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central nervous system Flashcards

1
Q

holoprosencephaly is due to a defect in-

A

SHH signaling

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2
Q

flow of CSF

A 
choroid plexus
lateral ventricles 
interventricular foramen of monro
3rd ventricle
cerebral aquduct
4th ventricle
subarachnoid space (Magendie and Luschka)
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3
Q

most common cause of hydrocephalus in newborns

A

cerebral aqueduct stenosis

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4
Q

dandy-walker malformation

A

failure of cerebellar vermis to form, leads to massive dilation of the 4th ventricle

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5
Q

AC type I

A

low lying cerebellar tonsils- later in life with HA, dizziness

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6
Q

AC type II

A

congenital herniation of tonsils and vermis, presents in infancy with hydrocephalus

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7
Q

AC type I can lead to development of

A

syringomyelia

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8
Q

syringomyelia presentation

A

loss of pain and temp sensation along the arms bilaterally (shaw sign)

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9
Q

expansion of syrinx can lead to 2 complications

A 
UE weakness (anterior motor horn)
Horner syndrome (lateral horn)
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10
Q

early sign of ALS

A

weakness and atrophy of hands

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11
Q

ALS is differentiated from syringomyelia in that it lacks

A

sensory sx

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12
Q

familial ALS is due to

A

mutation in SOD-1 that leads to increased free radical damage

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13
Q

degeneration of ___ leads to ataxia in Friederich’s ataxia

A

spinocerebellar tracts

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14
Q

inheritance/gene/problem of Friederich’s ataxia

A

AR
GAA repeat frataxin gene
impaired mitochondrial iron regulation leads to increased free radicals via Fenton reaction

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15
Q

classic triad of Friederich’s ataxia

A

ataxia, cardiomyopathy, kyphoscoliosis

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16
Q

brown-sequard presentation

A

hemisection of the cord

ipsilateral: PT loss at level, UMN signs and loss of vibe/light touch below
contralateral: loss of PT starting 2-3 segments below injury

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17
Q

tabes dorsalis symptoms (3)

A

impaired vibratory sense (destruction of dorsal columns), arygll-robinson pupils (accommodate but don’t react), +rhomberg

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18
Q

fungal meningitis CSF

A

lymphocytes, low glucose

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19
Q

areas of the brain most susceptible to ischemia (4)

A

watershed areas
pyramidal neurons in layers 3/5/6 cortex
pyramidal neurons in hippocampus
Purkinje cells of the cerebellum

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20
Q

thromboembolic stroke- m/c source, type of infarct

A

m/c source- plaque in carotid artery

pale infarct

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21
Q

embolic stroke- m/c source, type of infarct

A

m/c source- atrial fibrillation

hemorrhagic infarct

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22
Q

lacunar stroke- pathophysiology

A

hyaline arteriolosclerosis of the lenticulostriate branches of MCA secondary to chronic hypertension

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23
Q

histologic changes after ischemia- day 0

A

12 hours- red neurons (eosinophilic, pyknosis, cell shrinking)

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24
Q

histologic changes after ischemia- day 1

A

24 hours- liquefactive necrosis
1-3 days- neutrophils
4-7 days- macrophages (microglia)

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25
histologic changes after ischemia- 1 week
granulation-like tissue
26
histologic changes after ischemia- 1 month
reactive astrocytes yield gliosis
27
hemorrhagic strokes are also called
intraparenchymal hemorrhages
28
m/c cause of intraparenchymal hemorrhages
rupture of charcot-bouchard aneurysms
29
charcot-bouchard aneurysm pathophysiology
develop secondary to hyaline arteriolosclerosis, complication of long-standing HTN
30
presentation of intraparenchymal hemorrhage
focal neurologic signs, headache
31
presentation of SAH
sudden, severe HA | nuchal rigidity
32
m/c cause of SAH
rupture of berry aneurysm
33
common sites of berry aneurysm
bifurcations- ACA and anterior communicating artery (due to lack of intima media layer)
34
conditions associated with increased risk of berry aneurysms
ADPKD | EDS
35
long term neurologic deficits related to SAH are secondary to
vasospasm (prevent with nimodipine)
36
intraventricular hemorrhage-
premature babies (less than 32 weeks) in the first 72 hours of life
37
epidural hematoma
temporal bone fracture- rupture of middle meningeal a, blood between dura and skull, lucid interval, lens shaped
38
subdural hematoma
rupture of bridging veins, blood between dura and arachnoid, slow bleed, crescent shaped
39
3 populations with increased subdural hematomas
shaken baby syndrome elderly alcoholic
40
subfalcine herniation + 1 complication
cingulate gyrus under falx cerebri, leads to infarction of ACA
41
uncal herniation + 3 complications
uncus of temporal lobe under tantrum cerebelli, compression of CN III (fixed dilated pupil, down and out eye), compression of PCA (contralateral homonymous hemianopsia), rupture of paramedian artery (Duret hemorrhage of brainstem)
42
tonsillar herniation + 1 complication
cerebellar tonsils into foramen magnum | cardiopulmonary arrest
43
metachromatic leukodystropy (inheritance, deficiency and consequences)
AR arylsulfatase accumulation of sulfatides in lysosomes
44
Krabbe disease (inheritance, deficiency and consequences)
AR galactocerebrosidase galactocerebroside accumulates in macrophages
45
Adrenoleukodystrophy
X-linked impaired addition of Co-A to LCFA accumulation of FA in adrenals and white matter
46
MS HLA association
DR2
47
MS lumbar puncture
lymphocytosis | Oligoclonal IgG bands
48
central pontine myelinolysis- caused by, results in
rapid correction of hyponatremia | locked in syndrome
49
AB amyloid pathophysiology
abnormal APP is degraded by b-secretase that leads to b-product = AB amyloid
50
APO increased and decreased risk of AD
increased- APO e4 | decreased- APO e2
51
familial AD
presenilin 1/2
52
neuritic plaques (location, composition)
extracellular | AB amyloid and neuritic processes
53
neurofibrillary tangles ((location, composition)
intracellular | hyperphosphorylated Tau
54
area of the brain that exhibits greatest atrophy in AD
hippocampus
55
4 brain changes in AD:
cerebral atrophy neuritic plaques neruofibrillary tangles loss of ACH from nucleus basalis
56
cerebral amyloid angiopathy
AB amyloid deposition around blood vessels, increases risk of hemorrhage
57
vascular dementia is characterized by (2)
focal neuro deficits | step wise progression
58
Picks disease main impairments (2)
language (temporal) and behavior (frontal)
59
lewy bodies contain
a-synuclein
60
HD is caused by
loss of GABA neurons in caudate nucleus
61
HD inheritance, defect
AD | CAG repeat in huntingtin gene on chromosome 4
62
in trinucelotide repeat disorders, anticipation is due to expansion of repeats during-
spermatogenesis
63
triad of NPH
ataxia dementia urinary incontinence
64
pathogenesis of NPH symptoms
stretching of descending cortical fibers that line the ventricles
65
pathogenesis of prion diseases
prion protein takes an altered B-pleated sheet configuration that cannot be degraded and accumulates
66
CJD is characterized by (4)
rapid onset dementia, startle myoclonus, ataxia, sharp waves on EEG
67
characteristic appearance of metastatic brain tumors
multiple, well circumscribed lesions at the gray-white junction
68
most common primary CNS tumor of adults
glioblastoma multiforme
69
most common primary CNS tumor of children
pilocytic astrocytoma
70
whorled pattern with psammoma bodies
meningioma
71
perivascular pseudorosettes
ependymoma
72
rosenthal fibers
pilocytic astrocytoma
73
pesudopallisading tumor cells surrounding areas of necrosis
glioblastoma multiforme
74
s100+ with highly cellular areas mixed with mixed regions of low cellularity
schwannoma
75
fried-egg appearance
oligodendroglioma
76
small, round blue cells in homer-write rosettes
medulloblastoma
77
glioblastoma multiforme
malignant, astrocytes | butterfly lesion that crosses corpus callosum
78
meningioma
ER+ (more common in women) | does not invade cortex, but may compress
79
schwannoma
m/c affects CN VIII leading to hearing loss and tinnitus
80
bilateral schwannomas are associated with
NF2
81
schwannoma staining
S100+ (neural crest cell derived)
82
oligodendroglioma imaging
calcified mass, usually in frontal lobe
83
VHL associated masses
hemangioblastoma of the cerebellum renal cysts RCC
84
pilocytic astrocytoma imaging
cystic lesion with mural nodule
85
ependymoma presentation
hydrocephalus
86
histologic finding in AIDS dementia
microglial nodules

path block 6 (8 decks)

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