Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

NEURO MODULE > Pathoma - CNS Pathology > Flashcards

Pathoma - CNS Pathology Flashcards

1
Q

what do neural crests become?

A

PNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What becomes the CNS system?

A

neural tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is LOW before conception of neural tube defect?

A

FOLATE is low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

anencephaly

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

polyhydramnios

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

spina bifida

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

spina bifida occulta

A

no herniation small dimple or patch of hair above defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

meningomyelocele

A

herniation of meninges and spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

hydrocephalus

A

accumulation of CSF (or fluid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what parts of spine does syringomyelia affect?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

horner syndrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what spinal cord lesion is horner sydrome associated with?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

how is ALS different from syringomyelia?

A

in ALS you retain pain and T sensation!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
early sign of ALS?
atrophy and weakness in hands
26
what mutation can cause ALS and what is its mechanism
SOD1 mutation SOD1 = superoxide dismutase --\> without this, free radical injury increases in neurons
27
friedrich ataxia
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
28
what causes friedrich ataxia
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
29
frog like fetus?
anencephaly - disrupted cranial end of neural tube -- absence of brain/skull
30
spinal tracts and their effects -spinothalmic -dorsal column-medial lemniscus -lateral corticospinal -hypothalamospinal
-pain and temperature -pressure, touch, vibration, proprioreception -voluntary movement -sympathetic input to face
31
meningitis
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
32
how to perform lumbar puncture?
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!
33
what three agents cause meningitis in neonates? in nonvaccinated infants?
e coli group b streptococci listeria monocytogenes - H influenza
34
what causes meningitis in teenagers? adults? immunocompromised?
teens - N meningitidis adults - strep pneumoniae immuno - fungi
35
lab results of CSF in: viral meningitis bacterial meningitis fungal meningitis
v - lymphocytes with normal glucose b - neutrophils with low glucose and gram stain f - lymphocytes with low glucose
36
global cerebral ischemia
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
37
what causes global cerebral ischemia?
low perfusion (like atherosclerosis) low blood flow (shock) hypoxia (anemia) recurrent hypoglycemia
38
ischemic stroke
focal ischemia to brain with neurologic deficits lasting longer than 24 hrs --three types = thrombotic, embolytic, and lacunar --leads to liquefactive necrosis
39
transient ischemic attack
focal ischemia with neurologic deficits lasting less than 24 hrs
40
thrombotic stroke
rupture of atherosclerotic plaque --\> pale infarct in cortex periphery
41
embolic stroke
due to thromboemboli, usually w middle cerebral artery --\> hemorrhagic infarct in cortex periphery
42
lacunar stroke
hyaline arteriolosclerosis due to diabetes or HTN --\> narrowed lumen and low blood flow --involves lenticulostriate vessels --leads to cystic gliosis
43
lacunar stroke with thalamus involvement--\>
pure sensory stroke
44
earliest change seen with ischemic stroke?
red neurons (12-24 hrs)
45
progression of ischemic stroke
12 hrs - red neurons 1 day - neutrophils 1 week - macrophages/microglial cells 1 month - granulation like tissue --\> cystic space with gliosis (astrocytes)
46
intracerebral hemorrhage
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
what are symptoms of intracerebral hemorrhage?
headache nausea vomiting eventual coma
48
subarachnoid hemorrhage
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
common site of subarachnoid hemorrhage?
anterior circle of willis at branch points of the anterior communicating artery
50
epidural hematoma
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
subdural hematoma
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
who has increased risk of subdural hematoma?
the elderly age related cerebral atrophy can stretch the veins
53
tonsillar herniation
displacement of cerebellar tonsils into the foramen magnum --\> can compress brainstem and lead to cardiopulmonary arrest
54
subfalcine herniation
displacement of the cingulate gyrus under the falx cerebri --could compress anterior cerebral artery --\> infarction
55
uncal herniation
displacement of temporal lobe uncus underneath the tentorium cerebelli
56
effects of uncal herniation
--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
oligodendrocytes
myelinate the CNS
58
leukodystrophies
problem in the white (myelinated) matter --mutations in the enzymes necessary for production/maintenance of myelin
59
what leukodystrphy causes acumulation in macrphages? FA accumulation? myelin accumulation?
1- Krabbe disease 2- adrenoleukodystrophy 3- metachromatic leukodystrophy
60
multiple sclerosis
autoimmune destruction of CNS myelin and oligodendrocytes --20-30 yo, women\>men --associated with HLA-DR2 --relapsing neurological deficits with periods of remission
61
multiple sclerosis presents with:
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
how to diagnose multiple sclerosis
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
grey plaques in the white matter
multiple sclerosis
64
treat multiple sclerosis
high dose steroids and interferon beta
65
subacute sclerosing panencephalitis
pan = grey and white slow progressing and debilitating encephalitis leading to death --caused by persistent infection of the brain by measles virus
66
how does subacute sclerosing panencephalitis progress?
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
progressive multifocal leukoencephalopathy
JC viral infection in oligodendrocytes (white matter) immunosuppression leads to reactivation ----rapidly progressive neurologic signs (visual loss, weakness, dementia --\> death)
68
central pontine myelinolysis
focal demyelination of the pons (anterior brain stem) due to rapid IV correction of hyponatremia ---presents with lockedin syndrome (only eyes can move)
69
what presents with locked in sydrome?
central pontine myelinolysis
70
degeneration of cortex leads to
dementia
71
degeneration of brainstem and basal ganglia lead to
movement disorders
72
alzheimers disease
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
risks for sporadic alzheimers
elderly E4 allele of apoproteinE (APOE) increases risk E2 allele decreases risk
74
early onset alzheimers
AD, younger presenilin 1 and 2 mutations associated with Downs syndrome (trisomy 21)
75
why is alzheimers early onset associated with DOwns syndrome?
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
morphologic features of alzheimers
-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
TAU
a microtubule organizing protein -hyperphosphorylized in alzheimers
78
vascular dementia
infarction due to HTN, atherosclerosis or vasculitis 2nd cause of dementia
79
Pick Disease
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
round TAU aggregates? fiibers of TAU?
round - pick disease fibers - alzheimers
81
parkinsons disease
degeneration of dopaminergic neurons in substantia nigra of the basal ganglia -due to aging or MPTP exposure -late dementia
82
clinical features of parkinsons
TRAP tremor (pill rolling, disappears with movement) rigidity akinesia - slowed movement/expressionless face postural instability and shuffling gait
83
lewy body dementia
early onset dementia -dementia, hallucinations, parkinsonian features and lewy bodies
84
lewy body
round inclusions of alpha-synuclein in neurons -seen in parkinsons and lewy body dementia
85
histology of parkinsons
lewy bodies loss of pigmented neurons in substantia nigra
86
huntington disease
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
presentation of huntingtons disease
average age 40 -chorea (random movements) that progresses to dementia and depression
88
normal pressure hydrocephalus
increased CSF resulting in dilated ventricles that can cause dementia --triad of urinary incontinence, gait instability, and dementia (wet, wobbly, and wacky)
89
wet wobbly and wacky
normal pressure hydrocephalus -triad of urinary incontinence, gait instability, and dementia
90
treatment for normal pressure hydrocephalus
lumbar puncture and ventriculoperitoneal shunting
91
spongiform encephalopathy
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
intracellular vacuoles
damaged neurons and glial cells of spongiform encephalopathy
93
creutzfeldt-jakob disease (CJD)
most common spongiform encephalopathy --rapidly progressive dementia associated with ataxia (cerebellar involvement) and startle myoclonus -sharp waves on EEG
94
mad cow can cause
creutzfeldt-jakob disease (CJD)
95
familial fatal insomnia
inherited form of prion disease characterized by severe insomnia and exaggerated startle response
96
presentation of metastatic vs primary CNS tumors
metastatic - multiple, well circumscribed lesions at grey-white interface primary - locally destructive but rarely metastasize
97
glioblastoma multiforme (GBM)
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
most common primary malignancy in adults
glioblastoma multiforme
99
meningioma
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
schwannoma
benign tumor of schwann cells -involves cranial or spinal nerves - usualy CN VIII at cerebellopontine angle (loss of hearing) -S-100 Positive
101
S-100 +
schwannoma
102
oligodendroglioma
malignant tumor of oligodendrocytes -calcified tumor in white matter, usually frontal lobe -fried egg cells
103
pilocytic astrocytoma
benign tumor of astrocytes, usually in cerebellum -most common in kids -cystic lesion with mural nodule and rosenthal fibers -GFAP positive
104
medulloblastoma
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
drop metastasis
spread of medulloblastoma to the cauda equina
106
ependymoma
malignant tumor of ependymal cells -usually in kids -usually in 4th ventricle with hydrocephalus -perivascular pseudorosettes
107
perivascular pseudorosettes
ependymoma

NEURO MODULE (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions