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Neuro Module > Cerebral Vascular Disease > Flashcards

Cerebral Vascular Disease Flashcards

1
Q

Definition of cerebral ischemia

A

inadequate blood or oxygen to brain

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2
Q

mild or acute ischemia

A

syncope

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3
Q

severe or long-standing ischemia

A

whole brain = hypoxic-ischemia encephalopathy

focal region = stroke

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4
Q

systemic causes of short-lived cerebral ischemia

A

hypotension, vasovagal reaction, arrhythmia, MI

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5
Q

PE of stroke/TIA work up

A

BP, RR, pulse
Fundoscopy
Listen for bruits, murmurs, abnormal rhythms
Careful neuro exam

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6
Q

Labs to work up stroke/TIA

A

CBC, ESR, CMP, Lipid profile, Clotting studies (PT/PTT), serologic test for syphilis

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7
Q

Imaging to eval for possible embolic cause of stroke

A

carotid U/S, ECG, Holter monitor, ECHO, TEE, angiogram

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8
Q

Why is getting a CT/MRI important in work up of stroke?

A

only way to differentiate ischemic and hemorrhagic stroke

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9
Q

Difference in causes of ischemic and hemorrhagic strokes?

A

ischemic - thrombosis or embolic blockage of blood flow to brain

hemorrhagic - bleeding inside or around brain tissue

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10
Q

Non-modifiable RF for stroke

A

age, male, African American, hypercoaguable state

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11
Q

Modifiable RF for stroke

A
  • stop smoking and drinking
  • control DM, HTN
  • treat hyperlipidemia, hyper coagulability, sleep apnea
  • convert A-fib to sinus rhythm
  • reduce obesity
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12
Q

How to decrease risk of A-fib?

A

anti-coags

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13
Q

How are mitral valve defects and A fib ruled out as causes of stroke?

A

TEE r/o mitral defect

ECHO r/o A-fib

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14
Q

What are two types of stroke and which is more likely?

A

Ischemic (85%)

Hemorrhage (15%)

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15
Q

What is most likely cause of hemorrhagic stoke?

A

HTN

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16
Q

In a stroke, if blood quickly restored then it is a ______. But if prolonged ischemia _______.

A

TIA

tissue necrosis -> hemorrhagic stroke

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17
Q

RF specific to ischemic stroke

A

atherosclerosis, AGE, fhx, HTN, DM, tobacco, high lipids, A-fib, recent MI, valvular disease, patent foramen ovale, hypercoaguable states, systemic vascular disease, HIV/AIDS

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18
Q

What are some hypercoaguable states?

A

cancer, thrombocytosis, factor V Leiden, oral contraceptives

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19
Q

When is tPA not appropriate for stroke treatment?

A 
hemorrhagic strokes (or other bleeds)
acute stroke tx
after 4.5 hours of sx onset
thrombolysis (on blood thinner)
uncontrolled HTN
pregnancy
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20
Q

How/when does tPA work?

A

= tissue plasminogen activator

breaks up clots; used in immediate treatment of stroke (within 4.5 hrs) or MI (within 12 hrs)

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21
Q

What tx is used for acute stroke symptoms and prevention?

A

anti-platelet tx: Aspirin/Clopidogrel

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22
Q

Medical management to reduce complications and prevent secondary stroke?

A
  • reduce RFs
  • take Aspirin
  • Save ischemic penumbra region
  • Rehab: PT/OT, speech pathologist, respiratory therapist, social worker, psychologist
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23
Q

What is major risk of having TIA?

A

15% risk of full stroke after TIA, esp first 2 days

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24
Q

amaurosis fagux

A

TIA with transient monocular blindness from emboli to central retinal artery of one eye (branch of internal carotid artery); high correlation with ipsilateral carotid stenosis

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25
Q

How is TIA defined?

A

stroke that resolves within 24 hours; usually less than 1 hr

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26
Q

Major causes of TIA

A
  • stenosis of major artery (carotid, vertebral)
  • embolic phenomena (A-fib)
  • thrombosis of smaller BV in brain
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27
Q

What is an important part of PE for TIA?

A

Listen to carotid arteries

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28
Q

What drug can reduce ICP?

A

Mannitol

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29
Q

TIA treatement

A

Urgent eval and tx!
Aspirin
Avoid tPA

Hospitalization for acute workup and availability of tPA if stroke occurs

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30
Q

________ are 20% of ischemic strokes.

A

small vessel strokes (Lacunar stroke)

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31
Q

5 classic signs of lacunar stroke?

A

1) Pure motor hemiparesis (hyperreflexia, +Babinski)
2) Pure sensory stroke (unilateral sensory loss)
3) Ataxia hemiparesis (pyramid signs, cerebellar ataxia)
4) Dysarthria & clumsy hand (unilat facial weakness, dysarthric speech, tongue deviation)
5) Mixed sensorimotor stroke (pyramid signs, sensory loss)

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32
Q

Where do small vessel strokes occur?

A

brainstem, thalamus, pons

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33
Q

What are the effects of a middle cerebral artery stroke?

A
  • contralateral hemiplegia (motor)
  • contralateral hemianesthesia (sensory)
  • ipsilateral gaze preference
  • dysarthria due to facial weakness
  • aphasia if L side
34
Q

What are the effects of a posterior cerebral artery stroke?

A

3rd nerve palsy (eye down & out, dilated pupil)
Ataxia
Cortical blindness
Hemianopia

35
Q

What part of brain is affected by posterior cerebral artery stroke?

A

midbrain, subthalamic, thalamic, cerebellum

36
Q

Signs/sx of hemmorhagic stroke

A

ELEVATED ICP -> HA, altered mentation, confusion, coma, vomiting (no nausea), seizures, papilledema, Cushing’s triad, irregular respirations, arrhythmias

37
Q

Cushing’s triad

A

high BP, low pulse, widening pulse pressure

38
Q

Where is intraparenchymal bleeding?

A

bleeding into substance of brain

39
Q

Where is subarachnoid bleeding?

A

bleeding between arachnoid and pia mater

40
Q

RFs and causes of intraparenchymal bleeding?

A

RFs: age, heavy alcohol, anticoags, cocaine, Asians/African Americans

Causes: HTN, trauma, cerebral amyloid angiopathy

41
Q

Causes of subarachnoid bleeding?

A
  • aneurism (spontaneous rupture of artery)

- occasionally trauma

42
Q

Most common site for intraparenchymal hemorrhage

A

basal ganglia

43
Q

signs/sx of basal ganglia hemorrhage

A

CONTRALATERAL HEMIPARESIS

mild = face sag, slurred speech, extremity weakness
progression = flaccid paralysis, upper brainstem compression (coma, irreg breathing, dilated ipsilateral pupil)
44
Q

signs/sx of thalamus hemorrhage

A

Contralateral hemiparesis/hemiparesis
Sensory defect involving all modalities
Aphasia
Anisocoria (different sized pupils) w/o light reflex

45
Q

signs/sx of cerebellar hemorrhage

A

Occipital headache
Repeated vomiting
Gait ataxia
Dizziness/vertigo

progression = stuporous, coma, brainstem compression

46
Q

signs/sx of pontine hemorrhage

A

Deep coma w/ quadriplegia over minutes
Decerebrate rigidity
Pinpoint pupils which react to light
Doll eye phenomena

47
Q

occipital lobe hemorrhage ->

A

hemianopia

48
Q

L temporal lobe hemorrhage ->

A

aphasia, delirium

49
Q

parietal lobe hemorrhage ->

A

hemisensory loss

50
Q

frontal lobe hemorrhage ->

A

arm weakness

51
Q

Effects of thalamus/midbrain compression

A

stupor, coma, herniation

52
Q

saccular aneurism aka _______.

A

“Berry” aneurism

53
Q

Chief complaint of saccular aneurism

A

abrupt onset of “worst headache of my life” = thunderclap HA

54
Q

Common location of saccular aneurisms

A

Circle of Willis

55
Q

RFs of saccular aneurism

A

congenital arterial wall weakness

Polycystic kidneys

56
Q

What is major cause of delayed death and morbidity in saccular aneurism?

A

cerebral vasospasm 4-14 days following initial bleed

  • 50-70% mortality, 70% morbidity
57
Q

Hallmark diagnostic finding of saccular aneurism?

A

Blood in CSF upon lumbar puncture

58
Q

Definitive dx of saccular aneurism

A

angiography (only if patient stable)

59
Q

What imaging is done for all suspected hemorrhagic strokes?

A

Head CT - better at viewing bleeding than MRI

60
Q

saccular aneurism management

A
  1. AIRWAY
  2. Control BP (150 systolic)

Bed rest, head elevation, mild sedation, analgesia, stool softener

Surgery: surgical clipping or endovascular coil

61
Q

Of those who survive initial bleed of saccular aneurism, _____ rebleed in 1 month.

A

30%

62
Q

Which brain bleeds involve venous blood?

A

subdural hematomas

63
Q

RF of subdural hemorrhage

A

alcohol, anti-coags, elderly

64
Q

Causes of acute subdural bleed

A 
Contusion
Shearing injury (e.g. shaken baby syndrome)

BUT trauma not always required if +RFs

65
Q

Signs of acute subdural hematoma

A

Rapid ICP increase
Unilateral headache with enlarged pupil on ipsilateral side (“blown pupil”)
Drowsy/comatose

66
Q

CT scan results of subdural hematoma

A

hematoma that layers out in crescent shape

67
Q

Acute vs Chronic Subdural Hematoma treatment

A

Acute: immediate Burr hole drainage or craniotomy

Chronic: “watchful waiting” (hematoma may reabsorb on its own) or surgical evacuation

68
Q

Pathophysiology of chronic subdural hematoma development

A

brain ages and atrophies -> small bridging veins stretch -> increased tear risk

chronic/older collection of blood between dura and brain

69
Q

Signs of chronic hematoma

A

headache, slowed thinking, drowsiness, personality changes, depression, dementia, seizures, motor/sensory deficits

70
Q

How long for chronic hematoma to develop?

A

variable; days to weeks to months

71
Q

Layers from skull to brain

A

skull, epidural space, dura mater, subdural space, arachnoid membrane, subarachnoid space, pia mater, brain

72
Q

Why is dramatically high BP a sign of saccular hemorrhage?

A

body’s attempt to profuse brain

73
Q

Causes of epidural bleeds

A

TRAUMA - laceration of middle meningeal artery with overlying skull fracture

74
Q

Compare epidural and acute subdural bleeding

A
  • Epidural more rapid in development
    Epidural rounded blood layer, whereas acute subdural blood crescent shaped
  • Same treatment (Burr hole, rapid evacuation) and presentation (comatose, dilated pupils, headache)
75
Q

Why is epidural hematoma more rounded on CT?

A

hematoma can’t expand past skull sutures

76
Q

Symptoms of AV Malformation

A

asx until it bleeds

+/- headache, seizures, pulsating noise in head

77
Q

Where is bleeding of AV Malformation

A

surface or deep within brain tissue = intraperenchymal

78
Q

Best imaging for AV Malformation

A

MRI > CT better to see tissue of vessels

79
Q

Gold standard of AV Malformation dx

A

angiography

80
Q

Treatment of AV Malformation

A

Surgical tx if accessible
Embolization
Stereotactic radiation (slow sclerosis of vessels over 2-3 yrs)

81
Q

What age is AV Malformation most common?

A

10-30 yo

Neuro Module (13 decks)

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