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Neuro > Cerebrovascular Diseases and Infections > Flashcards

Cerebrovascular Diseases and Infections Flashcards

1
Q

What vascular deficits causes UMN weakness, cortical-type sensory loss and contralateral hemiplegia (initially)

A

ACA (anterior cerebral artery)

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2
Q

What vascular deficit causes contralateral leg > arm and face?

A

ACA

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3
Q

Injury to what causes alien hand syndrome?

A

ACA

semiautomatic movements of contralateral arm not under voluntary control

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4
Q

What vascular deficit causes contralateral homonymous hemianopia (only see one side of eye in both eyes)?

A

PCA

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5
Q

What is the most common vascular place for infarct and ischemia? Why?

A

MCA (middle cerebral artery)

larger territory

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6
Q

What vascular defect causes aphasia, hemineglect, hemianopia, face/arm (more common) or face/arm/leg sensorimotor loss?

A

MCA

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7
Q

MCA ischemia/infarct causes gaze preference toward….

A

toward side of lesion

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8
Q

Define lacunes

A

small, deep infarct involving penetrating branches of MCA (lenticulostriae vessels)

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9
Q

What is the third leading cause of death in US?

A

cerebrovascular disease

heart, cancer, then brain dz

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10
Q

What are the 3 major categories of cerebrovascular diseases?

A

Thrombosis
Embolism
Hemorrhage

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11
Q

What cerebrovascular disease condition does stroke apply to clinically?

A

All (thrombosis, embolism, hemorrhage)

especially acute symptomatology

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12
Q

What is an infarction in terms of stroke?

A

resultant lesion of brain parenchyma from thrombosis, embolism or hemorrhage

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13
Q

What are the most common cerebrovascular disorders?

A

Global ischemia (whole brain)

Embolism

Hypertensive Intraparenchymal Hemorrhage (most common, people don’t take meds or not treated)

Ruptured Aneurysm

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14
Q

Does oxygen or metabolic substrate limit brain oxygenation?

A

oxygen

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15
Q

When blood flow is reduced, survival depends on ……

A

collateral circulation (circle of willis)

duration of ischemia (TIA vs stroke)

magnitude and rapidity of flow reduction (slow blood loss or hypoxia vs fast)

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16
Q

What are 2 types of reduction in blood flow to brain?

A

global ischemia–> generalized reduction of perfusion
~~~cardiac arrest, shock severe hypotension

focal ischemia–> localized area
~~~embolic or thrombotic arterial occlusion (atherosclerosis in HTN!!!!!!)

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17
Q

What is a watershed infarct?

A

blood supply to two adjacent cerebral arteries are compromised

**region between 2 vessels are most susceptible to ischemia and infarction

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18
Q

Describe the type of necrosis in a watershed infarct

A

sickle-shaped band of necrosis over cerebral convexity (goes to back of brain lateral to separation of hemispheres)

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19
Q

Occlusion of what arterial connection causes higher-order visual processing deficits?

A

MCA-PCA

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20
Q

What would be the sx of a ACA-MCA watershed infarct?

A

Proximal arm and leg weakness

transcortical aphasia (language issues)

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21
Q

What is a typical patient that would have an ACA-MCA watershed infarct?

A

occlusion of INTERNAL CAROTID artery (MCA is terminal branch of internal carotid)

patient with hypotension and carotid stenosis

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22
Q

Cartoid stenosis is seen with what progressive disease?

A

Atherosclerosis

leads to stenosis of internal carotid artery just beyond bifurcation

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23
Q

With atherosclerosis–> carotid stenosis, you hear _______ into ________

A

bruit that continues into diastole

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24
Q

Thrombi formed in carotid artery d/t atherosclerosis can embolize and travel _______

A

distally to MCA, ACA and ophthalmic artery (vision problems)

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25
Q

What are classic sx of carotid stenosis?

A

contralateral face-arm weakness

contralateral sensory changes

contralateral visual field defects

aphasia

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26
Q

What are the most common sites of thombus formation?

A

branch points:

carotid bifurcation

origin of MCA (terminal branch of internal carotid)

either end of basilar artery

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27
Q

What most often causes thrombotic occlusions?

A

atherosclerosis

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28
Q

What is an atheroma?

A

intimal lesion with lipid core covered by fibrous cap in vessels

–> will cause clot or thrombus if ruptured d/t exposure of thrombotic substance (lipid core) to blood

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29
Q

What clot/thrombus would you get from A-fib?

A

left atrial appendage clot

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30
Q

What clot/thrombus would you get from an MI?

A

clot in hypokinetic or akinetic areas

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31
Q

What clot/thrombus would you get from valvular disease in heart?

A

form on diseased leaflets or prosthetic parts

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32
Q

Where is the origin of an artery-to-artery emboli?

A

vertebral or internal carotid artery stenosis

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33
Q

What clot/thrombus would cause a dissection?

A

carotid or vertebral emboli

atherosclerosis of aortic arch

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34
Q

What clot/thrombus would you get from a patent foramen ovale?

A

paradoxical embolus (bypass lungs to brain)

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35
Q

What causes air emboli?

A

deep sea divers

iatrogenic introduction into circulation

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36
Q

What causes septic emboli?

A

bacterial endocarditis

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37
Q

What causes fat/cholesterol emboli?

A

trauma to long bones

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38
Q

What causes marantic emboli?

A

proteinaceous emboli from non-bacterial thrombotic endocarditis

hypercoag states (malignancy, amniotic fluid emboli in childbirth)

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39
Q

What artery is most affected by embolic infarct?

A

MCA

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40
Q

Where do emboli typically lodge?

A

branch point or luminal stenosis

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41
Q

What is a shower emboli?

A

multiple emboli from fat after long bone fracture

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42
Q

What can cause hypercoagulable states?

A

heritable coag factor disorders (protein S, C, antithrombin III deficiency)

dehydration

adenocarcinoma/malignancies

surgery, trauma, childbirth

DIC (disseminated intravascular coag)

Hematologic disorders (sickle cell, leukemia, polycythemia)

vasculitis

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43
Q

What are sx of TIA?

A

+ or -

motor, sensory, visual auditory, olfactory, kinesthetic, emotional, cognitive (pretty much anything neuro)

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44
Q

What can cause sx of TIA?

A

migraines

seizures

non-neuro conditions (cardiac arrhythmia, hypoglycemia in elderly)

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45
Q

Describe the criteria to label sx as a TIA

A

neuro deficit less than 24 hours caused by temporary brain ischemia

more typical is less than 10 minutes (more–>permanent cell death)

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46
Q

TIAs that last longer than 1 hour are d/t what?

A

small infarcts

complete recovery can occur within 1 day

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47
Q

Are TIAs a neurological emergency?

A

yes!!!

warning sign for potentially larger ischemic injury to the brain

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48
Q

Why do TIAs need emergent evaluation?

A

15% TIAs will have full on stroke–> persistent defects within 3 months

half of those patients have stroke within first 48 hours

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49
Q

How does a TIA happen?

A

embolus temporarily occludes then dissolves

in situ thrombus formation

vasospasm

ALL TEMPORARY

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50
Q

What are the 2 types of strokes?

A

hemorrhagic (red, emboli)
–> intracerebral or subarachnoid hemorrhage secondary to reperfusion of damaged vessels (directly via collateral or dissolution of occlusion)

ischemic (pale/anemia, thrombus)
–> no blood, however can have hemorrhagic conversion if fragile vessels rupture

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51
Q

What causes an ischemic stroke?

A

inadequate blood supply–> infarction/death of brain tissue

emboli (formed elsewhere, moves), thrombi (local formed) in large vessel or small vessel, lacunar infarcts

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52
Q

Lacunar infarcts are associated with _________

A

HTN

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53
Q

Lacunar infarcts affect that arteries?

A

lenticulostriate arteries

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54
Q

What does malignant HTN cause in the CNS?

A

hypertensive encephalopathy

deep brain parenchymal hemorrhages

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55
Q

What causes vascular dementia and what are the sx of it?

A

malignant HTN

dementia, gait abn, pseudobulbar signs (sudden uncontrollable laughing/crying)

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56
Q

What is binswanger disease?

A

large area of subcortical white matter with myelin and axon loss

caused by HTN

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57
Q

What are Charcot-Bouchard Microaneurysms?

A

CHRONIC HTN

minute aneurysms in basal ganglia

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58
Q

Cerebral amyloid angiopathy (CAA) is associated with Alzheimer’s and ______

A

hypertensive lobar hemorrhage

amyloid deposits in wall of vessels–> microbleeds

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59
Q

What is CADASIL?

A

Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy

recurrent strokes and dementia around 35 years (younger than infarcts just d/t HTN)

NOTCH 3 gene

PAS+

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60
Q

What are stroke risk factors?

A 
HTN
DM
HLD
smoking
family hx
valvular dz, a-fib, PFO
prior hx
hypercoag
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61
Q

What is the most frequent cause of the most clinically significant hemorrhage?

A

Saccular/berry aneurysm in ANTERIOR circulation most common—> subarachnoid hemorrhage

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62
Q

What is a basilar subarachnoid hemorrhage?

A

fusiform rupture

d/t atherosclerosis of circle of willis

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63
Q

Are aneurysms present at birth?

A

no

develop over time d/t defect in media of vessel (usually at bifurcations)

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64
Q

What age is most common for aneurysms to rupture?

A

50s
more frequent in females

(over 10mm have 50% risk of bleeding per year)

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65
Q

What are situations where aneurysms can rupture?

A

if over 10mm–> 50% chance of bleeding per year

1/3 d/t increased ICP:
straining at stool
orgasm

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66
Q

The worst headache I’ve ever had corresponds to________-

A

ANEURYSM–> subarachnoid hemorrhage

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67
Q

What is the prognosis of aneurysm with subsequent subarachnoid hemorrhage?

A

25-50% with first rupture

repeat bleeding common in survivors

first few days after hemorrhage, increased risk for vasospam (brain doesn’t like blood there, so causes edema)–> more ischemic injury

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68
Q

Where are AV malformations in the brain?

A

subarachnoid space but can extend into brain tissue

more often occur in MCA and posterior branches

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69
Q

What are 4 principle routes of CNS infection?

A

blood–> most common (arterial, retrograde facial veins)

direct implantation–> trauma, congenital (meningomyelocele)

local extension-> teeth, sinuses

peripheral nervous system–> viruses (rabies, herpes zoster)

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70
Q

What produces CSF?

A

choroid plexus of lateral 3rd and 4th ventricles

exchanged every 3-4 hours

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71
Q

Does the CSF have lymphatics?

A

NO, in epidural space

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72
Q

How do herpes simplex and zoster spread to brain?

A

latent in sensory ganglia, replicate in schwaan cells and ascent within sensory nerves to brain

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73
Q

How does rabies spread to brain?

A

bind near acetylcholine receptors at NMJ, ascend to brain via motor nerves

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74
Q

Infections of retropharyngeal, peritoneal or mediastinal spaces may produce ________ via spread through epidural lymphatics

A

spinal epidural abscesses

75
Q

Tuberulous meningitis develops by ______

A

seeding CSF from subepidural or submeningeal GRANULOMAS

76
Q

What is an important anatomical feature that prevents most antibiotics, immunoglobulins and complement from going into the brain?

A

capillaries (surrounded by astrocyte foot processes that make BBB)

77
Q

What causes aseptic meningitis?

A

acute or subacute viral infection

78
Q

What causes chronic meningitis?

A

TB

spirochetes (neurosyphilis, neuroborreliosis)

cryptococcus

79
Q

What is pyogenic meningitis and what can cause it?

A

suppurative exudate that covers brainstem and cerebellum

thickened leptomeninges

TB or neurosyphilis

80
Q

What happens to the BBB in cerebral edema?

A

lost

81
Q

How does cerebral edema develop?

A

accelerated by products of living bacteria and abx-lysed bacteria

82
Q

How to slow/reverse cerebral edema

A

corticosteroids

83
Q

Sx of acute suppurative meningitis

A

ha

meningeal irritation signs (Kernig, Brudzinski)

high fever

confusion and coma

84
Q

Brudzinski sign

A

lift head, legs come up with it

meningitis test

85
Q

Kernig sign

A

supine, flex leg at hip and knee

try to extend leg while hip is flexed–> + is pain or spasm in hamstring

86
Q

Where would you see pus from meningitis in the brain?

A

follows subarachnoid space in sulci (near vessels)

87
Q

Pneumonococcal meningitis vs H influenzae exudate location

A

Pneumo: over convexities near sagittal sinus

H influ: basal location

88
Q

What fills what space when you have a suppurative/bacterial meningitis?

A

neutrophils fill subarachnoid space

89
Q

What is focal cerebritis?

A

inflammatory cells infiltrate veins and go from subarachnoid space down into brain parenchyma

90
Q

What is ventriculitis?

A

infection of brain that extends into ventricles

91
Q

What is phelbitis?

A

venous thrombi–> hemorrhagic infarcts of brain

92
Q

Leptomeningeal (between arachnoid and pia where CSF flows) fibrosis leads to _______

A

hydrocephalus

93
Q

Pneumococcal meningitis can cause __________

A

chronic adhesive arachnoiditis (thick d/t capsular polysaccharide of bacteria–> gel-like)

94
Q

Complications of bacterial meningitis

A

seizures

encephalitis

hearing loss, blindness, paralysis

meningococcemia and rash
–> adrenal hemorrhage and
death
——–> AKA Waterhouse-Friderichsen Syndrome

95
Q

LP gram stain: gram negative diplococci

A

Neisseria meningitidis

96
Q

LP gram stain: gram positive diplococci

A

Strep pneumoniae (#1 cause meningitis)

97
Q

LP gram stain: gram negative pleomorphic

A

Haemophilus influenzae

98
Q

LP gram stain: gram positive cocci

A

Staph aureus

Staph epidermidis

Strep

99
Q

LP gram stain: gram negative bacilli

A

E coli

others

100
Q

Where to perform LP

A

between L3 and L4

101
Q

CSF findings in bacterial meningitis

A

very increased neutrophils (over 100)

very decreased glucose (half serum level)

increased protein

cloudy/turbid

102
Q

CSF findings in viral meningitis

A

increased lymphocytes (may see neutrophils early on)

increased protein (not as much as bacterial)

clear/colorless

normal glucose

103
Q

Who is at increased risk of meningitis?

A

below 5 or above 60

DM

immunosuppressed/HIV

contiguous infection (like sinusitis that can retrograde)

IV drug abuse

bacterial endocarditis

sickle cell anemia

104
Q

Common causes of acute meningitis in neonate

A

E coli

Group B Strep

105
Q

Common causes of acute meningitis in 3m-2 year UNVACCINATED kids

A

H influenze type B

106
Q

Common causes of acute meningitis in adolescents and YA

A

Neiserria meningitidis

107
Q

Common causes of acute meningitis in elderly

A

Strep pneumo

Listeria monocytogenes

108
Q

What are examples of acute focal suppurative infections?

A

brain abscess
subdural empyema
extradural abscess

109
Q

Describe how a brain abscess forms

A

same route as meningitis:

endocarditis–> multiple
abscesses

R–>L shunt

bronchiectasis

immunosuppression

strep and staph in non-immuno

110
Q

Brain abscess sx

A

progressive focal neuro deficits

increased ICP signs

LIQUEFACTIVE NECROSIS

111
Q

CSF of brain abscess

A

high WBC
high protein
normal glucose

112
Q

Complications of brain abscess

A

rupture with ventriculitis or meningitis, venous sinus thrombosis

113
Q

Treatment for brain abscess

A

surgical drainage and abx

114
Q

What is a subdural empyema?

A

bacteria/fungal infection of skull bones OR sinuses that spread to subdural space

115
Q

What is evidence of a subdural empyema?

A

thickened dura

116
Q

What is the sx and CSF findings of subdural empyema?

A

same as abscess

  • -> progressive focal neuro def
  • -> increased ICP signs
  • -> high WBC, protein, normal glucose
117
Q

Treatment for subdural empyema

A

surgical drainage

118
Q

Sx of untreated subdural empyema

A

focal neuro signs, lethargy, coma

119
Q

What are extradural abscesses usually associated with?

A

osteomyelitis

120
Q

What can extradural abscess cause?

A

cord compression if in spine–> neuro emergency

121
Q

What can you see with subdural empyema?

A

thrombophlebitis of bridging veins–> infarct

122
Q

How does Neisseria meningitidis colonize?

A

colonizes oropharynx of asymptomatic carriers

spread via direct contact with respiratory secretions

occurs in 2-3% of healthy individuals

123
Q

Where is there a higher proportion of Neisseria?

A

crowded populations–> dorms, barracks, prisons

124
Q

Clinical sx of neisseria meningitidis

A

rapidly progressive septicemia with F, hypotension, IDC, petechial and purpuric lesions

purpura fulminans can occur–> gangrene in distal limbs

Waterhouse-Friderichsen syndrome: hemorrhagic infarction of adrenal glands with above sx

125
Q

What gram stain is Neisseria and where is it located?

A

gram negative diplococci

in and out of cells

126
Q

CSF of chronic meningitis

A

elevated protein

lymphocytes

low glucose

127
Q

How do you diagnose chronic meningitis?

A

meningitis sx and CSF findings progress for at least 4 weeks

128
Q

What causes chronic meningitis?

A

TB

Neuroborreliosis (lyme disease)

Neurosyphilis

129
Q

Where does mycobacterium tuberculosis cause chronic meningitis?

A

subarachnoid space with gelatinous or fibrinous exudate

likes base of brain, obliterates cisterns and encases cranial nerves–> arachnoiditis, hydrocephalus, CN sx

130
Q

What is a tuberculoma?

A

well-circumscribed intraparenchymal mass with central caseous necrosis

may calcify

see with mycobacterium tb chronic meningitis

131
Q

What bacteria can you see obliterative endarteritis with?

A

mycobacterium tb (chronic meningitis)

132
Q

What bacteria can you see with acid-fast stain?

A

mycobacterium TB

133
Q

Describe sx and CSF seen in chronic meningitis caused by borrelia burgdordferi

A

AKA lyme disease

neuro sx follow rash by 4 weeks (central clearing/bullseye)

CN palsy and peripheral neuropathies

CSF have antibodies, see with PCR

Ab cross-react with infectious mono, RA, SLE, syphilis (cause false +)

134
Q

What is neurosyphilis and how many patients develop it?

A

TREPONEMA PALLIDUM

tertiary stage, only 10% of untreated syphilis patients develop it

135
Q

What is meningovascular neurosyphilis?

A

chronic meningitis that involves the base of the brain and causes communicating hydrocephalus

will see obliterative/Heubner endarteritis

136
Q

What is paretic neurosyphilis?

A

Delusions of grandeur with severe dementia (general paresis of the insane)

perivasuclar iron deposits

hydrocephalus with granular ependymitis

137
Q

Describe tabes dorsalis

A

damage to sensory nerves in dorsal roots d/t neurosyphilis

loss of pain sensation, ataxia, joint damage with lightening pains (Charcot joints)

absence of deep reflexes

138
Q

What is treponema pallidum?

A

spirochete

causes syphilis

139
Q

What causes 80% of aseptic meningitis?

A

enteroviruses

140
Q

Describe aseptic meningitis

A

no recognizable organism with meningeal irritation, F, altered LOC, relatively acute onset

less fulminant c/t bacterial

141
Q

CSF findings in aseptic meningitis

A

lymphocytic pleocytosis

moderate increase in protein

normal glucose

142
Q

Treatment for aseptic meningitis

A

self-limiting

symptomatic tmt

143
Q

How do viruses enter the CNS and cause meningitis and encephalitis?

A

via blood

nerves (olfactory, trigeminal sensory or motor nerves)

brain mounts response with lymphocytes that have been sensitized by the virus

latency

144
Q

What causes epidemic encephalitis?

A

arthropod-borne (mosquito vectors) viruses

145
Q

What causes a polio-like syndrome with paralsysi?

A

West Nile virus

146
Q

CSF of West Nile

A

colorless

slight increased pressure

increased protein

normal glucose

starts out with neutrophils–> rapidly progresses to lymphocytes

147
Q

Histology seen in West Nile encephalitis

A

multiple foci of necrosis in white and gray matter

neuronophagia (microglia around dying neuron)

microglial nodules (aggregate around necrosis)

148
Q

HSV-1 is seen in who?

A

children and young adults

149
Q

What effect does HSV-1 have on the brain?

A

necrotizing and hemorrhagic changes to inferior and medial TEMPORAL lobes in kids and young adults

also orbital gyri of frontal lobes

150
Q

What intranuclear inclusions are seen with HSV-1 infection?

A

Cowdry type A in neurons and glia

151
Q

HSV-2 infection of CNS is seen in who?

A

neonates born via vaginal delivery to moms with active HSV-2

152
Q

What does HSV-2 do to the brain?

A

in neonates (vag delivery with infected mothers)–> severe encephalitis

153
Q

Where is herpes zoster latent?

A

sensory or dorsal root of trigeminal ganglia

154
Q

Reactivation of herpes zoster causes ________

A

shingles

single or limited dermatome

155
Q

What is persistent postherpetic neuralgia syndrome?

A

persistent pain following nonpainful stimuli

seen in shingles: skin brushed with clothing is painful

156
Q

Where is cytomegalovirus found?

A

fetuses and AIDS patients

157
Q

What is the histology of CMV found in utero?

A

periventricular necrosis–> severe brain destruction–> microcephaly and periventricular calcification

158
Q

What does CMV cause in AIDS/immunocompromised patients?

A

subacute encephalitis (localizes in paraventricular subependymal regions)

can also see radiculoneuritis in lower spinal cord and roots

159
Q

What inclusions are seen with CMV?

A

intracytoplamic and intranuclear

prominent enlarged cells

160
Q

Sx of poliomyelitis

A

mononuclear cell perivascular cuffs and neuronophagia of anterior horn motor neurons–> FLACCID PARALYSIS

161
Q

What is post-polio syndrome?

A

25-35 years later: decreased muscle mass and pain

162
Q

What is the incubation period for rabies?

A

Lyssavirus of rhabdoviridae family

1-3 months

163
Q

How does rabies infect/cause sx?

A

ascend along peripheral nerves from wound–> negri bodies in purkinje cells

*paresthesia around wound is diagnostic sx (pins and needles)

nonspecific sx: malaise, ha, fever

flaccid paralysis, respiratory center failure

hydrophobia (foaming at mouth, aversion to swallowing)

164
Q

What can HIV cause in CNS?

A

aseptic meningitis within 1-2 weeks of seroconversion

dementia

primary CNS lymphoma

IRIS (immune reconstitution inflammatory syndrome) after antiviral therapy, paradoxical exacerbation of sx from opportunistic infections

165
Q

Histology of HIV aseptic meningitis

A

acute: perivascualr inflammation
chronic: microglial nodules with multinucleated giant cells

white matter: pallor, axonal welling, gliosis

166
Q

What is progressive multifocal leukoencephalopathy (PML)?

A

via JC polyomavirus (reactivated during immunosuppression)

affects oligodendrocytes–>demyelination

exclusively in IMMUNOSUPPRESSED people

subcortical area of demyel with lipid-laden macrophages in center (decreased # of axons)

167
Q

What is subacute sclerosing panencephalitis (SSPE)?

A

paramyxovirus

progressive cognitive decline, spasticity of limbs, seizures

children or YA that aren’t immunized: months to year after measles (rubeola) in youth

168
Q

Histology of subacute sclerosing panencephalitis (SSPE)

A

widespread gliosis and myelin degeneration

viral inclusions (paramyxovirus/measles)

neurofibrillary tangles

169
Q

What is fungal meningoencephalitis caused by?

A

candida albicans

mucor

aspergillus
–> ALL vascular invasion

cryptococcus
–>AIDS

170
Q

What causes fungal meningoencephalitis in DM patients?

A

mucormycosis

171
Q

What does cryptococcus look like on histo?

A

soap bubbles

172
Q

CSF finding of cryptococcal polysaccharide antigen points to what diagnosis?

A

chronic meningitis caused by cryptococcus neoformans

AIDS, immunosuppressive therapy

shows up on india ink stain

173
Q

What CNS infector is huge in HIV and pregnant patients?

A

toxoplasmosis gondii

174
Q

What does toxoplasmosis gondii cause in CNS?

A

brain abscess near gray-white junction and deep gray nuclei

central foci of necrosis with petechial hemorrhages and vascular proliferation

free tachyzoites and encysted bradyzoites at periphery of necrosis

175
Q

What is the brain-eating ameba?

A

naegleria fowleri

contaminates when water enters brain through nose

warm freshwater and soil

176
Q

What ameba causes chronic granulomatous meningoencephalitis?

A

acanthamoeba

177
Q

What does plasmodium falciparum (parasite) cause?

A

long-term cognitive defects if survive

type of malaria

178
Q

What causes Creutzfeldt-Jakob disease?

A

prion (PRP)

179
Q

Describe sx of Creutzfeldt-Jakob disease

A

rapidly progressive neurodegen disorder–> dementia

spongiform change with intracellular vacuoles

180
Q

Mad cow disease is

A

Creutzfeldt-Jakob disease

181
Q

Bovine spongiform encephalopathy was seen where?

A

UK in young adults, 1995

slower progression c/t CJD

kuru plaque (congo red and PAS+ )

182
Q

When do you see CJD?

A

70s

iatrogenic

rapidly progressive dementia with myoclonus

7 month survival

little evidence of brain atrophy but have microscopic spongiform changes

183
Q

Describe fetal familial insomnia

A

sleep disturbances cause this

less than 3 year survival

ataxia, autonomic disturbances, stupor

Neuro (18 decks)

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