Cns

Front 1

specific groups of neurons are singled out for destruction

Back 1

selective vulnerability

Front 2

cells derived from neuroectoderm or frm bone marrow

role in inflammation, repair, fluid balance, and energy metabolism

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glia

Front 3

glial cells found throughout CNS in boh gray and white matter

star shaped appearance; multipolar branching cytoplasmic proscesses containing GFAP

some processes directed toward neurons and their processes-> synapse/act as metabolic buffers/detox, suppliers of nutrients, electric insulators

principle cells responsible for repair/scar formation in the brain

Back 3

astrocytes

Front 4

cells with cytoplasmic processes that wrap around the axons of neurons to form myelin in a manner analogous to the schwann cells of teh PNS

recognizable by their small, rounded, lymphocyte like nuclei, often in linear array

Back 4

oligodendrocytes

Front 5

cells that line the ventricular system

closely related to the cuboidal cells comprising the choroid plexus

viral inclusions may be seen in these cells after injury

Back 5

ependymal cells

Front 6

mesoderm derived cells whose primary function is to serve as a fixed macrophage system in teh CNS

express CR3 and CD68

respond to injury by proliferation, developing elongated nuclei (rod cells), forming aggregates about small foci of tissue necosis, congregating around cell bodies of dying neurons

Back 6

microglia

Front 7

sectrum of serum changes that accompany acute CNS hypoxia/ischemia

evident 12-24 hour after an irreversible hypoxic/ischemic insut

shrinkage of the cell body, pyknosis of the nucleus, disappearance of the nucleolus adn loss of Nissl substance with intense eosinophilia of cytoplasm

often nucleus assumes an angulated shape

Back 7

red neuron

Front 8

situations leading to neuronal death occuring as a result of progressive disease process of some duration

cell loss, often selectively involving functionally related systems of neurons and reactive gliosis

Back 8

subacute/chronic neuronal injury (degeneration)

Front 9

destructive process that interrupts majority of afferent input to a group of neurons

Back 9

transsynaptic degeneration

Front 10

reaction within the cell body that attends regeneration of the axon

increased protein synthesis; axonal sprouting

enlargement and roundign up the cell body, peripheral displacement of the nucleus, enlargement of the nucleolus, and dispersion of Nissl substance from the center to periphery of the cell

Back 10

axonal reaction

Front 11

manifestation of aging, when there are intracytoplasmic accumulations of cytoplasmic lipids, proteins, or carbohydrates

Back 11

nuclear inclusions

Front 12

neuronal cell body becomes greatly swollen at first because of intracytoplasmic accumulation of abnormal metabolite

process culminates in death

Back 12

disorders of metabolism

Front 13

most important histopathologic indicator of CNS injury

astrocytes undergo hypertrophy and hyperplasia; nucleus enlarges and becomes vesicular adn nucleolus is prominent

cytoplasm expands; in long standing lesions the nuclei becom small and dark and lie in a dense net of processes

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gliosis

Front 14

proliferation of astrocytes residing between molecular adn granule cell layers of the cerebellum

regular accompaniment of anoxic injury and other conditions associeated withPurkinje cells

Back 14

Bergmann gliosis

Front 15

thick, elongated, brightly eosinophilic structures that are somewhat irregular in contour and occur within astrocytic processes

dense osmiophilic deposits taht contain alpha beta crystallin and hsp27 adn ubiquitin

found in regions of long standing gliosis

Back 15

Rosenthal fibers

Front 16

polyglucosan bodie are round faintly basophilic, PAS positive, concentrically lamellated structures ranging between 5 and 50 micrometre in diameter; located wherever there are astrocytic end processes, especially in subpial and perivascular zones

contain heat shock proteins and ubiquitin

Back 16

corpora amylacea

Front 17

silver positive meshes of intermediate filaments that contain alpha synuclein

characteristic of CNS degenerative disease

Back 17

Glial cytoplasmic inclusions

Front 18

gray matter astrocyte with large nucleus, pale staining central chromatin, intranuclear glycogen droplet, prominent nuclear membrane nucleolus

patients with long standing hyperammonemia due to chronic liver disease, Wilson disease, or hereditary metabolic disorder of the urea cycle

Back 18

Alzheimer type II astrocyte

Front 19

integrity of the normal BBB is disrupted and increased vascular permeability occurs allowing fluid to excape from the intravascular compartment predominantly into the inercellular spaces of the brain

impaired resorption of excess extracellular fluid

Back 19

vasogenic edema

Front 20

increase in the intracellular fluid secondaryto neuronal, glial, or endothelial cell membrane injury

Back 20

cytotoxic edema

Front 21

brain is softer than normal and often appears to overfill the cranial vault

gyri are flattened, intervening sulci narrowed, and ventricular cavities are compressed

herniation may occur

Back 21

cerebral edema

Front 22

unilateral or asymmetric expansion of a cerebral hemisphere displaces the cingulate gyrus under teh falx cerebri

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subfalcine herniation

Front 23

medial aspect of the temporal lobe is compressed against the free margin of teh tentorium cerbelli

third cranial nerve is compromised resulting in pupillary dilation and impairment of the ocular movements on the side of the lesion

Back 23

transtentorial herniation

Front 24

transtentorial herniation is large enough the contralateral cerebral peduncle may be compressed resulting in hemiparesis ipsilateral to the side of the herniation

Back 24

Kernohan's notch

Front 25

displacement of the cerebellar tonsils through the foramen magnum

causes brainstem compression adn compromises vital respiratory adn cardiac centers in the medulla oblongata

Back 25

tonsillar herniation

Front 26

accumulation of excess CSF within the ventricular system

expanded ventricles, elevation of intracranial pressure; enlarges the head if before suture closure

Back 26

hydrocephalus

Front 27

enlargement of a portion of the ventricular system

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noncommunicating hydrocephalus (impaired flow)

Front 28

enlargement of the entire ventricular system

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communicating hydrocephalus (excess production)

Front 29

dilation of ventricular system with compensatory increase in CSF volume secondary to loss of brain parenchyma

Back 29

hydrocephalu ex vacuo

Front 30

failure of a portion of the neural tube to close or reopening of a region of the tube that has successfully closed

Back 30

neural tube defect

Front 31

malformation of the anterior end of the neural tube with absence of the brain and clvarium

more common in females

flattened remnant of disorganized brain tissue, area cerebrovasculosa, wher forebrain should be

Back 31

anencephaly

Front 32

diverticulum of malformed CNS tissue extending through a defect in the cranium; most offten in the occipital region or posterior fossa

Back 32

encephalocele

Front 33

most common forms of neural tube defect in new borns

failure of closure/reopening of caudal portions of neural tube

elevated alpha fetoprotein and folate deficiency

Back 33

spinal dysraphism or spina bifida

Front 34

extension of CNS tissue through a defect in the vertebral column

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myelomeningocele

Front 35

asymptomatic bony defect form of spina bifida

Back 35

occulta

Front 36

meningeal extension through defect in the vertebral system

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menigocele

Front 37

loss of the normal external contour of the cerebral convolutions

gray matter is composed of four or less layers

may be induced by localized tissue injury durign the time of neuronal migration

Back 37

polymicrogyri

Front 38

absence of gyri leaving a smooth surfaced brain

Back 38

lissencephaly

Front 39

seizure, mental retardation, lissencephaly

absence LIS1

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Miller-Dieker syndrome

Front 40

lethal disease characterized by abnormally large hyperconvoluted temporal lobes and skeletal anomalies

Back 40

thanatorphoric dwarfism

Front 41

incomplete separation of cerebral hemispheres across the midline

may have cyclopia

sonic hedgehog mutations

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holoprosencephaly

Front 42

relatively common malformation in which there is an absence of white matter bundles

bat wing deformity

Back 42

agenesis of the corpus callosum

Front 43

x linked syndrome that is lethal in males in which it is associated with chorioretinal defects and seizures

Back 43

aicardi syndrome

Front 44

small posterior fossa, misshapen midline cerebellum with downward extension of the vermis through the foramen magnum

hydrocephalus and lumbar myelomeningocele

caudal displacement of the medulla, malformation of the tectum, aqueductal stenosis, cerebral heterotopias, hydromyelia

Back 44

Arnold chiari malformation

Front 45

low lying cerebellar tonsils extend down into vertebral canal adn may cause symptoms referable to obstruction of CSF flow and medullary compression

Back 45

Chiari I malformation

Front 46

enlarged posterior fossa

cerebellar vermis is absent or present only in rudimentary forms; in its place a large midline cyst that is lined by ependyma and is contiguous with the leptomeninges

Back 46

dandy walker formation

Front 47

discontinuous multisegmental or confluent expansion of the ependyma-lined central canal of the cord

Back 47

hydromyelia

Front 48

formation of a fluid filled cleft like cavity in the inner portion of the cord

2nd/3rd decades of life

progressive evolution of dissociated sensory loss of pain adn temperature sensation inthe upper extremities

Back 48

syringomyelia, syrinx

Front 49

syringomyelia that extend into the brainstem

Back 49

syringobulbia

Front 50

non progressive neurologic motor deficit characterized by spasticity, dystonia, ataxia/athetosis, paresis attributable to insults during prenatal/perinatal periods

signs and symptoms may not be apparent at birth

Back 50

cerebral palsy

Front 51

injury premature infants are at risk for

found within germinal matrix; often near the junction between the thalamus and the caudate nucleus

may be localized or extend into the ventricular system leading to hydrocephalu

Back 51

parenchymal hemorrhage

Front 52

chalky yellow plaques consisting of discrete regions of white matter necrosis and mineralization

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periventricular leukomalacia

Front 53

both gray and white matter are involved by extensive ischemic damage, large destructive cystic lesions develop througout the hemisphere

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multicystic encephalopathy

Front 54

depths of sulci bear brunt of injury

thinned out gliotic gyri present

Back 54

ulegyria

Front 55

fractures that cross sutures

Back 55

diastatic

Front 56

fracture in which the bone is displaced into teh cranial cavity by a distance greater than the thickness of teh bone

Back 56

displaced skull fracture

Front 57

skull fractures that follow a blow to the occiput

symptoms referable to the lower cranial nerves or cervicomedullary region adn presence of orbital or mastoid hematoma

CSF discharge from nose or ear and meningitis may follow

Back 57

basal skull fracture

Front 58

alteratino of consciousness secondary to head injury typically brought about by change in momentum of the head

transient neurologic dysfunction

Back 58

concussion

Front 59

area most susceptible to contusion

Back 59

crests of gyri of the frontal lobes along the orbital gyri and temporal lobes

Front 60

most common contusions of the occipital lobes, brainstem, cerebellum

Back 60

fracture contusion

Front 61

cerebral injury at point of contact

Back 61

coup

Front 62

cerebral injury to brain surface diametrically opposite to the point of contact

Back 62

contrecoup

Front 63

wedge shaped lesion with the broad base spannign the surface adn centered on the point of impact

earliest stages: edema and hemorrhage that is often pericapillary; later extravasation of blood extends throughout the cortex and into the white matter and subarachnoid space

axonal swelling in the vicinity fo the damaged neuros or at the great distances; appearance of neutrophils then macrophages

old lesion: depressed, retracted, yellowish brown patches involving the crests of the gyri most commonly at sites of contrecoup

gliosis and residual hemosiderin laden macrophages

Back 63

contusions/plaque jaune lesions

Front 64

wide but often asymmetric distribution of axonal swellings that appear within hours of the injury adn may persist for much longer

later increase numbers of microglia in related areas of cerebral cortex; subsequent degeneration of involved fiber tracts

Back 64

diffuse axonal injury

Front 65

temporary displacement of the skull bones leading to laceration of a vessel can occur in the absence of a skull fracture

accumulation of blood under arterial pressure can cause separation of dura from the inner surface of the skull

expanding hematoma has smooth contour that compresses the brain surface

patient may be lucid for several hours

Back 65

epidural hematoma

Front 66

tearing of the bridging veins

collection of freshly clotted blood along the contour of the brain surface without extension into the depths of the sulci

underlying brain is flattened; bleeding typically self limiting

organized hematoma develops over weeks; lesion may eventually retract as granulation tissue matures until there may only be a thin layer of reactive cnnective tissue remaining

most often become manifest in first 48 hours after injury

Back 66

subdural hematoma

Front 67

delayed posttraumatic bleeding

syndrome of sudden deep intracerebral hemorrhage that follows even minor head trauma by an interval of 1-2 weeks

Back 67

spat apoplexie

Front 68

obstruction of CSF resorption from hemrrhage into subarachnoid spaces

Back 68

post traumatic hydrocephalus

Front 69

dementia that follows repeated head trauma during a protracted period

hydrocephalus, thinning of corpus callosum, diffuse axonal injury, neurofibrillary tangles, diffuse A beta positive plaques

Back 69

posttraumatic dementia/punch drunk syndrome

Front 70

at level of injury the acute phase consists of hemorrhage, necrosis, and axonal swelling in the surrounding white matter; lesion tapers above and below teh level of the injury

central necrotic lesion becomes cystic and gliotic

secondary ascending and descending wallerian degeneration respectively, involving the long white matter tracts affected at the site of trauma

Back 70

spinal cord trauma

Front 71

generalized reduction of cerebral perfusion

cardiac arrest, shock, severe hypotension

Back 71

global ischemia

Front 72

reduction or cessation of blood flow to a localized area of brain due to large vessel disease (such as embolic or thrombotic arterial occlusion) or small vessel disease (vasculitis or occlusion)

Back 72

focal ischemia

Front 73

neurons are most sensitive; widespread neuronal death, irrespective of regional vulnerability

Back 73

global ischemia

Front 74

brain is swollen, gyri are widened, sulci are narrowed

poor demarcation between white and gray matter

early changes: microvacuolization, eosinophilia of neuronal cytoplasm, pyknosis and karyorhexis (red neurons)

subacute changes: necrosis of tissue, influx of macrophages, vascular proliferation, reactive gliosis

repair after 2 weeks

Back 74

global ischemia

Front 75

cells most susceptible to global ischemia of short duration

Back 75

pyramidal cells of Sommer sector of hippocampus, Purkinje of the cerebellum, pyramidal of the neocortex

Front 76

wedge shaped areas of infarction that occur in he regions of the brain and spinal cord that lie at teh most distal fields of arterial irrigation

MCA/ACA is at greatest risk

sickle-shaped band of necrosis over cerebral convexity

Back 76

border zone/watershed ifarcts

Front 77

amino acids neurotransmitters released during ischemia

cause damge by overstimulation and persistent opening of specific membrane channels

Back 77

excitatory such as glutamate

Front 78

most common sites of primary thrombosis causing cerebral infarction

Back 78

carotid bifurcation, origin of the MCA, either end of the basilar artery

Front 79

inflammatory disorder that involves multiple small to medium sized parenchymal and sub arachnoid vessels

chronic inflammation, multinucleated giant cells and destruction of teh vessel wall

Back 79

primary angiitis of the CNS

Front 80

rare hereditary strok caused by mutations of Notch3

recurrent strokes and dementia

concentric thickening of the media and adventitiA

Back 80

cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL)

Front 81

amyloidogenic peptides nearly alwasy the ame one found in Alzheimer disease deposit in the wall of medium and small caliber meningeal and cortical vessels

deposition can result in weakening of the vessel wall and risk of hemorrhage from sporadic CAA; presence of epsilon 2 or 4 increase teh risk of rebleeding

Back 81

Cerebral amyloid angiopathy

Front 82

familial form CAA

Back 82

hereditary cerebral hemorrhge with amyloidosis Dutch type

Front 83

multiple sometimes confluent petechial hemorrhages typically associated with embolic events

secondary to reperfusion of damaged vessels

Back 83

hemorrhagic infarction

Front 84

tissue pale, soft, and swollen at 48 hours/corticomedullary junctino becomes indistinct

brain becomes gelatinous and friable

after teh edema resolves the tissue liquifies, eventually leaving a fluid filled cavity lined by dark gray tissue which gradually expands as dead tissue is removed

Back 84

non hemorrhagic infarct

Front 85

ischemic neuronal change adn both cytotoxic and vasogenic edema predominate

endothelial and glial cells, mainly astrocytes, swell and myelinated fibers begin to disintegrate

neutrophilic emigration progressively increases then falls off; as liquefaction and phagocytosis proceeds astrocytes at the edges of teh legion progressively enlarge, divide and develop a prominent network of protoplasmic extension

dense feltwork of glial fibers admixed with new capillaries and a few perivascular connective tissue fibers

Back 85

non hemorrhagic infarct

Front 86

parallel ischemic infarctino with the addition of blood extravasation and resorption

may be associated with extensive intracranial hematomas

Back 86

hemorrhagic

Front 87

focal cerebral ischemia when there is selective necrosis of neurons with relative preservation of glia and supporting tissues

Back 87

incomplete infarction

Front 88

hypoperfusion or consequence of interruption of the feeding tributaries derived from the aorta

Back 88

spinal cord infarction

Front 89

may originate in the putamen, pons, thalamus, cerebellar hemispheres

ganglionic hemorrhages

extravasation of blood with compression of the adjacent parenchyma; old hemorrhages show an area of cavitary destruction of teh brain with a rim of brownish color

central core of clotted blood surrounded by a rim of brain tissue showing anoxic neuronal and glial changes and edema

pigment and lipid laden macrophages; proliferation of reactive astrocytes

Back 89

hypertensive intraparenchymal hemorrhage

Front 90

thin walled outpouching at an arterial branch point along the circle of willis

bright red, shiny surface and thin, translucent wall

rupture at the apex fo the sac with extravasation of blood into subarachnoid space , the substance of the brain, or both

wall adjacent to neck often shows intimal thickening and gradual attenuation of the media as it approaches the neck; at the neck of tehaneurysm the muscular wall and intimal elastic lamina stop short and are absent from the sac

Back 90

berry aneurysm

Front 91

vessels in the subarachnoid space extending into the brain parenchyma

may occur exclusively within the brain

network of wormlike vascular channels that have pulsatile arteriovenous shunt with high blood flow

greatly enlarged blood vessels separated by gliotoc tissue enlarged blood vessels separated by gliotic tissue often with evidence of prior hemorrhage

Back 91

arteriovenous malformation

Front 92

consist of greatly distended loosely organized vascular channels with thin nervous tissue

most often in the cerebellum

Back 92

cavernous hemangiomas

Front 93

microscopic foci of dilated thin-walled vasculr channels separated by relatively normal brain parenchyma

most frequent in the pons

Back 93

capillary telangiectasias

Front 94

aggregates of ectatic venous channels

Back 94

venous angiomas

Front 95

venous angiomatous malformation of the spinal cord and overlying meninges associated with ischemic myelomalcia and slowly progressive neurologic symptoms most often referable to the lumbosacral cord

Back 95

Foix-Alajouanin disease

Front 96

rupture of the small caliber penetrating vessels adn the deelopment of small hemorrhages; in time they resorb leaving behind cavity

Back 96

slit hemorrhage

Front 97

pattern of encephalopathic injury preferentially involving the large areas of the subcortical white matter with myelin and axon loss

Back 97

Binswanger disease