THE MOTOR SYSTEM

The motor system is commonly divided into upper and lower motor neurons. Lesions of the
lower motor neurons - the spinal and cranial motor neurons that directly innervate the muscles - are
associated with flaccid paralysis, muscular atrophy and absence of reflex responses (Figure 38).
Destruction of the upper motor neurons results in spastic paralysis and hyperactive, stretch
reflexes. There are however 3 types of "upper motor neurons" usually considered, namely, the
neurons of the pyramidal system, extrapyramidal system and those from cerebellum. Destruction
in the extrapyramidal posture regulating pathways causes spastic paralysis, but lesions limited to
pyramidal tracts produce weakness rather than spastic paralysis and the affected musculature is
generally hypotonic, whereas cerebellar lesions produce in-coordination. So, the unmodified term,
upper motor neuron is confusing and should not be used.
The motor system controls voluntary movement. In voluntary movement, a muscle can be
made to contract by impulses reaching it by:
1) Synapsing directly upon the alpha motorneurons themselves. This has the advantage of speed
and specificity. Motor neurons to skeletal muscles can be classified into alpha and gamma
motor neurons. These will be described fully later.

2) Synapsing on the muscle spindles via gamma motor neurons and influence the alpha motor
neurons indirectly. This pathway and the pathway above seem always to operate together
(alpha-gamma co-activation).

3) Synapsing on interneurons, the same ones subserving the local reflexes. Although this route is
not as fast as directly influencing motor neurons, it has the advantage of the co-ordination
built into the interneuron net-work as will be described later (e.g. recruitment of synergistic
muscles and reciprocal innervations).

The degree to which each of these three mechanisms is employed varies, depending upon the
nature of the motor task to be performed and the descending pathway that is utilized. As mentioned
already, the descending pathway can be divided mainly into the pyramidal (corticospinal) and
extrapyramidal (rubrospinal, reticulospinal, tectospinal, vestibulospinal) pathways. The first of these
is concerned with skilled, fine movement, the second with gross. The cerebellum and its connections
are concerned with co-ordinating and smoothing movement
Since alpha motor neurons are activated by upper motor neurons and involuntarily by spinal
reflex arrangements, they are called the final common pathway.

Motor axis of the nervous system

 The degree of muscle contraction depends on the number of motor neurons (supplying that
muscle) that are sending action potentials along the motor nerve to that muscle. Relaxation occurs
when there are no action potentials traveling along the motor nerve. (This is in contrast with smooth
muscle where relaxation is brought about by inhibitory transmitters). Whether a motor neuron
generates action potentials or not depends on the relative balance of excitatory and inhibitory inputs
onto the motor neuron cells that are active at any one instance in time. These excitatory and inhibitory
inputs come from nerve terminals of descending fibers from higher centers or from sensory neurons.
(Contract your biceps and then relax it - all you are doing is varying the excitability of the motor
neurons supplying your biceps by consciously activating excitatory pathways or inhibitory pathways!)

SPECTRUM OF MOVEMENTS
Let us now consider the types of movements we make. There is a spectrum of movements. At
one end of the spectrum are the simple automatic movements e.g. withdrawing a hand from a hot
object; at the other end of the spectrum there are highly sophisticated movements which require skill
to perform e.g., dancing, piano playing. Movements are either reflex in origin or are dependent on
innate motor programmes (i.e. the programmes are there at birth).
Reflex movements occur in response to a stimulus and the response is usually a stereotype
(e.g., withdrawal of a limb from a painful stimulus). The neural circuit involved is the reflex arc.
There are short lived and do not involve the conscious mind.
Programme-dependent movements are completely voluntary. They can be modified as they
are occurring (whereas reflexes cannot); they rarely occur in response to a stimulus; they are executed
over a longer period of time and they are affected by attention and motivation.
We are born with a number of motor programmes which are neural circuits within the
cerebral cortex e.g., a motor programme for throwing things. As we get older and use these
programmes repeatedly till the programmes themselves become more and more refined. The
champion darts thrower uses the same basic programme as a baby does when he throws toys out of his
push chair. However, with practice, the basic programme has become more and more sophisticated.
Many people can kick a ball, but very few with such effect as Ronaldo, the footballer! (Practice makes
perfect!), the sophisticated programmes replace the simple ones.
There are however a class of movements that are neither purely reflex nor completely under
voluntary control i.e., they are in the middle of the spectrum. Examples of such movements are those
that are rhythmic in nature e.g., walking, chewing, swimming breathing. These movements can be
initiated and terminated voluntarily (except breathing) but once they are initiated, they proceed
automatically. These rhythmic movements are controlled by the neural circuits called pattern
generators. These pattern generators are intrinsic systems which can be set in motion by sensory
stimuli (e.g., chewing rice and altering the pattern to chew a tough piece of meat) or alternatively by
command signals (i.e. instructions from the conscious mind). The pattern generator for respiration is
found in the brain stem- it is responsible for the rhythmic contraction and relaxation of the respiratory
muscles. (You can change your breathing depth and rate of breathing but you don't have to
consciously contract your muscles every time you want to breathe!). The pattern generator for
walking is found in the spinal cord.
Therefore, movements can be considered to range from the completely automatic to through
the semiautomatic (e.g., walking) to the completely volitional. However, as volitional movements
become more and more learned (e.g., riding a bicycle) they become more and more automatic i.e.,
they tend to move along the spectrum.

MOTOR SYSTEM HIERARCHY

The motor system can be regarded as a hierarchical system and four levels of hierarchy have
been identified. Let us now discuss each of these levels in turn (Figure 38).

The Spinal Cord

The lowest level of the hierarchy is the spinal cord. It possesses the circuitry for the simplest
reflex movements. They include maintenance of muscle tone in response to gravity, the withdrawal of
the hand from a hot object and a variety of autonomic reflexes e.g., bladder emptying. Even when the
cord is disconnected from the brain by injury, the spinal cord reflexes are still present.

The Brain Stem

The brain stem contains neural systems that are necessary for integrating motor commands
coming from the cortex as well as for processing information that ascends from the cord and senses.
The brain stem motor systems participate in more complex reflexes whose afferent fibers are from the
special senses as well as the somatic senses. Examples of reflexes coordinated at the brain stem are
the postural reflexes which enable us to keep our balance. Other reflexes that involve the brain stem
are the startle response i.e., the tensing of the body m response to an unexpected sensory stimulus.
The essence of the brain stem motor systems is also highlighted by the fact that all motor
pathways going down to the spinal cord originate in the brain stem except for one: the corticospinal
tract.

The Primary Motor Cortex

The primary motor cortex is in the premotor gyrus (Brodmann area 4). It is the third level in
the motor hierarchy. The primary motor cortex contains the cell bodies of the pyramidal tract
(corticospinal tract). The pyramidal tract descends and acts on the motor neurons in the spinal cord
i.e., it is the pathway along which command signals are sent to the spinal cord. The motor cortex (via
the corticobulbar tract) also influences the motor nuclei in the brain stem thus influencing the
extrapyramidal system. The primary motor cortex is like an executive organ - it is instructed what to
do (i.e. which pyramidal neurons to fire) by the higher centers like the premotor areas.

The Premotor Areas

The fourth and highest level of the motor hierarchy consists of premotor cortical regions in
Brodmann area 6. These areas are closely connected by association fibers to the prefrontal and
posterior parietal cortices. The premotor areas are responsible for identifying the targets in space, for
choosing a course of action, and for programming movements. The premotor areas act primarily on
the primary motor cortex.

The role of the Basal Ganglia and Cerebellum

In addition to the four levels of motor hierarchy, two other parts of the brain are important for
motor function: the basal ganglia and the cerebellum.
The basal ganglia are subcortical forebrain nuclei that include the caudate nucleus, globus
pallidus and substantia nigra. Neurons from the basal ganglia receive input from wide areas of the
cortex and send output to the reticular formation and cortex. The basal ganglia in co-operation with
the cortex execute subconscious but learned patterns of movements. Without the cerebral cortex,
discrete movements are lost. However, walking, equilibrium, eating, head rotation and every type of
postural movement remains unaffected. Damage to the basal ganglia or to the connections between
them and other motor centers results in a family of movement disorders called dyskinesias. Typically,
these disorders involve spontaneous, repeated, inappropriate movements of entire muscle groups.
Patients may fling their limbs around or exhibit writhing movements or tremors.
The cerebellum is an important destination for sensory information from the muscle spindles,
Golgi tendon organ, the vestibular system and the visual system. All of the output of the cerebellum is
inhibitory. The Cerebellum compares afferent information from the periphery with the motor output
from the cerebral hemispheres and the brain stem and is continually updating and correcting neural
output so that the movement has precision both in time and space. This helps to smoothen and
coordinate movements. Lesion to the cerebellum leads to motor activity that is rough, jerky and
uncoordinated especially for rapid movements.
Each of the above levels of motor control will be discussed in detail later beginning with the
cord.
MOTOR FUNCTION OF THE SPINAL CORD AND THE LOWER BRAIN STEM
We have so far, considered in detail the sensory functions of the central nervous system. To
make use of the sensory information, the nervous system employs the motor mechanism to control
muscles and some of the glands of the body which are collectively called the effectors. The purpose of
this section will be to discuss the motor mechanism beginning with the motor function of the spinal
cord and the lower brain stem. Though most people have an inherent intuition that it is only the
conscious element of the brain that causes muscle movement and other motor activities, this is farthest
from the truth, for perhaps the greater portion of our motor activities is actually controlled by the
lower region of the central nervous system especially the spinal cord and the lower brain stem which
operate primarily at the subconscious level.

Cross section of the spinal cord showing its organisation for motor functions
A cross section through the spinal cord shows that each spinal nerve is formed from two
nerve roots, the posterior nerve root and the anterior nerve root. As in other parts of the CNS, the
grey matter consists of clusters of nerve cell bodies. The white matter consists of nerve fibers. It is
white because of the myelin sheaths of the nerve fibers.
The grey matter is the integrative area for the spinal cord reflexes and other motor functions.
See Figure 39 for the typical organization of the cord grey matter in a single cord segment.

Sensory neuron, association neuron (interneuron) and somatic motor neuron at the spinal cord level

Posterior nerve root - sensory neurons

Sensory signals pass into the cord through the sensory neurons in the sensory roots or
posterior roots. After entering the cord, every sensory signal travels in two separate destinations.
First, either in the same segment of the cord or nearby segments to elicit local segmental responses -
e.g. reflexes. Second, the signals may travel to higher levels of the nervous system; e.g. brain stem
and cerebral cortex. It is these sensory signals that cause the conscious sensory experiences.

Anterior nerve root - alpha and gamma motor neurons

Apart from the sensory relay neurons, the other neurons are divided into two types, the
anterior motor, neurons and the interneurons (internuncial neurons). The anterior motor neurons send
out nerve fibers that leave the cord through the anterior roots and innervate the skeletal muscle fibers.
The motor fibers are of two types; the alpha motor neurons and the gamma motor neurons. The alpha
motor neurons give rise to large, type A alpha (Aα) nerve ranging from 9 to 20 μ in diameter and
passing through the spinal nerves to innervate the skeletal muscle fibers. Stimulation of a single nerve
fiber excites from 3 to 2000 (average of 180) skeletal muscle fibers. A single axon and the group of
muscle fibers it controls are collectively known the motor unit. In addition to the alpha motor
neurons that excite contraction of the skeletal muscle fibers, there are other smaller motor neurons
located along the alpha motor neurons also in the anterior horns. These are called type A gamma
fibers, averaging 5 microns in diameter and send impulses to special skeletal muscle fibers called
intrafusal fibers which make up the muscle spindle.

Interneurons are present in all areas of the cord grey matter - beginning from the dorsal
horns to the anterior horns. Only a few incoming sensory signals to the spinal cord or signals from
the brain terminate directly on the anterior motor neurons. Most of them are transmitted first through
interneurons where they are appropriately processed before stimulating the anterior motor neurons.

Convergence and Divergence: Only a few of the synaptic knobs on a postsynaptic neuron are endings
of any single presynaptic neuron. The inputs to the cell are multiple. In the case of spinal motor
neurons, for example some inputs come directly from the dorsal root, some from the long descending
spinal tracts and many from interneurons, the short interconnecting neurons of the spinal cord. Thus
many presynaptic neurons converge on any single postsynaptic neuron (Figure 40a). Conversely, the
axons of most presynaptic neurons divide into many branches that diverge to end on many
postsynaptic neurons (Figure 40b). So, in convergence, several afferent neurons can synapse on the
same efferent neuron and in divergence an afferent neuron can have branches and synapse on several
efferent neurons. Convergence and divergence allow various phenomena like summation,
facilitation, occlusion, inhibition and after discharge (reverberation) to take place in the central
nervous system.

Convergence and Divergence

After Discharge: This is the persistence of the response after the stimulus is over. This is due to
reverberatory circuits. See diagram (Figure 41) below. On stimulation, the primary path (input) elicits
a response but due to reverberatory circuit (R), which is longer, and carries back some of the output
signals, the excitation continues and the response persists.
After Discharge Circuit

Renshaw cell and recurrent inhibition: Special inhibitory interneurons (Renshaw cells) are found in
the ventral horn of the spinal cord and in close association with motor neurons (Figure 42). Renshaw
cells are stimulated by the terminals of recurrent or collateral branches of a motor neuron axon
returning to the spinal cord. The axon of the Renshaw cell in turn transmits inhibitory signals to
nearby motor neurons. Thus, stimulation of each motor neuron tends to inhibit the surrounding motor
neurons, an effect called recurrent inhibition. This effect is important for the following reason: It
shows that the motor system utilizes the principle of collateral or recurrent inhibition to focus, or
sharpen its signals i.e. to allow unhindered the transmission of the primary signal while suppressing
the tendency for the signals to spread to adjacent neurons.

Circuit diagram for recurrent inhibition of a motor neuron by a Renshaw cell.

Pathways of sensory neurons to motor neurons

Most of the sensory neurons entering each segment of the spinal cord terminate on
interneurons but a very small number of large sensory fibers from the spindles terminate directly on
the anterior motor neurons. So, there are two pathways in the spinal cord that cord reflexes can take:
either directly to the anterior motor neuron itself utilizing a monosynaptic pathway; or through one
or more interneurons first before passing to the anterior motor neuron, thus utilizing a polysynaptic
pathway respectively. The monosynaptic pathway provides an extremely rapid reflex feedback
system and is the basis of the very important stretch reflex. All other cord reflexes utilize bisynaptic
or polysynaptic pathway. Polysynaptic pathways can cause complex reflex patterns. For instance, the
very important protective reflexes called the withdrawal reflex (flexor reflex) and crossed extensor
reflex utilizes this type of pathway.

Multisegmental connections in the spinal cord:

Ascending and descending fibers (propriospinal fibers) of the spinal cord provide pathways
for multi segmental reflexes. These include many reflexes that co-ordinate movements in both the
forelimbs and hind limbs simultaneously.

REFLEXES
A reflex is a stereotype reaction of the central nervous system (CNS) to sensory stimuli.
There are three types of reflexes; the monosynaptic, bisynaptic and polysynaptic reflexes. The basic
unit of integrated neural activity is the reflex arc.

The reflex arc

This arc consists of the following:
i. Receptor (sense organ)
ii. Dorsal root sensory neuron (afferent neuron)
iii. One or more synapses in a central integrating station
iv. The ventral root motor neuron (the efferent neuron) and
v. The effector.

In humans, the connections between the afferent and efferent somatic neurons is in the spinal
cord or in the brain. The afferent neuron enters via the dorsal root or cranial nerves. They have their
cell bodies in the dorsal root ganglia or in the homologous ganglia on the cranial nerves. The efferent
fibers leave via the ventral roots or corresponding motor cranial nerves. The principle that in the
spinal cord the dorsal roots are sensory and the ventral roots are motor is known as the Bell-
Magendie Law.
At the receptor, at the synapse and at the myoneural junction in the arc, there is a non-
propagated graded response that is proportionate to the magnitude of the stimulus. Whereas in
portions of the arc specialized for transmission (axons, muscle membrane) the response is all or none
action potential.

Classification of reflexes
(1) Monosynaptic (2) Bisynaptic and (3) Polysynaptic reflexes.

Monosynaptic reflexes
This has only one central synapse. That means that the sensory fibers make monosynaptic
contacts with alpha motor neurons to the same (homonymous) muscle. It is involved in monosynaptic
stretch reflex. Clinical examples in the body include: knee jerk reflex, biceps reflex, triceps reflex,
supinator (brachioradialis), jerk reflex, jaw (masseter) jerk and angle jerk reflex. Stretch reflexes are
the only monosynaptic reflexes in the body (Figure 43).

Bisynaptic reflex
This has two central synapses. This means that the sensory fibers make bisynaptic contacts
with alpha motor neurons to the same (homonymous) muscle. An example is the Golgi tendon organ
reflex.

Polysynaptic reflex
There have many central neurons or synapses. Examples include: withdrawal (flexor) reflex,
locomotor reflex, sucking reflex, respiratory reflex, cough reflex, cardiovascular reflex, GIT reflexes,
sexual reflexes.
MONOSYNAPTIC REFLEX (THE STRETCH REFLEX)

The stretch reflex

Stimulus: is the stretch of the muscle and the response of the effector is the contraction of the muscle.
The sense organ is the muscle spindle. A muscle spindle measures the instantaneous length of the
muscle and also measures the rate of stretching the muscle. The basis of all muscle movements is the
stretch reflex.

Structure of the muscle spindle (Figures 44 and 45)

Each muscle spindle consists of 2 - 10 muscle fibers enclosed in a spindle shaped capsule.
These fibers are called intrafusal fibers; to distinguish them from the extrafusal fibers which are the
regular contractile units of the muscle. The intrafusal fibers are in parallel with the rest of the fibers.
The ends of the capsule of the spindle are attached to the end of the tendons at the end of the muscle
or to the sides of the extrafusal fibers.
Fiber types: There are two types of intrafusal fibers in the mammalian muscle spindle; the nuclear bag
and the nuclear chain fibers. The nuclear bag fibers contain many nuclei in a dilated central area. The
nuclear chain fiber is thinner and shorter and lacks a definite bag. The ends of the intrafusal fibers are
contractile, whereas the central portion is not.

Innervation
There are two sensory endings in each spindle; the primary (annulospiral) endings and the
secondary (flower spray) endings. The primary endings are the terminations of rapidly conducting
group of Ia afferent fibers that wrap round the nuclear bag and chain fibers. The secondary (flower
spray) endings are terminations of group II sensory fibers and are located nearer the ends of the
intrafusal fibers, probably only on the nuclear chain fibers. The spindles also have a motor nerve
supply on their own. These nerves are 3 – 6 u in diameter, constitute about 30% of the fibers in the
ventral roots and because of their size they are called the gamma efferents of Leksell or gamma motor
neurons.
The endings of the gamma efferent fibers are of two histologic types - the plate endings and
the trail endings. Plate endings are motor end plates on the nuclear bag fibers and the trail endings are
the endings that form extensive networks primarily on the nuclear chain fibers. The muscle spindle
receives two functional types of innervation - dynamic gamma efferents and static gamma efferents.
The dynamic gamma efferents terminate at plate endings and static gamma efferents terminate at trail
endings.
The knee Jerk as an example of stretch reflex.

Mode of operation of muscle spindle

When the muscle spindle is stretched, the primary endings are distorted and receptor
potentials are generated. This in turn sets up action potential in the sensory fiber at a frequency that is
proportionate to the degree of stretching. Since the spindle is in parallel with the extrafusal fibers,
passive stretching of the muscle also stretches the spindle. This initiates a reflex contraction of the
extrafusal fibers in the muscle. The spindle and its reflex connection constitute a feedback device that
operates to maintain muscle length; if the muscle is stretched, spindle discharge increases and reflex
shortening is produced, whereas if the muscle is shortened without a change in gamma efferent
discharge, spindle discharge decreases and the muscle relaxes. Both primary and secondary endings
are stimulated when the spindle is stretched but the pattern of response differs. The nerve from the
primary ending discharges most rapidly while the muscle is being stretched and less rapidly during
sustained stretch. The nerve from the secondary ending discharges at an increased rate throughout the
period when the muscle is in maintained stretch and non-responsive to when it is being stretched.
Thus, the primary ending responds to both changes in length and changes in the rate of stretching
while the secondary ending responds primarily to length alone, i.e. the primary measures length plus
velocity of stretch, and the secondary mainly length (Figure 46).
The importance of the dual response of the primary fiber is that prompt, marked phasic
response helps to dampen oscillations and jerkiness due to conduction delays in the feedback loop
regulating muscle length. These oscillations in this feedback loop are the physiological tremor,
which has a frequency of approximately 10 Hz. This tremor would have been worse if not for the
sensitivity of muscle spindle to the velocity of muscle stretch.

Effects of gamma efferent discharge:

Stimulation of gamma efferent system does not lead directly to detectable contraction of the
muscle, because the intrafusal fibers are not strong enough or plentiful enough to cause shortening.
However, stimulation causes the contractile ends of the intrafusal fires to shorten and therefore stretch
the nuclear bag portion of the spindle, deforming the annulospiral endings initiating impulses in the Ia
fibers. This in turn can lead to reflex contraction of the muscle.
In summary, there are two ways to elicit contraction of muscles. These are: i) via a
stimulation of the alpha motor neurons that innervate the extrafusal fibers, ii) via the gamma efferent
neurons that initiate contraction indirectly via the stretch reflex.
 There is considerable evidence that there is increased gamma efferent discharge along with
increase in the alpha motor neurons, which initiate movement. Because of this "alpha-gamma linkage
or coactivation", the spindle shortens (i.e. in slight tension) during muscle contraction. The existence
of dynamic and static efferents has already been mentioned. Stimulation of the dynamic gamma
efferents, which may end via plate endings on nuclear bag fibers increases spindle sensitivity to the
rate of change of stretch. Stimulation of the latter, possibly via trail endings on nuclear chairs fibers,
increases spindle sensitivity to steady maintained stretch. It is thus possible to adjust separately the
responses to phasic and tonic events.
The purpose of contracting muscle spindle same time as large skeletal muscle fibers:
1) keeps the length of the receptor portion of the spindle from changing and therefore keeps the
muscle spindle from opposing muscle contraction
2) maintains proper damping function of the muscle spindle regardless of change in muscle
length. For instance, if the muscle spindle should not contract and relax along with the large
muscle fibers, the receptor portion of the spindle would sometimes be flail and at other times
be overstretched, in neither instance operating under optimal conditions for spindle function.

Muscle spindle, showing its relation to the large extrafusal skeletal muscle fibers. Note also both the
motor and the sensory innervations of the muscle spindle and the extrafusal large muscle fibers
Simplified diagram of the central region of the muscle spindle to show the relation to the two kinds of
afferent ending to the two kinds of intrafusal fiber

Diagrammatic comparison of the typical responses of primary and secondary endings to large
stretches applied in the absence of fusimotor activity

Clinical significance of eliciting the stretch reflex

If the reflex can be demonstrated, it is certain that all the components of the reflex are
working well. Both sensory and motor connections are intact between the muscle and the spinal cord.
For example, in tabes dorsalis, the dorsal fibers of the stretch reflex are destroyed, the patient has
marked disturbance in posture. Also, in poliomyelitis the ventral root containing the alpha motor
neuron is destroyed by virus. Poliomyelitis results in muscle paralysis. In these disorders where the
ventral root or dorsal roots are destroyed, the knee jerk is absent. The presence of knee jerk also
indicates that the lumbar level (L2, 3, 4) of the spinal cord and the muscle fibers of the rectus femoris
are fine. Similarly, ankle jerk tests L5 to S2, Jaw jerk tests Pons and V, Biceps jerk tests C5 and C6,
Triceps jerk tests C7 and C8.
The stretch reflex also helps to determine the degree of excitability of the spinal cord. When a
large number of facilitatory impulses are being transmitted from the brain to the spinal cord e.g. by
lesion in the contralateral areas of the cerebral cortex and basal ganglia caused by tumour or stroke.
The stretch reflex will be so active at times that simply tapping the patellar tendon with the tip of
one's finger might make the leg jump a foot or more. On the other hand, the cord may be intensely
inhibited by other impulses from the brain, in which case almost no degree of stretch can elicit a
response.
Using this method of assessment, it is possible to test the function of many spinal nerves and
spinal cord segments and some of the cranial nerves and brain segments in a short time. If
abnormality of excitability is detected, further tests are required to determine the nature and location
of the pathologic process.

Role of stretch reflex in muscle tone and posture

The natural stimulus for stretch reflex is gravity. In patellar tendon reflex, the quadriceps
muscle is under maintained pull by gravity and this induces repetitive firing of stretch receptors
(muscle spindle) and results in sustained, smooth contraction (muscle tone) which is of significance to
posture. So, muscle tone (tonic contraction) of the muscle which is a consequence of the stretch reflex
helps to maintain posture.

BISYNAPTIC REFLEX
 A good example is the Golgi tendon organ reflex (Figure 47). It can also be called inverse
stretch reflex or clasp knife reflex. This stimulus is due to increase in muscle tension generated
during muscle contraction. These receptors are Golgi tendon organs, which occur in the tendons of
skeletal muscles just beyond the point where muscle fibers and tendon tissues fuse. In contrast to the
spindle, receptors which are connected in parallel to muscle fibers, the Golgi tendon organs are
attached "in line" or in "in series" with the muscle cells. There is only one interneuron in the spinal
cord. This interneuron is inhibitory. Contraction of the muscle exerts a direct pull on the Golgi tendon
organ. The sensory fibers (I b) that supply Golgi organs respond by firing more frequently. These
sensory nerve fibers transmit their action potentials to the spinal cord where they synapse with the
inhibitory interneurons. These inhibitory interneurons inhibit the alpha motor neurons that cause the
muscle to relax.

Function of the Golgi tendon organ reflex

They protect against overloading of the muscle, thereby preventing damage of the tendon. If
the tension generated by the muscle becomes extreme e.g. by excessive muscle contraction, the high
level of activity of the Golgi organs can cause a sudden relaxation of the muscle by blocking large
numbers of alpha motor neurons.

Golgi tendon organ reflex

POLYSYNAPTIC REFLEXES

The flexor reflex or withdrawal reflex

Excitation of pain endings of a limb via pin prick, heat or some other painful reason may
probably cause the flexor muscle of the limb to contract strongly, thereby withdrawing the limb from
the stimulus. This is called the flexor reflex, nociceptive reflex, pain reflex or withdrawal reflex. Note
that the receptors for this reflex are pain receptors in the skin.

Neuronal mechanism of the flexor reflex

The pathways for eliciting the flexor reflex do not pass directly to the anterior motor neurons,
but instead, pass first into the interneuron pool of neurons and then to the motor neurons. The shortest
possible circuit is a three-neuron arc; however, most of the signals of the reflex pass through many
more neurons than this and involve the following types of circuit (Left hand portion of Figure 48):

(1) diverging circuits to spread the reflex to the necessary muscle for withdrawal;
(2) circuits to inhibit the antagonist muscles called reciprocal inhibition circuits for example
stimulation of the sensory nerve of the right limb results in simultaneous stimulation of the
 ipsilateral (same side) flexor motor neuron (F) via excitatory interneurons (2a &b) and
inhibition of the ipsilateral extensor motor neuron (E) via inhibitory interneuron (1); see
diagram (Figure 48) below.
(3) circuits to cause a prolonged repeated firing called after-discharge even after the stimulus is
over. This after discharge is due to continued bombardment of motor neurons by impulses
arriving by complicated and circuitous polysynaptic paths.
Thus the flexor reflex results in contraction of the flexor and relaxation of the extensor and
the effect is withdrawal of the stimulated part from the painful stimulus. Furthermore, because of the
after discharge it will hold the irritated part away from the stimulus for as long as I to 3 seconds even
after the irritation is over. During this time, other reflexes and actions of the central nervous system
can move the entire body away from the painful stimulus.

The crossed extensor reflex

Soon (0.2 to 0.5 sec.) after a strong stimulus elicits a flexor reflex in one limb, the opposite
limb begins to extend. This is known as crossed extensor reflex. Extension of the opposite limb
obviously can push the object causing the painful stimulus away from the body. The receptors are also
pain receptors.

Neuronal mechanism of the crossed extensor reflex

The right hand portion of Figure 48 (below) illustrates the neuronal circuit responsible for the
crossed extensor reflex, showing that signals from the sensory nerves decussate to the opposite side of
the cord to cause exactly opposite reactions to those that cause the flexor reflex. Because the crossed
extensor reflex usually does not begin until many milliseconds (200 - 500 milliseconds - or 0.2 to 0.5
seconds) following the initial pain stimulus, it is certain that many internuncial neurons are in the
circuit between the incoming sensory neuron and the motor neuron of the cord responsible for the
crossed extension. Thus, the crossed extensor reflex results in extension of the limb on the side
opposite of the stimulation and the effect is withdrawal of the body from the painful stimulus.
Moreover, after removal of the the painful stimulus, the crossed extensor reflex persists for
even longer period of after discharge than that of the flexor reflex. The prolonged after discharge is of
huge importance in keeping the entire body away from the painful object until other neurogenic
reactions should cause the body to move away. The crossed extensor reflex is adaptive in that it helps
prevent falls by shifting the weight of the body from the affected to the unaffected limb.

Reciprocal inhibition
A very important feature of most reflexes, especially illustrated by the flexor and crossed
extensor reflex is the phenomenon called reciprocal inhibition (Figure 48). That is, when a reflex
stimulates a muscle, it ordinarily restrains the antagonist muscle at the same side. Even in the stretch
reflex (Figure 49), the antagonist muscle is inhibited by reciprocal innervation. Using the flexor reflex
as an example, when the flexor reflex excites the biceps muscle it simultaneously inhibits the
opposing triceps muscle. Also, the crossed extensor reflex excites the triceps but inhibits the biceps.
All parts of the body where opposing muscles exist, a corresponding reciprocal inhibition circuits is
present in spinal cord. This obviously allows greater ease in the performance of desired activities. The
nerve pathway for reciprocal inhibition is called reciprocal innervation.
All the reflexes mentioned above can be modified by influences descending from higher
centers e.g. the brain. For instance, if you touch a hot plate and do not want to drop and break it, you
can keep holding it at the expense of burning your fingers. The stretch reflex can also be modified by
higher centers. For instance, when it is difficult to elicit stretch reflexes in some healthy individuals,
ask them to clench their teeth as you are tapping and you will find that the reflex becomes
exaggerated. This is the Jendrassik maneuvre and is due to descending pathways that activate
gamma motor neurons.
Spinal cord circuitry responsible for the flexion reflex. Stimulation of the cutaneous receptors in the
foot leads to activation of spinal cord local circuits that withdraw (flex) the stimulated extremity and
extend the other extremity to provide compensatory support

Circuit diagram of a monosynaptic stretch reflex showing reciprocal inhibition

Autonomic Reflexes
By analogy with the somatic motor system in which the motor neuron is the final common
pathway, the preganglionic sympathetic and the parasympathetic neurons can be regarded as the final
common pathway of the autonomic system. The afferents are the same for both somatic and
autonomic systems (except proprioceptive afferents). Most reflexes have an autonomic and somatic
component. An example of an autonomic reflex is vomiting and the baroreceptor reflex. Micturition
and defaecation are autonomic reflexes which have a somatic component and involve the spinal cord.
EFFECTS OF SURGICAL REMOVAL OF THE HIGHER NERVOUS CENTERS
Normally, the operations of the spinal cord are strongly controlled by signals from the brain.
Therefore, to study the isolated reflexes, it is necessary to separate the cord from the higher centers.
This is usually done in two different types of preparations namely: (1) the Spinal animal (2) the
Decerebrate animal.

The spinal animal is prepared by severing the spinal cord at any level above which the
reflexes are to be studied. For a variable period of time depending on the animal, the cord reflexes are
depressed (spinal shock). Spinal shock is the result of the sudden withdrawal of the descending
impulses from the higher brain centers e.g. via reticulospinal, vestibulospinal and corticospinal tracts.
This lasts few minutes in frogs, 1-2 hours in cats, and a minimum of 2 weeks in man, before the cord
reflexes become progressively more active and can be studied independently of control by the higher
levels of the nervous system. Cord reflexes especially, flexor and crossed extensor reflexes are
usually more excitable after this preparation. The animal is able to support its weight for a short
period of time (spinal standing). This is because spinal animals exhibit positive supporting
reactions. For example, if your finger is placed on the sole of the foot of a spinal animal, the limb
usually extends following the finger as it is withdrawn (positive supporting reaction). It involves
proprioceptive as well as tactile afferents and transforms the limb into a rigid pillar to resist gravity
and support the animal. If the animal is suspended in the air, alternating flexion and extensions of the
legs are seen (spinal stepping). Other effects include:

a) loss of voluntary movement below the level of section;

b) loss of sensation;
c) spinal autonomic reflexes become automatic i.e. micturition reflexly occur when the bladder
is full, due to loss of control of external sphincter (voluntary muscle);
d) mass reflex - mild noxious sensory stimuli lead to irradiation to the spinal autonomic centers
resulting in sweating, increase in blood pressure, defaecation and micturition. There is also
strong flexor spasm.
The centers for these reflexes (supporting reaction, mass reflexes, spinal autonomic reflexes) are in
the spinal cord.
In the Decerebrate preparation (Figure 50), the brain stem is usually transected between the
superior and inferior colliculi of the midbrain. The transection removes the influence of the voluntary
control centers of the forebrain as well as the inhibitory influence of the basal ganglia. The excitatory
output of the reticular formation below the transection is left unhindered. Removal of the inhibition of
the basal ganglia and the retention of the excitatory effect of the reticular formation cause immediate
increase in the activity of the cord reflexes especially the extensors that help the animal hold itself
against gravity. In contrast to spinal animal, it is capable of standing for a very long period of time
and may even walk. The animal has greater control of posture but cannot right itself when placed on
its back or side i.e. righting reflexes are absent. So, decerebration uncovers the tonic stretch reflex
mechanisms that .support the animal against gravity. It also exhibits tonic labyrinthine reflexes
and tonic neck reflexes.

Decerebrate rigidity
Tonic labyrinthine reflexes
To demonstrate the role of the labyrinths in tonic postural reflexes, a plaster of Paris around
the neck of the animal is used to fix the head in relation to the trunk, so that the neck proprioceptors
will not be stimulated. The tone of the various muscles of the body varies depending on whether the
animal is lying in the prone, supine or lateral position. For instance, if the animal is placed on its
back, the extension of all the four limbs is maximal. When it is prone, it is minimal. When it is
sideways it is intermediate. These changes in rigidity (tonic labyrynthine reflexes) are initiated by the
action of gravity (stimulus) on the otholithic organs (receptors) and are effected through
vestibulospinal tracts. Their physiologic significance is unknown.

Tonic neck reflexes (Figure 51)

The tone of the muscles of the body also varies depending on the position of the head in
relation to the trunk. If the labyrinths of decerebrate animals are destroyed and the neck is free to
move, it is found that changing the position of the head in relation to the trunk evokes a reflex
redistribution of tone in various muscle groups. For instance, if the head is moved relative to the body
(stimulus), the input from neck proprioceptors (receptors) produces tonic neck reflexes. For instance,
if the head is tilted upwards and backwards, the hind limbs become flexed and the animal sits down. If
the head is tilted down, the forelegs bend and the animal adopts a posture reminiscent of feeding. If
the head is rotated upon the neck,, the ipsilateral forelimb flexes and the contralateral forelimb
extends. Other effects include:
a) loss of sensation
b) respiration and cardiovascular control are retained.
The centers for these (i.e., tonic labyrinthine reflexes and tonic neck reflexes, respiration and CVS
controls) are in the medulla.
These two preparations namely, the spinal and decerebrate animals show that a greater
portion of our motor activities are actually controlled by the lower region of the central nervous
system, especially the spinal cord and the lower brain stem which operate primarily at the
subconscious level.

Tonic neck reflexes

ROLE OF THE BRAIN STEM IN CONTROL OF MOTOR FUNCTION

Physiologic anatomy of the brain stem

The brain stem links spinal cord and cerebrum and is composed of three regions - the medulla
oblongata, pons and midbrain.
The medulla oblongata is continuous with the spinal cord and contains the same fibre tracts.
The Grey mater, however, is not organised in a continuous column but is broken into discrete nuclei,
including motor and sensory nuclei for the pharynx, mouth and neck, and nuclei involved in the
control of the respiratory and cardiovascular systems and of movement and posture.
The pons may be recognised on the ventral surface by the bulged brainstem formed by axons
descending from the cerebrum and turning up into the cerebellum which, in the intact brain, conceals
the dorsal surface of the pons. The pons is continuous with the medulla and contains the same
ascending and descending tracts in the reticular grey mater (reticular formation). It also contains
nuclei that are involved in the control of respiratory system and in motor and sensory function of the
face.
The midbrain, the smallest part of the brain stem is continuous with the pons below and the
diencephalon above. The ventral surface usually referred to as tegmentum or covering is characterised
by the large cerebral peduncles lying laterally and carrying axons from the cerebrum to the brain stem
and to cerebellum. Substantia nigra (of the basal ganglia mainly located in the white matter of the
cerebrum) lies in the ventral surface of the mid brain. The ventral surface i.e. tegmentum also contains
the red nucleus. The dorsal surface usually referred to as the tectum or roof may be recognised by two
pairs of the superior and inferior colliculi. The superior collicular neurons are concerned with of
visual information and the inferior collicular neuron with auditory signals. The midbrain also contains
nuclei concerned with the state of wakefulness of the brain and ascending tract from the spinal cord
on their way to the diencephalon.
From the brainstem, the various cranial nerves have their superficial origin at different levels.
There are twelve pairs of these and they innervate the skin and muscles of the face, structures in the
head and neck and, in the case of vagus (X) nerve, the thoracic and many other abdominal viscera.
Strictly speaking, the olfactory (I) nerves are connected to the fore brain, and not the brain stem. The
optic (II) nerves are joined to the diencephalon by "the optic chiasma. Cranial nerves pairs III and IV
emerge from the mid brain, V - VIII from the pons and the remaining four pairs from the medulla.
The nuclei from which these cranial nerves have their origin may extend through a
considerable length of the brain stem. Note that many of these nerves contain a mixture of fibres,
motor and sensory, somatic and autonomic. (Table 6)
The afferent fibres (mainly V, VIII, IX, X) arise from ganglion cells outside the brain stem
(c.f. dorsal root ganglion in spinal cord) and send branches to "nuclei of termination" on each side in
the brain stem grey mater. These nuclei send fibres in the reticular formation to the thalamus and to
the cerebellum and motor cortex.
The efferent fibres arise directly from nuclei of origin which are discrete clumps of cell
bodies in the brain stem (III, IV, V, VI, VII, XII) or from the nucleus ambiguus in the medulla (IX, X,
XI), All these motor nuclei receive descending crossed cortico-nuclei fibre connections.

Special interest
For years, anatomy students have used the following mnemonic (memory) device to
remember the names and associated number of the cranial nerves: "on old Olympus tiny tops, a
Finn and German viewed some hops." The sentence has twelve words. Note the first letter of each
consecutive word in the sentence is the same as the first letter of cranial nerves I and XII:
Olfactory (I), sensory
Optic (II), sensory
Oculomotor (III), motor
Trochlear (IV), motor
Trigeminal (V), both (mixed)
Abducens (VI), motor
Facial (VII), both (mixed)
Acoustic (vestibulocochlear, VIII), sensory
Glossopharyngeal (IX), both (mixed)
Vagus (X), both (mixed)
Spinal accessory (XI), motor
Hypoglossal (XII), motor
Cranial nerve VIII is sometimes called the acoustic nerve, emphasizing its hearing function.
Another mnemonic device is similarly used for the functional classification of the cranial
nerves I-XII as sensory, motor, or both (mixed): Sister say marry money, but my brother say bad
business marry money."

Functions of the brain stem include the following:

1. Control of respiration
2. Control of the cardiovascular system
3. Control of gastrointestinal function
4. Control of many stereotyped movements of the body
5. Control of equilibrium
6. Control of eye movement
Finally, the brain stem serves as a way station for "command signals" from still higher centers that
control functions throughout the body.

The cranial nerves

S/No NAME FIBRES COMMENTS ORIGIN IN BRAIN
I Olfactory nerve Afferent Tract of brain. Carries input from receptors in Forebrain
olfactory (smell) epithelium.
II Optic nerve Afferent Tract of brain. Carries input from receptors in Diencephalon via optic
eye. chiasma
III Oculomotor nerve Efferent Innervates skeletal muscles that move eyeball up,
(Autonomic) down, and medially and raise upper eyelid;
innervates smooth muscles that constrict pupil
and alter lens shape for near and far vision. Midbrain
IV Trochlear nerve Efferent Innervates skeletal muscles that move eyeball
downwards and laterally (superior oblique).
V Trigeminal nerve Efferent Innervates skeletal chewing muscles.
Afferent Transmits information from receptors in skin of
chin, auricle and temporal region; skeletal
muscles of face, nose, and mouth; and teeth
sockets.
VI Innervates skeletal muscles that move eyeball Pons
Abducens nerve Efferent laterally (lateral rectus).

VII Innervates skeletal muscles of facial expression

Facial nerve Efferent and swallowing; innervates nose, palate, and
(Autonomic) lacrimal and salivary glands.
Afferent Transmits information from taste buds in front of
tongue and mouth.
VIII Vestibulocochlear Afferent Transmits information from receptors in ear
Nerve hearing and balance).
IX Efferent Innervates skeletal muscles involved in
Glossopharyngeal swallowing and parotid salivary gland.
nerve Afferent Transmits information from taste buds at back of
(Autonomic) tongue and receptors in auditory-tube skin. Medulla
X Vagus nerve Efferent Innervates skeletal muscles of pharynx and
(Autonomic) larynx and smooth muscle and glands of thorax
and abdomen.
 Afferent Transmits information from receptors in thorax
and abdomen.
XI Accessory nerve Efferent Enervates neck skeletal muscles.

XII Hypoglossal nerve Efferent Innervates tongue, skeletal muscles.

Motor control function of the brain stem

In the following sections, we discuss the role of the brain stem in controlling whole-body
movement and equilibrium. Especially important for these purposes are the brain stem's reticular
nuclei and vestibular nuclei.

Support of the body against gravity - Roles of the Reticular and Vestibular Nuclei
Excitatory-Inhibitory Antagonism between Pontine and Medullary Reticular Nuclei
Figure 53 below shows the locations of the reticular and vestibular nuclei. The recticular
nuclei are divided into two major groups: (a) the pontine reticular nuclei located slightly posteriorly
and slightly laterally in the pons and extending into the mesencephalon (mid brain) and (b) the
medullary reticular nuclei, which extend the entire extent of the medulla, lying ventrally and medially
near the midline. These two sets of nuclei function mainly antagonistically, to each other, the pontine
exciting the antigravity muscles and the medullary inhibiting them. The pontine reticular nuclei
transmit excitatory signals downward into the cord through the pontine reticulospinal tract, located in
the anterior column of the cord as shown in Figure 53. The fibers of this pathway terminate on the
medial anterior motor neurons that excite the axial muscles of the body, which support the body
against gravity - that is, the muscles of the vertebral column and the extensor muscles of the limbs.
The reticulospinal fibres end in the gamma motor neurons of the anterior gray horn through
internuncial neurons.

la) Pontine Reticular system

The pontine reticular nuclei have a high degree of natural excitability. In addition, they
receive especially strong excitatory signals from the vestibular nuclei as well as from the deep nuclei
of the cerebellum. Therefore, when the pontine reticular excitatory system is unopposed by the
medullary reticular system it causes powerful excitation of the antigravity muscles (i.e. muscles of the
vertebral column and extensors of the limbs) throughout the body, so much so that four-legged
animals can then be placed in a standing position, supporting the body against gravity without any
signals from still higher levels of the brain.

Ib) Medullary Reticular System

The medullary reticular nuclei, however, transmit inhibitory signals to the same antigravity
anterior motor neurons by way of a different tract, the medullary reticulospinal tract, located in the
lateral column of the cord, as also shown in Figure 53. The medullary reticular nuclei receive strong
input collaterals from (1) the corticospinal tract, (2) the rubrospinal tract, and (3) other motor
pathways. These normally activate the medullary reticular system, so that under normal conditions,
the body muscles are not abnormally tense.
Yet signals from higher areas of the brain can "disinhibit" the medullary system to cause
standing. At other times, excitation of the medullary reticular system can inhibit antigravity muscles
in certain portions of the body to allow those portions to perform special motor activities, which
might be impossible if the antigravity muscles opposed the necessary movements.
Therefore, the excitatory and inhibitory reticular nuclei constitute a controllable system that is
manipulated by motor signals from the cortex and elsewhere to provide the necessary background
muscle contractions for standing against gravity and yet to inhibit appropriate groups of muscles as
needed so that other functions can be performed as required.

2) Vestibular Nuclei in motor function.

The vestibular nuclei usually function in association with the pontine reticular nuclei to excite
the antigravity muscles (i.e. muscles of the vertebral column and extensors of the limbs). The lateral
vestibular nuclei transmit strong excitatory signals by way of both the lateral and the medial
(anterior} vestibulospinal tracts in the anterior column of the spinal cord as shown in Figure 53. In
fact, without this support of the vestibular nuclei, the pontine reticular system loses much of its
excitation of the axial antigravity muscles. The vestibular nuclei receive impulses concerned with
muscle tone and posture from vestibular apparatus and cerebellum. The specific role of the vestibular
nuclei, however, is to control selectively the excitatory signals to the different antigravity muscles to
maintain equilibrium in response to signals from the vestibular apparatus and cerebellum. The medial
vestibulospinal tract however stops at cervical spine. Lesion of reticulospinal or vestibulospinal tracts
affects the ability to maintain erect posture.

3) Rubrospinal tract
This tract arises from cells of the posterior part of the red nucleus in the midbrain. It is so
called because it is highly vascularised. The large diameter fibers cross immediately and run down the
contralateral side of the brainstem and spinal cord. Their terminals are distributed similarly to those of
the corticospinal tract. The red nucleus receives input from the cerebral cortex and the dentate and
intermediate nuclei of the cerebellum. It is one of the descending tracts through which the cerebellum
influences movement (Figure 53). This tract exhibits facilitatory influence upon the flexors.

4) Tectospinal tract
This tract originates in the rnidbrain in the region of the superior colliculus. It is a crossed
pathway and the fibers terminate on interneurons in the cervical cord. At its origin, it receives input
from the cerebral cortex, especially the occipital lobe, and from the superior colliculus. The pathway
seems to generate head movements to help direct one's gaze at a particular point. This tract projects no
further than the cervical spine (Figure 53).

Decerebrate rigidity
The relationship between the cerebral cortex, the reticular formation, and the gamma motor
neurons can be demonstrated by separating the cerebral hemispheres from the brain stem (Figure 54).
This is done by sectioning between the superior and inferior colliculi of the mid brain
(Decerebration). This operation removes the inhibitory centers notably, the basal ganglia above the
cut leaving the pontine and medullary reticular system as well as the vestibular system intact. The
animal develops a condition called decerebrate rigidity.
The extensor muscles are particularly affected by the unimpeded excitatory output of the
reticular formation acting on the gamma motor neurons. The continuous firing of these motor neurons
results in the tetanic contractions of the muscles by way of the gamma loop.
The reflexes exhibited by the decerebrate animal have already been described under spinal
cord reflexes. We shall see later that other types of rigidity occur in other neuromotor diseases
especially lesions in the basal ganglia.
 (a)

The principal motor pathways arising in the brain: (a) shows the arrangement of the major
descending motor tracts and the approximate location of the main motor nuclei, (b) shows the
position of the major pyramidal and extrapyramidal descending pathways within the spinal cord.

CORTICAL CONTROL OF MOTOR FUNCTION

The cerebral cortex is a paired structure in the forebrain that is found only in mammals and is
largest (relative to body size) in humans. Its most distinctive anatomical features are (i) the very
extensive internal connections between one part and another part, and (ii) its arrangement as a six-
layered sheet of cells, many of which cells are typical Pyramidal cells. Although the crumpled, folded
surface of this sheet is responsible for the very characteristic appearance of the brains of large
mammals, the cortex of small mammals tends to be smooth and unfolded. Where folds occur, each
fold or gyrus is about ½ cm in width.
 All "voluntary" movements initiated by the cerebral cortex are achieved by cortical activation
of “patterns" of function stored in lower brain areas - in the cord, brain stem, basal ganglia, and
cerebellum. These lower centers in turn send specific activating signals to the muscles.
Yet, for a few types of movements, the cortex does have almost a direct pathway to the
anterior motor neuron of the cord, bypassing other motor centers on the way, especially for control of
the dexterous movements of the fingers and hands.

Functional Histology of the Cerebral Cortex

More than 90% of the cerebral cortex is of this basic 6-layered type, which in phylogeny first
appears with the mammals and therefore is called neocortex; because of its structure, it is also called
isocortex. The phylogenetically older allocortex has a basically 3-layered structure. Located deep in
the temporal lobe, it is not visible from outside the brain. It includes the archipallium (fascia dentate,
Ammon's horn, subiculum), the paleopallium (prepiriform region, periamygdalar region, entorhinal
region) and the cortical derivatives claustrum and amygdala. The layers in the isocortex, counting
from the surface down, are as follows (Figure 55).
Layer I. Molecular layer, which contains numerous dendrites, axons, and glia cells.
Layer II. External granule layer, consisting of small densely packed cells (granules) which are round,
polygonal, or triangular in shape.
Layer III. External pyramidal layer, which contains large pyramidal cells, usually increasing in size
from without inwards.
Layer IV. Internal granule layer, resembling layer II.
Layer V. Internal pyramidal layer. Basically composed of medium-sized and large pyramidal cells,
especially large in the precentral gyrus (Betz's giant pyramidal cells). Like all pyramidal cells these
have long apical dendrites, extending as far as the molecular layer, whereas the basal dendrites spread
out more or less tangential to the surface.
Layer VI. Fusiform-cell layer, predominantly spindle-shaped neurons. The inner part of this layer (VI
b) merges with the white matter

Cortical maps: Although the basic structural pattern of the isocortex is uniform, there can be
considerable local variation. On jthe basis of cortical cytoarchitectonics alone – that is the density,
arrangement and shape of the neurons – Brodmann subdivided the cerebral cortex into about 50 areas
(see Figure 12). Other maps are still more detailed (VON ECONOMO and VOGT). To a certain
extent, these histologically defined areas match the areas to which particular functions are ascribed on
the basis of physiological experiments and clinical observations.

Homotypical and heterotypical isocortex

VON ECONOMO grouped the cytoarchitectonic cortical areas into five types (Figure 55).
The types 2, 3 and 4 in the diagram of the Figure confirm (to varying extents) all 6 layers, and
therefore are called homotypical. By contrast, in mature cortex of types 1 and 5 fewer than 6 layers
are clearly identifiable; the cortex is heterotypical. In the heterotypical cortex of type 1 there are no
distinct granular layers (II and IV), whereas in 5 these layers are especially conspicuous, and the
pyramidal-cell layers (III and V) are very poorly developed. Therefore type 1 is called agranular
cortex and type 5, granular cortex or koniocortex (Greek konios = dusty, from the dark band of
granular cells in layer IV).
Agranular cortex is found particularly in regions where cortical efferents originate, for
example, in the pre-central gyrus and rostral to it. It can thus be regarded as the prototype of the
motor cortex. Conversely, the granular or koniocortex is found especially in areas in which the major
sensory pathways terminate. It can therefore be classified as the prototype of the sensory cortex. The
unspecific cortex comprises the various forms of homotypical cortex. There are gradual transitions
between the different types of cortex. The parts of the frontal cortex labeled "2" in Figure 55 and the
anterior half of the cingulated gyrus are now thought to be better classified as heterotypic cortex and
are called dysgranular.
Diagram of the five fundamental types of structure found in the cerebral cortex. (Economo.
Cytoarchitectonics of the Human Cerebral Cortex)

The motor cortex

Anterior to the central cortical sulcus, occupying approximately the posterior one third of the
frontal lobes, is the motor cortex. Posterior to the central sulcus is the somatosensory cortex, an area,
which feeds into the motor cortex many of the signals that initiate motor activities. The motor cortex
itself is further divided into three sub-areas, each of which has its own topographical representation of
muscle groups and specific motor functions of the body: (1) the primary motor cortex, (2) the pre-
motor area, and (3) the supplementary motor area.
Afferent projections to the motor cortex (Incoming fiber pathways to the motor cortex). The
motor cortex receives information from many parts of the brain and spinal cord:
1. Dorsal column afferents from skin touch receptors and proprioceptors via the thalamus
2. Intracortical projections from the somatosensory cortex
3. The posterior parietal cortex (this coordinates information from all sense organs), including
visual and auditory cortices
4. From the cerebellum via the thalamus.
5. From the basal ganglia via the thalamus.

Efferent projections from the motor cortex (fiber pathways from the motor cortex include the
tracts of the following areas) (Figure 56):
1. To spinal interneurones and motor neurons via the pyramidal tract (or corticospinal tract) also
give motor signals to the basal ganglia, brain stem and cerebellum.
2. To cranial nerve nuclei via the corticonuclear tract.
3. To brain stem motor nuclei via the corticobulbar tract.
4. To the striatum (part of the basal ganglia) via the corticostriatal tract.
5. To the cerebellum via the cortico-pontine-cerebellar tract
Major efferent projections from the motor cortex

Primary Motor Area

The primary motor area or cortex lies just in front of the central sulcus or groove mostly in
the precentral gyrus or ridge. It corresponds to Brodmann's area 4. It is sometimes simply called
"Motor Cortex". It has a topographical representation of the different muscle areas of the body (Motor
homunculus). The degrees of representation of the different muscle area shows that it has a large
presentation for fingers and thumb as well as muscle of speech (These muscles are in constant use).
The primary motor cortex controls contralateral movements, mainly the distal limbs and digits for
discrete movements (Figures 14 and 57).

Motor and somatosensory functional areas of the cerebral cortex. The numbers 4, 5, 6, and 7 are
Brodmann's cortical areas

Premotor Area (Motor Association Area)

The premotor area (Brodmann's area 6) lies immediately anterior to the primary motor cortex,
projecting 1 to 3 centimeters anteriorly and extending inferiorly into the Sylvian fissure and superiorly
into the longitudinal fissure, where it abuts the supplementary motor area, which has functions similar
to those of the premotor area. The topographical organization of the premotor cortex is roughly the
same as that of the primary motor cortex, with the mouth and face areas located most laterally and
then moving upward, the hand, arm, trunk, and leg areas.
Nerve signals generated in the premotor area cause much more complex “patterns" of
movement than the discrete patterns generated in the primary motor cortex. For instance, the "pattern"
may be to position the shoulders and arms so that the hands become properly oriented to perform
specific tasks. To achieve these results, the posterior premotor cortex then sends its signals either
directly to the primary motor cortex to excite multiple groups of muscles or, often, by way of the
basal ganglia and then back through the thalamus to the primary motor cortex. Thus, the premotor
cortex, basal ganglia, thalamus, and primary motor cortex constitute a complex overall system for
control of the body's complex patterns of coordinated muscle activity (Figure 57).

Supplementary Motor Area

The supplementary motor area has still another topographical organization for control of
motor function. It lies mainly in the longitudinal fissure but extends a few centimeters onto the
superior frontal cortex; Superior portion of Brodmann's area 6. Contractions elicited by stimulating
this area are often bilateral rather than unilateral: For instance, stimulation frequently leads to bilateral
grasping movements of both hands simultaneously. In general, this area functions in concert with the
premotor area to provide attitudinal movements, fixation movements of the different segments of the
body, positional movements of the head and eyes, and so forth, as background for the finer motor
control of the arm and hands by the area and primary motor cortex (Figure 57). (Attitudinal movement
= postural movement of the body).

Pyramidal and Extrapyramidal systems

As outlined previously (Figure 56), motor signals are transmitted directly from the cortex to
the spinal cord through the pyramidal or corticospinal tract and indirectly through extrapyramidal
tracts that involve tracts from the brain stem to the spinal cord, basal ganglia and cerebellum. The four
important extrapyramidal tracts to the spinal cord (reticulospinal, vestibulospinal, rubrospinal and
tectospinal tracts) are described above. In general, the direct pathways are concerned more with
discrete and detailed movements, especially of the distal segments of the limbs, particularly the hands
and fingers. The extrapyramidal tracts are mainly involved in the control of posture.

Organization of Corticospinal Tract (Pyramidal Tract)

The most important output pathway from the motor cortex is the corticospinal tract, also
called the pyramidal tract, shown in Figure 58 below.
The human corticospinal tract consists of about one million axons of which about 30%
originate in the primary motor cortex, 30% in the premotor and supplementary motor area and 40% in
the somatosensory cortex. These axons descend through the subcortical white mater, they form
internal capsule (between thalamus and basal ganglia),and the cerebral peduncle (Figure 58). As the
fibers of the corticospinal tract descend, they form the medullary pyramids, prominent protuberances
on the ventral surface of the medulla, and thus the entire projection is sometimes called the pyramidal
tract.
Like the ascending somatosensory system, the descending corticospinal tract crosses to the
opposite side of me spinal cord. Most of the corticospinal fibers cross the midline in the medulla at a
location known as the pyramidal decussation. These fibers are known as lateral corticospinal tracts.
However, about 20% of the fibers do not cross until they reach the neck or thoracic level of the spinal
cord before they cross and terminate (ventral corticospinal tracts).
The corticospinal tract makes monosynaptic connections with motor neurons, connections
that are particularly important for individuated finger movements. It also forms synapses with
interneurons in the spinal cord. These indirect connections are important for coordinating larger
groups of muscles in behaviors such as reaching and walking.
The motor information carried in the corticospinal tract is significantly modulated by both
sensory information and information from other motor regions. This includes a continuous stream of
tactile, visual and proprioceptive information needed to make voluntary movement both accurate and
properly sequenced. In addition, the output of the motor cortex is under the substantial influence of
other motor regions of the brain, including the cerebellum and basal ganglia, structures that are
essential for smoothly executed movements.
The most impressive fibers in the pyramidal tract are a population of large myelinated fibers
with a mean diameter of 16 micrometers. These fibers originate from the giant pyramidal cells, called
betz cells that are found only in the primary motor cortex. These cells are about 60 micrometers in
diameter, and their fibers transmit nerve impulses to the spinal cord at a velocity of about 70 m/sec,
the most rapid rate of transmission of any signal from the brain to the cord. There are about 34,000 of
these large Betz cell fibers in each corticospinal tract. The total number of fibers in each corticospinal
tract is more than 1 million, so these large fibers represent only 3 per cent of all of them. The other 97
per cent are mainly fibers smaller than 4 micrometers in diameter that conduct (1) background tonic
signals to the motor areas of the cord and (2) feedback signals from the cortex to control the
intensities of various sensory signals going to the brain.

The corticospinal tracts

Effect of Lesions in the Motor Cortex or in the Corticospinal Pathway - The "Stroke"
The motor control system can be damaged especially by the common abnormality called a
"stroke". This is caused either by a ruptured blood vessel that hemorrhages into the brain or by
thrombosis of one of the major arteries supplying the brain, in either case causing loss of blood supply
to the cortex or to the corticospinal tract where it passes through the internal capsule.

Lesion of the Primary Motor Cortex (the Area Pyramidalis)

Removal of a portion of the primary motor cortex - the area that contains the giant Betz
pyramidal cells - in a monkey causes varying degrees of paralysis of the represented muscles. If the
sublying basal ganglia and adjacent premotor and supplementary motor areas are not damaged, gross
postural and limb "fixation" movements can still be performed, but the animal loses voluntary control
of discrete movements of the distal segments of the limbs, especially of the hands and fingers. This
does not mean that the hand and finger muscles themselves cannot still contract, but that the animal's
ability to control the fine movements is gone. From these results, one can conclude that the area
pyramidalis is essential for voluntary initiation of finely controlled movements, especially of the
hands and fingers.

Babinski sign
While tactile stimulation of the foot pad normally evokes plantar (downward, flexion of the
toes), after lesion of the precentral primary motor cortex or pyramidal tract, the same stimulus evokes
upward movement of the foot, and toes (Babinski sign). Babinski sign has become a classic clinical
test for damage to the pyramidal system. In babies (0-2 years), the normal sign is the Babinski sign
since their upper motor neurons are not well developed.

Decortication (damage of large areas of motor cortex) produces muscle spasticity.

Ablation of the primary motor cortex alone causes hypotonia, not spasticity, because of
stimulatory effect on the motor neurons of the spinal cord; when this stimulatory effect is removed,
hypotonia results.
 Conversely, most lesions of the motor cortex (decorticate preparation), especially those
caused by a stroke, involve not only primary motor cortex but also adjacent cortical areas and deeper
structures of the cerebrum, especially the basal ganglia. So, few if any lesions affect only the
pyramidal tract; thus a pure lesion of the pyramidal tract virtually does not exist. In these instances,
muscle spasm almost invariably occurs in the afflicted muscle areas on the opposite side of the body
(because the motor pathways cross to the. opposite side). This spasm is not caused by the loss of
primary motor cortex function or by blockage corticospinal fibers to the cord.
Instead, the spasm results mainly from damage to accessory pathways from the nonpyramidal
portions of the cortex. These pathways normally inhibit the vestibular and reticular brain stem motor
nuclei. When these nuclei cease their state of inhibition (i.e., are "disinhibited"), they become
spontaneously active and cause excessive spastic tone in the involved muscle areas of the body. This
is the spasticity that normally accompanies a "stroke" in the human being. Initially, following a
stroke, there is hypotonia before spasticity sets in. The spasticity is with hypertonia in flexors of the
arm and extensors of the leg. Removal of the entire motor cortex produces the signs as damage to
large areas adjacent to the motor cortex that is, maximal paralysis and spasticity flexors of the arm
and extensors of the leg. There is also loss of certain superficial abdominal reflexes and appearance of
Babinski sign.
As described previously, motor lesions are often divided into damage to upper or lower motor
neurons. Lower motor neuron refers to α-motor neurons or nerves; thus, they are located in the spinal
ventral horn cranial motor nuclei. Damage to lower motor neurons is characterized by decreased
muscle tone, muscle atrophy, fasticulations of single muscles, absence of tendon reflexes, and no
Babinski sign. Upper motor neuron refers to corticospinal neurons or extrapyramidal tracts or
neurons. Lesions of upper motor neurons are most often characterized by increased muscle tone,
although tone can also decrease (depending on region damaged). Other signs are derangements of
groups of muscles, enhanced tendon reflexes, presence of a Babinski sign, and muscle atrophy
(rarely). There is also a loss of certain abdominal reflexes.

THE BASAL GANGLIA IN CONTROL OF MOTOR FUNCTION

The basal ganglia are composed of large masses of neurons located deep in the substance of
the cerebrum and in the upper part of the mesencephalon (mid brain). They include the caudate
nucleus (tailed nucleus), the putamen, the globus pallidus (pale body), the substantia nigra (black
matter), and several other less important nuclei (Figure 59).
The caudate nucleus and putamen are sometimes referred to as corpus striatum (striped body).
The putamen and globus pallidus make up the lentiform nucleus (Table 6). As with the motor cortex,
nuclei on the left side, control movements on the right side of the body and vice versa. The basal
ganglia like the cerebellum are also the accessory motor systems and exert profound influences on
movement. Unlike the cerebellum, however, the basal ganglia receive no direct input from primary
sensory systems. Information used by the basal ganglia is derived primarily from the cerebral cortex.
It functions not by itself but always in close association with the cerebral cortex and the corticospinal
system. In fact, the basal ganglia receive virtually all their input signals from the cortex itself and in
turn return almost all their output signals back to the cortex. The motor deficits that follow damage to
the basal ganglia vary depending on the particular type of cells that are used.

The basal ganglia

Caudate nucleus
Striatum
Putamen

Lenticular
nucleus
Globus pallidus (pallidum)

Subthalamic nucleus (body of Luys)

Substantia nigra
The basal ganglia

The symptomatology leads to two general disorders. It may be an inability to suppress

involuntary motor activity (hyperkinetic syndromes e.g. chorea, athetosis and hemiballismus) or it
may be inability to generate rapid voluntary movements (hypokinetic syndromes e.g. parkinsonism).
Connections between various basal ganglia nuclei have been well defined and the transmitter
substances involved identified. One circuitry that is present and important is the following: the whole
of the cerebral cortex (including association cortices) sends information back to the motor cortex via
the motor nuclei of the thalamus. Another connection with clinical relevance is the dopaminergic
nigro-striatal pathway (Figure 60).

Basal ganglia connections (BG receive information from all cerebral cortex, sends information to premotor
and motor cortex via thalamus

Control of subconscious movements by the Basal ganglia

Before attempting to discuss the function of the basal ganglia in man, we should speak briefly
of their better known function in lower animals. In birds, for instance, the cerebral cortex is very
poorly developed while the basal ganglia are highly developed. These ganglia perform essentially all
motor functions, even controlling the voluntary movements in much the same manner than the motor
cortex of the human being controls voluntary movement. In the cats, and to a less extent in the dogs,
removal of the cerebral cortex prevents discrete types of motor function but does not interfere with the
cats’ ability to walk perfectly well, to Figureht, and to develop rage, and to have periods of sleep and
wakefulness, and even to participate naturally in sexual activities. However, if a major portion of the
basal ganglia is destroyed, only gross stereotype movements remain, which are controlled by the very
primitive lower areas in the brain stem.
In the human being, many of the potential functions of the basal ganglia are suppressed by the
cerebral cortex, but if the cerebral cortex becomes destroyed in a young human being, many of the
voluntary functions do develop. The person will never be able to develop discrete movements,
particularly of the hands, but he can learn to walk, to control his equilibrium, to eat, rotate his head, to
perform almost any type of postural movement and to carry out other subconscious movements. On
the other hand, destruction of a major portion of the caudate nucleus almost totally paralyses the
opposite side of the body, except a few stereotype reflex movements integrated in the cord or lower
brain stem. So, the basal ganglia in co-operation with the cortex execute subconscious but learned
patterns of movements. It also plans multiple parallel and sequential patterns of movement for a
purposeful task.
Unfortunately, little is known about the function of the individual basal ganglia other than the
fact that they operate together in a loosely knit unit to perform the subconscious movements. Yet the
following are a few of the discrete bits of information that are known about their individual functions;
(1) The caudate nucleus in co-operation with the motor cortex controls gross intentional movements
of the body, these occurring mainly subconsciously but aiding in the overall control of the body
movements (e.g. writing of alphabets, cutting paper with scissors, hammering nails, passing a
football, shoveling dirt). It also helps to plan patterns of movement that the mind must put together to
achieve a goal (i.e. cognitive control of motor activity, e.g. response to sudden sight of a lion, where
the individual instinctively decides to turn away, run and climb a tree). The caudate nucleus also
assists in changing the timing and scaling the intensity of movements e.g. determines how rapidly and
how large a movement is made.

(2) The putamen operates in conjunction with the caudate nucleus to control gross intentional
movements. Both of these nuclei also function in cooperation with the motor cortex to control the
patterns of movement.

(3) The globus pallidus probably controls the background positioning of the gross parts of the body
when a person begins to perform a complex movement pattern. That is, if a person wishes to perform
very exact function with one of his hands, he first positions his body appropriately and then tenses the
muscles of the upper arm. These functions are said to be initiated by the globus pallidus.

(4) The subthalamic nucleus controls walking movement and perhaps other types of gross rhythmic
body motions.

Transmission of signals from the basal ganglia through the extrapyramidal system
In previous sections, we noted that signals from the cerebral cortex to the spinal cord that
cause voluntary motor activities are transmitted through the pyramidal tract (called also the
corticospinal ract). The basal ganglia on the other hand, do not transmit their motor signals through
this tract but instead over short pathways into neuronal centers of the lower brain stem. From there the
signals are relayed down to the cord through the (1) reticulospinal tracts, (2) vestibulospinal tracts,
and (3) rubrospinal tract, and (4) propiospinal tracts (non specific tracts running up and down the
spinal cord).
The basal ganglia receive large numbers of fibers from the secondary motor areas which lie in
front of the motor cortex and sensory cortex. The entire system for transmitting motor signals down
the axis of the nervous system is called the Extrapyramidal system because it does not utilize the
pyramidal tract (corticospinal tract) as does the system for direct control of voluntary muscle
movement, as explained earlier. In general, one can say that Extrapyramidal system controls the
various postural movements and the back ground tone of the different muscles in contrast to the
control of discrete voluntary movements by the corticospinal system.

Abnormalities associated with damage of the basal ganglia

Even though we do not know all the precise functions of the basal ganglia, we do know many
abnormalities that develop when portions of the basal ganglia are destroyed as follows:
 Chorea: is random uncontrolled sequence of motor movement, beginning first at the joints
then the entire body, occurring one after the other. Normal progression of body movements cannot
occur. Instead, the person may perform a normal sequence of movements for a few seconds and then
jump to a new sequence, thus jumping to a new sequence occurring again and again without stopping
is caused by widespread damage in the caudate nucleus and putamen, which produce inhibitory
GABA. The loss of inhibition leads to spontaneous outbursts of Globus pallidus and Substantia nigra
that cause distortional movements. The accompanying dementia is due to loss of ACh-secretory
neurons.
Athetosis: Athetosis is characterized by slow, writhing movements of peripheral parts of the
body. For instance neck, face, hand or arm may undergo worm-like movements, such as twisting of
the arm to one side, then to the other side, then backwards, then forward, repeating the same activity
over and over again. The damage is always the globus pallidus. The abnormal movements usually
involve the hands and less frequently the lips, the tongue or occasionally the neck and foot.
Hemiballismus: Hemiballismus is an uncontrollable succession of violent movements of
large areas of the body. For instance, a leg may kick forward, and this may be repeated once in many
minutes. The damage that causes this is in the subthalamus. (Ballismus is a violent flinging of the
limbs).
Parkinson's disease: This disease is characterized by tremor and rigidity of the musculature
in either widespread areas or isolated areas of the body. A typical person with full blown Parkinson's
disease walks in a crouch like an ape, except that his muscles are obviously tense, his face is mask-
like and he jerks all over with a violent tremor of approximately 3 to 6 times per second. Yet when he
attempts to perform voluntary movement the tremor stops temporarily. This disease is paused by
destruction of the substantia nigra, one of the less conspicuous basal ganglia that extend downward
into the mesencephalon. Loss of dopamine secretion from the substantia nigra (SN) into caudate
nucleus and putamen leads to loss of balance between the excitatory and inhibitory system and may
result in tremor and Bradikinesia or akinesia. So, this is due to damage to the dopaminergic-
nigrostriatrial system. Administration of L-dopa that crosses the blood brain barrier ameliorates the
condition. The brain converts L-dopa to dopamine that does not cross the blood-brain barrier. It can
be treated by transplantation of aborted fetal dopamine secreting cells into caudate nucleus and
putamen cells. It only lasts for few months. It can also be treated with L-Deprenyl which inhibits
monoamine oxidase that destroys dopamine. Better results are obtained in combination with L-Dopa.
It is also treated by destruction of some nuclei in the thalamus by electro-coagulation to block some
back loops that cause some tremor. It can also be treated by transplantation of aborted fetal secreting
cells into the caudate nucleus and putamen. The remedy only lasts for a few months.
WAKEFULNESS AND SLEEP

The reticular activating system

The reticular formation extends through the upper medulla, pons, and midbrain with profuse
ascending connections to the thalamus and cerebral cortex and descending connections to the spinal
cord. The reticular formation receives sensory input from all the peripheral receptors, including those
of the muscles and joints, pain nerve endings, and visceral receptors, and the visual and auditory input
from the eye and ear. Consequently, this collection of neural subcenters is in an excellent position to
monitor all incoming and outgoing information (Figure 65).

The reticular formation receives sensory input from receptors and relays this information to the midbrain,
limbic system, and neocortex. The response of the neocortex can be seen in the electroencephalogram (EEC).
Visceral changes can be seen in the recordings of respiration and blood pressure.

Stimulation of the reticular formation activates the cerebral cortex, and so it is often referred
to as the reticular activating system (RAS). The physiological mechanisms for RAS stimulation are
through the profuse sensory input. Pain receptors are particularly effective for eliciting the arousal
response; this is probably an evolutionary mechanism of benefit for survival.
Several positive feedback mechanisms are involved in the RAS. The aroused cerebral cortex
further stimulates the RAS, particularly through the barrage of impulses from the motor cortex; this
results in further RAS stimulation of spinal motor neurons. The increased muscle tone and increased
level of autonomic activity feed back through peripheral afferent pathways to maintain the level of
excitement of the RAS. Movement is a particularly effective stimulus for the RAS, and wakefulness
can be maintained by muscle activity, as evinced by the wriggling of sleepy, bored students.

Attention. Although impulses from the brainstem portion of the RAS cause generalized excitation
through the cerebral cortex, more specific mechanisms involving the thalamic portion of the RAS
stimulate selected areas of the cortex, permitting us to concentrate on the desired aspects of the
sensory input and to ignore extraneous information.

Sleep-Wake cycle: After the brain remains activated for many hours, even the neurons in the RAS
become fatigued. Consequently, the positive feedback between the neurons in the RAS and cortex
would fade and the inhibitory effects of the sleep centers would take over leading to rapid transition
from wakefulness to sleep. One could also postulate that during prolonged sleep, excitatory neurons
of RAS gradually become more and more excitable because of the prolonged rest, whereas the
inhibitory neurons of the sleep centers become less excitable because of their over activity thus,
leading to a new cycle of wakefulness. This is the passive theory of sleep. Also the ability to fall
asleep may be due to the action of specific neurotransmitters that inhibit the activity of the RAS e.g.
serotonin, muramyl peptide, etc. This is the active inhibitory process of sleep.
Drugs and the RAS: Certain drugs can either stimulate or depress the RAS. General anaesthetics and
tranquilizers depress it. On the other hand, ammonia and other irritants send action potentials via the
terminal nerve endings to arouse an unconscious patient.

Sleep
Sleep is defined as unconsciousness from which the person can be aroused by sensory or
other stimuli. It is to be distinguished from coma, which is unconsciousness from which the person
cannot be aroused.
Approximately two hours after we fall asleep, our eyes begin to quiver quickly backward and
forth under the eyelids. The observation of this phenomenon led scientists to divide sleep into two
basic phases or types: REM (Rapid eye movement) sleep and non REM sleep. Non-REM sleep can be
subdivided into four stages of progressively deeper sleep. During a healthy night's sleep, REM sleep
occurs several times alternating with non-REM sleep.
Most dreaming occurs during REM sleep. The body also experiences maximum muscle
relaxation, which allows the sleeper to wake up feeling physically refreshed. In addition, some
researchers believe that newly acquired information is consolidated as part of our long-term memory
during this sleep stage. REM sleep is accompanied in males, by periodic penile erections. There is
increased heart rate and blood pressure and rapid eye movement and hence the name. REM sleep
appears to be deeper than Non-REM sleep, for the arousal threshold is higher. So, the person is more
difficult to arouse than in non REM sleep. However, the brain is very active in REM sleep but the
brain activity is not channeled in the proper direction for the person to be fully aware of his
surroundings and therefore the person is truly asleep. Prolonged deprivation of REM sleep may result
in hallucinations, aberrant behavior and memory impairment. It is a restorative process, and
consequently there must be a need for it. The waves are similar to those in wakefulness (with eyes
open) i.e. Beta waves (>14cps) hence, the synonyms paradoxical sleep, desynchronized sleep and beta
wave sleep (Figure 66).
Non REM sleep as stated earlier is divided into four stages. A person falling asleep enters into
stage I ( drowsiness stage) which is characterized by low amplitude high frequency EEG activity.
Then he enters stage 2 (light-sleep) marked by the appearance of sleep spindles (bursts of alpha
waves). Stages 3 and 4 are deep and deeper stages of Non REM sleep with lower frequency and
increased amplitude of the EEG waves. During deep sleep (non REM sleep stages 3 and 4), our blood
pressure and heart rate reach lower ranges, providing rest for the circulatory system and helping to
ward off cardiovascular disease. In addition, the production of growth hormone peaks during non-
REM sleep, with some teenagers producing as much as 50 times more growth hormone at night than
during the day. This sleep is deep, dreamless, exceedingly relaxed and associated with decrease in
blood pressure, respiratory rate, BMR, muscle tone and almost other vegetative functions of the body.
If recordings are made of brain waves at this stage of sleep, the electroencephalogram (EEG) shows
slow cortical waves of less than 3.5 cycles per second (cps) i.e. delta waves. These brain waves are of
large amplitude and are found mainly in the frontal and associated areas. Non-REM sleep is also
called deep restful sleep, dreamless sleep, delta wave sleep, normal sleep or slow wave sleep (Figures.
66 and 67).

Vital for Health

Sleep plays a role in the maintenance of a higher level of performance of tasks since during
sleep, there is selective activation of neural areas associated with the performance of these tasks.
Sleep also seems to affect our appetite. Our brain interprets a lack of sleep as a lack of food. While we
sleep, our adipose tissue secretes leptin, the hormone that normally lets our body know that we have
eaten enough. When we stay awake longer than we should, our body produces less leptin, and we feel
a craving for more carbohydrates. So sleep deprivation can lead to increased carbohydrate
consumption, which in turn can lead to obesity. Sleep makes it easier for our body to metabolize free
radicals – molecules that are said to increase the aging of cells and even cause cancer. Sleep
deprivation even affects the production of white blood cells and the hormone cortisol, making a
person more prone to infections and circulatory diseases.

The effects of sleep deprivation

Short term effects

Drowsiness
Sudden mood swings
Loss of short-term memory
Loss of capacity to create, plan and carry out activities
Loss of concentration

Long term effects

Obesity
Premature aging
Fatigue
Increases risk of infections, diabetes, cardiovascular diseases, and gastrointestinal disease
Chronic memory loss

An afternoon nap
Have you ever felt an uncontrollable drowsiness after lunch? It is normal to feel sleepy in the
early afternoon because of a natural drop in body temperature in addition, scientists have recently
discovered a protein called hypocretin or orexin produced in the brain and helps keep us awake.
There is a connection between hypocretin and food. When we eat, the body’s adipose tissue produces
a peptide called leptin. But leptin inhibits the production of hypocretin. In other words, the more
leptin there is in the brain, the less hypocretin and the greater the feeling of drowsiness. Perhaps that
is why in some countries people take a siesta – a break in the workday that allows people to sleep a
little after lunch.

Sleep problems
Today, millions of people have difficulty sleeping well. An estimated 35 percent of the
world’s population suffer from insomnia (insomnia is the inability to enjoy normal and sufficient
sleep).
One of the most common causes of chronic insomnia among adultsis related to snoring. If
you have ever slept near someone who snores, you know that this can be extremely uncomfortable.
Snoring can be a symptom of obstructive sleep apnea syndrome (OSAS), in which the closure of
the throat temporarily prevents a sleeper from sucking air into his lungs. Initial steps in treating OSAS
include weight loss, avoidance of alcoholic beverages and avoidance of muscle-relaxing drugs.
Specialists may also prescribe specific medication for the use of dental appliances or a continuous
positive airway pressure machine. In more severe cases, surgical correction of the throat, jaw, tongue
or nose may be necessary in order to make it easier for air to enter and leave during the breathing
process.
Sleepwalking (somnambulism) and bed wetting (nocturnal enuresis) have been shown to
occur during slow-wave sleep, or more specifically during arousal from slow–wave sleep. They are
not associated with REM sleep. Episodes of sleep walking are more common in children than adults
and occur predominantly in males. They may last several minutes. Somnambulists walk with their
eyes open and avoid obstacles but when awakened, they cannot recall the episodes.
Narcolepsy is a not uncommon disease of unknown cause in which there is an eventually
irresistible urge to sleep during daytime activities. In some cases, it has been shown to start with the
sudden onset of REM sleep. REM sleep almost never occurs without previous slow wave sleep in
normal individuals.
 Cataplexy (from kataplesseein, meaning to strike down). A paroxysmal disorder of postural
tone in which in response to an emotional stimulus such as pleasure, laughter, anger or excitement,
there is a sudden loss of function of some or all of the voluntary muscle. Consciousness and
awareness are preserved throughout the attack. The condition usually occurs in association with
narcolepsy and is believed to be due to hypersensitivity of one part of the reticular inhibitory system.
It bears no relationship to epilepsy.

Recordings made from the neck muscle, eye muscle and respiratory rate during wakefulness, slow wave sleep
and REM sleep. Note the rapid eye movements characteristic of REM sleep and the loss of muscle tonus that
occurs during this period

EEG during wakefulness, different stages of NON REM sleep and REM sleep

Brain structures needed for sleep

Surgical lesions of different parts of the brain have shown that REM sleep and slow wave
sleep depend on different structures (Figure70). REM sleep is dependent on clusters of neurons in the
roof (tegmentum) of the pons, forming the nucleus locus ceruleus. These neurons have been shown by
histochemical fluorescent techniques to contain norepinephrine, bilateral destruction of these nuclei
impairs REM sleep but not slow wave sleep. Slow wave sleep is abolished, however, if the cerebral
cortex is removed. .
Another distinct group of neurons implicated in sleep is located in the midline, of the pons.
These cells form the raphe nuclei, and they contain serotonin. If these raphe nuclei are destroyed, a
permanent state of insomnia results. Parachlorophenylalamine, a drug that depletes brain serotonin
causes insomnia in cats, and this effect is overcome by administration of 5-hydroxyltryptophan which
restores serotonin content of the neurons to normal.
Jouvet (1969) has proposed a linkage between the norepinephrine-containing neurons of the
locus ceruleus and the raphe nuclei, which contain serotonin. He suggested that the serotonin-
containing neurons trigger the norepinephrine neurons to induce REM sleep. This is a rather
complicated mechanism, involving cholinergic interneurons, but it may explain why REM sleep will
only appear after a certain level of slow wave sleep has been attained (equivalent to more than 15 per
cent of the day).

Brain structures needed for sleep include the raphe nuclei, which, through the production of serotonin,
depress the arousal effect of the reticular formation. The norepinephrine-producing cells of the locus
ceruleus are needed for REM sleep.

Electroencephalogram
The synaptic potentials produced at the cell bodies and dendrites of the cerebral cortex create
electrical currents, which can be measured by electrodes placed on the scalp. A record of these
electrical currents is called an electroencephalogram, or EEG. Deviations from normal EEG patterns
can be used clinically to diagnose epilepsy and localize brain tumors, and the absence of an EEG can
be used to detect brain death. It is also used in the diagnosis of the various stages of sleep.
There are normally four types of EEG patterns (Figure 68).
Alpha waves are best recorded from the parietal and occipital regions while a person is awake and
relaxed but with the eyes closed. These waves are rhythmic oscillations of about 8-13 cycles/second.
The alpha rhythm of a child younger than eight years old occurs at a slightly lower frequency of 4-7
cycles/second.
Beta waves are strongest from the frontal lobes, especially the area near the precentral gyrus. These
are produced by visual stimuli and mental activity (eyes are open). Because they respond to stimuli
from receptors and are superimposed on the continuous activity patterns, they constitute evoked
activity. The frequency of beta waves is 13-25 cycles/second. They also occur during REM or
paradoxical sleep.
Theta waves are emitted from the temporal and occipital lobes. They have a frequency of 4-7 and are
common in newborn infants. The recording of theta waves in adults generally indicate severe
emotional stress and can be a forewarning of a nervous breakdown.
Delta waves are seemingly emitted in a general pattern from the cerebral cortex. These waves have a
frequency of 1-3.5 cycles/second and are common during slow wave sleep in the adult, and in an
awaked infant. The presence of delta waves in an awake adult indicates brain damage.

Types of electroencephalograms (Brain waves) of Normal individuals.

Abnormal potentials – Epilepsy

Discharges associated with Epilepsy
Epilepsy is a brain disorder characterized by convulsive seizures or loss of consciousness or
both. It occurs due to excessive discharge of impulses from some part of the brain particularly
cerebral cortex. Convulsive seizures mean the sudden uncontrolled involuntary muscular contractions.
The person with epilepsy remains normal in between seizures. The epileptic attack develops only
when the excitability of the neuron is increased, causing excessive neuronal discharge. The persons
affected by epilepsy are known as epileptics.

Types of Epilepsy
Epilepsy is divided into two categories namely:
A. Generalized epilepsy or general onset seizure or general onset epilepsy. This is due to
excessive discharge of impulses from all parts of the brain and
B. Localized epilepsy or local seizure or local epilepsy. This occurs because of excessive
discharge of impulses from one part of brain.

A. Generalized epilepsy
This is subdivided into three types viz:
1. Grand mal epilepsy
2. Petit mal epilepsy
3. Psychomotor epilepsy
1. The grand mal epilepsy is the most severe and is characterized by extreme neuronal
discharges in all areas of the brain including the RAS, where discharges are transmitted to the
spinal cord causing tonic convulsion of the entire body and alternating muscular contraction,
the person falls to the ground. The cause of the extreme neuronal over-activity is due to
massive activation of many reverberating pathways throughout the brain precipitated by
strong emotional stimuli, alkalosis, drugs, fever, convulsion and loud noise. These occur in
persons genetically predisposed; but may be contributed by traumatic brain lesion. Strong
emotional stimuli, high fever and drugs can also cause it. This form of epilepsy is stopped by
fatigue of the neurons following their intense activity and by active inhibition through
feedback circuits through inhibitory areas of the brain especially the cerebellum. Fast waves
with a frequency of 15 – 30Hz per second are seen during the tonic state.
2. Petit mal epilepsy
In this, the person becomes unconscious suddenly without any warning. The unconsciousness
last for a very short period of 3 to 30 seconds. Convulsions do not occur. However, the
muscles of face show twitch like contractions and there is blinking of eyes. Afterwards, the
person recovers automatically and becomes normal. The frequency of attack may be once in
many months or many attacks may appear in rapid series. It usually occurs in late childhood
and disappears completely at the age of 30 or above. The EEG recording shows slow and
large waves during the attack. A sharp spike follows each wave. This type of waves appears
from recording over any part of the cerebral cortex indicating the involvement of whole
brain. Delta waves appear in between the seizures.
3. Psychomotor epilepsy
This is characterized by emotional outbursts such as abnormal rage, sudden anxiety, fear or
discomfort. There may be amnesia or a confused mental state for some period. Some persons
have the tendency to attack others bodily or rubbing their own face vigorously. In most cases,
the persons are very well aware of the actions, but still the abnormal actions cannot be
controlled. The causes of the psychomotor epilepsy are the abnormalities in temporal lobe
and tumor in hypothalamus and other regions of limbic system like amygdala and
hippocampus. The EEG recordings show a low frequency rectangular waves, ranging
between 2 and 4 per second.

B. Localized Epilepsy
It is otherwise known as local or focal epilepsy. This involves only a localized area of
cerebral cortex or the deeper parts of cerebellum which are affected by tumor, abscess or
vascular defects. The abnormality starts from a particular area and may spread to adjacent
areas, developing slow spreading muscular contractions. The contractions usually start in the
mouth region and spread down towards the legs. This type of seizure is also known as
Jacksonian epilepsy.
Anticonvulsants are used to alleviate epilepsy. These drugs potentiate sympathetic inhibition
mediated by GABA or benzodiazepines and barbiturates. Others block voltage dependent ion
channels in neuronal membranes e.g. phenytoin for sodium and barbiturates for calcium.
Electronencephalograms in different types of epileptics. The neurons involved are hyperactive and
this hyperactivity appears to be autonomous.