps, from node to node along the length of
the fiber; this occurs because no electrical current can flow across the axon membrane
where there is fatty myelin insulation.
The Nerve Impulse Pathway
 Resting membrane electrical conditions. The external face of the membrane is slightly

positive; its internal face is slightly negative; the chief extracellular ion is sodium,
whereas the chief intracellular ion is potassium; the membrane is relatively permeable to
both ions.
 Stimulus initiates local depolarization. A stimulus changes the permeability of a
“patch” of the membrane, and sodium ions diffuse rapidly into the cell; this changes the
polarity of the membrane (the inside becomes more positive; the outside becomes more
negative) at that site.
 Depolarization and generation of an action potential. If the stimulus is strong enough,
depolarization causes membrane polarity to be completely reversed and an action
potential is initiated.
 Propagation of the action potential. Depolarization of the first membrane patch causes
permeability changes in the adjacent membrane, and the events described in (b) are
repeated; thus, the action potential propagates rapidly along the entire length of the
membrane.
 Repolarization. Potassium ions diffuse out of the cell as the membrane permeability
changes again, restoring the negative charge on the inside of the membrane and the
positive charge on the outside surface; repolarization occurs in the same direction as
depolarization.
Communication of Neurons at Synapses
The events occurring at the synapse are arranged below.
 Arrival. The action potential arrives at the axon terminal.

 Fusion. The vesicle fuses with plasma membrane.
 Release. Neurotransmitter is released into synaptic cleft.
 Binding. Neurotransmitter binds to receptor on receiving neuron’s end.
 Opening. The ion channel opens.
 Closing. Once the neurotransmitter is broken down and released, the ion channel close.
Autonomic Functioning
Body organs served by the autonomic nervous system receive fibers from both divisions.
 Antagonistic effect. When both divisions serve the same organ, they cause antagonistic
effects, mainly because their post ganglionic axons release different transmitters.
 Cholinergic fibers. The parasympathetic fibers called cholinergic fibers, release
acetylcholine.
 Adrenergic fibers. The sympathetic postganglionic fibers, called adrenergic fibers,
release norepinephrine.
 Preganglionic axons. The preganglionic axons of both divisions release acetylcholine.
Sympathetic Division
The sympathetic division is often referred to as the “fight-or-flight” system.
 Signs of sympathetic nervous system activities. A pounding heart; rapid, deep

breathing; cold, sweaty skin; a prickly scalp, and dilated pupils are sure signs sympathetic
nervous system activities.
 Effects. Under such conditions, the sympathetic nervous system increases heart rate,
blood pressure, and blood glucose levels; dilates the bronchioles of the lungs; and brings
about many other effects that help the individual cope with the stressor.
 Duration of the effect. The effects of sympathetic nervous system activation continue
for several minutes until its hormones are destroyed by the liver.
 Function. Its function is to provide the best conditions for responding to some threat,
whether the best response is to run, to see better, or to think more clearly.
Parasympathetic Division
The parasympathetic division is most active when the body is at rest and not threatened in any
way.
 Function. This division, sometimes called the “resting-and-digesting” system, is chiefly

concerned with promoting normal digestion, with elimination of feces and urine, and with
conserving body energy, particularly by decreasing demands on the cardiovascular
system.
 Relaxed state. Blood pressure and heart and respiratory rates rate being regulated at
normal levels, the digestive tract is actively digesting food, and the skin is warm
(indicating that there is no need to divert blood to skeletal muscles or vital organs.
 Optical state. The eye pupils are constricted to protect the retinas from excessive
damaging light, and the lenses of the eye are “set” for close vision.
II. Application of the Nursing Process

A. ASSESSMENT
1. Subjective Data
a. Nursing History
Weakness A common manifestation of neurologic disease. It frequently coexists with
other symptoms of disease and can affect a variety of muscles, causing a
wide range of disability. It can be sudden and permanent, as in stroke, or
progressive, as in neuromuscular diseases such as amyotrophic lateral
sclerosis. Any muscle group can be affected
Numbness Abnormal sensation is a neurologic manifestation of both central and
peripheral nervous system disease. Altered sensation can affect small or
large areas of the body. It is frequently associated with weakness or pain
and is potentially disabling. Lack of sensation places a person at risk for
falls and injury
Paresthesia A sensation of numbness or tingling or a “pins and needles” sensation.
Depending on the cause, the sensation of paresthesia can be short-term and
disappear quickly, such as when it occurs due to hyperventilation, an
anxiety attack or from lying on the arm while asleep. It happens when
sustained pressure is placed on a nerve. The feeling quickly goes away
once the pressure is relieved. Some individuals may experience chronic
paresthesia.
Chronic paresthesia is often a symptom of an underlying neurological
disease or traumatic nerve damage. Paresthesia can be caused by disorders
affecting the central nervous system, such as stroke and transient ischemic
attacks (mini-strokes), multiple sclerosis, transverse myelitis, and
encephalitis.
Headache Cephalalgia
Caused by tension or by displacement of pain-sensitive structures, dilation
of intracranial arteries, inflammation in a pain-sensitive structure of the
head, and direct pressure on certain cranial nerves.
.Pain Considered an unpleasant sensory perception and emotional experience
associated with actual or potential tissue damage or described in terms of
such damage. Pain can be acute or chronic.
Acute pain lasts for a relatively short period of time and remits as the
pathology resolves. May be associated with BRAIN HEMMORHAGE,
SPINAL DISK DISEASE, or TRIGEMINAL NEURALGIA.
Chronic pain extends for long periods of time and may represent a
broader pathology. This type of pain can occur with many degenerative
and chronic neurologic conditions (e.g. MULTIPLE SCLEROSIS)
Altered thinking An alteration in mental status refers to general changes in brain function,
such as confusion, amnesia (memory loss), loss of alertness, disorientation
(not cognizant of self, time, or place), defects in judgment or thought,
unusual or strange behavior, poor regulation of emotions, and disruptions
in perception, psychomotor skills, and behavior.
Speech Difficulty Dysarthria is a condition in which the muscles you use for speech are weak
or you have difficulty controlling them. Dysarthria often is characterized

by slurred or slow speech that can be difficult to understand. Common
causes of dysarthria include nervous system (neurological) disorders such
as stroke, brain injury, brain tumors, and conditions that cause facial
paralysis or tongue or throat muscle weakness. Certain medications also
can cause dysarthria.
Vomiting Vomiting, along with nausea, is a symptom of an underlying disease rather
than a specific illness itself.
Emesis is the medical term for vomiting.
Vomiting is the forcible emptying of the stomach in which the stomach has
to overcome the pressures that are normally in place to keep food and
secretions within the stomach.
Vertigo An illusion of movement, usually rotation
Vertigo is usually a manifestation of vestibular dysfunction.
Result in spatial disorientation, lightheadedness, loss of equilibrium
(staggering), and nausea and vomiting.
Ataxia Impaired coordination of movements or inability to coordinate muscle
movements resulting in difficulty in walking, talking, and performing self-
care activities
Fainting The temporary loss of consciousness due to a sudden decline in blood flow
to the brain. It may be caused by an irregular cardiac rate or rhythm or by
changes of blood volume or distribution. Syncope can occur in otherwise
healthy people. The patient feels faint, dizzy, or lightheaded (presyncope),
or loses consciousness (syncope).
Seizures The result of abnormal paroxysmal discharges in the cerebral cortex, which
then manifest as an alteration in sensation, behavior, movement,
perception, or consciousness. The alteration may be short or longer
duration. Seizures can occur as isolated events, such as when induced by a
high fever, alcohol, or drug withdrawal, or hypoglycemia. It may also be
the first obvious sign of a brain lesion.
Loss of Loss of consciousness is a partial or complete loss of the perception of
Consciousness yourself and all that around you.
Altered Sleep Disturbed sleeping patterns

patterns
Aphasia Or aphemia, is a loss of the ability to produce and/or comprehend

language, due to injury to brain areas specialized for these functions. It is
not a result of deficits in sensory, intellect, or psychiatric functioning.
Depending on the area and extent of the damage, someone suffering from
aphasia may be able to speak but not write, or vice versa, or display any of
a wide variety of other deficiencies in language comprehension and
production, such as being able to sing but not speak. Aphasia may co-occur
with speech disorders such as dysarthria or apraxia of speech.
Change in Partial or complete loss of memory caused by a physical or psychological
memory or condition
memory events
Change in ability Difficulty concentrating is a normal and periodic occurrence for most
to concentrate people. Tiredness and emotional stress can cause concentration problems
in most people. Hormonal changes, such as those experienced
during menopause or pregnancy, can also affect how we think and
concentrate. Concentration problems, when present to an excessive degree,
are also characteristic of certain physical and psychological conditions.
b. Functional Health Patterns

2 Objective Data
a. Assessing Neurologic Function
 Mental Status Assessment
The mental status examination (MSE) is a component of all medical exams and may be
viewed as the psychological equivalent of the physical exam. It is especially important in
neurologic and psychiatric evaluations. The purpose is to evaluate, quantitatively and
qualitatively, a range of mental functions and behaviors at a specific point in time. The MSE
provides important information for diagnosis and for assessment of the disorder’s course and
response to treatment. Observations noted throughout the interview become part of the MSE,
which begins when the clinician first meets the patient. Information is gathered about the
patient’s behaviors, thinking, and mood.
Major Components of the Mental Status Examination

Appearance  Age (chronological age and whether person looks this age)
 Sex, Race
 Body build (thin, obese, athletic, medium)
 Position (lying, sitting, standing, kneeling)
 Posture (rigid, slumped, slouched, comfortable, threatening)
 Eye contact (eyes closed, good contact, avoids contact, stares)
 Dress (what individual is wearing, cleanliness, condition of clothes,
neatness, appropriateness of garments)
 Grooming (malodorous, unkempt, dirty, unshaven, overly
meticulous, hairstyle, disheveled, makeup)
 Manner (cooperative, guarded, pleasant, suspicious, glib, angry,
seductive, ingratiating, evasive, friendly, hostile)
 Attentiveness to examiner (disinterested, bored, internally
preoccupied, distractible, attentive)
 Distinguishing features (scars, tattoos, bandages, bloodstains,
missing teeth, tobacco-stained fingers)
 Prominent physical irregularity (missing limb, jaundice, profuse
sweating, goiter, wheezing, coughing)
 Emotional facial expression (crying, calm, perplexed, stressed, tense,

screaming, tremulous, furrowed brow)
 Alertness (alert, drowsy, stupor, confused)
Motor/Behavior  Retardation (slowed movements)
 Agitation (unable to sit still, wringing hands, rocking, picking at
skin or clothing, pacing, excessive movement, compulsive)
 Unusual movements (tremor, lip smacking, tongue thrust,
mannerisms, grimaces, tics)
 Gait (shuffling, broad-based, limping, stumbling, hesitation)
 Catatonia (stupor, excitement)
Speech  Rate (slowed, long pauses before answering questions, hesitant,
rapid, pressured)
 Rhythm (monotonous, stuttering)
 Volume (loud, soft, whispered)
 Amount (monosyllabic, hyper-talkative, mute)
 Articulation (clear, mumbled, slurred)
 Spontaneity
Mood/Affect  Stability (stable, fixed, labile)
 Range (constricted, full)
 Appropriateness (to content of speech and circumstance)
 Intensity (flat, blunted, exaggerated)
 Affect (depressed, sad, happy, euphoric, irritable, anxious, neutral,
fearful, angry, pleasant)
 Mood (reported by patient/client)
Thought Content  Suicidal or homicidal ideations (intent, plan, access to means, time-

frame)
 Depressive cognition (guilt, worthlessness, hopelessness)
 Obsessions (persistent, unwanted, recurring thought)
 Ruminations
 Phobias (strong, persistent, fear of object or situation)
 Ideas of reference
 Paranoid ideation
 Magical ideation
 Delusions (false belief kept despite no supportive evidence)
 Overvalued ideas
 Thought broadcasting, insertion or withdrawal
 Other major themes discussed by patient/client
Thought Process  Coherence (coherent, incoherent)

 Logic (logical, illogical)
 Stream (goal-directed, circumstantial, tangential [diverges suddenly
from a train of thought], looseness of associations, flight of ideas,
rambling, word salad)

 Perseveration (pathological repetition of a sentence or word)
 Neologism (use of new expressions, phrases, words)
 Blocking (sudden cessation of flow of thinking and speech related to
strong emotions)
 Attention (distractibility, concentration)
Perception  Hallucinations (auditory [including command, running
commentary], visual, olfactory [smelling], gustatory [taste], tactile)
 Illusions (misinterpretation of actual external stimuli)
 Depersonalization
 Déjà vu, Jamais vu
Cognition  Orientation (time, person, place)
 Memory (short-term, long-term)
 Intellect
 Abstract thought
 Capacity to read and write
 Level of consciousness
Insight/Judgement  Awareness of illness (insight)
 Ability to make a decision wisely considering pros and cons for a
course of action
Level of Consciousness
Level of consciousness (LOC) can lie anywhere along a continuum from a state of alertness to
coma. A fully alert client responds to questions spontaneously; a comatose client may not
respond to verbal stimuli. The Glasgow Coma Scale was originally developed to predict recovery
from a head injury; however, it is used by many professionals to assess LOC. It tests in three
major areas: eye response, motor response, and verbal response. An assessment totaling 15
points indicates the client is alert and completely oriented. A comatose client scores 7 or less
Levels of Consciousness: Glasgow Coma Scale

FACULTY MEASURED RESPONSE SCORE
Eye opening Spontaneous 4
To verbal command 3
To pain 2 2
No response 1
Motor response To verbal command 6
To localized pain 5
Flexes and withdraws 4
Flexes abnormally 3
Extends abnormally 2
No response 1
Verbal response Oriented, converses 5
Disoriented, converses 4
Uses inappropriate words 3
Makes incomprehensible sounds 2
No response 1
 Cranial Nerve Assessment
The cranial nerve exam is part of the neurological examination. Proper assessment of these
nerves provides insightful and vital information about a patient’s nervous system. Examine
patient while he or she is sitting over the edge of the bed or examination table.
Cranial Nerve Assessment

CN I: Olfactory nerve  Not always tested.
 Assess for a rash or deformity of the nose.
 An upper respiratory infection is the most frequent cause of
dysfunction.
 To test, offer the patient something familiar to smell and identify,
for example, an orange or lemon peel, coffee, or vinegar. You can
also use essence bottles of vanilla or peppermint.
CN II: Optic nerve Acuity
 Use a Snellen chart, or have patient read something in the room.
 Assess with and without patient’s vision aids.
 Wiggle fingers and move hand medially, starting one-foot
lateral from patient’s ears; ask the patient to say when they see
the examiner’s fingers.
Color
 Use Ishihara plates to identify patients who are color blind.
Visual Field
 Ask the patient to look directly at examiner while examiner
wiggles one of their fingers in each of the four quadrants. Then,
ask the patient to identify which finger is moving.
Visual Reflexes
 Place one hand vertically along the patients nose to block any
light from entering the eye which is not being tested and shine a
light into each eye observing for pupillary reflexes.
Fundoscopy
 Use a fundoscope to examine the structures of each eye.
CN III, IV, VI:  Test the 6 cardinal points in an H pattern by asking the patient to
Oculomotor nerve, follow your finger with only his eyes without moving his head.
trochlear nerve, and  Look for failure of movement, nystagmus, eyelid drooping, and ask
abducens the patient if he experiences any double vision.
 Inspect pupils for size, equality, and regularity. Observe pupil size
with a shined light.
CN V: Trigeminal Test sensory branches:
nerve  Lightly touch the face with a piece of cotton followed by a blunt
pin in three places on each side of face: around jawline, on
cheek, on forehead.
 Assess corneal reflex by lightly touching each cornea with small
piece of cotton. This should cause the patient to blink.
Test motor branches:

 Have patient open his mouth against your resistance, or simulate
chewing gum
 Perform the jaw jerk by placing left index finger across patient’s
chin and striking finger with a tendon hammer. This should
normally cause slight protrusion of the jaw.
CN VII: Facial nerve  Test by asking patient to crease up forehead (raise eyebrows), close
eyes and keep closed against resistance, puff out cheeks and reveal
teeth.
 Assess taste by touching both sides of patient’s tongue with piece of
gum or peppermint stick. Can they taste it?
CN VIII: Acoustic  Stand to the side or behind the patient and whisper to him. Ask him
nerve (also known as to repeat what you whispered.
vestibulocochlear  The Rinne and Weber tests can also be used to assess hearing and
nerve) differentiate conductive and sensorineural hearing loss.
 Rinne test:
o Place sounding tuning fork on patient’s mastoid process
and then, next to the ear, ask which is louder (normal
hearing patient will find the second position the loudest).
 Weber test:
o Place sounding tuning fork base down in the center of the
patient’s forehead and ask if it is louder in either ear
(should be heard equally in both ears).
CN IX, X:  Ask the patient to swallow or attempt to elicit gag reflex with
Glossopharyngeal tongue depressor.
nerve and vagus nerve  Assess phonation by listening to vocal sounds as the patient speaks.
 Offer patient a piece of gum or peppermint stick to assess taste.
CN XI: Spinal  Ask the patient to shrug his shoulders and turn his head against
Accessory your resistance.
CN XII: Hypoglossal  Have the patient stick out tongue and observe for deviations to
either side.
 Cerebellar Function
Although the cerebellum does not initiate movements, it interrelates with many brainstem
structures in executing various movements, including maintaining proper posture and balance;
walking and running; fine voluntary movements as required in writing, dressing, eating, and
playing musical instruments; and smooth tracking movements of the eyes.
1. Equilibratory Coordination
2. Non-equilibratory
The cerebellum controls the property of movements, such as speed, acceleration, and trajectory.
Checking cerebellar functioning includes testing balance, coordination, and skilled movements.
Assessment of Cerebellar Function: Gait & Romberg’s Test
Gait: Have the patient walk heel to toe in a straight line ‐ forwards and backwards. Assess for
abnormalities such as stiff posture, staggering, wide base of support, lack of arm swing, unequal
steps, dragging or slapping of foot, and presence of ataxia (lack of co‐ordination).
Romberg’s Test: With eyes closed, have the patient stand with feet together and arms extended
to the front, palms up. Your patient should be able to maintain their balance. Stay next to the
patient when they are performing this test in particular, so if they begin to fall, you can catch
them. Balance should be maintained (Jarvis, 2011).
Assessment of Cerebellar Function: Rapid Alternating Movements
To further assess cerebellar function, rapid alternating movements are assessed, using a variety
of quick tests:
The Alternating Palm Slap Test: Have your patient rapidly slap one hand on the palm of the
other, alternating palm up and then palm down ‐ test both sides. Abnormal findings might be lack
of coordination, or slow, clumsy movements.
The Finger to Finger Test: To perform, have the patient touch your index finger with their
index finger, as you move your index finger in the space around them. Patients should be able to
do this without missing the mark.
Assessment of Cerebellar Function: Rapid Alternating Movements
The Finger to Nose Test: To perform, have your patient touch their nose with their index finger
of each hand with eyes shut. Patients should be able to do this without missing the mark.
The Heel to Shin Test: While standing, have your patient touch the heel of one foot to the knee
of the opposite leg. While maintaining this contact, have the patient run the heel down the shin to
the ankle. Test each leg. If your patient misses the mark, lower extremity coordination may be
impaired.
 Sensory Function
Assessment of the Sensory System Testing
The sensory system checks the intactness of peripheral nerves, sensory tracts, and higher cortical
discrimination. Have your patient close his eyes while checking sensory perception.
 Light Touch: Can your patient feel light touch equally on both sides of the body?
 Sharp/Dull: Can your patient distinguish between a sharp or dull object on both sides of
the body?
 Hot/Cold: Can your patient distinguish between a hot or cold object on both sides of the
body
Assessing the Spinothalamic Tract
Checking the spinothalamic tract tests your patient’s ability to sense pain, temperature, and light
touch.
 Presence of Pain: Pain can be tested by a simple pin prick with the patient’s eyes closed.
Abnormal findings would include hypalgesia, hypoalgesia, and analgesia.
 Temperature: Temperature should be tested only if pain test is normal. Hot and cold
objects may be placed on the patient’s skin at various locations bilaterally to test for
temperature sensation.
 Light touch: With a cotton ball or soft side of a Q‐tip, touch the patient’s body bilaterally
with their eyes closed. Ask them to indicate when you have touched them. Abnormal
responses include hypoesthesia, anesthesia, and hyperesthesia.
Assessing the Posterior Column Tract
Assessing the posterior column tract may identify lesions of the sensory cortex or vertebral
column.
 Vibration: Test the patient’s ability to feel vibrations by placing a tuning fork over
various boney locations on the patient’s toes and feet. If these areas are normal, then you
may assume the proximal areas are also normal.
 Position: Position or kinesthesia is tested by having the patient close their eyes and move
their big toe up and down. The patient should be able to tell you which way their toes are
moving.
Assessing the Posterior Column Tract
 Tactile discrimination
Tactile discrimination tests the discrimination ability of the sensory cortex. Stereognosis tests
the patient’s ability to recognize objects by feeling them. You can place car keys, a spoon, a
pencil, or other common object in your patient’s hand. They should be able to identify that
object by feel only. Graphesthesia is the ability to “read” a number “written” in your palm.
 Two point discrimination
Two point discrimination tests the brain’s ability to detect two distinct pin pricks on the skin.
An increase in the distance it normally takes to identify two distinct pricks occurs with
sensory cortex lesions
 Motor Function
Inspection and Palpation of the Motor System
A comprehensive inspection and palpation of the motor system includes evaluation of muscle
size, strength and tone of muscles.
Inspection and Palpation: Muscle Size
 Begin the inspection and palpation of the motor system by examining muscle size.
 Does your patient have appropriate size muscles for body type, age, and gender?
 Atrophy is abnormally small muscles with a wasted appearance. This can occur
with disuse, injury, motor neuron diseases, and muscle diseases.
 Hypertrophy (increased size) occurs with athletes and body builders. It is
characterized by increased size and strength of muscles
Inspection and Palpation: Muscle Strength Test
Muscle strength against a resistance, using a 0 ‐ 5 scale, with 0 = no movement and 5 = strong
muscle strength. Muscle strength should be equal bilaterally.
When testing muscle strength in the arms ask your patient to do the following against resistance:
 Lift arms away from side

 Push arms towards side
 Pull forearm towards upper arm
 Push forearm away from upper arm
 Lift wrist up; push wrist down
 Squeeze examiners finger
 Pull fingers apart
 Squeeze fingers together (Jarvis, 2011)
Inspection and Palpation: Muscle Tone
When testing muscle strength in the legs ask your patient to do the following against resistance:
 Lift legs up
 Push legs down
 Pull legs apart
 Push legs together
 Pull lower leg towards upper leg
 Push lower leg away from upper leg
 Push feet away from legs
 Pull feet towards legs
When testing muscle strength, abnormalities in muscle tone will become more evident.
Abnormal muscle tone findings can include:
 Limited range of motion

 Pain on motion
 Decreased resistance (flaccidity) or increased resistance (rigidity), or spasticity (Jarvis,
2011)
Involuntary Movements:
Tics, tremors, and fasciculation (involuntary contraction of a muscle) are all examples of
abnormal involuntary movements you may note on exam (Jarvis, 2011; Shaw, 2012).
 Reflexes
Reflexes are involuntary actions in response to a stimulus sent to the central nervous system.
Alterations in reflexes are often the first sign of neurological dysfunction such as upper motor
neuron disease, diseases of the pyramidal tract, or spinal cord injuries.
Stretch or Deep Tendon Reflexes: Deep tendon reflexes, also known as muscle stretch reflexes,
are reflexes elicited in response to stimuli to tendons. Normally, when a specific area of the
muscle tendon is tapped with a soft rubber hammer, the muscle fibers contract. Abnormal
responses may indicate injury to the nervous system pathways that produce the deep tendon
reflex. Deep tendon reflexes can be influenced by age, metabolic factors such as thyroid
dysfunction or electrolyte abnormalities, and anxiety level of the patient.
Reflexes & Spinal Nerve Roots
The main spinal nerve roots involved in testing the deep tendon reflexes are summarized in the
following table:
Reflex Main Spinal Nerve Roots Involved

Biceps C5, C6
Brachioradialis C6
Triceps C7
Patellar L4
Achilles Tendon S1
Reflexes & Spinal Nerve Roots

Check the deep tendon reflexes with a reflex hammer to stretch the muscle and tendon. The
limbs should be in a relaxed and symmetric position. Strike the reflex hammer across the
selected tendon with a moderate tap. If you cannot elicit a reflex, you can sometimes bring it out
by certain reinforcement procedures. For example, have the patient grit their teeth then try to
elicit the reflex again. Or you may have them clench their fists together when checking lower
extremity reflexes.
Rating Deep Tendon Reflexes
When reflexes are very brisk, clonus is sometimes seen. This is a repetitive vibratory contraction
of the muscle that occurs in response to muscle and tendon stretch.
Deep tendon reflexes are often rated according to the following scale:
Rating Reflex Response

0 Absent reflex
1+ Race, or seen only with reinforcement
2+ Normal
3+ Brisk
4+ Non-sustained clonus (i.e., repetitive vibratory movements
5+ Sustained clonus
Deep tendon reflexes are considered normal if they are 1+, 2+, or 3+. Reflexes that are
asymmetric, or there is a large difference between the arms and legs, or are rated as 0, 4+, or 5+
abnormal
Absence of superficial reflexes or unilateral suppression of superficial reflexes often results from
upper motor lesions subsequent to a stroke. Presence of primitive reflexes in adults is often a
sign of frontal lobe lesions.
Superficial Reflexes
The following superficial reflexes are considered normal in adults:
 Upper Abdominal: Ipsilateral contraction of abdominal muscles on the stroked side.
 Lower Abdominal: Ipsilateral contraction of abdominal muscles on the stroked side.
 Cremasteric: Stroke inner thigh, elicits elevation of testes.
b. Diagnostic Examination
b.1 Non-invasive Test
Structure:
Test Purpose
Skull X-ray A skull X-ray is an imaging test doctors
use to examine the bones of the skull,
including the facial bones, the nose, and
the sinuses.
A skull X-ray is typically done after

a traumatic head injury.
Computed Tomography (CT) Scan Computed tomography (CT scan) uses

X-rays to produce two-dimensional images of
organs, bones, and tissues.
A CT scan can aid in proper diagnosis
by showing the area of the brain that is
affected. CT scans can be used to quickly
detect hemorrhage in the brain and to
determine if someone who has had a stroke can
safely receive intravenous treatment to
dissolve clots.
CT scans also may be used to detect
bone and vascular irregularities, brain tumors
and cysts, brain damage from head injury,
hydrocephalus, brain damage causing epilepsy,
and encephalitis, among other disorders.
A contrast dye may be injected into the
bloodstream to highlight the different tissues in
the brain.
A CT of the spine can be used to show
herniated discs, spine fractures, or spinal
stenosis (narrowing of the spinal canal).
Magnetic Resonance Imaging (MRI) Magnetic resonance imaging

(MRI) uses computer-generated radio waves
and a powerful magnetic field to produce
detailed images of body tissues. Using
different sequences of magnetic pulses, MRI
can show anatomical images of the brain or
spinal cord, measure blood flow, or reveal
deposits of minerals such as iron.
MRI is used to diagnose stroke,
traumatic brain injury, brain and spinal cord
tumors, inflammation, infection, vascular
irregularities, brain damage associated with
epilepsy, abnormally developed brain regions,
and some neurodegenerative disorders. MRI is
also used to diagnose and monitor disorders
such as multiple sclerosis. A contrast dye may
be injected into the vein to enhance visibility
of certain areas or tissues.
Function:
Test Purpose
Electroencephalography Monitors the brain’s electrical activity through the skull. EEG
(EEG) is used to help diagnose seizure disorders and metabolic,
infectious, or inflammatory disorders that affect the brain’s
activity. EEGs are also used to evaluate sleep disorders,
monitor brain activity when a person has been fully
anesthetized or loses consciousness, and may be used to
confirm brain death.
Evoked Potential Studies Also called evoked response, measure the electrical signals to
the brain generated by hearing, touch, or sight. Evoked

potentials are used to test sight and hearing (especially in
infants and young children) and can help diagnose such
neurological conditions as multiple sclerosis, spinal cord
injury, and acoustic neuroma (small tumors of the acoustic
nerve). Evoked potentials are also used to monitor brain
activity among coma patients, and confirm brain death.
 Auditory evoked potentials (also called brain stem
auditory evoked response) can assess hearing loss and
damage to the acoustic nerve and auditory pathways in the
brainstem, and detect acoustic neuromas. The person being
tested sits in a soundproof room and wears headphones.
Clicking sounds are delivered one at a time to one ear while
a masking sound is sent to the other ear. Each ear is usually
tested twice, and the entire procedure takes about 45
minutes.
 Visual evoked potentials detect loss of vision from optic
nerve damage (for example from multiple sclerosis). The
person sits close to a screen and is asked to focus on the
center of a shifting checkerboard pattern. One eye is tested
at a time. Each eye is usually tested twice. Testing takes
30-45 minutes.
 Somatosensory evoked potentials (SSEPs) measure
responses from electrical stimuli to the nerves. In addition
to electrodes on the scalp, electrodes are pasted to the arms,
leg, and back to measure the signal as it travels from the
peripheral nerves to the brain. Tiny electrical shocks are
delivered by electrodes pasted to the skin over a nerve in an
arm or leg. SSEPs may be used to help diagnose multiple
sclerosis, spinal cord compression or injury, and certain
metabolic or degenerative diseases. SSEP tests usually take
longer than an hour.
Neuropsychological Testing Neuropsychological tests are specifically designed
tasks used to measure a psychological function known to be
linked to a particular brain structure or pathway. They usually
involve the systematic administration of clearly defined
procedures in a formal environment. Neuropsychological tests
are typically administered to a single person working with an
examiner in a quiet office environment, free from distractions.
As such, it can be argued that neuropsychological tests at times
offer an estimate of a person's peak level of cognitive
performance. Neuropsychological tests are a core component
of the process of conducting neuropsychological assessment.
Positron Emission Test Positron emission tomography (PET) scans provide
(PET) two- and three-dimensional pictures of brain activity by
measuring radioactive isotopes that are injected into the
bloodstream. PET scans of the brain are used to detect or

highlight tumors and diseased tissue, show blood flow, and
measure cellular and/or tissue metabolism.
PET scans can be used to evaluate people who have
epilepsy or certain memory disorders, and to show brain
changes following injury. PET may be ordered as a follow-up
to a CT or MRI scan to give the physician a greater
understanding of specific areas of the brain that may be
involved with problems. A low-level radioactive isotope, also
called a tracer, is injected into the bloodstream and the tracer’s
uptake in the brain is measured.
Functional MRI Functional MRI (fMRI) uses the blood’s magnetic properties
to produce real-time images of blood flow to particular areas of
the brain. fMRI can pinpoint areas of the brain that become
active and show how long they stay active. This imaging
process may be used to localize brain regions for language,
motor function, or sensation prior to surgery for epilepsy.
Researchers use fMRI to study head injury and degenerative
disorders such as Alzheimer’s disease.
Vascular Abnormalities Also called ultrasonography, uses high-frequency sound waves
Ultrasonography to obtain images inside the body. Ultrasound can be used to
 Doppler Scanning assess changes in the anatomy of soft tissues, including muscle
and nerve. It is more effective than an x-ray in displaying soft
tissue changes, such as tears in ligaments or soft tissue masses.
In pregnant women, ultrasound can suggest the diagnosis of
conditions such as chromosomal disorders in the fetus. The
ultrasound creates a picture of the fetus and the placenta.
Ultrasound also may be used in newborns to diagnose
hydrocephalus (build-up of cerebrospinal fluid in the brain) or
hemorrhage.
 Carotid Doppler ultrasound is used to measure flow in

arteries and blood vessels in the neck.
 Transcranial Doppler ultrasound is used to view blood
flow in certain arteries and blood vessels inside the
skull. Carotid Doppler and transcranial Doppler are
used to assess the risk of stroke.
 Duplex ultrasound refers to ultrasound studies that are
combined with anatomical ultrasound.
b.2 Invasive Tests

Structure:
Test Purpose
Lumbar Puncture Cerebrospinal fluid analysis involves the

removal of a small amount of the fluid that
surrounds the brain and spinal cord. The
procedure is commonly called a lumbar puncture
or spinal tap.
The fluid is tested to detect evidence of brain

hemorrhage, infection, multiple sclerosis,
metabolic diseases, or other neurological
conditions Pressure inside the skull can be
measured to detect conditions such as a false
brain tumor. The lumbar puncture may be done
as an inpatient or as an outpatient procedure.
Myelography Myelography involves the injection of contrast

dye into the spinal canal to enhance imaging of
the spine, by CT or by X-ray. Myelograms have
mostly been replaced by MRI, but may be used
in special situations. For example, myelograms
may be used to diagnose tumors of the spine or
spinal cord or spinal cord compression from
herniated discs or fractures..
Cerebral Angiography Angiography is a test that involves injecting dye

into the arteries or veins to detect blockage or
narrowing.
A cerebral angiogram can show narrowing or

obstruction of an artery or blood vessel in the
brain, head, or neck. It can determine the
location and size of an aneurysm or vascular
malformation. Angiograms are used in certain
strokes where there is a possibility of unblocking
the artery using a clot retriever. Angiograms can
also show the blood supply of a tumor prior to
surgery or embolectomy (surgical removal of a
blood clot or other material that is blocking a
blood vessel).
Digital Venous Angiograpghy Also called Digital Subtraction Angiography
Provides an image of the blood vessels in the

brain to detect a problem with blood flow. The
procedure involves inserting a catheter (a small,

thin tube) into an artery in the leg and passing it
up to the blood vessels in the brain. A contrast
dye is injected through the catheter and X-ray
images are taken of the blood vessels.
Function:
Test Purpose
Peripheral Nerve Studies Nerve Conduction Study
An EMG is usually done in conjunction with a nerve

conduction study (NCS). An NCS measures the nerve’s
ability to send a signal, as well as the speed (nerve conduction
velocity) and size of the nerve signal through peripheral
nerves.
Electromyography Or EMG, is used to diagnose nerve and muscle disorders,
spinal nerve root compression, and motor neuron disorders
such as amyotrophic lateral sclerosis. EMG records the
electrical activity in the muscles. Muscles develop abnormal
electrical signals when there is nerve or muscle damage.
Nerve Conduction Velocity A nerve conduction velocity test (NCV) is an
electrical test that is used to determine the adequacy of
the conduction of the nerve impulse as it courses down
a nerve. This test is used to detect signs of nerve injury.
Muscle of Nerve Biopsy Biopsy involves the removal and examination of a small piece
of tissue from the body. Muscle or nerve biopsies are used to
diagnose neuromuscular disorders.
A skin biopsy can be used to measure small nerve fibers or to
test for certain metabolic disorders. A small piece of skin is
removed under local anesthesia, usually in an office setting.
A brain biopsy, used to determine tumor type or certain
infections, requires surgery to remove a small piece of the
brain or tumor. A brain biopsy is an invasive procedure that
carries its own risks.

Genetic (Cellular Assessment) Genetic testing of people with a family history of a
neurological disease can determine if they are carrying one of
the genes known to cause the disorder. Genetic counseling
may be recommended for patients, or parents of children
being tested, to help them understand the purpose of the tests
and what the results could mean.
 The mother’s blood can be screened for abnormalities that
suggest a risk for a genetic disorder. Cell-free DNA from
the mother’s blood can also be used to look for Down
syndrome and some chromosomal disorders.
 Doctors may also use a type of blood test called a triple

screen in order to identify some genetic disorders,
including trisomies (disorders such as Down syndrome in
which the fetus has an extra chromosome) in an unborn
baby. A blood sample is taken from a pregnant woman
and tested for three substances: alpha-fetoprotein, human
chorionic gonadotropin, and estriol. The test is performed
between the 15th and 20th week of pregnancy. It usually
takes several days to receive results from a triple screen.
Abnormal results of a triple screen may indicate a possible
problem such as spina bifida (the incomplete development
of the brain, spinal cord, or the cord’s protective
coverings) or a chromosome abnormality. However, the
test has many false positive results, so additional testing is
needed to confirm if there is a problem.
 Amniocentesis is usually done at 14-16 weeks of

pregnancy. It tests a sample of the amniotic fluid in the
womb for genetic defects (the cells found in the fluid and
the fetus have the same DNA). Under local anesthesia, a
thin needle is inserted through the woman’s abdomen and
into the womb.
 Chorionic villus sampling is performed by removing and

testing a very small sample of the placenta during early
pregnancy. The sample, which contains the same DNA as
the fetus, is removed by catheter or fine needle inserted
through the cervix or by a fine needle inserted through the
abdomen.
b.3 Laboratory Examinations

Laboratory screening tests of blood, urine, or other body fluids may help doctors diagnose
disease, understand disease severity, and monitor levels of therapeutic drugs.
Test Purpose
Complete Blood Count (CBC) A complete blood count (CBC) is a blood test used to
evaluate your overall health and detect a wide range of
disorders, including anemia, infection and leukemia.
A complete blood count test measures several components

and features of blood
Abnormal increases or decreases in cell counts as revealed

in a complete blood count may indicate that you have an
underlying medical condition that calls for further
evaluation.
Prothrombin Time (PT) A prothrombin time test measures how quickly your blood
clots. Sometimes called a PT or pro time test, a prothrombin
time test uses a sample of your blood.
Prothrombin is a protein produced by your liver. It is one of

many factors in your blood that help it to clot appropriately.
Partial Thromboplastin Time A partial thromboplastin time (PTT) test measures the time
(PTT) it takes for a blood clot to form. Normally, when you get a
cut or injury that causes bleeding, proteins in your blood
called coagulation factors work together to form a blood
clot. The clot stops you from losing too much blood.

Check the function of specific coagulation factors. If any
of these factors are missing or defective, it can mean you
have a bleeding disorder. Bleeding disorders are a group
of rare conditions in which blood doesn't clot normally.
The most well-known bleeding disorder is hemophilia.
 Find out if there is another reason for excessive bleeding
or other clotting problems. These include
certain autoimmune diseases that cause the immune
system to attack coagulation factors.
 Monitor people taking heparin, a type of medicine that
prevents clotting. In some bleeding disorders, the blood
clots too much, rather than too little. This can
cause heart attacks, strokes, and other life-threatening
conditions. But taking too much heparin can cause
excessive and dangerous bleeding.
International Normalized Ratio This blood test looks to see how well your blood clots.
(INR)
The international normalized ratio (INR) is a standardized
number that's figured out in the lab. If you take blood
thinners, also called anti-clotting medicines or

anticoagulants, it may be important to check your INR. The
INR is found using the results of the prothrombin time (PT)
test. This measures the time it takes for your blood to clot.
The INR is an international standard for the PT.
Electrolytes and Blood Glucose A basic metabolic panel is a blood test that measures your
sugar (glucose) level, electrolyte and fluid balance,
and kidney function.
Glucose is a type of sugar your body uses for energy.

Electrolytes keep your body's fluids in balance. They also
help keep your body working normally, including your heart
rhythm, muscle contraction, and brain function.
 BUN - A blood urea nitrogen (BUN) test measures the

amount of nitrogen in your blood that comes from the
waste product urea. Urea is made when protein is broken
down in your body. Urea is made in the liver and passed
out of your body in the urine. A BUN test is done to see
how well your kidneys are working.
 Calcium - A test for calcium in the blood checks the

calcium level in the body that is not stored in the bones.
 Carbon Dioxide - This test measures the level of

bicarbonate in a sample of blood from a vein.
Bicarbonate is a chemical that acts as a buffer. It keeps
the pH of blood from becoming too acidic or too basic.
 Chloride - A chloride test measures the level of chloride

in your blood or urine. Chloride is one of the most
important electrolytes in the blood. It helps keep the
amount of fluid inside and outside of your cells in
balance. It also helps maintain proper blood volume,
blood pressure, and pH of your body fluids. Tests for
sodium, potassium, and bicarbonate are usually done at
the same time as a blood test for chloride
.
 Creatinine and Creatinine Clearance - Creatinine and
creatinine clearance tests measure the level of the waste
product creatinine in your blood and urine. These tests
tell how well your kidneys are working.
 Blood glucose - A blood glucose test measures the

amount of a type of sugar, called glucose, in your blood.
Glucose comes from carbohydrate foods.
 Potassium - A potassium test checks how much

potassium is in the blood. Potassium is both
an electrolyte and a mineral. It helps keep the water (the
amount of fluid inside and outside the body's cells) and
electrolyte balance of the body. Potassium is also
important in how nerves and muscles work.
 Sodium - A sodium test checks how much sodium is in

the blood. Sodium is both an electrolyte and mineral. It
helps keep the water (the amount of fluid inside and
outside the body's cells) and electrolyte balance of the
body. Sodium is also important in how nerves and
muscles work.
Coagulation Studies Coagulation tests measure your blood’s ability to clot, and
how long it takes to clot. Testing can help your doctor
assess your risk of excessive bleeding or developing clots
(thrombosis) somewhere in your blood vessels.
Serum Osmolarity The serum or plasma osmolality is a measure of the
different solutes in plasma. Among other applications,
serum osmolality is indicated to evaluate the etiology of
hyponatremia and may be used to screen for alcohol
intoxication by means of the osmolal gap.
Toxicology A toxicology test looks for traces of drugs in
your blood, urine, hair, sweat, or saliva.
B. ANALYSIS/NURSING DIAGNOSIS
1. Ineffective Tissue Perfusion Cerebral as evidence by level of consciousness changes,

cognitive defects, and inaccurate interpretation of stimuli including confusion,
comprehension, problem solving, abstraction and memory deficits.
2. Impaired verbal communication as evidence by inability/ difficulty in speaking or

understanding spoken or written words.
3. Powerlessness as evidence by expression of frustration regarding inability to control

their illness, recovery rate or care.
4. Acute Confusion as evidence by restlessness, hallucinations, disorientation, anxiety
5. Impaired Swallowing (Nutritional – Metabolic)
6. Impaired Physical Mobility (Activity – Exercise)
C. PLANNING FOR HEALTH PROMOTION, RESTORATION, AND MAINTENANCE

1. Planning for Health promotion

 Proper nutrition
a. Essential fluids and electrolytes, particularly calcium is required for normal
nerve irritability and muscle contractions.
b. Thiamine and niacin are required for the breakdown of glucose and the
support of the nervous tissue. Deficiencies may be first noted when peripheral
nerves become irritable and fail to function normally.
c. All four basic food groups are required to ensure adequate intake of these
essential coenzymes.
d. Vitamin B6 is another important element that supports nervous system
functioning. Deficiencies may be evidenced by nervous irritability and even
seizures.
e. Vitamin B12 has a significant role in the metabolism of nervous tissue;
deficiencies create poor coordination, and in some cases, slow down mental
functioning.
 Physical Fitness/Exercise
a. Regular exercise is essential for developing normal neuromuscular control and
coordination.
b. Weight control is also a vital element to control atherosclerosis phenomenon
and reduce the risk of cardiovascular disease.
 Risk Management
Risk is a probability/threat of damage, injury, liability loss that is caused by
vulnerabilities and that may be avoided through pre-emptive action/s. For the
protection of the patient, side rails are padded. Two rails are kept in the raised
position. Care should be taken to prevent injury from invasive lines and
equipment, and other potential sources of injury should be identified, such as
restraints, tight dressings, environmental irritants, damp bedding or dressings,
and tubes and drains.
 Personal Safety
a. Protective headgear when engaging in certain sports and motorcycling could
significantly reduce many serious neurological injuries.
b. Practice proper body mechanics routinely.
c. Use seatbelts on a regular basis.
2. Planning for Health maintenance and restorations

 Maintaining a patent airway
a. This is the highest priority of nursing care.
b. Oral airway may be placed in the oral cavity; suctioning and positioning are
the measures to maintain a patent airway.
c. Nasopharyngeal and oral secretions must be aspirated as frequently as
necessary.
d. Turn frequently the client from the right lateral to left lateral and the semi-
prone positions to facilitate drainage of secretions from the oral cavity and
prevent the tongue from falling back that could obstruct the airway. Supine
position should never be used because it favors aspirations of secretions.
e. Dentures should be removed
f. Nostrils should be kept clean.
 Monitoring vital signs and neurological status

a. In assessing the vital signs, the nurse must not only assess the rate of the pulse
and respirations but also observe their quality and rhythms so that the proper
therapy can be implemented before a complication sets in.
b. Neurological assessment should be made. Assessment includes:
a. Level of Consciousness
b. Pupillary Reaction
c. Motor Strength
d. Sensory Function
 Maintaining integrity of the skin

Pressure Ulcer Formation:
a. Factors in Pressure ulcer formation
Pressure is considered as the primary factor in ulcer formation.
o Most likely to have ulcer formation are the areas that lie over bony
prominence.
 Iliac crest
 Ischial tuberosities
 Great femoral trochanters
 Scapular
 Heels
 Sacrum
o Intensity – low pressure for long periods of time produces more damage
than high pressure for short periods.
o Shearing force
o Excessive moisture
b. Stages of Pressure Formation
o Ischemia – characterized by blanching.
o Hyperemia – redness on and increased temperature of the pressured area.
Cell destruction and hemorrhage have already occurred.
o Ulceration – the last stage of pressure formation.
 Stage 1: Non-blanching erythema, warmth and tenderness.
 Stage 2: Skin breakdown limited to the dermis excoriation, blistering,
drainage, more sharply defined erythema, variable skin temperature,
local swelling, and edema.
 Stage 3: Ulcer formation into the subcutaneous tissues, crater
formation, slough, eschar, and/or drainage.
 Stage 4: Ulcers extend beyond the deep fascia into the muscle or bone,
decayed area may be larger than visible apparent wound, osteomyelitis
or sepsis may be present, granulation tissue and epithelialization may
be present at wound margins.
 Maintaining joint mobility

o Positioning prevents deformities of the extremities.
o Exercise: range of motion exercises provide full movement for all joints of
the body; prevent joint and muscular contractions and, thereby, facilitate
maintenance of joint mobility. They keep muscle tone and improve venous
and lymphatic circulation.
Types of Range of Motion
 Passive range of motion – performed at the client at a time the
client cannot do them
 Active range of motion – performed by the client without
assistance from other individuals or mechanical means. It
maintains muscle strength/
 Active assistance exercises – performed by the client, exercises or
self-assisted or with assistance from another person or by
mechanical means.
 Maintaining sensory function

a. The nurse observes the characteristics of the eyes on the affected side and
reports any changes so that measures can be prescribed to protect the eye.
b. Special ophthalmic solutions may be prescribed for irrigation or instillation,
three to four times a day.
c. Butterfly gauzed may be used to keep the eye closed.
d. Nurse must communicate as though the client can hear.
e. Family must be informed about the possibility that the client still has hearing
ability.
f. The nurse must speak to client, providing the information about all the aspects
of care
g. Explanation must be kept simple until the client is responsive, and the nurse
assured that he/she can understand more detailed explanations.
 Maintaining fluid and Nutritional status

a. Administer 3000 mL/day of fluids and electrolyte intravenously
b. NGT may be inserted for feeding
c. Determine the frequency of the amount of each feeding.
d. Test if gag reflex returns by touching the posterior pharynx with cotton swab
and observe whether or not the client swallows. If gag reflex has returned:
fluid can be given by mouth, solid foods may be gradually added, and client
should be spoon fed.
e. Oral hygiene should be administered by feeding and after every 2 hours to
prevent drying of the mucous membrane and parotitis.
f. Dentures should be removed
g. Accurate recording of intake, output and weight is important to determine the
degree of fluid balance.
 Maintaining bowel and bladder function
a. Catheter is prescribed and usually remains until the client regains

consciousness.
b. Maintenance and principles of asepsis should be applied to prevent infections.
c. Monitor I and O
d. Encourage diet high in bulk and increase fluid intake to prevent constipation
or impaction
e. Provide a regular bowel movement an give privacy to client.
 Caring for clients with surgical procedure

o Craniotomy
Post-operative care for neurological clients having supratentorial and

infratentorial procedures
Positioning
a. Supratentorial: Semi-fowler’s position is used because lowering the head
can cause venous congestion and bleeding. Position flat only when the
client is in shock. No Trendelenburg position, which would increase
intracranial pressure.
b. Commonalities: keep off operative site, turn every 2 hours; keep head on
small pillow; mouth in dependent situation to drain secretions.
c. Infratentorial: position flat on either side, keep off back because of
impaired swallowing and gag reflexes; head may be gradually elevated on
the third post-operative day.
Vital Signs
a. Commonalities: Monitor vital signs, monitor neurological signs; observe
for shock and increased ICP
b. Infratentorial: oberve for respiratory difficulty
Foods and Fluids
a. Supratentorial: limit to 1500 ml during first 24 hours to control edema;
food diets are tolerated after return of swallowing and gag reflexes.
b. Commonalities: Record I and O
c. Infratentorial: no oral fluids or solids for 24 hours; begin oral fluids and
diet on second post-operative day after ascertaining presence of
swallowing and gag reflexes.
Other Measures
a. Check dressing for clear drainage and excessive bleeding and reinforce as
necessary. Restraint client if necessary to prevent disturbance of dressing.
b. Suction as necessary to clear mouth or airway, being careful not to
stimulate the cough reflex, since this facilitates increasing ICP
c. Encourage deep breathing; coughing should be discouraged.
d. Apply ice bag to head as necessary for headache
e. Monitor bowel and bladder elimination. Catheterize if necessary. Avoid

enemas, since they may increase ICP
f. Give analgesics, anticonvulsants, stimulants or steroids as ordered.
g. Follow eye care regimen if corneal reflex is absent
h. Facilitate advance activities as indicated.
3. Common Health Problems

a. Responses to Altered Neurological Function
Disturbances in Cerebral Function
Intracranial Disorders
Altered Level of Consciousness (LOC)
 An altered level of consciousness (LOC) is apparent in the patient who is not oriented,
does not follow commands, or needs persistent stimuli to achieve a state of alertness.
 Coma is a clinical state of unarousable unresponsiveness in which there are no
purposeful responses to internal or external stimuli, although nonpurposeful responses to
painful stimuli and brain stem reflexes may be present
 Akinetic mutism is a state of unresponsiveness to the environment in which the patient
makes no voluntary movement.
 Persistent vegetative state is a condition in which the unresponsive patient resumes
sleep–wake cycles after coma but is devoid of cognitive or affective mental function.
 Locked-in syndrome results from a lesion affecting the pons and results in paralysis and
the inability to speak, but vertical eye movements and lid elevation remain intact and are
used to indicate responsiveness
Level of Consciousness
 Alert or Conscious – attends to the environment, responds appropriately to commands
and questions with minimal stimulation.
 Confused – disoriented to the surroundings, may have impaired judgment, and may need
cues to respond to commands.
 Lethargic – drowsy, need gentle verbal or touch stimulation to initiate response
 Obtunded – responds slowly to external stimulation, and needs repeated stimulation to
maintain attention and response to the environment
 Stuporous – responds only minimally with vigorous stimulation, may only moan as a
verbal response
 Comatose – no observable response to any external stimuli.
Causes of altered LOC
1. Structural
 Trauma – concussion, contusion, traumatic intracerebral hemorrhage, cerebral
edema, subdural and epidural hematoma.
 Vascular disease - infarction, intracerebral hemorrhage, subarachnoid hemorrhage
 Infection – meningitis, encephalitis, brain abscess
 Neoplasms – primary brain tumor, metastatic tumors.
2. Metabolic
 Systemic metabolic derangement – hypoglycemia, DKA, HHNK, uremia, hepatic
encephalopathy, hyponatremia, myxedema

 Hypoxic encephalopaties – severe CHF, COPD, severe anemia, prolonged
hypertension
 Toxicity – heavy metals, carbon monoxide drugs (opiates, barbiturates and alcohol)
 Extremes of body temperature – heat stroke, hypothermia
 Seizures
Complications
 Respiratory distress or failure
 Pneumonia
 Aspiration
 Pressure ulcer
 Deep vein thrombosis (DVT)
 Contractures
Increased Intracranial Pressure
 The rigid cranial vault contains brain tissue (1400 g), blood (75 mL), and CSF (75 mL).
The volume and pressure of these three components are usually in a state of equilibrium
and produce the ICP.
 The intracranial pressure (ICP) is the pressure within the cranium of the skull. Due to
the fixed nature of the cranium, an increase in volume of any one of the intracranial
components will also cause an increase in pressure.
 The normal value for intracranial pressure is 5–15mmHg. A value above 20mmHg
usually signifies the point at which intervention may be required to avoid significant or
life-threatening consequences.
CAUSES
 Tumor
 Head Injury
 Inflammatory Diseases of the nervous system e.g. encephalitis
 Conditions characterized by arteriolar spasm – the volume of blood circulating in the
capillaries are reduced and becomes permeable. The conditions occur in acute nephritis
and malignant hypertension, and result in edematous brain.
 Anything that blocks partly or completely causing the normal course of CSF pressure to
rise.
Symptoms
 headache
 nausea
 vomiting
 increased blood pressure
 decreased mental abilities
 confusion about time, and then location and people as the pressure worsens
 double vision
 pupils that don’t respond to changes in light
 shallow breathing
 seizures
 loss of consciousness
 coma
Complications
 Brain Stem Herniation
 Diabetes Insipidus
 Syndrome Of Inappropriate Antidiuretic
 Hormone (SIADH)
Headache (Cephalalgia)
 Caused by tension or by displacement of pain-sensitive structures, dilation of
intracranial arteries, inflammation in a pain-sensitive structure of the head, and direct
pressure on certain cranial nerves.
 Primary headache is one for which no organic cause can be identified. These types of
headache include migraine, tension-type, and cluster headaches
 Secondary headache is a symptom associated with an organic cause, such as a brain
tumor or an aneurysm.
Cause: Cranial Arteritis
Cranial arteritis often begins with general manifestations, such as fatigue, malaise, weight loss,
and fever. Clinical manifestations associated with inflammation (heat, redness, swelling,
tenderness, or pain over the involved artery) usually are present. Sometimes a tender, swollen, or
nodular temporal artery is visible. Visual problems are caused by ischemia of the involved
structures.
Clinical Manifestations (Migraine)
 Prodromal phase: depression, irritability, feeling cold, food cravings, anorexia, change
in activity level, increased urination, diarrhea, or constipation.
 Aura Phase - Visual disturbances (ie, light flashes and bright spots) are most common
and may be hemianopic (affecting only half of the visual field); numbness and tingling of
the lips, face, or hands; mild confusion; slight weakness of an extremity; drowsiness; and
dizziness.
 Headache phase – photophobia, nausea and vomiting
 Recovery Phase (Termination and postdrome) – muscle contraction in the neck and
scalp, with associated muscle ache and localized tenderness, exhaustion, and mood
changes.
Classification
a. Muscle contraction headache – the most common type of headache. It is generally
considered to be a psychogenic origin and most often associated with anxiety or
depression. It is managed by gentle massage, analgesics; tranquilizers, and hot
application to the head.
b. Vascular headache – precipitated by various allergies from food products containing
tyramine and monosodium glutamate (found in wine and cheese), emotional stress,
fatigue, vasodilating drugs, and herediraty factors.
 Migraine (Sick Headache)
Cause: Constriction and then dilation of cerebral arteries. The person who develops
migraine is usually one who works hard and strives for perfection. It often follows a
period of too much work and stress.
Treatment:
 Ergotamine tartrate (Gynergen) – a vasoconstrictor given at the beginning of the
attack.
 Ergotamine tartrate with caffeine (Cafergot)
 Ice packs; quiet, darkened room, psychotherapy
 Cluster Headache (Histamine headache) – often severe; maybe functional or organic
in nature
 Traction and Inflammatory headache – less common; more intense in the morning or
upon awakening and generally involves the entire head.
Seizure and Epilepsy
Seizures
 are episodes of abnormal motor, sensory, autonomic, or psychic activity (or a
combination of these) that result from sudden excessive discharge from cerebral neurons
Epilepsy
 A group of seizures characterized by unprovoked, recurring seizures (AANN, 2007)
 A disease diagnosed primarily from a history of seizure episodes because of increased
basal level of excitability of the CNS
 Epilepsy is a central nervous system (neurological) disorder in which brain activity
becomes abnormal, causing seizures or periods of unusual behavior, sensations, and
sometimes loss of awareness.
Epileptic Syndromes are classified by specific patterns of clinical features, including:
 Age at onset
 Family history
 Seizure type
Classification
GRAND MAL
 Abrupt onset produced by an aura (any peculiar feeling, sight, sound, taste, smell, or
twitching and spasm of small muscle groups).
 Child falls to the ground, becomes pale, and pupils dilate with upward rolling of the
eyeballs. Head is thrown backward or to one side; chest and abdominal muscles are rigid;
limbs are rigid and contracted (tonic phase)
 As air is forced out of a closed glottis by sudden contraction of the diaphragm, the child
lets out a short, starting cry; the tongue may be bitten
 Involuntary urination and defecation will follow
 The 20 to 40 second tonic phase is followed by clonic activity involving spams of the
entire body.
 The child sleeps after the episode. Upon awakening, he or she appears drowsy and
stuporous, and accomplishes routine task in an automatic fashion.
 When seizures are so frequent that they appear to be constant, the condition is called
STATUS EPILEPTICUS, a medical emergency which may result in brain damage
because of decreased oxygen supply to the cerebrum.
PETIT MAL
 Transient losses of consciousness
 Eye-rolling; drooping or fluttering of eyelids; drooping of the head; quivering of limb or
trunk muscles
 After the seizure, the child immediately resumes activity without knowledge of what
happened.
 It can be precipitated by hyperventilation or induced by a blinking light.
JACKSONIAN
 Convulsion starts with a muscle or group of muscles and then spreads to other parts of the
body.
FOCAL SEIZURES
FOCAL SEIZURES WITHOUT LOSS OF CONSCIOUSNESS
 Simple partial seizures, don't cause a loss of consciousness
 They may alter emotions or change the way things look, smell, feel, taste or sound.
 They may also result in involuntary jerking of a body part, such as an arm or leg, and
spontaneous sensory symptoms such as tingling, dizziness and flashing lights.
FOCAL SEIZURES WITH IMPAIRED AWARENESS
 Complex partial seizures, these seizures involve a change or loss of consciousness or
awareness.
 During a complex partial seizure, you may stare into space and not respond normally to
your environment or perform repetitive movements, such as hand rubbing, chewing,
swallowing or walking in circles.
GENERALIZED SEIZURES
ABSENCE SEIZURES
 Previously known as petit mal seizures, often occur in children and are characterized
by staring into space or subtle body movements such as eye blinking or lip smacking.
 These seizures may occur in clusters and cause a brief loss of awareness.
TONIC SEIZURES
 Cause stiffening of your muscles
 These seizures usually affect muscles in your back, arms and legs and may cause you
to fall to the ground.
ATONIC SEIZURES
 Also known as drop seizures, cause a loss of muscle control, which may cause you to
suddenly collapse or fall down.
CLONIC SEIZURES
 Are associated with repeated or rhythmic, jerking muscle movements.
 These seizures usually affect the neck, face and arms.
MYOCLONIC SEIZURES
 Usually appear as sudden brief jerks or twitches of your arms and legs.
TONIC-CLONIC SEIZURES
 previously known as grand mal seizures, are the most dramatic type of epileptic
seizure and can cause an abrupt loss of consciousness, body stiffening and shaking,
and sometimes loss of bladder control or biting your tongue.
SYMPTOMS
 Temporary confusion
 A staring spell
 Uncontrollable jerking movements of the arms and legs

 Loss of consciousness or awareness
 Psychic symptoms such as fear, anxiety or déjà vu
*Symptoms vary depending on the type of seizure.
CAUSES
 Genetic influence
 Head trauma
 Brain conditions
 Infectious diseases
 Prenatal injury
 Developmental disorders
RISK FACTORS
 Age
 Family history
 Head injuries
 Stroke and other vascular diseases
 Dementia
 Brain infections
 Seizures in childhood
COMPLICATIONS
 Falling
 Drowning
 Car accidents
 Pregnancy complications
 Emotional health issues
LIFE-THREATENING COMPLICATIONS
STATUS EPILEPTICUS
 Occurs if you're in a state of continuous seizure activity lasting more than five minutes or
if you have frequent recurrent seizures without regaining full consciousness in between
them. People with status epilepticus have an increased risk of permanent brain damage
and death.
SUDDEN UNEXPECTED DEATH IN EPILEPSY (SUDEP)
 People with epilepsy also have a small risk of sudden unexpected death. The cause is
unknown, but some research shows it may occur due to heart or respiratory conditions.
People with frequent tonic-clonic seizures or people whose seizures aren't controlled by
medications may be at higher risk of SUDEP. Overall, about 1 percent of people with
epilepsy die of SUDEP.
Head Injury
 A broad classification that includes injury to the scalp, skull, or brain.
 Traumatic brain injury (TBI) or head injury refers to any injury to the scalp, skull
(cranium or facial bones) or brain that disrupts the function of the brain, patients’ life and
the lives of their families and caregivers
Primary injury is the initial damage to the brain that results from the traumatic event. This may
include contusions, lacerations, and torn blood vessels due to impact, acceleration/deceleration,
or foreign object penetration.
Secondary injury evolves over the ensuing hours and days after the initial injury and results
from inadequate delivery of nutrients and oxygen to the cells
TBI can also be divided into:
 the primary injury (induced by a mechanical force):
 acceleration injury – the head is struck by a moving object
 deceleration injury – the head hits a stationary object
 acceleration–deceleration injury – the head hits an object and the brain ‘rebounds’
within the skull
 injuries to the brain including concussion, contusion and diffuse axonal injury
 intracranial hemorrhage, including hematomas; this can be extradural, subdural or
intracerebral
 injuries to the skull (including fractures)
 secondary injuries:
 occurring after the initial injury as a result of progression events, which affect the
perfusion and oxygenation of the brain cells
 most commonly occurring as a result of brain swelling, with an increase in ICP
 if the raised ICP is left untreated, a decrease in cerebral perfusion leads to ischemia
 The ability to cope with an increase in ICP differing from person to person and
ultimately being dependent on the compliance of the brain tissue.
Scalp Laceration
 Isolated scalp trauma is generally classified as a minor injury.
 Trauma may result in an abrasion (brush wound), contusion, laceration, or hematoma
beneath the layers of tissue of the scalp (subgaleal hematoma).
 A large avulsion (tearing away) of the scalp may be potentially life-threatening and is a
true emergency.
 Diagnosis of a scalp injury is based on physical examination, inspection, and
palpation.
 Scalp wounds are potential portals of entry for organisms that cause intracranial
infections.
Skull Fractures
 A skull fracture is a break in the continuity of the skull caused by forceful trauma.
 It may occur with or without damage to the brain. Skull fractures can be classified as
simple, comminuted, depressed, or basilar.
 A simple (linear) fracture is a break in the continuity of the bone.
 A comminuted skull fracture refers to a splintered or multiple fracture line.
 Depressed skull fractures occur when the bones of the skull are forcefully displaced
downward and can vary from a slight depression to bones of the skull being splintered
and embedded within brain tissue.
 A fracture of the base of the skull is called a basilar skull fracture
Symptoms (head injury)
 Persistent, localized pain
 Area of ecchymosis may be seen over the mastoid (Battle’s sign)

 Hemorrhage from the nose, pharynx, or ears, and on conjunctiva
Clinical manifestations (Brain injury)

 Altered level of consciousness
 Confusion
 Pupillary abnormalities (changes in shape, size, and response to light)
 Altered or absent gag reflex
 Absent corneal reflex
 Sudden onset of neurologic deficits
 Changes in vital signs (altered respiratory pattern, widened pulse pressure, bradycardia,
tachycardia, hypothermia, or hyperthermia)
 Vision and hearing impairment
 Sensory dysfunction
 Headache
 Seizures
Types of Brain Injury

Concussion (mild TBI)
 A temporary loss of neurologic function with no apparent structural damage.
 two types of concussion: mild and classic; Mild concussion may lead to a period of
observed or self-reported transient confusion, disorientation, or impaired consciousness;
signs and symptoms of neurologic or neuropsychological dysfunction may include
seizures, headache, dizziness, irritability, fatigue, or poor concentration; classic
concussion is an injury that results in a loss of consciousness; characteristically, this
usually lasts less than 6 hours. This loss of consciousness is always accompanied by
some degree of posttraumatic amnesia.
Contusion
 a moderate to severe head injury, the brain is bruised and damaged in a specific area
because of severe acceleration-deceleration force or blunt trauma.
 Contusions are characterized by loss of consciousness associated with stupor and
confusion. Other characteristics can include tissue alteration and neurologic deficit
without hematoma formation, alteration in consciousness without localizing signs, and
hemorrhage into the tissue that varies in size and is surrounded by edema.
Diffuse Axonal Injury
 Diffuse axonal injury (DAI) results from widespread shearing and rotational forces that
produce damage throughout the brain—to axons in the cerebral hemispheres, corpus
callosum, and brain stem.
 The patient with DAI in severe head trauma experiences no lucid interval, immediate
coma, decorticate and decerebrate posturing (see Fig. 61-1 in Chapter 61), and global
cerebral edema.
Intracranial Hemorrhage
 Hematomas are collections of blood in the brain that may be epidural (above the dura),
subdural (below the dura), or intracerebral (within the brain)
 Subdural Hematoma: A subdural hematoma is a collection of blood between the dura
and the brain, a space normally occupied by a thin cushion of fluid.
 Epidural Hematoma: After a head injury, blood may collect in the epidural (extradural)
space between the skull and the dura mater.
 Acute and Subacute Subdural Hematoma. Acute subdural hematomas are associated
with major head injury involving contusion or laceration. Subacute subdural hematomas
are the result of less severe contusions and head trauma.
 Chronic Subdural Hematoma. Chronic subdural hematomas can develop from
seemingly minor head injuries and are seen most frequently in the elderly.
 Intracerebral Hemorrhage and Hematoma. Intracerebral hemorrhage is bleeding into
the substance of the brain. It is commonly seen in head injuries when force is exerted to
the head over a small area (eg, missile injuries, bullet wounds, stab injuries).
Cerebral Infections/Inflammatory
Meningitis
 Meningitis is inflammation of the arachnoid and pia mater of the brain and spinal cord.
 Meningitis is caused by bacterial and viral organisms, although fungal and protozoal
meningitis also occurs.
 Cerebrospinal fluid is analyzed to determine the diagnosis and the type of meningitis.
Transmission
 Transmission is by direct contact, including droplet spread.
 Transmission occurs in areas of high population density, crowded living areas, and
prisons.
Causes
 Meningitis is most frequently caused by bacterial or viral agents.

 In newborns, Streptococcus pneumoniae is the most frequent bacterial organism; in other
age groups, it is S. pneumonia and Neisseria meningitidis. Haemophilus influenzae is the
most common organism in unvaccinated children and adults who contract meningitis.
 Viral meningitis is caused by many viruses. Depending on the cause, isolation
precautions may be indicated early in treatment. There has been a decrease in viral
meningitis in locations where immunizations have become routine.
Predisposing Factors
 Skull fractures
 Brain or spinal surgery
 Sinus or upper respiratory infections
 Use of nasal sprays
 Individuals with a compromised immune system
Assessment
 Mild lethargy
 Memory changes
 Short attention span
 Personality and behavior changes
 Severe headache
 Generalized muscle aches and [pains
 Nausea and vomiting
 Fever and chills
 Tachycardia
 Deterioration in the level of consciousness
 Photophobia
 Signs of meningeal irritation such as nuchial rigidity and positive Kernig’s sign and
Brudzinski’s sign
 Red, macular rash with meningococcal meningitis
 Abdominal and chest pain with viral meningitis
Possible Complications
 Brain damage
 Hearing loss or deafness
 Hydrocephalus
 Loss of vision
Brain Abscess
 A brain abscess is a collection of infectious material within the tissue of the brain.
 Bacteria are the most common causative organisms. An abscess can result from intra-
cranial surgery, penetrating head injury, or tongue piercing.
 Organisms causing brain abscess may reach the brain by hematologic spread from the
lungs, gums, tongue, or heart, or from a wound or intra-abdominal infection. It can be a
complication in patients whose immune systems have been suppressed through therapy or
disease.
Prevention
 To prevent brain abscess, otitis media, mastoiditis, rhinosinusitis, dental infections, and
systemic infections should be treated promptly.

Clinical Manifestations
 Generally, symptoms result from alterations in intracranial dynamics (edema, brain shift),
infection, or the location of the abscess.
 Headache, usually worse in morning, is the most prevailing symptom.
 Fever, vomiting, and focal neurologic deﬁcits (weakness and decreasing vision) occur as
well.
 As the abscess expands, symptoms of increased intracranial pressure (ICP) such as
decreasing level of consciousness and seizures are observed.
Herpes Simplex Virus Encephalitis
 Encephalitis is an acute inflammatory process of the brain tissue.
 Herpes simplex virus (HSV) is the most common cause of acute encephalitis in the
United States.
 There are two herpes simplex viruses: HSV-1 and HSV-2. HSV-1 typically affects
children and adults. HSV-2 most commonly affects neonates
Pathophysiology
 The pathology of encephalitis involves local necrotizing hemorrhage that becomes more
generalized, followed by edema. There is also progressive deterioration of nerve cell
bodies.
 fever
 headache
 confusion
 behavioral changes
 focal seizures
 dysphasia
 hemiparesis
 altered LOC
Arthropod-Borne Virus Encephalitis
 Arthropod vectors transmit several types of viruses that cause Encephalitis. The primary
vector in North America is the mosquito. In cases of West Nile virus, humans are the
secondary host; birds are the primary host.
 Arbovirus infection (transmitted by arthropod vectors) occurs in specific geographic
areas during the summer and fall. In the United States, West Nile and St. Louis are the
most common types of arboviral encephalitis; both are members of the Japanese
encephalitis serogroup. West Nile virus develops in 1 out of 150 cases of encephalitis
Pathophysiology
 Viral replication occurs at the site of the mosquito bite. The host immune response
attempts to control viral replication. If the immune response is inadequate, viremia will
ensue. The virus gains access to the central nervous system (CNS) via the cerebral
capillaries, resulting in encephalitis. It spreads from neuron to neuron, predominantly
affecting the cortical gray matter, the brain stem, and the thalamus. Meningeal exudates
compound the clinical presentation by irritating the meninges and increasing ICP.
 Arboviral encephalitis begins with early flulike symptoms, but specific neurologic
manifestations depend on the viral type.
 A unique clinical feature of St. Louis encephalitis is SIADH with hyponatremia.
 Signs and symptoms specific to West Nile encephalitis include a maculopapular or
morbilliform rash on
 the neck, trunk, and arms; enlarged lymph nodes and legs; and flaccid paralysis
 Both West Nile and St. Louis encephalitis can result in parkinsonian-like movements,
reflecting inflammation of the basal ganglia. Seizures, a poor prognostic indicator, are
present in both types of encephalitis but are more common in the St. Louis type
Fungal Encephalitis
 Fungal infections of the CNS occur rarely in healthy people. The presentation of fungal
encephalitis is related to geographic area or to an immune system that is compromised
due to disease or immunosuppressive medication.
Causes
 Cryptococcus neoformans
 Blastomyces Dermatitidis
 Histoplasma capsulatum
 Aspergillus fumigatus,
 Candida
 Coccidioides immitis
Pathophysiology
 The fungal spores enter the body via inhalation. They initially infect the lungs, causing
vague respiratory symptoms or pneumonitis. The fungi may enter the bloodstream,
causing a fungemia. If the fungemia overwhelms the person’s immune system, the fungus
may spread to the CNS. The fungal invasion may cause meningitis, encephalitis, brain
abscess, granuloma, or arterial thrombus
 Fever
 Malaise
 Headache
 meningeal signs
 change in LOC or cranial nerve dysfunction
 Symptoms of increased ICP related to hydrocephalus often occur.
 C. neoformans and C. immitis are associated with specific skin lesions.
 H. capsulatum is associated with seizures
 A. fumigatus may cause ischemic or hemorrhagic strokes.
Creutzfeldt-Jakob Disease
 A degenerative brain disorder that leads to dementia and, ultimately, death. Symptoms of
Creutzfeldt-Jakob disease (CJD) can resemble those of other dementia-like brain
disorders, such as Alzheimer's. But Creutzfeldt-Jakob disease usually progresses much
more rapidly.
 CJD captured public attention in the 1990s when some people in the United Kingdom
developed a form of the disease — variant CJD (vCJD) — after eating meat from
diseased cattle. However, "classic" Creutzfeldt-Jakob disease hasn't been linked to
contaminated beef
Symptoms
 Personality changes
 Anxiety
 Depression
 Memory loss
 Impaired thinking
 Blurred vision or blindness
 Insomnia
 Difficulty speaking
 Difficulty swallowing
 Sudden, jerky movements
Causes
 Creutzfeldt-Jakob disease and its variants belong to a broad group of human and animal
diseases known as transmissible spongiform encephalopathies (TSEs). The name derives
from the spongy holes, visible under a microscope, that develop in affected brain tissue.
 The cause of Creutzfeldt-Jakob disease and other TSEs appears to be abnormal versions
of a kind of protein called a prion. Normally these proteins are harmless. But when
they're misshapen, they become infectious and can harm normal biological processes.
Transmission
 Sporadically
 By inheritance
 By contamination
Risk Factors
 Age
 Genetics
 Exposure to contaminated tissue
Cerebrovascular Disorders
CVA (Stroke)
Cerebrovascular Disorders
 An umbrella term that refers to a functional abnormality of the central nervous system
(CNS) that occurs when the normal blood supply to the brain is disrupted.
Two Major Categories of Cerebrovascular Disorders
 Ischemic Stroke, in which vascular occlusion and significant hypoperfusion occur
 Hemorrhagic Stroke, in which there is extravasation of blood into the brain or
subarachnoid space.
ISCHEMIC STROKE
Other terms: Cerebrovascular accident (CVA) or “brain attack”
Definition: A sudden loss of function resulting from disruption of the blood supply to a part of
the brain.
Brain attack: A term that is being used to suggest healthcare practitioners and the public that a
stroke is an urgent healthcare issue similar to a heart attack.
Subdivisions of Ischemic Stroke
 Large artery thrombotic strokes are caused by atherosclerotic plaques in the large
blood vessels of the brain. Thrombosis formation and occlusion at the site of
atherosclerosis result in ischemia and infarction.
 Small penetrating artery thrombotic strokes affects one or more vessels and are the
most common type of ischemic attack. It is also called lacunar strokes because of the
cavity that is created after the death of infarcted brain tissue.
 Cardiogenic embolic strokes are associated with cardiac dysrhythmias, usually atrial
fibrillation. Emboli originate from the heart and circulate to the cerebral vasculature,
most commonly the left middle cerebral artery, resulting in a stroke.
 Cryptogenic strokes, which have no known causes
 Strokes from other causes, such as illicit drugs, coagulopathies, migraine, and
spontaneous dissection of the carotid or vertebral arteries.
 Numbness or weakness of the face, arm, or leg, especially on one side of the body
 Confusion or change in mental status
 Trouble speaking or understanding speech
 Visual disturbances
 Difficulty walking, dizziness, or loss of balance or coordination
 Sudden severe headache
Neurologic Deficits Manifestations

Visual Field Deficits
Homonymous Hemianopsia (loss of half of the  Unaware of persons or objects on

visual field) inside of visual loss
 Neglect of one side of the body
Loss of peripheral vision  Difficulty judging distances
Diplopia  Difficulty seeing at night

 Unaware of objects or the borders of
objects
 Double Vision
Motor Deficits
Hemiparesis  Weakness of the face, arm, and leg

on the same side (due to a lesion in
the opposite hemisphere)
 Paralysis of the face, arm, and leg on

the same side (due to a lesion on the
opposite side)
Ataxia  Staggering, unsteady gait

 Unable to keep feet together; needs a
broad base to stand
Dysarthria  Difficulty in forming words
Dysphagia  Difficulty in swallowing

Sensory Deficits
Paresthesia (occurs on the side opposite the

lesion)
 Numbness and tingling of extremity
 Difficulty with proprioception
Verbal Deficits
Expressive aphasia  Unable to perform words that are

understandable; may be able to speak
in single-word responses
Receptive aphasia  Unable to comprehend the spoken
word; can speak but may not make
sense
Global (mixed) aphasia  Combination of both receptive and
expressive aphasia
Cognitive Deficits  Short-term and long-term memory
loss
 Decreased attention span
 Impaired ability to concentrate
 Poor abstract reasoning
 Altered judgment
Emotional Deficits
 Loss of self-control
 Emotional liability
 Decreased tolerance to stressful
situations
 Depression
 Withdrawal
 Fear, hostility, and anger
 Feeling of Isolation
Comparison of Left and Right Hemispheric Strokes

Left Hemispheric Strokes Right Hemispheric Strokes
Paralysis or weakness on right side of body Paralysis or weakness on left side of body
Right visual field deficit Left visual field deficit
Aphasia (expressive, receptive, or global) Spatial-perceptual deficits
Altered intellectual ability Increased distractibility
Slow, cautious behavior Impulsive behavior and poor judgment
Lack of awareness of deficits
*Agnosias - deficits in the ability to recognize previously familiar objects perceived by one or
more of the senses.
*TRANSIENT ISCHEMIC ATTACK
Definition: a neurologic deficit typically lasting less than 1 hour; “mini stroke”
Clinical Manifestation: Sudden loss of motor, sensory, or visual function
Non-modifiable factors
 Age
 Gender
 Race
Modifiable factors
 Hypertension
 Atrial fibrillation
 Hyperlipidemia
 Obesity
 Smoking
 Excessive alcohol consumption
 Diabetes
 Asymptomatic carotid stenosis
 Valvular heart disease (endocarditis, prosthetic heart valves)
Prevention
 not smoking
 maintaining a healthy weight
 following a healthy diet (including modest alcohol consumption)
 daily exercise
HEMORRHAGIC STROKE
Definition: Hemorrhagic strokes account for 15% to 20% of cerebrovascular disorders and are
primarily caused by intracranial or subarachnoid hemorrhage.
Cause: bleeding into the brain tissue, the ventricles, or the subarachnoid space
Types of Hemorrhagic Stroke
 Intracerebral Hemorrhage: An intracerebral hemorrhage, or bleeding into the brain
tissue, is most common in patients with hypertension and cerebral atherosclerosis,
because degenerative changes from these diseases cause rupture of the blood vessel.
Bleeding occurs most commonly in the cerebral lobes, basal ganglia, thalamus, brain
stem (mostly the pons), and cerebellum.
 Intracranial (Cerebral) Aneurysm: An intracranial (cerebral) aneurysm is a dilation of

the walls of a cerebral artery that develops as a result of weakness in the arterial wall. The
cause of aneurysms is unknown, although research is ongoing. An aneurysm may be due
to atherosclerosis, which results in a defect in the vessel wall with subsequent weakness
of the wall; a congenital defect of the vessel wall; hypertensive vascular disease; head
trauma; or advancing age.
 Arteriovenous Malformations: Most AVMs are caused by an abnormality in embryonal
development that leads to a tangle of arteries and veins in the brain that lacks a capillary
bed (see Fig. 62-5). The absence of a capillary bed leads to dilation of the arteries and
veins and eventual rupture. AVM is a common cause of hemorrhagic stroke in young
people.
 Subarachnoid Hemorrhage: A subarachnoid hemorrhage (hemorrhage into the
subarachnoid space) may occur as a result of an AVM, intracranial aneurysm, trauma, or
hypertension. The most common causes are a leaking aneurysm in the area of the circle
of Willis and a congenital AVM of the brain.
 Same with ischemic stroke
 Severe headache
 vomiting
 an early sudden change in level of consciousness
 possibly focal seizures due to frequent brain stem involvement
Clinical Manifestation of patient with an intracranial aneurysm or AVM
 Rupture of an aneurysm or AVM usually produces a sudden, unusually severe headache
and often loss of consciousness for a variable period of time.
 Pain and rigidity of the back of the neck (nuchal rigidity) and spine due to meningeal
irritation.
 Visual disturbances (visual loss, diplopia, ptosis) occur if the aneurysm is adjacent to the
oculomotor nerve.
 Tinnitus, dizziness, and hemiparesis may also occur.
Risk Factors: Age, male gender, and excessive alcohol intake.
Complications:
 Re-bleeding or hematoma expansion
 cerebral vasospasm resulting in cerebral ischemia
 acute hydrocephalus, which results when free blood obstructs the reabsorption of
cerebrospinal fluid (CSF) by the arachnoid villi
 Seizures
 Cerebral hypoxia and decreased blood flow
 Increased Intracranial Pressure
 Hypertension
Prevention: managing hypertension and ameliorating other significant risk factors.
Arteriovenous Malformations
 A brain arteriovenous malformation (AVM) is a tangle of abnormal blood vessels
connecting arteries and veins in the brain
Symptoms
 Hemorrhage – first sign

In people without hemorrhage, signs and symptoms of a brain AVM may include:
 Seizures
 Headache or pain in one area of the head
 Muscle weakness or numbness in one part of the body
Some people may experience more-serious neurological signs and symptoms, depending on the
location of the AVM, including:
 Severe headache
 Weakness, numbness or paralysis
 Vision loss
 Difficulty speaking
 Confusion or inability to understand others
 Severe unsteadiness
One severe type of brain AVM, called a vein of Galen defect, causes signs and symptoms that
emerge soon or immediately after birth. The major blood vessel involved in this type of brain
AVM can cause fluid to build up in the brain and the head to swell. Signs and symptoms include
swollen veins that are visible on the scalp, seizures, failure to thrive and congestive heart failure.
Risk Factors
 Being male
 Family History\
Complications
 Bleeding in the brain (hemorrhage)
 Reduced oxygen to brain tissue.
 Thin or weak blood vessels.
 Brain damage
Disturbance in Peripheral Nerve Function

Cranial Nerve Disorders
Trigeminal Neuralgia
 Trigeminal neuralgia is a chronic pain condition that affects the trigeminal nerve, which
carries sensation from your face to your brain. If you have trigeminal neuralgia, even
mild stimulation of your face — such as from brushing your teeth or putting on makeup
— may trigger a jolt of excruciating pain.
Symptoms
 Episodes of severe, shooting or jabbing pain that may feel like an electric shock
 Spontaneous attacks of pain or attacks triggered by things such as touching the face,
chewing, speaking or brushing teeth
 Bouts of pain lasting from a few seconds to several minutes
 Episodes of several attacks lasting days, weeks, months or longer — some people have
periods when they experience no pain
 Constant aching, burning feeling that may occur before it evolves into the spasm-like
pain of trigeminal neuralgia
 Pain in areas supplied by the trigeminal nerve, including the cheek, jaw, teeth, gums, lips,
or less often the eye and forehead
 Pain affecting one side of the face at a time, though may rarely affect both sides of the
face
 Pain focused in one spot or spread in a wider pattern
 Attacks that become more frequent and intense over time
Causes
 In trigeminal neuralgia, also called tic douloureux, the trigeminal nerve's function is
disrupted. Usually, the problem is contact between a normal blood vessel — in this case,
an artery or a vein — and the trigeminal nerve at the base of your brain. This contact puts
pressure on the nerve and causes it to malfunction.
Triggers
A variety of triggers may set off the pain of trigeminal neuralgia, including:
 Shaving
 Touching your face
 Eating
 Drinking
 Brushing your teeth
 Talking
 Putting on makeup
 Encountering a breeze
 Smiling
 Washing your face
Bell’s palsy
 Bell’s palsy (facial paralysis) is due to peripheral involvement of the seventh cranial
nerve on one side, which results in weakness or paralysis of the facial muscles.
 The cause is unknown, but possible causes may include vascular ischemia, viral disease
(herpes simplex, herpes zoster), autoimmune disease, or a combination.
 Bell’s palsy may represent a type of pressure paralysis in which ischemic necrosis of the
facial nerve causes a distortion of the face, increased lacrimation (tearing), and painful
sensations in the face, behind the ear, and in the eye.
 The patient may experience speech difﬁculties and may be unable to eat on the affected
side owing to weakness.
 Most patients recover completely, and Bell’s palsy rarely recurs.
Guillaine-Barre Syndrome
 Also known as polyradiculoneuritis.
 It is an acute inflammatory polyneuropathy of the peripheral sensory and motor and nerve
roots.
 Affected nerves are demyelinated with possible axonal degeneration.
 It’s exact cause is unknown, Guillain-Barré Syndrome is believed to be an autoimmune
disorder that may be triggered by viral infection, Campylobacter diarrheal illness,
immunization, or other precipitating event.
 The syndrome is marked by acute onset of symmetric progressive muscle weakness, most
often beginning in the legs and ascending to involve the trunk, upper extremities, and
facial muscles. Paralysis may develop.
 Complications may include respiratory failure, cardiac arrhythmias, and complications of
immobility.
Pathophysiology
 GBS results from an autoimmune (cell-mediated and humoral) attack on peripheral nerve
myelin proteins (substances speeding conduction of nerve impulses). The Schwann cell
(which produces myelin in the peripheral nervous system) is paired in GBS, allowing for
remyelination in the recovery phase of the disorder.
Assessment
 Acute onset (hours to weeks) of progressive, usually ascending muscle weakness and
fasciculation, possibly leading to paralysis (maximal weakness is reached within 2
weeks).
 Paresthesia and painful sensations.
 Possible hypoventilation due to chest muscle weakness.
 Difficulty with swallowing, chewing, speech, and gag, indicating fifth (trigeminal) and
ninth (glossopharyngeal) cranial nerve movement.
 Reduce or absent deep tendon reflexes, position and vibratory perception.
 Autonomic dysfunction with orthostatic hypotension and tachycardia.
Peripheral Nerve Impulse Disorders

Multiple Sclerosis
 Multiple sclerosis is a chronic, progressive, non- contagious, degenerative disease of the
CNS characterized by demyelinization of the neurons.
 Multiple sclerosis usually occurs between the ages of 20 and 40 and consists of periods of
remissions and exacerbations.
 The causes are unknown, but the disease is thought to be a result of an autoimmune
response or viral infection.
 Precipitating factors include pregnancy, fatigue, stress, infection, and trauma.
 Electroencephalogram findings are abnormal
 A lumbar puncture indicates increased gamma globulin, but the serum globulin level is
normal.
Assessment
 Fatigue and weakness
 Ataxia and vertigo
 Tremors and spasticity of the lower extremities
 Parasthesias
 Blurred vision and diplopia
 Nystagmus
 Dysphasia
 Decreased perception to pain, touch, and temperature
 Bladder and bowel disturbances, including urgency, frequency, retention, and
incontinence
 Abnormal reflexes, including hyperreflexia, absent reflexes, and a positive Babinski’s
reflex
 Emotional changes such as apathy, euphoria, irritability, and depression
 Memory changes and confusion
Parkinson’s Disease
 Parkinson’s disease is a degenerative disease caused by depletion of dopamine, which

interferes with the inhibition of excitatory impulses.
 Parkinson’s disease results in a dysfunction of the extrapyramidal system.
 Parkinson’s disease is a slow, progressive disease that results in a crippling disability.
 The debilitation can result in falls self-care deficits, failure of body systems, and
depression.
 Mental deterioration occurs late in the disease.
Cause
The majority of all cases of classic Parkinson’s disease are primary, or idiopathic, Parkinson’s
disease (IPD). The cause is unknown; a few cases suggest a hereditary pattern. Secondary, or
iatrogenic, Parkinson’s disease is drug- or chemical-related. Dopamine-depleting drugs such as
reserpine, phenothiazine, metoclopramide, tetrabenazine, and the butyrophenones (droperidol
and haloperidol) can lead to secondary Parkinson’s disease.
Assessment
 Bradykinesia, abnormal slowness of movement, and sluggishness of physical and mental
responses.
 Akinesia
 Monotonous speech
 Handwriting that becomes progressively smaller
 Tremors in hands and fingers at rest (pill rolling)
 Tremors increasing when fatigued and decreasing with purposeful activity or sleep.
 Rigidity with jerky interrupted movements
 Restlessness and pacing
 Blank facial expression-mask –like facies
 Drooling
 Difficulty swallowing and speaking
 Loss of coordination and balance.
 Shuffling steps, stooped position, and propulsive gait.
Myasthenia Gravis
 Myasthenia Gravis is a neuromuscular disease characterized by considerable weakness
and abnormal fatigue of the voluntary muscles.
 A defect in the transmission of nerve impulses at the myoneural junction occurs.
 Causes include insufficient secretion of acetylcholine, excessive secretion of
cholinesterase, and unresponsiveness of the muscle fibers to acetylcholine.
Causes
 MG, thought to be an autoimmune disorder, is caused by a loss of acetylcholine (ACh)
receptors in the postsynaptic neurons at the neuromuscular junction. About 80% of all
MG patients have elevated titers for ACh receptor antibodies, which can prevent the ACh
molecule from binding to these receptor sites or can cause damage to them. MG is often
associated with thymic tumors.
Assessment
 Weakness and fatigue
 Difficulty chewing
 Dysphagia
 Ptosis
 Diplopia
 Weak, hoarse voice
 Difficulty breathing
 Diminished breath sounds
 Respiratory paralysis and failure
Complications
Myasthenic Crisis
 This sudden onset of muscle weakness is usually the result of undermedication or no
cholinergic medication at all. Myasthenic crisis may result from progression of the
disease, emotional upset, systemic infections, medications, surgery, or trauma. The crisis
is manifested by sudden onset of acute respiratory distress and inability to swallow or
speak.
Cholinergic Crisis
 Caused by overmedication with cholinergic or anticholinesterase drugs, cholinergic crisis
produces muscle weakness and the respiratory depression of myasthenic crisisas well as
gastrointestinal symptoms (nausea, vomiting, diarrhea), sweating, increased salivation,
and bradycardia.
Diagnostic Evaluation
 Injection of edrophonium (Tensilon) is used to confirm the diagnosis (have atropine
available for side effects). Improvement in muscle strength represents a positive test and
usually confirms the diagnosis
Amyotrophic Lateral Sclerosis
 Amyotrophic lateral sclerosis (ALS) is a disease of unknown cause in which there is a
loss of motor neurons (nerve cells controlling muscles) in the anterior horns of the spinal
cord and the motor nuclei of the lower brain stem.
 It is often referred to as Lou Gehrig’s disease.
Risk Factors
 Autoimmune
 Free radical damage
 Oxidative stress
 Cigarette smoking
Pathophysiology
 As motor neuron cells die, the muscle fibers that they supply undergo atrophic changes.
Neuronal degeneration may occur in both the upper and lower motor neuron systems.
 The leading theory held by researchers is that over excitation of nerve cells by the
neurotransmitter glutamate leads to cell injury and neuronal degeneration.
Assessment/Clinical Manifestations/Signs and Symptoms
The signs and symptoms presented depend on the location of the affected neuron. Generally, the
following presentations are evident:
 Fatigue
 Progressive muscle weakness
 Cramps
 Twitching
 Incoordination
Anterior horns
 Progressive weakness
 Muscle atrophy (arms, trunk, legs)
 Spasticity
 Brisk or overreactive muscle reflexes
Cranial nerves
 Muscle weakness
 Difficulty talking
 Difficulty swallowing
 Difficulty breathing
 Soft palate and upper esophageal weakness
 Weakness on the posterior tongue
Bulbar muscles
 Progressive difficulty in speaking
 Difficulty in swallowing
 Articulation and speech effects
 Compromised respiratory function
Huntington’s Chorea
 Huntington’s disease (also called Huntington’s chorea) is a rare abnormal hereditary disorder
of the CNS. It is characterized by chronic progressive chorea (involuntary purposeless, rapid
movements) and mental deterioration that results in dementia.
 Chorea, the Greek word meaning “dance”.
Risk Factors
 Hereditary (autosomal dominant gene transmission)
 Idiopathic
Pathophysiology
 There is destruction of cells in the caudate nucleus and putamen areas of the basal ganglia
and extrapyramidal motor system. The neurotransmitters, gamma-aminobutyric acid (GABA)
and Ach are decreased. Dopamine is not affected, but the decrease of Ach cause relative
increase of dopamine in the basal ganglia. The excess dopamine causes uncontrolled
movement in Huntington’s chorea.
Assessment/Clinical Manifestations/Signs and Symptoms
 Intellectual decline
 Abnormal movements
 Restlessness, forgetfulness, clumsiness, frequent falls
 Problems with speech, coordination and balance
 Depression, memory loss, emotional lability and impulsiveness
 Facial grimaces, protrusion of the tongue, jerky movements of the arms and legs
 Gait disturbances, patient at risk for falls
Complications
 Weight loss
 Pneumonia
 Congestive heart failure
 Incapacitated
 Bed sore
Disturbances in Spinal Cord Function

Spinal Cord Injury
 A spinal cord injury — damage to any part of the spinal cord or nerves at the end of the
spinal canal (cauda equina) — often causes permanent changes in strength, sensation and
other body functions below the site of the injury.
Symptoms
The lowest normal part of your spinal cord is referred to as the neurological level of your injury.
The severity of the injury is often called "the completeness" and is classified as either of the
following:
 Complete. If all feeling (sensory) and all ability to control movement (motor function)
are lost below the spinal cord injury, your injury is called complete.
 Incomplete. If you have some motor or sensory function below the affected area, your
injury is called incomplete. There are varying degrees of incomplete injury.
Additionally, paralysis from a spinal cord injury may be referred to as:
 Tetraplegia. Also known as quadriplegia, this means that your arms, hands, trunk, legs
and pelvic organs are all affected by your spinal cord injury.
 Paraplegia. This paralysis affects all or part of the trunk, legs and pelvic organs.
Spinal cord injuries of any kind may result in one or more of the following signs and symptoms:
 Loss of movement
 Loss or altered sensation, including the ability to feel heat, cold and touch
 Loss of bowel or bladder control
 Exaggerated reflex activities or spasms
 Changes in sexual function, sexual sensitivity and fertility
 Pain or an intense stinging sensation caused by damage to the nerve fibers in your spinal
cord
 Difficulty breathing, coughing or clearing secretions from your lungs
Emergency signs and symptoms
 Emergency signs and symptoms of a spinal cord injury after an accident may include:
 Extreme back pain or pressure in your neck, head or back
 Weakness, incoordination or paralysis in any part of your body
 Numbness, tingling or loss of sensation in your hands, fingers, feet or toes
 Loss of bladder or bowel control
 Difficulty with balance and walking
 Impaired breathing after injury
 An oddly positioned or twisted neck or back
Causes
 Motor vehicle accidents
 Falls
 Acts of violence.
 Sports and recreation injuries.
 Alcohol
 Diseases. Cancer, arthritis, osteoporosis and inflammation of the spinal cord also can
cause spinal cord injuries.
Risk Factors
 Being male
 Being between the ages of 16 and 30
 Being older than 65
 Engaging in risky behavior
 Having a bone or joint disorder
Complications
 Bladder control
 Bowel control
 Skin sensation
 Circulatory control
 Respiratory system
 Muscle tone
 Fitness and wellness
 Sexual health.
 Pain
 Depression
Herniated Intervertebral Disk
 A herniated disk refers to a problem with one of the rubbery cushions (disks) that sit
between the individual bones (vertebrae) that stack to make your spine.
 A spinal disk has a soft, jellylike center (nucleus) encased in a tougher, rubbery exterior
(annulus). Sometimes called a slipped disk or a ruptured disk, a herniated disk occurs
when some of the nucleus pushes out through a tear in the annulus.
Symptoms
 Arm or leg pain
 Numbness or tingling
 Weakness
Risk Factors
 Weight
 Occupation
 Genetics
 Smoking
 Complications
 Worsening symptoms
 Bladder or bowel dysfunction
 Saddle anesthesia
Disk Cord Tumor
 A spinal tumor is a growth that develops within your spinal canal or within the bones of
your spine. A spinal cord tumor, also called an intradural tumor, is a spinal tumor that
that begins within the spinal cord or the covering of the spinal cord (dura). A tumor that
affects the bones of the spine (vertebrae) is called a vertebral tumor.
 Spinal cord tumors may be classified as one of three different types depending on where
they occur relative to the protective membranes of the spinal cord.

These are the main types of intradural tumors:
 Intramedullary tumors begin in the cells within the spinal cord itself, such as gliomas,
astrocytomas or ependymomas.
 Extramedullary tumors grow in either the membrane surrounding the spinal cord or the
nerve roots that reach out from the spinal cord. Although they don't begin within the
spinal cord itself, these types of tumors may affect spinal cord function by causing spinal
cord compression and other problems. Examples of extramedullary tumors that can affect
the spinal cord include meningiomas, neurofibromas, schwannomas and nerve sheath
tumors.
Tumors from other parts of the body can spread (metastasize) to the vertebrae, the supporting
network around the spinal cord or, in rare cases, the spinal cord itself.
Spinal tumors or growths of any kind can lead to pain, neurological problems and sometimes
paralysis. A spinal tumor can be life-threatening and cause permanent disability.
Treatment for a spinal tumor may include surgery, radiation therapy, chemotherapy or other
medications.
Types
 Astrocytoma - a type of cancer that can form in the brain or spinal cord. Astrocytoma
begins in cells called astrocytes that support nerve cells.
 Chordoma - a rare type of bone cancer that happens most often in the bones of the spine
or the skull. It most often forms where the skull sits atop the spine (skull base) or at the
bottom of the spine (sacrum).
 Ependymoma - a type of tumor that can form in the brain or spinal cord. Ependymoma
begins in the ependymal cells in the brain and spinal cord that line the passageways
where the fluid (cerebrospinal fluid) that nourishes your brain flows.
 Glioma - a type of tumor that occurs in the brain and spinal cord. Gliomas begin in the
gluey supportive cells (glial cells) that surround nerve cells and help them function.
 Meningioma - a tumor that arises from the meninges — the membranes that surround
your brain and spinal cord. Although not technically a brain tumor, it is included in this
category because it may compress or squeeze the adjacent brain, nerves and vessels.
Meningioma is the most common type of tumor that forms in the head.
 Neurofibroma - a type of nerve tumor that forms soft bumps on or under the skin. A
neurofibroma can develop within a major or minor nerve anywhere in the body. This
common type of benign nerve tumor tends to form more centrally within the nerve.
Sometimes it arises from several nerve bundles (plexiform neurofibroma).
 Schwannoma - a type of nerve tumor of the nerve sheath. It's the most common type of
benign peripheral nerve tumor in adults. It can occur anywhere in your body, at any age.
Symptoms
 Pain at the site of the tumor due to tumor growth
 Back pain, often radiating to other parts of your body
 Feeling less sensitive to pain, heat and cold
 Loss of bowel or bladder function
 Difficulty walking, sometimes leading to falls
 Back pain that's worse at night
 Loss of sensation or muscle weakness, especially in your arms or legs
 Muscle weakness , which may be mild or severe, in different parts of your body
Risk factors
Spinal cord tumors are more common in people who have:
 Neurofibromatosis 2. In this hereditary disorder, benign tumors develop on or near the
nerves related to hearing. This may lead to progressive hearing loss in one or both ears.
Some people with neurofibromatosis 2 also develop spinal canal tumors.
 Von Hippel-Lindau disease. This rare, multisystem disorder is associated with blood
vessel tumors (hemangioblastomas) in the brain, retina and spinal cord and with other
types of tumors in the kidneys or adrenal glands.
Disturbances in Neurologic Function

Degenerative Disorders
Multiple Sclerosis
Parkinson’s Disease
Huntington’s Disease
Amyotrophic Lateral Sclerosis
Dementia
 Dementia describes a group of symptoms affecting memory, thinking and social abilities
severely enough to interfere with your daily life. It isn't a specific disease, but several
different diseases may cause dementia.
Symptoms
Cognitive changes
 Memory loss, which is usually noticed by a spouse or someone else
 Difficulty communicating or finding words
 Difficulty with visual and spatial abilities, such as getting lost while driving
 Difficulty reasoning or problem-solving
 Difficulty handling complex tasks
 Difficulty with planning and organizing
 Difficulty with coordination and motor functions
 Confusion and disorientation
Psychological changes
 Personality changes
 Depression
 Anxiety
 Inappropriate behavior
 Paranoia
 Agitation
 Hallucinations
Cause
 Damage to or loss of nerve cells and their connections in the brain. Depending on the
area of the brain that's affected by the damage, dementia can affect people differently and
cause different symptoms.
Progressive dementias
Types of dementias that progress and aren't reversible include:

 Alzheimer's disease. Alzheimer's disease is the most common cause of dementia
 Vascular dementia. This second most common type of dementia is caused by damage to
the vessels that supply blood to your brain
 Lewy body dementia. Lewy bodies are abnormal balloonlike clumps of protein that have
been found in the brains of people with Lewy body dementia, Alzheimer's disease and
Parkinson's disease. This is one of the more common types of progressive dementia
 Frontotemporal dementia. This is a group of diseases characterized by the breakdown
(degeneration) of nerve cells and their connections in the frontal and temporal lobes of
the brain, the areas generally associated with personality, behavior and language.
 Mixed dementia. Autopsy studies of the brains of people 80 and older who had dementia
indicate that many had a combination of several causes, such as Alzheimer's disease,
vascular dementia and Lewy body dementia.
Other disorders linked to dementia
 Huntington's disease. Caused by a genetic mutation, this disease causes certain nerve
cells in your brain and spinal cord to waste away.
 Traumatic brain injury (TBI). This condition is most often caused by repetitive head
trauma. People such as boxers, football players or soldiers might experience TBI.
 Creutzfeldt-Jakob disease. This rare brain disorder usually occurs in people without
known risk factors. This condition might be due to deposits of infectious proteins called
prions.
 Parkinson's disease. Many people with Parkinson's disease eventually develop dementia
symptoms (Parkinson's disease dementia).
Risk Factors
 Age
 Family History
 Down Syndrome
Complications
 Poor Nutrition
 Pneumonia
 Inability to perform self-care tasks
 Personal safety challenges
 Death
Alzheimer’s Disease
 Alzheimer’s disease is an irreversible, progressive brain disease that slowly destroys
memory and thinking skills, and eventually even the ability to carry out the simplest
tasks. In most people with Alzheimer’s, symptoms first appear after age 60.
Characteristics/ Signs and Symptoms
The disease course is divided into four stages, with progressive patterns of cognitive and
functional impairments.
 Pre-dementia
Stage 1 is characterized by recent memory loss, increased irritability, impaired judgment, loss of
interest in life, decline of problem-solving ability, and reduction in abstract thinking. Remote
memory and neurological exam remain unchanged from baseline.
 Early
Stage 2 lasts 2 to 4 years and reveals a decline in the patient’s ability to manage personal and
business affairs, an inability to remember shapes of objects, continued repetition of a
meaningless word or phrase (perseveration), wandering or circular speech patterns
(circumlocution dysphasia), wandering at night, restlessness, depression, anxiety, and
intensification of cognitive and emotional changes of stage 1.
 Moderate
Stage 3 is characterized by impaired ability to speak (aphasia), inability to recognize familiar
objects (agnosia), inability to use objects properly (apraxia), inattention, distractibility,
involuntary emotional outbursts, urinary or fecal incontinence, lint-picking motion, and chewing
movements. Progression through stages 2 and 3 varies from 2 to 12 years.
 Advanced
Stage 4, which lasts approximately 1 year, reveals a patient with a masklike facial expression, no
communication, and apathy, and withdrawal, eventual immobility, assumed fetal position, no
appetite, and emaciation.
D. Implementation
1. Pharmacological Therapeutics
a. Autonomic Nervous System Drugs
AUTONOMIC DRUGS
There are several drugs affecting the autonomic nervous system which, for a better
understanding of specific drugs, are classified into groups.
1. Drugs acting on the sympathetic nervous system
a) Sympathomimetics or adrenergic drugs: are drugs that mimic the effects of
sympathetic nerve stimulation.
b) Sympatholytics: are drugs that inhibit the activity of sympathetic nerve or that of
sympathomimetics.
2. Drugs acting on the parasympathetic nervous system
a) Parasympathomimetics or cholinergic drugs: are drugs which mimic acetylcholine or
the effects of parasympathetic nerve stimulation.
b) Parasympatholytics: are drugs that inhibit parasympathetic nervous system activity or
that of cholinergic drugs.
ADRENERGIC
As their name suggests, these drugs resemble sympathetic nerve stimulation in their effects; they
may be divided into two groups on the basics of their chemical structure.
1. Catecholamines: -these are compounds which have the catechol nucleus.
Catecholamines have a direct action on sympathetic effectors cells through interactions with
receptor sites on the cell membrane.
The group includes adrenaline, noradrenaline, dopamine, isoprenaline, and dobutamine.

Noncatecholmines: - lack the catechol nucleus.
They may directly act on the receptors or may indirectly release the physiologic
catecholaminese.g. Ephedrine, phenylephrine, amphetamine
Adrenergic drugs, like cholinergic drugs, can be grouped by mode of action and by the spectrum
of receptors that they affect.
a. Direct mode of action: directly interact with and activate adrenoreceptors, e.g., adrenaline and
noradrenaline
b. Indirect mode of action: their actions are dependent on the release of endogenous
catecholamines. This may be
i. Displacement of stored catecholamies from the adrenergic nerve endings, e.g.,
amphetamine, tyramine
ii. Inhibition of reuptake of catecholamines already released, e.g. cocaine,
tricyclic antidepressants
Both types of sympathomimetic, direct and indirect, ultimately cause activation of
adrenoreceptors leading to some or all characteristic effects of the catecholamines.
Organ-system Effects of Activation of the Adrenergic System
1. CVS:
a. Heart: increased rate and force of contraction, increased cardiac output, myocardial demand,
and AV conduction
b. Blood Vessels and Blood pressure: constriction of blood vessels in the skin and mucous
membranes
- Dilatation of skeletal muscle vessels
- Adrenaline increases systolic and decreases diastolic blood pressure at low doses but
increases both at higher doses
- Noradrenaline increases both systolic and diastolic blood pressure
2. Smooth Muscle:
a. Bronchi: relaxation.
b. Uterus: relaxation of the pregnant uterus
c. GIT: relaxation of wall muscles and contraction of sphincters
d. Bladder: relaxation of detrusor muscle; contraction of sphincter and trigone muscle
3. Eye: mydriasis; reduction of intraocular pressure in normal and glacucomatous eyes

4. Respiration: Bronchodilatation; relief of congestion; mild stimulation of respiration
5. Metabolic: Increased hepatic glycogenolysis; decreased peripheral glucose intake; increased
free fatty acids in the blood (lipolysis)
6. CNS: excitement, vomting, restlessness
7. Skeletal muscle: facilitation of neuromuscular transmission and vasodilatation
Drugs Acting on the Adrenergic Receptor Subtypes

α1 α2 β1 β2
Agonist Phenylephrine Clonidine Dobutamine Salbutamol
Methoxamine Oxymetazoline Isoproterenol Terbutaline
Terbutaline Isoetharine
Antagonist Prazosin Yohimbine Propranolol Propranolol
Phentolamine Phentolamine Pindolol Pindolol
Phenoxybenzamin Phenoxybenzamine Atenolol Butoxamine
e Metoprolol Timolol
Timolol
Adrenaline stimulates all the four receptor subtypes.
Noradrenaline stimulates both alpha receptors and beta1 but has very poor affinity for beta2
receptors. Labetalol blocks all beta receptors as well as some alpha receptors.
ADRENALINE
This is the prototype of adrenergic drugs and is produced in the body by the cells of the Adrenal
medulla and by chromaffin tissues.
Pharmacokinetics
Adrenaline is rapidly destroyed in the gastrointestinal tract, conjugated, and oxidized in the liver.
It is therefore ineffective when given orally and should be given intramuscularly or
subcutaneous. Intravenous injection is highly dangerous and is likely to precipitate ventricular
fibrillation. The drug may however, be given by nebulizer for inhalation when its relaxing effect
on the bronchi is desired or it may be applied topically to mucus membranes to produce
vasoconstriction. Because of the extensive metabolism of the drug in liver, little is excreted
unchanged in the urine.
Pharmacodynamics
Adrenaline directly stimulates all the adrenergic receptors both and brings about effects of
sympathetic nerve stimulation. Its action may be divided in to two, depending on the type of
receptor stimulated. The α effects consist of vasoconstriction in skin and viscera, mydriasis,
platelet aggregation and some increase in blood glucose. The ß effects consists of increased
contractility and rate of heart with a decreased refractory period (ß1), vasodilatation in muscles
and coronary vessels (ß2), bronchial relaxation (ß2) uterine relaxation (ß2), hyperglycemia, lactic
acidemia and increased circulating free fatty acids.
Indications
1. Acute bronchial asthma
2. Anaphylaxis
3. Local haemostatic to stop bleeding in epistaxis
4. with local anesthesia to prolong the action
5. Cardiac arrest
Adverse reactions
1. Anxiety, restlessness, headache tremor
2. Anginal pain
3. Cardiac arrhythmias and palpitations
4. Sharp rise in blood pressure
5. Sever vasoconstriction resulting in gangrene of extremities
6. Tearing, conjunctival hyperemia
Contraindications
1. Coronary diseases
2. Hyperthyroidism
3. Hypertension
4. Digitalis therapy
5. Injection around end arteries
NOR ADRENALINE
Nor adrenaline is the neurochemical mediator released by nerve impulses and various drugs from
the postganglionic adrenergic nerves. It also constitutes 20% of the adrenal medulla
catecholamine output.
Pharmacokinetics
Like adrenaline, noradrenaline is ineffective orally so it has to be given intravenously with
caution. It is not given subcutaneous or intramuscularly because of its strong vasoconstrictor
effect producing necrosis and sloughing. The metabolism is similar to adrenaline; only a little is
excreted unchanged in urine.
Pharmacodynamics
Nor adrenaline is a predominantly α receptor agonist with relatively less β agonist action when
compared to adrenaline.
Indication
Nor adrenalines is used as hypertensive agent in hypotensive states
E.g. During spinal anesthesia or after sympathectomy.
Adverse effects include:
- Anxiety, headache, bradycardia are common side effects
- Severe Hypertension in sensitive individuals
- Extravasation of the drug causes necrosis and sloughing.
ISOPRENALINE DOPAMINE, DOBUTAMINE. These are the other catecholamines which
have similar properties to adrenaline and noradrenaline.
Dopamine is naturally occurring and is a precursor of noradrenaline. The other two-isoprenaline
and dobutamine- are synthetic. These drugs have advantage over the others because they are
more selective in their action so that they have fewer side effects than adrenaline and nor
adrenaline. Dopamine and dobutamine are very useful drugs for the treatment of shock.
NON- CATECHOLAMINES
Most of the non- catecholamines function by releasing the physiologic catecholamines from the
postganglionic nerve endings EPHEDRINE.
Pharmacokinetics
Ephedrine in absorbed from the gastrointestinal tract and from all parenteral sites. It has a good
distribution throughout the body and is resistant to hydrolysis by the liver enzymes. Major
proportion of the drug is excreted unchanged in the urine. Because of its stability to metabolism
it has long duration of action than the catecholamines.
Pharmacodynamics
Ephedrine stimulates both α and β receptors. This effect is partly by a direct action on the
receptors and partly indirectly by releasing noradrenaline from its tissue stores the effect of the
drug to various organs and systems is similar to that of adrenaline. It is also a mild CNS
stimulant.
Indications:
1. Bronchial asthma: - usually as a prophylactic for prevention of attacks
2. Nasal decongestion
3. Mydriasis
4. Heart block
5. Nocturnal enuresis
Side effects
The side effects are similar to those of adrenaline; but in addition it may produce insomnia and
retention of urine.
Contraindications
They are the same as Adrenaline.
Based on their selectivity to specific receptors the rest of the catecholamines, are classified but it
is very difficult to exhaust all the drugs. More over their effect and pharmacology is discussed
where they are clinically indicated.
ADRENERGIC BLOCKERS
Adrenergic receptor blockers may be considered in two groups:
1. Drugs blocking the ą adrenergic receptor
2. Drugs blocking theβ Adrenergic receptor
These drugs prevent the response of effectors organs to adrenaline, noradrenaline and other
sympathomimetic amines whether released in the body or injected. Circulating catecholamines
are antagonized more readily than are the effects of sympathetic nerve stimulation. The drugs act
by competing with the catechoamines for α or β receptors on the effectors organs. They don’t
alter the production or release of the substances.
α- Adrenergic blockers
Alpha adrenergic receptor antagonists may be reversible or irreversible. Reversible antagonists
dissociate from the receptors e.g. phentolamine, tolazoline, prazosin,yohimbine, etc. Irreversible
antagonists tightly bind to the receptor so that their effects may persist long after the drug has
been cleared from the plasma e.g. phenoxybenzamine
Pharmacologic Effects:
Alpha receptor antagonist drugs lower peripheral vascular resistance and blood pressure. Hence,
postural hypotension and reflex tachycardia are common during the use of these drugs. Other
minor effects include miosis, nasal stuffiness, etc.
Prazosin
This is an effective drug for the management of hypertension. It has high affinity for alpha1
receptor and relatively low affinity for the alpha2 receptor. Prazosin leads to relaxation of both
arterial and venous smooth muscles due to the blockage of alpha1 receptors. Thus, it lowers
blood pressure, reduces venous return and cardiac output. It also reduces the tone of internal
sphincter of urinary bladder.
Indications:
- Essential hypertension
- Raynaud’s syndrome
- Benign prostatic hyperplasia
β - ADRENERGIC BLOCKING DRUGS
The β - adrenergic receptor blocking drugs in use may be classified by their selectivity for
receptors in different tissues.
1. Drugs blocking all the β receptor effects of adrenaline (non-selective beta blockers) e.g.
propanalol, pinadolol, timolol etc
2. Drugs blocking mainly the β1 effects (those on the heart) with less effect on the bronchi and
blood vessels (beta1-selective blockers), e.g. atenolol, practalol acebutalol, etc.
PROPRANOLOL
Propranolol is a non- selective β adrenergic blocker; it has also other actions like membrane
stabilization.
Pharmacokinetics
Propranolol is almost completely absorbed following oral administration. However, the liver,
leaving only 1/3 rd of the dose to reach the systemic circulations, metabolizes most of the
administered dose. It is bound to plasma to the extent of 90-95%. It is excreted in the urine.
Pharmacodynamics
The drug has the following main actions.
1. Cardiovascular system: Bradycardia, reduces force of contraction, reduces blood pressure
2. Respiratory system :Bronchoconstriction
3. Metabolic system: Hypoglycemia
4. Central nervous system : Anti-anxiety action
5. Eye: Decrease the rate of Aqueous humor production
6. Kidneys: Decrease renin secretion
Indications
 Cardiac arrhythmias
 Hypertension
 Prophylaxis against angina
 Myocardial infarction
 Thyrotoxicosis
 Anxiety states (suppression of the physical manifestations of situational anxiety)

 Prophylaxis against migraine attacks
 Glaucoma
Adverse reactions
 GI disturbances like nausea, vomiting

 Heart failure
 Heart block
 Hypotension and severe bradycardia
 Bronchospasm
 Allergic reaction
 Vivid dreams night mare and hallucinations
 Cold hands
 Withdrawal symptoms in case of abrupt discontinuation
 Masking of hypoglycemia in diabetic patients
Contraindications and Precautions:
 Bronchial asthma
 Diabetes mellitus
 Heart failure
 Peripheral vascular disease
CHOLINERGIC DRUGS
Cholinergic drugs are also called parasympathomimetics because their effect mimics the effect of
parasympathetic nerve stimulation. Administration of these drugs will result in an increase in the
parasympathetic activities in the systems innervated by cholinergic nerves.
There are two groups of cholinergic drugs:
1. Direct-acting: bind to and activate muscarinic or nicotinic receptors (mostly both) and include
the following subgroups:
a. Esters of choline: methacholine, carbachol, betanechol
b. Cholinergic alkaloids: pilocarpine, muscarine, arecoline, nicotine
2. Indirect-acting: inhibit the action of acetylcholinesterase enzyme
a. Reversible: neostigmine, physostigmine, edrophonium
b. Irreversible: Organophosphate compounds; echothiophate
The actions of acetylcholine may be divided into two main groups:
1. Nicotinic actions- those produced by stimulation of all autonomic ganglia and the
neuromuscular junction
2. Muscarinic actions- those produced at postganglionic cholinergic nerve endings

ESTERS OF CHOLINE
ACETYLCHOLINE is the prototypical cholinergic agent. It functions as neurotransmitter at all
cholinergic sites in the body; because of its unique pharmacokinetic properties, it has never been
used in medical therapeutics.
Pharmacokinetics
Acetylcholine is poorly absorbed from the gastric mucosa; therefore it is ineffective if given
orally. The recommended way of administration is parenteral. In the blood it is rapidly
hydrolyzed by the enzyme cholinesterase into acetic acid and choline; this makes its duration of
action very short and unreliable for therapeutic purposes.
Pharmacodynamics
As mentioned earlier it has two types of actions: nicotinic and muscarinic; the muscarinic actions
are of main interest and are discussed below.
 Cardiovascular system
Heart - slow heart rate
Blood vessels - vasodilator
Blood pressure - falls because of the effect on the heart and blood revels
i) Gastrointestinal tract It stimulates the tone and motility of the Gl tract but the sphincters will
be relaxed
ii) Urinary tract It stimulates the detrusor muscle and relaxes the internal urethral sphincter
resulting in evacuation of bladder
iii) Bronchioles It increase bronchial secretion and brings about bronchoconstriction
iv) Eye- It has two effects- miosis and accommodation for near objects because of stimulation of
the constrictor pupillae and ciliary muscles respectively.
v) Exocrine glands- it stimulates salivary, gastric, bronchial, lachrymal and sweat gland
secretions.
SYNTHETIC CHOLINE ESTERS
These are synthetic derivatives of choline and include metacholine, carbachol and betanechol.
These drugs have the following advantages over acetylcholine:
 They have longer duration of action

 They are effective orally as well as parenterally
 They are relatively more selective in their actions.
CARBACHOL
Pharmacokinetics
It is completely absorbed from the gastro intestinal tract and is stable towards hydrolysis by
cholinesterase enzyme; therefore it can be given both orally and parenterally with almost similar
dosage.
Pharmacodynamics
It has similar actions to those of acetylcholine with pronounced effects on the gastro intestinal
tract and the urinary bladder
Indications
 Glaucoma
 Retention of urine (postoperative)
 Paralytic ileus
BETANECHOL
This drug is similar to carbachol in all parameters, i.e., pharmacokinetics, pharmacodynamics
and clinical indications; it has a better advantage over carbachol because it has fewer side effects
as a result as lack of nicotinic actions.
Contra indications to the use of choline esters
1. Bronchial asthma because they may induce bronchial constriction and increase bronchial
secretions
2. Hyperthyroidism because of the danger of inducing atrial fibrillation
3. Peptic ulcer disease because of the increase in gastric acid secretion
4. Coronary insufficiency because the hypertension produced will further compromise coronary
blood flow
5. Mechanical intestinal and urinary outlet obstruction
CHOLINERGIC ALKALOIDS
1. Those with chiefly nicotinic actions include nicotine, lobeline etc.
2. Those with chiefly muscarinic actions include muscarine, pilocarpine, etc.
PILOCARPINE
Pharmacokinetics
This drug is readily absorbed from the gastrointestinal tract and it is not hydrolyzed by
cholinesterase enzyme. It is excreted partly destroyed and partly unchanged in the urine.
Pharmacodynamics
The drug directly stimulates the muscarinic receptors to bring about all the muscarinic effects of
acetylcholine.
Indications: Glaucoma
ANTICHOLINESTERASE DRUGS
The commonly used cholinesterase inhibitors fall into three chemical groups:
1. Simple alcohols bearing quaternary amines, e.g., edrophonium
2. Carbamate and related quaternary or tertiary amines, e.g., neostigmine, physostigmine
3. Organic derivatives of phosphates, e.g., isofluorophate, echothiophate
PHYSOSTIGMINE
Pharmacokinetics
This drug is completely absorbed from the gastrointestinal and is highly distributed throughout
the body; it can pass the blood brain barrier.
Pharmacodynamics
Inhibits the enzyme cholinesterase; therefore, it increases and prolongs the effect of endogenous
acetylcholine at the different sites. It has no direct effect on cholinergic receptors.
Indications
 Glaucoma
 Atropine over dosage
NEOSTIGMINE
Pharmacokinetics
This drug is poorly absorbed from the gastro intestinal tract and is poorly distributed throughout
the body; it cannot pass the blood brain barrier.
Pharmacodynamics
Just like physostigmine, it inhibits cholinesterase enzyme; but unlike physostigmine, it has a
direct nicotinic action on skeletal muscles.
Indications
 Myasthenia gravis
 Paralytic Ileus
 Reversal of effect of muscle relaxants, e.g. tubocurarine
 Post-operative urine retention
Organophosphates such as echothiophate, isofluorophate, etc. combine with cholinesterase
irreversibly and thus hydrolysis is very slow.
They may be used in glaucoma. Other organophosphates like parathion and malathion are used
as insecticides. Poisoning with organophosphates is an important cause of morbidity and
mortality all over the world. It usually results from:
 Occupational exposure as in persons engaged in spraying insecticides,

 Accidental exposure, and
 Ingestion of any of these compounds with suicidal intent
ANTICHOLINERGICS
Anticholinergics block the effects of acetylcholine and other cholinergic drugs at cholinergic
receptors of effector cells. Anticholinergics fall into two major families:
1. Antinicotinics which include ganglion blockers such as hexamethonium, trimethaphan, etc.,
and neuromuscular blockers such as gallamine, tubocurarine, pancuronium, etc.
2. Antimuscarinics include tertiary amines such as atropine, scopolamine, tropicamide, etc,
andquaternary amines such as propantheline, ipratropium, benztropine, etc.
ATROPINE
Atropine is found in the plant Atropa belladonna and it is the prototype of muscarinic
antagonists.
Pharmacokinetics
Atropine is absorbed completely from all sites of administration except from the skin wall, where
absorption is for limited extent; it has good distribution. About 60% of the drug is excreted
unchanged in urine.
Pharmacodynamics
Atropine antagonizes the effect of acetylcholine by competing for the muscarinic receptors
peripherally and in the CNS; therefore the effects of atropine are opposite to the acetylcholine
effects.
Organ-system Effects:
 CNS: - lower doses produce sedation - higher doses produce excitation, agitation and
hallucination
 Eyes: - relaxation of constrictor pupillae (mydriasis) - relaxation or weakening of ciliary
muscle (cycloplegia-loss of the ability to accommodate)
 CVS: - blocks vagal parasympathetic stimulation (tachycardia) - vasoconstriction
 Respiratory: - bronchodilatation and reduction of secretion
 GIT: - decreased motility and secretions
 GUS: - Relaxes smooth muscle of ureter and bladder wall; voiding is slowed.
 Sweat Glands: - suppresses sweating
Clinical Indications
 Pre anesthetic medication -to reduce the amount of secretion and to prevent excessive
vagal tone due to anesthesia.
 As antispasmodic in cases of intestinal, biliary, and renal colic
 Heart block
 Hyperhidrosis
 Organophosphate poisonings
Side effects
 Dryness of the mouth, tachycardia and blurred vision

 Retention of urine
Contraindications
 Glaucoma
 Bladder outlet obstruction
HYOSCINE (SCOPOLAMINE)
This drug has the same effect as atropine except for some differences which includes:-
- It has shorter duration of action
- It is more depressant to the CNS.
- All other properties are similar to atropine. It has certain advantage over atropine. These
include:
3. Better for preanesthetic medication because of strong antisecretory and antiemetic action and
also brings about amnesia
4. Can be used for short- travel motion sickness
SYNTHETIC ATROPINE DERIVATIVES
There are a number of synthetic atropine derivatives, which are used in the treatment of various
conditions, their actions are similar to that of atropine but have fewer side effects. These groups
of drugs include
1. Mydriatic atropine substitutes, this group of drugs have shorter duration of action than
atropine and are used locally in the eye; drugs included: Homatropine, Eucatropine etc.
2. Antiseccretory antispasmodic atropine substitutes: - Effective more localized to the Gl. Drugs
include: propantheline and hyoscine
3. Antiparkinsonian atropine substitute: - drugs like Benztropine, Trihexyphenidyl
4. Atropine substitutes which decrease urinary bladder activity like oxybutynin
5. Atropine substitutes used in bronchial asthma drugs like ipratropium
ANALGESICS
Opioid Analgesics
Opioid is any substance that can produce morphine like effects. Opium is an extract of the juice
of the poppy Papaver somniferum. Opium contains many alkaloids related to morphine. The
main group of drugs that are discussed in section are divided into two; morphine analogues and
synthetic derivatives.
Morphine analogues. Compounds closely related in structure to morphine. They may be agonist
(codeine and heroin), partial agonists (nalorphine) or antagonists (naloxone).
Synthetic derivatives. Pethidine, fentanyl, methadone, pentazocine are examples of synthetic
derivatives.
Opioid receptors. Three receptors mediate the main pharmacological effects of opiates. mu
receptors are responsible for the analgesic and major unwanted effects (respiratory depression,
sedation and dependance). Delta for analgesia and peripheral effects of opiates and kappa
contribute to analgesia at spinal level and dysphoria.
Agonists and antagonists of opioid receptors
Pure agonists. They all have high affinity to mu receptors and varying affinity to delta and
kappa receptors (codeine, methadone, dextropropoxyphene). Partial antagonists and mixed
agonist-antagonists: Nalorphine, and pentazocine.
Pharmacokinetics: Most opioid analgesics are well absorbed from subcutaneous and
intramuscular sites as well as from the mucosal surfaces of the nose or mouth. Although
absorption from the gastrointestinal tract is rapid, some opioids given by this route are subject to
first-pass metabolism by glucuronidation in the liver. All opioids bind to plasma proteins with
varying degrees of affinity, the drugs rapidly leave the blood and localize in highest
concentrations in tissues that are highly perfused. The opioids are converted in large part to polar
metabolites, which are then readily excreted by the kidneys.
Pharmacodynamics
A. Mechanism of Action: Opioid agonists produce analgesia by binding to specific receptors,
located primarily in brain and spinal cord regions involved in the transmission and
modulation of pain.
Effects of morphine and its synthetic derivatives
1. Central nervous system effects - The principal effects of the opioid analgesics with affinity
for mu receptors are on the central nervous system; the more important ones include analgesia,
euphoria, sedation, and respiratory depression. With repeated use, a high degree of tolerance
occurs to all of these effects except respiratory depression. They also cause addiction and
dependence.
a. Analgesia-Pain consists of both sensory and affective (emotional) components. Opioids can
change both aspects of the pain experience. In most cases, these drugs have a relatively greater
effect on the affective component.
b. Euphoria-After a dose of morphine, a typical patient in pain experiences a pleasant floating
sensation and freedom from anxiety and distress. Dysphoria is a state characterized by
restlessness and a feeling of malaise.
c. Sedation-Drowsiness and clouding of mentation are frequent concomitants of opioid action.
d. Respiratory depression-All of the opioid analgesics can produce significant respiratory
depression by inhibiting brain stem respiratory mechanisms.
e. Cough suppression-Suppression of the cough reflex is a well-recognized action of opioids.
However, cough suppression by opioids may allow accumulation of secretions and thus lead to
airway obstruction and atelectasis. e.g. codeine.
f. Miosis-Constriction of the pupil is seen with virtually all opioid agonists.
g. Nausea and vomiting-The opioid analgesics can activate the brain stem chemoreceptor trigger
zone to produce nausea and vomiting.
2. Peripheral effects
a. Cardiovascular system: Hypotension effects; has been attributed to a number of mechanisms
including central depression of vasomotor-stabilizing mechanisms and release of histamine.
b. Gastrointestinal tract: Constipation. Opioid receptors exist in high density in the
gastrointestinal tract, and the constipating effects of the opioids are mediated through an action
on the local enteric nervous system as well as the central nervous system.
c. Biliary tract: The opioids constrict biliary smooth muscle, which may result in biliary colic.
The sphincter of Oddi may constrict, resulting in reflux of biliary and pancreatic secretions and
elevated plasma amylase and lipase levels.
d. Genitourinary tract: Renal function is depressed by opioids. It is believed that in humans this
is chiefly due to decreased renal plasma flow.
e. Uterus: The opioid analgesics may prolong labor.
f. Neuroendocrine: Opioid analgesics stimulate the release of antidiuretic hormone, prolactin,
and somatotropin but inhibit the release of luteinizing hormone.
B. Effects of mixed agonist-antagonists: Pentazocine and other opioids with agonist actions at
some opioid receptors and antagonist actions at others usually produce sedation in addition to
analgesia when given in therapeutic doses. At higher doses, sweating, dizziness, and nausea are
common, but severe respiratory depression may be less common than with pure agonists.
Clinical use of opioid analgesics
Opioids are used in severe, constant pain, acute pulmonary edema (pulmonary edema associated
with left ventricular failure), cough suppression, diarrhea, and preanaesthetic medication.
CNS stimulants: As compared to CNS depressants the stimulants of the centeral nervous system
are therapeutically not as useful as they lack selectivity of action. Further, excessive stimulation
of CNS is followed by its depression.
CNS stimulant can be classified into:
1. convulsants and respiratory stimulants eg. Srychnine picrotoxin, nikethaimide
2. psychomotor stimulants Eg. Amphetamine, cocaine, caffeine
3. psychotomimetic drug Eg. Lysergic and diethylamide (LSD) psilocybin, phencyclidine.
Convulsants and respiratory stimulants: these are diverse group or drugs and have little
clinical use. Certain short acting respiratory stimulants like doxapram, amiphenazole can be used
in respiratory failure. Strychnine, picrotoxin and leptazole are used as chemical tools in
experimental pharmacology in various animal models.
Psychomotor stimulants: Drugs like amphetamine cause increased motor activity, euphoria,
excitement and anorexia due to release of noradrerline and dopamine.
Clinical uses: Amphaetamine is useful in the treatment of narcolepsy and attention deficit in
children. Cocaine is occasionally used as a local aneasthetic, mainly in ophthalmology and minor
nose and throat surgery.
Khat is another drug that belongs to this group and it is a major drug of abuse in Ethiopia. As
drugs of abuse amphetamine khat and cocaine produce strong psychological dependence and
carry a high risk of adverse reactions.
Psycho mimetic drugs: Drugs like LSD, phencyclidine and psilocybin cause sensory changes,
hallucinations and delusions, resembling symptoms of acute schizophrenia. They are not used
clinically but are important as drugs of abuse.
Drug dependence and drug abuse
There are many drugs that human beings consume because they choose to, and not because they
are advised to by physicians. Society in general disapproves, because in most cases there is a
social cost; for certain drugs, this is judged to out-weigh the individual benefit and their use is
banned in many countries.
SEDATIVE AND HYPNOTIC DRUGS
Anxiolytic drugs are used to treat the symptoms of anxiety, whereas hypnotic drugs used to treat
insomnia. The same drugs are used for both purposes.
Classes of anxiolytic and hypnotic drugs: The main groups of the drugs are:
1. Benzodiazepines. Benzodiazepines are the most important group, used as sedative and
hypnotic agents.
2. 5- HT1A receptor agonist (e.g. buspirone). It is recently introduced anxiolytic.

3. Barbiturates (phenobarbitone). They are nowadays less commonly used as sedativehypnotics.
4. β -adrenoceptor antagonists (e.g. propranolol). They are used to treat some forms of anxiety,
where physical symptoms (sweating, tremor, and tachycardia), are troublesome. They are not
used as hypnotics.
5. Miscellaneous drugs (chloral hydrate, paraldehyde, and diphenhydramine). These drugs are
not commonly recommended for axiety or insomia.
Benzodiazepines
Benzodiazepines are well absorbed when given orally. They bind strongly to plasma proteins,
however, many of them accumulate gradually in the body fat (i.e. they are highly lipid soluble).
Benzodiazepines are inactivated by the liver and excreted in the urine.
Based on their duration of action roughly divided into short acting (flurazepam, triazolam),
medium acting (alprazepam, lorazepam) and long acting compounds (diazepam,
chlordiazepoxide, clonazepam).
Pharmacodynamics
Act by binding to a specific regulatory site on the GABAA receptor, thus enhancing the
inhibitory effects of GABA. Central nervous system effects of benzodiazepines include:
1. Reduction of anxiety and aggression.
2. Sedation and induction of sleep.
3. Reduction of muscle tone and coordination.
4. Anticonvulsant effects.
Clinical Uses
 Treatment insomnia
 Anxiety
 Preoperative mediations
 Acute alcohol withdrawal
 As anticonvulsants
 Chronic muscle spasm and spasticity
Unwanted effects
 Toxic effects due to acute overdosage causes prolonged sleep.

 Unwanted effects occurring during normal therapeutic use includes: drowsiness,
confusion, amnesia, and impaired motor coordination.
 Tolerance and dependance: Pharmacokinetic and tissue tolerance and also cause physical
dependance. i.e. stopping benzodiazepines treatment after weeks or months causes an
increase in symptoms of anxiety.
5 - HT1A receptor agonist
Buspirone is a potent agonist of. 5 - HT1A receptors. Anxiolytic effects take days to weeks to
develop. Buspirone does not cause sedation, motor incoordiation and withdrawal effects. The
main side effects are nausea, dizziness, headache, and restlessness.
Barbiturates
They are non-selective CNS depressants, which produce effects ranging from sedation and
reduction of anxiety, to unconsciousness and death from respiratory and cardiovascular failure.
Barbiturates act by enhancing action of GABA, but less specific than benzodiazepines. They are
potent inducers of hepatic drug metabolizing enzymes, hence likely to cause drug interaction.
Tolerance and dependence occur, more than benzodiazepines.
ANTICONVULSANTS
Mechanism of action
Anticonvulsant drugs act by two mechanisms: by reducing electrical excitability of cell
membrane and by enhancing GABA mediated synaptic transmission.
The main drugs used in the treatment of epilepsy are phenytoin, carbamazepine, valproate,
ethosuximide and phenobarbitone.
Phenytoin
It is commonly used antiepileptic drug. It is effective against different forms of partial and
generalized seizures; however it is not effective in absence seizures. Well absorbed when given
orally. It is metabolized by the liver. It is liver enzyme inducer and therefore, increases the rate
of metabolism of other drugs.
Main side effects are sedation, confusion, gum hyperplasia, skin rash, anaemia, nystagmus, and
diplopia.
Carbamazepine
It is derived from tricyclic antidepressant. Its pharmacological action resembles those of
phenytoin, however, it is chiefly effective in the treatment of partial seizure. It is also used in the
treatment of trigeminal neuralgia and manic-depressive illness.
It is powerful inducer of liver microsomal enzymes, thus accelerates the metabolism of
phenytoin, warfarin, oral contraceptives and corticosteroids. Carbamazepine causes sedation,
mental disturbances and water retention.
Valproate
Valproate is chemically unrelated to the other antiepileptic drugs. The mechanism of action is
unknown. It is used in grand mal, partial, petit mal and myoclonic seizure. Relatively has few
side effects, however, it is potentially hepatotoxic. It is non-sedating.
Ethosuximide
Has fewer side effects and used in the treatment of absence seizures.
Phenobarbitone
It is well absorbed after oral administration and widely distributed. Renal excretion is enhanced
by acidification of the urine. Phenobarbitone is liver enzyme inducer and hence accelerates the
metabolism of many drugs like oral contraceptives and warfarin.
The clinical use of phenobarbitone is nearly the same as that of phenytoin. The most important
unwanted effect is sedation. Benzodiazepines: Clonazepam and related compounds, clobazam
are claimed to be relatively selective as antiepileptic drugs. Sedation is the main side effect of
these compounds, and an added problem may be the withdrawal syndrome, which results in an
exacerbation of seizures if the drug is stopped.
AGENTS FOR ALZHEIMER’S
DRUG PHARMACOLOGIC DOSAGE TARGET MINIMUM

ACTIONS DOSAGE* THERAPEUTIC
DOSAGE†
Donepezil Acetylcholinesterase Start at 5 mg 10 mg once 5 mg daily
(Aricept) inhibitor once daily, daily
taken at
bedtime; after 6
weeks, increase
to 10 mg once
daily.
Rivastigmine Acetylcholinesterase Start at 1.5 mg 6 mg twice 3 mg twice daily
(Exelon) inhibitor twice daily, daily
Butyrylcholinesterase taken with
inhibitor food; at 2-week
intervals,
increase each
dose by 1.5 mg,
up to a dosage
of 6 mg twice
daily.
Galantamine Acetylcholinesterase Start at 4 mg 12 mg twice 8 mg twice
(Reminyl) inhibitor twice daily daily daily§
Nicotinic receptor with food; at 4-
actions week intervals, *§—This dosage
increase each can be used in
dose by 4 mg, patients with
up to a dosage moderate hepatic

of 12 mg twice or renal disease;
daily. galantamine is
not
recommended
for use in
patients with
severe hepatic or
renal disease.
2. Complementary and Alternative Therapy
a. Gingko Biloba
Ginkgo biloba has many health benefits. It’s often used to treat mental health
conditions, Alzheimer’s disease, and fatigue. It’s been used in traditional Chinese medicine for
about 1,000 years. It came on the Western culture scene a few centuries ago, but has enjoyed a
surge of popularity over the last few decades.
Uses of ginkgo biloba
Ginkgo is used as an herbal remedy to treat many conditions. It may be best known as a
treatment for dementia, Alzheimer’s disease, and fatigue. Other conditions it’s used to treat are:
 anxiety and depression
 schizophrenia
 insufficient blood flow to the brain
 blood pressure problems
 altitude sickness
 erectile dysfunction
 asthma
 neuropathy
 cancer
 premenstrual syndrome
 attention deficit hyperactivity disorder (ADHD)
 macular degeneration
Like many natural remedies, ginkgo isn’t well-studied for many of the conditions it’s used for.
Health benefits of ginkgo biloba
Ginkgo’s health benefits are thought to come from its high antioxidant and anti-inflammatory
properties. It may also increase blood flow and play a role in how neurotransmitters in the brain
operate; reduce the risk of peripheral artery disease caused by poor blood circulation; and can be
considered an adjuvant therapy for schizophrenia; may improve erectile dysfunction caused by
antidepressant medication; and may help relieve premenstrual syndrome (PMS) symptoms.
Ginkgo biloba risks
 Ginkgo may cause an allergic reaction in some people. Your risk may be higher if you’re
allergic to urushiols, an oily resin found in poison ivy, sumac, poison oak, and mango
rind.
 Ginkgo may increase bleeding. Don’t use ginkgo if you have a bleeding disorder or take
medications or use other herbs that may increase your risk of bleeding. To limit your
bleeding risk, stop taking ginkgo at least two weeks before undergoing a surgical
procedure.
 Don’t take ginkgo if you’re on any medications that alter clotting. Don’t take it if you’re
taking NSAIDS like ibuprofen, too. Ginkgo can have serious side effects. If you’re on
any medication, let your doctor know the dose you plan on taking.
 Ginkgo may lower blood sugar. Use with caution if you have diabetes or hypoglycemia
or if you take other medications or herbs that also lower blood sugar.
 Don’t eat ginkgo seeds or unprocessed ginkgo leaves; they’re toxic.
 Due to the potential bleeding risk, don’t use ginkgo if you’re pregnant. Ginkgo hasn’t
been studied for use in pregnant women, breastfeeding women, or children.
Other potential side effects of ginkgo are:
 headache
 vomiting
 diarrhea
 nausea
 heart palpitations
 dizziness
 rash
b. Co-enzyme Q10 supplements
Coenzyme Q10 (CoQ10) is a nutrient that occurs naturally in the body. CoQ10 is also in many
foods we eat. CoQ10 acts as an antioxidant, which protects cells from damage and plays an
important part in the metabolism.
CoQ10 has also been studied as a preventive treatment for migraine headaches, though it may
take several months to work. It was also been studied for low sperm
count, cancer, HIV, muscular dystrophy, Parkinson’s disease, gum disease, and many other
conditions. However, the research has not found any conclusive benefits. Although CoQ10 is
sometimes sold as an energy supplement, there is no evidence that it will boost energy in a
typical person.
The amounts of CoQ10 in found naturally in food is much lower than that found in supplements.
Good food sources of CoQ10 include:
 Cold water fish, like tuna, salmon, mackerel, and sardines
 Vegetable oils
 Meats
Side effects from CoQ10 seem to be rare and mild. They include diarrhea, nausea,

and heartburn.
Risks. People with chronic diseases such as heart failure, kidney or liver problems,
or diabetes should be wary of using this supplement. CoQ10 may lower blood sugar
levels and blood pressure. Doses of more than 300 milligrams may affect liver enzyme
levels.
Interactions. People taking blood thinners and thyroid medications as well as chemotherapy
should check with their doctors before using CoQ10 supplements.
Given the lack of evidence about its safety, CoQ10 supplements are not recommended for
children or for women who are pregnant or breastfeeding.
3. Nutritional Diet Therapy

a. Low-carbohydrate or Ketogenic Diet
Ketogenic diet:
 Carbs are limited to 50 grams or less per day.

 Protein is often restricted.
 A major goal is to increase blood levels of ketones, molecules that can partly replace
carbs as an energy source for the brain.
Low-carb diet:
 Carbs can vary from 25–150 grams per day.

 Protein is usually not restricted.
 Ketones may or may not rise to high levels in the blood.
On a ketogenic diet, the brain is mainly fueled by ketones. These are produced in the liver when
carb intake is very low.
On a standard low-carb diet, the brain will still be largely dependent on glucose, although it may
burn more ketones than on a regular diet.
b. Vitamin E Supplements
 Deficiency of vitamin E can produce neurologic disorders, some of which can improve
following administration of vitamin E.
 Vitamin E has antioxidant and neuroprotective effects.
 Vitamin E has been found to be beneficial in the management of some neurologic
disorders not characterized by deficiency of vitamin E.
 Vitamin E is effective as a prophylactic in preventing neurologic complications of some
disorders where its deficiency has been proven to play a causative role.
c. High Dose of Vitamin B12

 Vitamin B12 is a water-soluble vitamin that is naturally present in some foods, added to
others, and available as a dietary supplement and a prescription medication. Vitamin B12
exists in several forms and contains the mineral cobalt, so compounds with vitamin B12
activity are collectively called “cobalamins”. Methylcobalamin and 5-
deoxyadenosylcobalamin are the forms of vitamin B12 that are active in human
metabolism.
 Vitamin B12 is required for proper red blood cell formation, neurological function, and
DNA synthesis. Vitamin B12 functions as a cofactor for methionine synthase and L-
methylmalonyl-CoA mutase. Methionine synthase catalyzes the conversion of
homocysteine to methionine. Methionine is required for the formation of S-
adenosylmethionine, a universal methyl donor for almost 100 different substrates,
including DNA, RNA, hormones, proteins, and lipids. L-methylmalonyl-CoA mutase
converts L-methylmalonyl-CoA to succinyl-CoA in the degradation of propionate, an
essential biochemical reaction in fat and protein metabolism. Succinyl-CoA is also
required for hemoglobin synthesis.
 A deficiency in vitamin B12 causes an accumulation of homocysteine in the blood and
might decrease levels of substances needed to metabolize neurotransmitters
4. Client Education
a. Disease Process
b. Physical Activity
c. Meal Planning
d. Medication Compliance
e. Monitoring Laboratory Test
f. Risk Reduction
g. Psychosocial
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Ervous Ystem: Structural Classification

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NERVOUS SYSTEM

 Monitoring changes. Much like a sentry, it uses its millions of sensory receptors to

 Sensory division. The sensory, or afferent division, consists of nerves (composed of

 Functional classification. Functional classification groups neurons according to the

 Structures. Its structures are the midbrain, pons, and the medulla oblongata.

 Contents. The CSF contains less protein and more vitamin C, and glucose.

 Length. The spinal cord is approximately 17 inches (42 cm) long.

Gray Matter of the Spinal Cord and Spinal Roots

 Projections. The two posterior projections are the dorsal, or posterior, horns; the two

 Endoneurium. Each fiber is surrounded by a delicate connective tissue sheath, an

Spinal Nerves and Nerve Plexuses

 Composition. It is composed of a specialized group of neurons that regulate cardiac

 Preganglionic neurons. The preganglionic neurons of the parasympathetic division are

 Electrical conditions of a resting neuron’s membrane. The plasma membrane of a

 Resting membrane electrical conditions. The external face of the membrane is slightly

 Arrival. The action potential arrives at the axon terminal.

 Signs of sympathetic nervous system activities. A pounding heart; rapid, deep

 Function. This division, sometimes called the “resting-and-digesting” system, is chiefly

II. Application of the Nursing Process

or you have difficulty controlling them. Dysarthria often is characterized

Altered Sleep Disturbed sleeping patterns

Aphasia Or aphemia, is a loss of the ability to produce and/or comprehend

b. Functional Health Patterns

Major Components of the Mental Status Examination

 Emotional facial expression (crying, calm, perplexed, stressed, tense,

Thought Content  Suicidal or homicidal ideations (intent, plan, access to means, time-

Thought Process  Coherence (coherent, incoherent)

rambling, word salad)

Levels of Consciousness: Glasgow Coma Scale

Cranial Nerve Assessment

Test motor branches:

Assessment of Cerebellar Function: Gait & Romberg’s Test

 Lift arms away from side

 Limited range of motion

Reflex Main Spinal Nerve Roots Involved

Reflexes & Spinal Nerve Roots

Rating Reflex Response

A skull X-ray is typically done after

Computed Tomography (CT) Scan Computed tomography (CT scan) uses

Magnetic Resonance Imaging (MRI) Magnetic resonance imaging

the brain generated by hearing, touch, or sight. Evoked

bloodstream. PET scans of the brain are used to detect or

 Carotid Doppler ultrasound is used to measure flow in

b.2 Invasive Tests

Lumbar Puncture Cerebrospinal fluid analysis involves the

The fluid is tested to detect evidence of brain

Myelography Myelography involves the injection of contrast

Cerebral Angiography Angiography is a test that involves injecting dye

A cerebral angiogram can show narrowing or

Provides an image of the blood vessels in the

procedure involves inserting a catheter (a small,

An EMG is usually done in conjunction with a nerve

carries its own risks.

 Doctors may also use a type of blood test called a triple

 Amniocentesis is usually done at 14-16 weeks of

 Chorionic villus sampling is performed by removing and

b.3 Laboratory Examinations

A complete blood count test measures several components

Abnormal increases or decreases in cell counts as revealed