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NEURO MODULE > Pathoma - CNS Pathology > Flashcards

Pathoma - CNS Pathology Flashcards

1
Q

what do neural crests become?

A

PNS

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2
Q

What becomes the CNS system?

A

neural tube

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3
Q

what is LOW before conception of neural tube defect?

A

FOLATE is low

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4
Q

during pregnancy what can be measured to indicated neural tube defect?

A

elevated AFP (alpha-fetoprotein) in both amniotic fluid and maternal blood

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5
Q

anencephaly

A

absence of skill and brain due to disruption of cranial end of neural tube –> frog like fetus + polyhydramnios

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6
Q

polyhydramnios

A

impaired fetal swallowing due to lack/defect in brain swallowing centers

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7
Q

spina bifida

A

failure of posterior vertebral arch to close; disruption of caudal end of neural tube

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8
Q

spina bifida occulta

A

no herniation small dimple or patch of hair above defect

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9
Q

two types of spina bifida

A

meningocele - herniation of meninges (dura and arachnoid) through vertebral defect meningomyelocele - herniation of both meninges and spinal cord

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10
Q

meningomyelocele

A

herniation of meninges and spinal cord

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11
Q

cerebral aqueduct stenosis

A

stenosis of cerebral aqueduct from the 3rd to the 4th ventricle —leads to accumulation of CSF (causes hydrocephalus) –> enlarging head circumference in newborns

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12
Q

hydrocephalus

A

accumulation of CSF (or fluid)

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13
Q

dandy-walker malformation

A

failure of cerebellar vermis (mid portion) to form –> presents as one large dilated 4th ventricle with ABSENCE of cerebellum – can also have hydrocephalus

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14
Q

arnold - chiari malformation

A

downward displacement (herniation) of cerebellar vermis and tonsils through the foramen magnum type 1 - no symptoms type 2 - CSF obstruction –> hydrocephalus (can also have meningomyelocele)

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15
Q

syringomyelia

A

cystic degeneration of the spinal cord at C8-T1 level –due to trauma or with arnold chiari –upper extremity sensory loss of pain and temperature but spares fine touch/position sensing

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16
Q

what parts of spine does syringomyelia affect?

A

anterior white commisure of spinothalmic tract –> SPARES dorsal column (fine touch)

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17
Q

how can syringomyelia progress?

A

syrinx expansion –> anterior horn = lower motor neurons = muscle weakness/atrophy and impaired reflexes –> lateral horn = hypothalamospinal tract (input to face) = HORNER syndrome (ptosis, myosis, anhydrosis)

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18
Q

horner syndrome

A

ptosis (droopy eyelid) myosis (constricted pupil) anhydrosis (decreased sweating)

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19
Q

what spinal cord lesion is horner sydrome associated with?

A

syringomyelia (when it expands to the lateral horn of hypothalamospinal tract)

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20
Q

poliomyelitis

A

damage to the anterior motor horn due to poliovirus infection –lower motor neuron signs = flaccid paralysis, muscle atrophy, impaired reflexes and negative (downward) babinski sign

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21
Q

what has the same effects as poliomyelitis? how is it different?

A

werdnig-hoffman disease INHERITED (AR) degeneration of anterior motor horn –> presents as floppy baby syndrome and causes death

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22
Q

werdnig-hoffman disease

A

inherited (AR) degeneration of anterior motor horn –> causes floppy baby syndrome at birth (lack of muscle tone) and death

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23
Q

ALS

A

amyotrophic lateral sclerosis – degeneration of upper AND lower motor neurons of the corticospinal tract –usually sporadic in middle aged adults; can be due to SOD1 mutation –anterior motor horn degeneration causes lower motor signs (flaccid paralysis, atrophy, impaired reflexes, less muscle tone, negative babinski) –lateral corticospinal tract degeneration causes upper motor neuron signs = spastic paralysis, hyperreflexia, increased tone, positive babinski

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24
Q

how is ALS different from syringomyelia?

A

in ALS you retain pain and T sensation!

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25
Q

early sign of ALS?

A

atrophy and weakness in hands

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26
Q

what mutation can cause ALS and what is its mechanism

A

SOD1 mutation SOD1 = superoxide dismutase –> without this, free radical injury increases in neurons

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27
Q

friedrich ataxia

A

degeration of cerebellum and spinal cord – presents in early (AR) childhood and patients are wheelchair bound -loss of cerebellum –> ataxia (lack of muscle control) -loss of spinal cord –> loss of vibration sense, proprioception, weakness in Lower ext., and loss of deep tendon reflexes

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28
Q

what causes friedrich ataxia

A

Autosomal recessive expansion of trinucleotide repeat (GAA) in the FRATAXIN gene – frataxin is essential for mitochondrion iron regulation so without it –> iron buildup –> free radical damage

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29
Q

frog like fetus?

A

anencephaly - disrupted cranial end of neural tube – absence of brain/skull

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30
Q

spinal tracts and their effects -spinothalmic -dorsal column-medial lemniscus -lateral corticospinal -hypothalamospinal

A

-pain and temperature -pressure, touch, vibration, proprioreception -voluntary movement -sympathetic input to face

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31
Q

meningitis

A

inflammation of the leptomeninges (pia and arachnoid layers) due to infectious agent (virus, bacteria, or fungi) -symptoms = triad ofheadache, neck stiffness (nuchal rigidity), and fever can also cause photophobia, vomiting, and altered mental status

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32
Q

how to perform lumbar puncture?

A

at L4/L5 level because spinal cord ends at L2 so you can go in near cauda equina to sample CSF you cross skin, ligaments, epidural space, dura and arachnoid BUT DO NOT PIERCE THE PIA!

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33
Q

what three agents cause meningitis in neonates? in nonvaccinated infants?

A

e coli group b streptococci listeria monocytogenes - H influenza

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34
Q

what causes meningitis in teenagers? adults? immunocompromised?

A

teens - N meningitidis adults - strep pneumoniae immuno - fungi

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35
Q

lab results of CSF in: viral meningitis bacterial meningitis fungal meningitis

A

v - lymphocytes with normal glucose b - neutrophils with low glucose and gram stain f - lymphocytes with low glucose

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36
Q

global cerebral ischemia

A

global ischemia to brain mild - transient confusion and prompt recovery moderate - infarcts in watershed areas (last areas to be perfused) severe - diffuse necrosis –> vegetative state or death

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37
Q

what causes global cerebral ischemia?

A

low perfusion (like atherosclerosis) low blood flow (shock) hypoxia (anemia) recurrent hypoglycemia

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38
Q

ischemic stroke

A

focal ischemia to brain with neurologic deficits lasting longer than 24 hrs –three types = thrombotic, embolytic, and lacunar –leads to liquefactive necrosis

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39
Q

transient ischemic attack

A

focal ischemia with neurologic deficits lasting less than 24 hrs

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40
Q

thrombotic stroke

A

rupture of atherosclerotic plaque –> pale infarct in cortex periphery

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41
Q

embolic stroke

A

due to thromboemboli, usually w middle cerebral artery –> hemorrhagic infarct in cortex periphery

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42
Q

lacunar stroke

A

hyaline arteriolosclerosis due to diabetes or HTN –> narrowed lumen and low blood flow –involves lenticulostriate vessels –leads to cystic gliosis

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43
Q

lacunar stroke with thalamus involvement–>

A

pure sensory stroke

44
Q

earliest change seen with ischemic stroke?

A

red neurons (12-24 hrs)

45
Q

progression of ischemic stroke

A

12 hrs - red neurons 1 day - neutrophils 1 week - macrophages/microglial cells 1 month - granulation like tissue –> cystic space with gliosis (astrocytes)

46
Q

intracerebral hemorrhage

A

bleeding into brain pernchyma due to rupture of charcot-bouchard microaneurysms of lenticulostriate vessels of middle cerebral artery –complication of HTN (hyaline arteriolosclerosis) –usually at basal ganglia

47
Q

what are symptoms of intracerebral hemorrhage?

A

headache nausea vomiting eventual coma

48
Q

subarachnoid hemorrhage

A

bleeding into subarachnoid space –“worst headache of my life” + neck stiffness –bleeding on the bottom of brain –due to rupture of berry aneurysm (lack of media layer)

49
Q

common site of subarachnoid hemorrhage?

A

anterior circle of willis at branch points of the anterior communicating artery

50
Q

epidural hematoma

A

blood between the dura and skull due to fracture of temporal bone and rupture of middle meningeal artery –lens shaped on CT that separates dura from skull –lucid interval before neurological signs

51
Q

subdural hematoma

A

blood underneath the dura caused by trauma that tears the bridging veins between dura and arachnoid –crescent shaped lesion on CT –progressive neurologic signs

52
Q

who has increased risk of subdural hematoma?

A

the elderly age related cerebral atrophy can stretch the veins

53
Q

tonsillar herniation

A

displacement of cerebellar tonsils into the foramen magnum –> can compress brainstem and lead to cardiopulmonary arrest

54
Q

subfalcine herniation

A

displacement of the cingulate gyrus under the falx cerebri –could compress anterior cerebral artery –> infarction

55
Q

uncal herniation

A

displacement of temporal lobe uncus underneath the tentorium cerebelli

56
Q

effects of uncal herniation

A

–compression of CN III (oculomotor)–> eye moving down and out, dilated pupils –compressed posterior cerebral artery –> occipital lobe infarction –rupture of paramedian artery –> Duret (brainstem) hemorrhage

57
Q

oligodendrocytes

A

myelinate the CNS

58
Q

leukodystrophies

A

problem in the white (myelinated) matter –mutations in the enzymes necessary for production/maintenance of myelin

59
Q

what leukodystrphy causes acumulation in macrphages? FA accumulation? myelin accumulation?

A

1- Krabbe disease 2- adrenoleukodystrophy 3- metachromatic leukodystrophy

60
Q

multiple sclerosis

A

autoimmune destruction of CNS myelin and oligodendrocytes –20-30 yo, women>men –associated with HLA-DR2 –relapsing neurological deficits with periods of remission

61
Q

multiple sclerosis presents with:

A

blurred vision (optic nerve) vertigo and scanning speech (like a drunk) (brainstem) -internuclear opthalmoplegia (medial longitudinal fasciculus) -hemiparesis/loss of sensation (cerebral white matter) -lower extr. loss of sensation (spinal cord) -bowel/bladder/sex dysfunctions (ANS)

62
Q

how to diagnose multiple sclerosis

A

MRI - plaques (mhite matter demyelination) Lumbar puncture - increased lymphocytes, increased immunoglobulins w oligoclonal IgG bands, and myelin basic protein exam –> grey plaques in thewhite matter

63
Q

grey plaques in the white matter

A

multiple sclerosis

64
Q

treat multiple sclerosis

A

high dose steroids and interferon beta

65
Q

subacute sclerosing panencephalitis

A

pan = grey and white slow progressing and debilitating encephalitis leading to death –caused by persistent infection of the brain by measles virus

66
Q

how does subacute sclerosing panencephalitis progress?

A

infection as a baby and neurologic signs show up later in childhood —-brain shows viral inclusions within neurons (grey matter) and oligodendrocytes (white matter)

67
Q

progressive multifocal leukoencephalopathy

A

JC viral infection in oligodendrocytes (white matter) immunosuppression leads to reactivation —-rapidly progressive neurologic signs (visual loss, weakness, dementia –> death)

68
Q

central pontine myelinolysis

A

focal demyelination of the pons (anterior brain stem) due to rapid IV correction of hyponatremia —presents with lockedin syndrome (only eyes can move)

69
Q

what presents with locked in sydrome?

A

central pontine myelinolysis

70
Q

degeneration of cortex leads to

A

dementia

71
Q

degeneration of brainstem and basal ganglia lead to

A

movement disorders

72
Q

alzheimers disease

A

degeneration of cortex - most common cause of dimentia –slow onset memory loss and progressive disorientation, with loss of language and motor skills –become mute and bedridden, die due to infection usually

73
Q

risks for sporadic alzheimers

A

elderly E4 allele of apoproteinE (APOE) increases risk E2 allele decreases risk

74
Q

early onset alzheimers

A

AD, younger presenilin 1 and 2 mutations associated with Downs syndrome (trisomy 21)

75
Q

why is alzheimers early onset associated with DOwns syndrome?

A

because APP (amyloid precursor protein) is encoded on chromosome 21 when APP undergoes B cleavage instead of usual alpha cleavage, it results in AB amyloid which accumulates as deposits

76
Q

morphologic features of alzheimers

A

-cerebral atrophy - narrowing of gyri, widened sulci, and ventricle dilation -neuritic plaques (extracellular AB amyloid with entangled neuritic processes) -neurofibrillary tangles (intracellular aggregate of hyperphosphosylated TAU protein)

77
Q

TAU

A

a microtubule organizing protein -hyperphosphorylized in alzheimers

78
Q

vascular dementia

A

infarction due to HTN, atherosclerosis or vasculitis 2nd cause of dementia

79
Q

Pick Disease

A

degeneration of the frontal and temporal cortex (spares parietal and occipital) –round aggregates of TAU protein (pick bodies) in neurons –early behavior and language symptoms –> dementia eventually

80
Q

round TAU aggregates? fiibers of TAU?

A

round - pick disease fibers - alzheimers

81
Q

parkinsons disease

A

degeneration of dopaminergic neurons in substantia nigra of the basal ganglia -due to aging or MPTP exposure -late dementia

82
Q

clinical features of parkinsons

A

TRAP tremor (pill rolling, disappears with movement) rigidity akinesia - slowed movement/expressionless face postural instability and shuffling gait

83
Q

lewy body dementia

A

early onset dementia -dementia, hallucinations, parkinsonian features and lewy bodies

84
Q

lewy body

A

round inclusions of alpha-synuclein in neurons -seen in parkinsons and lewy body dementia

85
Q

histology of parkinsons

A

lewy bodies loss of pigmented neurons in substantia nigra

86
Q

huntington disease

A

degeneration of GABAergic neurons in the caudate nucleus of the basal ganglia -AD disorder of ch. 4 with expanded CAG trinucleotide repeats in huntingtingene -further expansion leads to anticipation

87
Q

presentation of huntingtons disease

A

average age 40 -chorea (random movements) that progresses to dementia and depression

88
Q

normal pressure hydrocephalus

A

increased CSF resulting in dilated ventricles that can cause dementia –triad of urinary incontinence, gait instability, and dementia (wet, wobbly, and wacky)

89
Q

wet wobbly and wacky

A

normal pressure hydrocephalus -triad of urinary incontinence, gait instability, and dementia

90
Q

treatment for normal pressure hydrocephalus

A

lumbar puncture and ventriculoperitoneal shunting

91
Q

spongiform encephalopathy

A

degeneration due to prion protein that is converted from its usual helical PrP to a B-pleated PrPsc -pathologic protein is not degradable and converts normal protein to bad form = vicious cycle –> intracellular vacuoles (damaged neurons and glial cells)

92
Q

intracellular vacuoles

A

damaged neurons and glial cells of spongiform encephalopathy

93
Q

creutzfeldt-jakob disease (CJD)

A

most common spongiform encephalopathy –rapidly progressive dementia associated with ataxia (cerebellar involvement) and startle myoclonus -sharp waves on EEG

94
Q

mad cow can cause

A

creutzfeldt-jakob disease (CJD)

95
Q

familial fatal insomnia

A

inherited form of prion disease characterized by severe insomnia and exaggerated startle response

96
Q

presentation of metastatic vs primary CNS tumors

A

metastatic - multiple, well circumscribed lesions at grey-white interface primary - locally destructive but rarely metastasize

97
Q

glioblastoma multiforme (GBM)

A

malignant tumor of astrocytes -cerebral hemisphere and crosses the corpus callosum (butterfly lesion) -regions of necrosis surrounded by pseudopalisading tumor cells -GFAP positive poor prognosis

98
Q

most common primary malignancy in adults

A

glioblastoma multiforme

99
Q

meningioma

A

benign tumor of arachnoid cells -women>men -seizures = tumor compresses but does not invade cortex -round mass attached to dura with whorled cell pattern

100
Q

schwannoma

A

benign tumor of schwann cells -involves cranial or spinal nerves - usualy CN VIII at cerebellopontine angle (loss of hearing) -S-100 Positive

101
Q

S-100 +

A

schwannoma

102
Q

oligodendroglioma

A

malignant tumor of oligodendrocytes -calcified tumor in white matter, usually frontal lobe -fried egg cells

103
Q

pilocytic astrocytoma

A

benign tumor of astrocytes, usually in cerebellum -most common in kids -cystic lesion with mural nodule and rosenthal fibers -GFAP positive

104
Q

medulloblastoma

A

malignant tumor from granular cells of the cerebellum -usually kids -small round blue cells and homer wright rosettes -poor prognosis, spreads fast through CSF

105
Q

drop metastasis

A

spread of medulloblastoma to the cauda equina

106
Q

ependymoma

A

malignant tumor of ependymal cells -usually in kids -usually in 4th ventricle with hydrocephalus -perivascular pseudorosettes

107
Q

perivascular pseudorosettes

A

ependymoma

NEURO MODULE (2 decks)

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