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Neuro V Flashcards

1
Q

Most common site of berry aneurysm

A

Junction of anterior communicating and ACA.

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2
Q

berry aneurysm RF’s

A

1) advanced age
2) HTN
3) smoking
4) race (increased risk in blacks)

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3
Q

Locations of charcot-bouchard aneurysms

A

Micro aneurysms in basal ganglia + thalamus

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4
Q

Imaging and charcot-bouchard aneurysms

A

They’re too small to see on angiograms.

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5
Q

Etiology of charcot-bouchard aneurysms

A

HTN

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6
Q

Complications of ACA berry aneurysms?

A

1) compression of ACA can lead to bitemporal hemianopia; visual acuity deficits.
2) ACA rupture can lead to lower extremity hemiparesis, sensory deficits.

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7
Q

Complications of PCA berry aneurysms?

A

Compression may cause CN III palsy (blown pupil).

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8
Q

Complications of MCA berry aneurysms?

A

Rupture may cause ischemia in MCA distribution –> contralateral upper extremity and facial hemiparesis, sensory deficits.

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9
Q

What is central post-stroke pain syndrome? Presentation? Epidemiology?

A

1) Neuropathic pain due to thalamic lesions.
2) Initial paresthesias followed in weeks to months by allodynia (ordinarily painless stimuli cause pain) and dysesthesia.
3) happens to 10% of stroke patients.

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10
Q

Epidural hematomas due too.

A

middle meningeal artery rupture

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11
Q

middle meningeal branches from…

A

maxillary artery

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12
Q

Epidurals and suture lines?

A

DO NOT cross

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13
Q

epidural setting

A

often secondary to skull fracture

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14
Q

epidural complications

A

Rapid expansion under systemic arterial pressure can lead to transtentorial herniation + CN III palsy.

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15
Q

lucid interval…

A

epidural

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16
Q

Subdural hematoma etiology…

A

ruptured bridging veins

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17
Q

Chronic vs acute subdural on CT

A

1) acute (traumatic, high-energy impact) –> hyper dense on CT
2) Chronic –> hypodense on CT

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18
Q

Subdurals seen in..

A

1) mild trauma or high-energy trauma
2) cerebral atrophy
3) elderly
4) alcoholism
5) shaken babies

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19
Q

Subdurals and suture lines?

A

Cross suture lines.

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20
Q

Impt clinical finding for subarachnoid hemorrhage

A

bloody or yellow (xanthochromic) spinal tap.

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21
Q

When does vasospasm occur?

A

4-10 days after subarachnoid

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22
Q

Other impt subarachnoid sequela…

A

Communicating and/or obstructive hydrocephalus.

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23
Q

Intraparenchymal hemorrhage caused by…

A

1) most commonly systemic HTN
2) amyloid angiopathy
3) vasculitis
4) neoplasm
5) secondary to repercussion injury in ischemic stroke.

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24
Q

Location of intraparenchymal hemorrhage…

A

Typically basal ganglia + internal capsule but can be lobar.

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25
Charcot-Bouchard and intraparenchymal hemorrhage
Rupture charcot-bouchard in lenticulostriate vessels in internal capsule can cause intraparenchymal hemorrhage.
26
When does irreversible damage occur after a stroke?
5 minutes of hypoxia
27
Most vulnerable brain regions to ischemic stroke
1) hippocampus 2) neocortex 3) cerebellum 4) watershed areas
28
Stroke algorithm
1) get imaging: Noncontrast CT to exclude hemorrhage | 2) tPA
29
When can CT detect ischemic changes?
6-24 hrs
30
When can diffusion-weighted MRI detect ischemia?
3-30 minutes
31
Histologic features 12-48 hours after infarct in brain:
red neurons
32
Histologic features 24-72 hours after infarct in brain:
necrosis + neutrophils
33
Histologic features 3-5 days after infarct in brain:
macrophages (microglia)
34
Histologic features 1-2 weeks after infarct in brain:
Reactive gliosis + vascular proliferation
35
Histologic features >2 weeks after infarct in brain:
Glial scar
36
Most common location of thrombotic stroke
MCA
37
Where do thrombotic strokes usually occur?
on top of atherosclerotic plaques
38
Common scenario for hypoxic stroke:
Common during cardiovascular surgery
39
Window for tPA treatment
within 3-4.5 hours of onset, proved no hemorrhage risk
40
How do you reduce stroke risk
1) aspirin + clopidogrel 2) control BP 3) get blood sugars under control 4) control lipids 5) treat conditions that increase risk (a fib)
41
TIA prognosis
Most resolve in less than 15 minutes but you can get deficits due to focal ischemia.
42
Venous sinus thrombosis presentation
signs/symptoms of increased ICP (eg. headache, seizures, focal neurologic deficits).
43
Venous sinus thrombosis sequela
venous hemorrhage
44
Venous sinus thrombosis associations
Hyper coagulable states (pregnancy, OCP use, factor V leaden)
45
Identify all venous sinuses
470
46
Where does internal jugular vein pass through?
jugular foramen
47
cerebral aqueduct connects
3rd ventricle --> 4th ventricle
48
foramen of monro connect
lateral ventricles with 3rd ventricle
49
psuedotumor cerebri
idiopathic intracranial HTN. Increased ICP with no apparent cause on imaging.
50
RFs for pseudotumor cerebri
1) being a woman of childbearing age 2) vitamin A excess 3) danazol 4) tetracycline
51
pseudotumor cerebri presentation
1) headache 2) diplopia (usually from CN VI palsy) 3) *no change in mental status 4) papilledema 5) increased opening pressure on LP, which will also relieve headache.
52
pseudotumor cerebri treatment
1) weight loss 2) acetazolamide 3) topiramate 4) invasive procedures for refractory cases (eg, repeat LP, CSF shunt placement, optic nerve fenestration surgery).
53
hydrocephalus caveat
ICP not always increased
54
Common cause of communicating hydrocephalus
arachnoid scarring post-meningitis
55
communicating hydrocephalus presentation
1) increased ICP 2) papilledema 3) herniation
56
NPH characteristics
1) *episodic CSF pressure elevation. | 2) *No increase in subarachnoid space volume.
57
pathophys of NPH
Expansion of ventricles distorts the fibers of the corona radiate.
58
Characteristic finding in NPH other than triad?
Magnetic gait (feet appear stuck to floor)
59
dysesthesia
abnormal sensation
60
uncal/transtentorial herniation
uncal is a common type of transtentorial herniation.

STEP (85 decks)

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