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    Pathology of The Central Nervous System (CNS)

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    This document discusses the pathology of the central nervous system (CNS). It describes the anatomy of the CNS, including the different cell types found in the brain parenchyma. It then discusses the basic reactions of the CNS to injury, including the reactions of neurons and glia cells, as well as cerebral edema. It also covers increased intracranial pressure and herniation, hydrocephalus, and CNS trauma.

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    Pathology of The Central Nervous System (CNS)

    Uploaded by

    Rikizu Hobbies
    20 views53 pages
    This document discusses the pathology of the central nervous system (CNS). It describes the anatomy of the CNS, including the different cell types found in the brain parenchyma. It then discusses the basic reactions of the CNS to injury, including the reactions of neurons and glia cells, as well as cerebral edema. It also covers increased intracranial pressure and herniation, hydrocephalus, and CNS trauma.

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    Neuropathology 01

    Original Title

    Neuropathology

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    This document discusses the pathology of the central nervous system (CNS). It describes the anatomy of the CNS, including the different cell types found in the brain parenchyma. It then discusses the basic reactions of the CNS to injury, including the reactions of neurons and glia cells, as well as cerebral edema. It also covers increased intracranial pressure and herniation, hydrocephalus, and CNS trauma.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    20 views53 pages

    Pathology of The Central Nervous System (CNS)

    Uploaded by

    Rikizu Hobbies
    This document discusses the pathology of the central nervous system (CNS). It describes the anatomy of the CNS, including the different cell types found in the brain parenchyma. It then discusses the basic reactions of the CNS to injury, including the reactions of neurons and glia cells, as well as cerebral edema. It also covers increased intracranial pressure and herniation, hydrocephalus, and CNS trauma.

    Copyright:

    © All Rights Reserved
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    of 53

    PATHOLOGY OF THE

    CENTRAL NERVOUS SYSTEM


    (CNS)
    Anatomy
    Brain parenchyma is composed of
    • neurons
    • glia cells
    • endothelial cells
    • cells of choroid plexus
    Neurons: highly specialized postmitotic cells in the cortex, basal
    ganglia, anterior horns of the spinal cord; have dendrits and
    axons; are very sensitive to ischemia

    Bielschowsky-silver
    Glia cells:
    • Astrocytes (found both in GM and white matter
    [WM]): their cytoplasmic processes fix the
    neurons; important elements of the blood-brain
    barier; responsible for scar formation in the brain

    • Oligodendroglia cells (located in the WM): form


    myelin sheaths of axon

    • Microglia cells: fixed macrophages derived from


    bone marrow; become activated in encephalitis
    •
    • Ependyma cells: line ventricles
    Neurons and astrocytes in the gray matter
    • Adult neural stem cells are found in the
    hippocampus; are capable of generating neurons,
    astrocytes, and oligodendroglia cells

    • Their role in health and disease is not known


    BASIC REACTIONS OF CNS TO INJURY

    • Reactions of neurons

    • Reactions of glia cells

    • Edema
    REACTIONS OF NEURONS

    • Acute injury secondary to global hypoxia or


    arterial-occlusion induced ischemia

    • The neurons do not tolerate O2 deprivation

    • The neurons are selectively vulnerable to O2


    deprivation  the injury within minutes!! turns
    into irreversible

    • Hypoxia affects more prominently the pyramidal


    neurons of neocortex and hippocampus, and the
    cerebellar Purkinje cells than other neurons
    LM
    • Red neurons (indicate dead cell): become evident
    12 to 24 hours after irreversible hypoxic/ischemic
    insult. Features: shrinkage of the cell body, pyknosis
    of the nucleus, loss of Nissl substance, intense
    eosinophilia of the cytoplasm

    • Laminar necrosis: high sensitivity and rapid death of


    neurons within layers III and V of the neocortex

    • Border zone infarct: wedge-shaped area of


    infarction at the border zone between the anterior
    and the middle cerebral artery distribution, usually a
    few centimeters lateral to the interhemispheric
    fissure; may be visible grossly
    The patient had myocardial infarction-induced ventricular
    fibrillation. He was reanimated, and died 4 days after the
    cardial event. Red neurons (*) in the gray matter.

    *
    *
    Chronic injury in
    neurodegenerative
    disorders

    • Neuronal inclusions
    (arrow) associated with
    aggregated proteins

    • Neuronal death: apoptosis;


    accompanied by reactive
    gliosis (not shown)
    REACTIONS OF GLIA CELLS (astrocytes, microglial
    cells)

    Glial scar

    • Phagocytosis of lipids of white matter at site of


    injury (e.g., infarction) is carried out by
    macrophages derived from the circulation  turn
    into foamy ma-s

    • Foamy ma-s are replaced by reactive astrocytes


    (gliosis), resulting in a glial scar: consists of
    cytoplasmic processes of astrocytes, and is devoid
    of collagen
    Foamy macrophages at site of infarction
    Proliferation of astrocytes  glial scar

    Foamy
    macrophages

    Astrocytes

    Astrocytes
    Microglia in encephalitis

    Microglia cells proliferate, form aggregates around


    necrotic foci (microglial nodules), and phagocytose
    dying neurons (neuronophagia)
    Microglial nodule (encircled) and neuronophagia (arrow)
    in encephalitis: microglia cells have cigar-shaped nuclei
    CEREBRAL EDEMA

    Types

    Vasogenic edema - extracellular


    • Due to  vascular permeability (blood-brain
    barrier dysfunction)  fluid escapes from the
    vessels into the IS space localizing between the
    neurons and glial cells
    • Causes: inflammation, neoplasm
    Cytotoxic edema – intracellular

    • Due to hypoxic/ischemic injury to neurones and


    glia cells
    • Fluid accumulation inside the cells (hydropic
    swelling)

    In many instances, vasogenic and cytotoxic


    mechanisms act in parallel
    Manifestations of brain edema

    • Focal: induced by mass lesion (tumor, hemorrhage,


    abscess) or infarction

    • Diffuse: induced by global hypoxia


    Morphology of diffuse brain edema

    • The brain is heavier (>1350 g) and softer than


    normal

    • Flattened broad gyri, narrowed slitlike sulci

    • Compressed lateral ventricles

    • On sectioning, fluid sweeps from the cut


    surfaces

    • + signs of tonsillar herniation


    Diffuse brain
    edema: ventricular
    spaces are
    severely
    narrowed

    Prof. Barzó Pál, Neurosurgery


    INCREASED INTRACRANIAL PRESSURE AND
    HERNIATION

    • The volume of the intracranial contents is fixed


    by the skull. Neoplasm, hemorrhage, abscess,
    etc. lead to an  in pressure 
    • Papilloedema (swelling of the optic nerve head),
    nausea and vomiting, headache, and
    impairment of consciousness;

    • If left untreated, herniation of certain parts of the


    brain occurs
    Sites of herniation

    • Underneath the falx cerebri: subfalcine

    • Underneath the free edge of the cerebellar


    tentorium: transtentorial

    • Into the foramen magnum: tonsillar


    1. Subfalcine herniation
    Unilateral mass lesion
    forces the ipsilateral
    cingulate gyrus to be
    compressed Subfalcine
    underneath the falx herniation
    cerebri
     focal necrosis and
    hemorrhage in the
    herniated tissue
    +
    compression of the
    anterior cerebral artery
    Kumar, Cotran, Robbins: Basic
    Pathology 2003
    2. Transtentorial herniation
    • Expansion of the
    hemisphere  the uncal
    gyrus of hippocampus is
    herniated underneath the
    free edge of the cerebellar
    tentorium

    Transtentorial
    herniation
    2. Transtentorial herniation
    •The ipsilateral oculomotor
    nerve undergoes
    compression: ipsilateral
    fixed pupil
    • Posterior cerebral artery
    compression  occipital
    infarction, cortical
    blindness
    • Cerebral peduncle
    compression  upper
    motor neuron signs
    • Brainstem compression 
    cardiorespiratory failure,
    Transtentorial
    death herniation
    3. Tonsillar herniation
    The cerebellar tonsils are
    forced into the foramen
    magnum and compress
    the respiratory and
    cardiac centers within the
    medulla 
    cardiorespiratory failure,
    death

    Transtentorial
    herniation
    Tonsillar
    herniation
    Compression of cerebellar tonsils and medulla
    oblongata by the foramen magnum
    Striped hemorrhages in the pons in response to tearing
    of small vessels(Duret hemorrhages)
    HYDROCEPHALUS (HC)

    • Cerebrospinal fluid (CSF): produced by the choroid


    plexus, circulates through the ventricular system, enters
    the cisterna magna through the foramina of Luschka and
    Magendie. Subarachnoid CSF is absorbed by the
    arachnoid granulations.

    • Accumulation of excess quantity of CSF within the


    ventricular system

    • Primary HC
    • Secondary HC
    Primary hydrocephalus
    • Accumulation of CSF is accompanied by an 
    in intracranial pressure, due to
    • congenital
    • acquired obstruction to CSF flow
    Acquired obstruction - sites and causes

    • CSF flow through the lateral ventricles and third


    ventricle can be obstructed by intracranial or
    intraventricular neoplasms

    • The cerebral aqueduct, the fourth ventricle, and


    the foramina can be obstructed by neoplasm,
    organised blood clot or inflammatory exsudate

    • The subarachnoid space and arachnoid


    granulations can be impaired by organised
    inflammatory exsudate or hemorrhage
    Consequences

    • When HC develops before closure of cranial


    sutures, there is enlargement of the head
    Hydrocephalus

    Preparation of late
    Prof Dr. Gellért Albert
    SZTE Anatomy Department
    Consequences

    • When HC develops before closure of cranial


    sutures, there is enlargement of the head

    • HC developing after fusion of the sutures is


    associated with  intracranial pressure,
    expansion of the ventricles, and pressure
    atrophy of the brain

    • HC can be treated via insertion of a ventricular


    shunt with a one-way valve system to drain CSF
    into the peritoneum
    Hydrocephalus: severe enlargement of the ventricles,
    atrophy of the brain
    Sec. (compensatory) hydrocephalus

    The increase in
    CSF volume
    occurs following
    brain atrophy:
    HC ex vacuo

    The intracranial
    pressure is
    normal
    CNS TRAUMA

    Frequent, may manifest in:

    • Concussion
    • Contusion and laceration
    • Diffuse axonal injury
    • Traumatic intracranial hemorrhage
    • Spinal cord injury
    Concussion

    • A clinical sy brought about closed head injury


    characterized by sudden onset and transient
    neurologic dysfunction: loss of consciousness,
    respiratory arrest, and loss of reflexes

    • Associated with WM (axonal) injury

    • Recovery is complete, amnesia (loss of


    memory) for the events persists
    Contusion and laceration

    • Contusion (bruising): hemorrhagic necrosis of


    superficial cortex, resulting from rapid
    deceleration or acceleration of the skull and
    brain; it involves a coup lesion at the site of
    impact of force and a contre-coup lesion,
    diametrically opposite to it

    • Associated with laceration (tearing of tissue)


    and disruption of vessels  intracerebral
    hemorrhage
    • Skull fracture is usually present
    • Outcome: healing with gliosis; if extensive, may
    be lethal
    Fracture contusion with necrosis of GM and WM,
    hemorrhage and brain oedema

    Contre-coup
    Coup
    Diffuse axonal injury
    (DAI)

    Rotational movements
    of the brain within
    the skull lead to
    shearing and tensile
    strains on neuronal
    processes  DAI in
    deep WM regions
    (corpus callosum,
    paraventricular and
    hippocampal areas
    and the brainstem)
    • Morphology: axonal swelling and focal
    hemorrhages

    • Clinical features: instantaneous deep coma,


    usually fatal

    • In survivors, damaged axons undergo


    degeneration  loss of fibers in the WM
    TRAUMATIC INTRACRANIAL HEMORRHAGE

    Hemorrhage is a frequent component of CNS


    trauma

    Hemorrhage (sometimes in combination) may be


    • epidural
    • subdural
    • subarachnoid
    • intraparenchymal

    • Without neurosurgical intervention, death in


    significant number of patients
    The branches of middle meningeal artery run between the dura
    mater and the skull
    Epidural hematoma
    • Temporal bone fracture  rupture of middle
    meningeal artery  accumulation of arterial blood
    between the dura and the skull: EH
    • Lucid interval followed by a rapid  in intracranial
    pressure

    Prof. Barzó Pál, Neurosurgery


    The bridging veins between the dura mater and the arachnoid membrane
    Subdural hematoma
    Rupture of bridging veins
    between the brain and superior
    sagittal sinus due to torsion
    forces  accumulation of venous
    blood between the dura and the
    arachnoid: SH

    Prof. Barzó Pál, Neurosurgery


    Subdural hematoma.
    In this patient, the midline structures are shifted to the right

    • Acute: rapid increase in


    intracranial pressure

    • Chronic: change in
    personality, memory
    loss and confusion,
    particularly in
    elderly and
    alcoholics

    Prof. Barzó Pál, Neurosurgery


    Subarachnoidal hemorrhage

    • Rupture of arteries of the circle of Willis 


    accumulation of arterial blood in the subarachnoid
    space

    • Meningeal irritation with a rapid increase in


    intracranial pressure
    Intraparenchymal hemorrhage

    • Rupture of small intrinsic vessels in the setting of


    brain trauma with contusions and lacerations

     intracran. pressure with focal neurologic deficits;


    may be fatal
    Outcome of CNS trauma
    Minor head injury: satisfactory recovery

    Severe head injury: good recovery or patients


    remain disabled:
    • Post-traumatic epilepsy
    • Post-traumatic hydrocephalus: organization of
    subarachnoid hemorrhage  disturbed CSF
    resorption
    • Post-traumatic dementia: due to neuronal loss
    and axonal damage; frequent in boxers who
    have repeated head trauma during several years
    • Persistent vegetative state: in patients with
    diffuse axonal injury
    Spinal cord injury

    • Fracture/dislocation of the vertebral column 


    contusions, nerve fibre transection, hemorrhagic
    necrosis in the cord
    • Lesions involving the thoracic vertebrae or
    below lead to paraplegia
    • Cervical lesions result in tetraplegia
    • Consequences: incontinence, urinary tract and
    pulmonary infections, pressure sores and
    muscle wasting

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