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NEURO > Cerebrovascular Disease > Flashcards

Cerebrovascular Disease Flashcards

1
Q

ischemia vs hemorrhage

A

ischemia=no blood flow (more common), vs. hemorrhage=ICH, SAH
-byproducts of CV dz manifest as sudden, focal neurological deficits related to specific vascular territories of the CNS

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2
Q

causes of impairment or LOC

A
  • global deficit

- usually d/t cerebral hypoperfusions, vasovagal syncope, or toximetabolic d/o

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3
Q

TIA

A
  • transient ischemic attack
  • sudden focal neurological deficits which completely resolve within 24hrs
  • serious warning of high stroke risk
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4
Q

STROKE

A
  • refers to a sudden focal neurological deficit which does NOT completely resolve within 24hr
  • may variable improve over several weeks to months
  • most often caused by ISCHEMIC infarction
  • pts with suspected acute stroke should initially receive a head CT sans contrast to rule out hemorrhage
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5
Q

RF for atherosclerosis (which most pts with CV dz have)

A
  • HTN/HL
  • heart dz
  • DM
  • smoking
  • FHx of vascular dz
  • minor: obesity, lack of exercise, xs EtOH consumption
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6
Q

Atherosclerotic changes

A
  • predominate at bifurcation pts of large, major cervical and intracranial arteries
  • d/t turbulent blood flow at these sites
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7
Q

intravascular atheromas or arterial plaques

A
  • over years develop from subintimal lipid deposition, smooth muscle proliferation, and fibrosis.
  • enlarging ones may narrow or occlude an artery or may ulcerate
  • ulceration disrupts intima, coagulation process initiated
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8
Q

once coagulation process initiated:

A

-leads to local occlusion (thrombosis) or distal propagation (embolization) of blood clot, platelets, fibrin, cholesterol, or calcified elements (emboli)

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9
Q

What are the two basic mechanisms of ischemic infarction?

A
  1. local arterial THROMBOSIS of an atheroma (form in vessel at site)
  2. EMBOLIC arterial occlusions from proximal sources (travel to site)
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10
Q

collateral blood flow

A

-enhanced by congenitally complete CoW at base of brain

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11
Q

cool branches of external carotid artery

A

-can supply blood in reverse direction through the ophthalmic artery to the CoW

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12
Q

cool vertebrobasilar

A

VB flow ending in PCA may continue through patent posterior communicating branches of the CoW and supple MCA and ACA

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13
Q

microscopically within 12-36 hours of clinical stroke

A
  • ischemic neurons shrink and appear eosinophilic (“pink neurons”)
  • days later: macrophages scavenge necrotic debris and cyst formation occurs with astrocytes at the periphery of the infarction.
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14
Q

perforator or lenticulostriate arteries

A
  • arise abruptly from BASILAR artery and proximal ACA, MCA

- supply deeper structures with significant functions (basal ganglia, internal capsule, thalamus, corona radiata)

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15
Q

What deeper structures are vascularized by the perforator or lenticulostriate arteries

A
  • BASAL GANGLIA
  • internal capsule
  • thalamus
  • corona radiata
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16
Q

lacunar infarcts

A

small artery occlusions caused by THROMBOSIS (form in vessel at site)

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17
Q

general path of TIA

A
  • an embolus from an arterial of cardiac source obstructs a branch of an internal carotid or vertebrobasilar artery
  • clinical deficit depends on location of ischemic area
  • deficit resolves quickly as embolus fragments or disintegrates=re-establish flow before permanent damage is done
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18
Q

amaurosis fugax (monocular blindness)

A
  • is a type of carotid territory TIA involving ophthalmic artery or its retinal branches
  • pt says: “lowered dark shade” in one eye which gradually lightens up
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19
Q

what can carotid TIAs do?

A

-causes hemispheral ischemia leading to hemiparesis or aphasia

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20
Q

vertebrobasilar territory TIAs

A

-cause ischemia of: brainstem, cerebellum, or visual (occipital) cortex, producing symptoms of ataxia, homonymous hemianopsia, or hemiparesis associated with “crossed” brain stem syndromes

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21
Q

completed ischemic infarction

A
  • certain stroke syndromes suggest occlusion of larger arteries or branches
    1a. precentral MCA: hemiparesis with greater weakness of face and upper limb
    1b. postcentral MCA: sensory deficits limited to face and upper limb

2a. precentral ACA: hemiparesis with greater weakness of lower limb
2b. postcentral ACA: sensory deficits limited to lower limb

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22
Q

crossed brainstem syndromes

A
  • Weber and Wallenberg

- occur with occlusion of large vertebrobasilar arterial branches

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23
Q

Lacunar syndromes

A

-pure motor hemiplegia, ataxic-hemiparesis, clumsy hand-dysarthria=lacunar syndromes from tiny infarcts in the internal capsule, corona radiata, or basilar pons

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24
Q

pure sensory stroke

A

-a lacunar syndrome from a small vessel occlusion involving the thalamus

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25
Q

What about the heart?

A

It can be a source of emboli causing TIAs or ischemic infarction in large artery territories

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26
Q

Where can emboli arise from with the heart? (echo helps determine cardiac sources)

A
  1. f/m endocardial clot associated with an acute MI
  2. f/m poorly contracting LV
  3. f/m LA clot created d/r afib
  4. infected/septic emboli from endocarditis
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27
Q

venous clots

A

-in adults with PFO, can pass from R–>LA into cerebral circulation

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28
Q

arterial lesions

A

usually consist of atherosclerotic plaques or stenoses which locally thrombose or embolize distally (lacunar infarctions from small vessel atherosclerotic occlusions are thrombotic in nature)

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29
Q

hypercoaguable states (hereditary or acquired)

A
  • can cause occlusions of large and small arteries in addition to cortical veins
  • ex: sickle cell anemia, polycythemia vera, antiphospholipid antibody syndrome.
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30
Q

non-atherosclerotic arterial lesions (rare)

A
  • traumatic or spontaneous arterial dissections
  • inflammation (vasculitis)
  • degenerative occlusive disease (fibromuscular dysplasia)
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31
Q

how can carotid TIAs be evaluated?

A
  • with ultrasound imaging of the cervical internal carotid artery
  • also: MRA, CTA, or move invasive catheter angiography
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32
Q

Who benefits from carotid endarterectomy (surgical removal of atheromatous plaque)?

A

-pts w/ symptomatic atheromatous lesions of 70-99% stenosis at the origin of the internal carotid artery
(smaller risk reduction in symptomatic 50-69% and asymptomatic 60-99%)

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33
Q

What percent stenotic lesion precludes surgery

A

complete or 100% stenotic lesions (at origin of internal carotid artery) since its thrombotic occlusion extends from the neck to the base of the skull

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34
Q

what are other neurointerventional procedures to tx cervical internal carotid stenotic dz?

A

arterial stenting and angioplasty via intravascular catheters.

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35
Q

What are the benefits of warfarin therapy?

A

helps reduce the stroke risk in pts with chronic afib (target INR 2.5) <>

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36
Q

tx for non-afib TIA pts?

A

stroke reduction with antiplatelet drugs such as:

  • ASA 50-325mg daily
  • Clopidogrel (Plavix) 75mg daily
  • ASA 25mg/Dipyridamole 200mg
  • Statins (reduce r/o stroke even sans HL)
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37
Q

Treatment of ischemic infarction

A

-iv tPA (tissue plasminogen activator)-thrombolytic administered within THREE HOURS of stroke onset

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38
Q

What are conditions that prohibit tPA?

A
  • rapidly improving (TIA) or post-ictal deficits (sz)
  • presence of hemorrhage (inc bleed risk) on CT
  • uncontrollable HTN
  • extreme hypo- or hyperglycemia
  • concurrent use of warfarin (inc bleed risk)
  • inc bleeding risk f/m recent sx or invasive procedures
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39
Q

What is the greatest risk of using tPA?

A

(potentially fatal) intracranial hemorrhage

40
Q

What if ischemic stroke pt cannot receive tPA?

A

-brain CT or MRI scans help indicate whether a LARGE artery occlusion occurred in which case embolic sources must be investigated for possible need for warfarin, carotid endarterectomy, or interventional procedures (vs. small guy use anti-platelet drugs and medical therapy)

41
Q

hyperglycemia during an acute ischemic infarction

A
  • associated with poorer prognosis
  • preferred initial iv fluid: saline sans dextrose
  • insulin may be need to ensure nml glucose levels
42
Q

besides glucose levels what else needs to be closely monitored?

A

BP

43
Q

indications for warfarin therapy

A
  • pts with afib

- ischemic infarction related to: antiphospholipid syndrome, arterial dissection, cerebral venous thrombosis

44
Q

when warfarin is not indicated what is used

A

antiplatelet medication

45
Q

When a pt with a recent cerebral infarction develops impaired consciousness in the absence of hypoglycemia what must be considered?

A

increased ICP

  • in 3-5d of an extensive cerebral infarction brain edema can develop
  • even earlier, hemorrhagic transformation of an initially ischemic infarct can occur
46
Q

what is the relationship between mechanical hyperventilation and inc ICP?

A

if an obtunded pt requires tracheal intubation for airway protection, mechanical hyperventilation to a pCO2 of 30-35mmHg helps reduce inc ICP
-hypocapnia induces cerebral vasoconstriction which reduces cerebral blood volume

47
Q

besides mechanical hyperventilation what is another means of reducing elevated ICP

A

iv mannitol; 0.25gm/kg every 6h if serum osm < 310
-corticosteroids DO NOT reduce inc ICP from ischemic infarction or hemorrhage, but do counteract the elevated ICP from tumor or infection

48
Q

what happens when there is a sudden rupture of arterial blood into the brain parenchyma?

A

since arterial bp normally exceeds ICP, there will be an abrupt increase in ICP causing severe HA, impairment or LOC and a focal neurological deficit-dependent on the location of the bleeding

49
Q

what happens when ICP increases and the edema around the hematoma worsens

A

there is potentially fatal shifting or herniation of the brain and perfusion around the area of the hematoma is impaired

50
Q

deeply located vs. superficial hemorrhage

A
  • deeply located: suggest HTN as cause

- superficial, at the poles of the frontal, temporal, or occipital lobes: head trauma

51
Q

pathologically how does a cerebral hemorrhage appear?

A

dark red clot with surrounding edema and occasional dissection into the ventricular system if the bleeding is deep and extensive

52
Q

Subdural hematoma path in elderly

A
  • mild head trauma may tear taut bridging cortical veins which empty into larger venous sinuses
  • venous bleeding accumulates in subdural space
  • progressive expansion may impair cognition and consciousness, and create focal neurological deficits
53
Q

how are most cerebral hemorrhages readily seen?

A

noncontrasted CT brain scan

54
Q

why is it indicated to screen the urine for illicit drugs?

A

cocaine or other sympathomimetic drugs which abruptly increase bp may also cause cerebral hemorrhage

55
Q

What is the most common cause of cerebral hemorrhage

A

HTN!!

  • the weakened walls of small lenticulostriate arteries rupture, bleeding most often into the striatum (putamen and caudate) and thalamus <>
  • tx: control bp and increased ICP
56
Q

What appears white on CT?

A

acute blood appears dense or “white” on CT, as do calcified structures such as the skull

57
Q

What is cerebral amyloid angiopathy

A
  • leads to recurrent lobar hemorrhages usually in the posterior cerebral hemispheres
  • hereditary condition where arterial walls are weakened by amyloid deposits
58
Q

which congenital vascular abnormality carries a r/o rupture and hemorrhage?

A

AVMS (abnml connection of cerebral a to v, sans intervening capillary bed which enlarge over time)
-can be visualized on a brain MRI scan

59
Q

ischemic infarcts and cerebral hemorrhages

A
  • cerebral hemorrhages may occur within brain tumors or ischemic infarcts
  • damaged, ischemic endothelium may leak or ooze blood if reperfusion occurs in an ischemic infarction
60
Q

what is the m/c c/o bleeding into the subarachnoid space

A

TRAUMA (in the absence of trauma, a ruptured congenital berry aneurysm)

61
Q

congenital berry or saccular aneurysms

A
  • arise in the CoW at the base of the brain, especially anteriorly
  • berry enlarge overtime with greater risk of rupture beyond 7-10 mm in size
  • some pts have a sentinel HA or “warning leak” from a mild to moderate amount of bleeding
62
Q

why is SAH the WHOML

A
  • d/t increased ICP and meningeal irritation by the blood
  • also: nuchal rigidity and meningeal signs
  • n/v/impaired consciousness
  • no localizing neuro signs since hemorrhage doesnt involve brain parenchyma itself
63
Q

third cranial (oculomotor) nerve palsy

A

-this suggests that the berry aneurysm is near the posterior communicating artery

64
Q

if a pt is suspected of having SAH from aneurysmal rupture what test should they have done?

A

noncontrasted CT brain scan-which often shows blood in cisterns and sulci around the base of the brain
-If the CT brain scan appears nml, LP is necessary to exclude small volume of subarachnoid blood

65
Q

Xanthochromia

A

-yellow coloration of CSF indicating breakdown of blood within the CSF prior to the LP; blood constant from tube to tube (vs traumatic LP blood amt decreases)

66
Q

What can be used to locate an aneurysm

A

emergent angiography, preferably conventional catheter angiography for optimal imaging

67
Q

what can help prevent some future rebleeding

A

neck of the berry aneurysm should be surgically clipped OR an intravascular catheter may be used to occlude the aneurysm with metallic coils

68
Q

whats a serious complication of SAH

A

cerebral vasospasm-reduced blood flow from cerebral vasospasm creates ischemic infarctions and is more likely after a large volume SAH

69
Q

How do you minimize cerebral vasospasm postoperatively

A

Triple H therapy:

  1. HTN-induced vasopressor medication
  2. hypervolemia-generous iv hydration
  3. hemodilution (phlebotomy to remove blood)
    also. ..oral nimodipine (CCB) improves pt outcome; neuroprotective
70
Q

CUBS and BEAMS

A

CUBS: crescent, subdural, bridging veins
BEAM: epidural, MMA, lucid

71
Q

presentation within 3.5-4 hours of symptom onset and no contraindications

A

iv alteplase

72
Q

stroke with no prior antiplatelet therapy

A

ASA

73
Q

stroke on ASA therapy

A

ASA + dipyridamole OR Clopidogrel

74
Q

stroke on ASA therapy and pt with intracranial large artery atherosclerosis

A

ASA + Clopidogrel

75
Q

stroke with evidence of afib

A

long-term anticoagulation (warfarin, dabigatran, rivaroxaban)

76
Q

amaurosis fugax

A
  • painless, rapid, transient monocular vision loss
  • curtain descending over the visual field
  • mc etiology: retinal ischemia d/t atherosclerotic emboli originating from ipsi carotid artery
  • pts with vascular rf should receive duplex US of the neck
77
Q

lacunar stroke of posterolateral thalamus

A
  • sudden onset contra sensory loss involving all sensory modalities (pure sensory stroke)
  • wk to mo later pt can develop thalamic pain syndrome=paroxysmal burning pain over affected area that is exacerbated by light touch
78
Q

basal ganglia (putamen)

A
  • common site of hypertensive intraparenchymal brain hemorrhage
  • internal capsule that lies adjacent to the putamen is almost always involved=contra hemiparesis, contra sensory loss, conjugate gaze deviation toward the side of lesion (gaze palsy)
79
Q

cerebellum hemorrhage

A
  • usually NO hemiparesis
  • facial weakness
  • ataxia and nystagmus
  • occipital HA and neck stiffness
80
Q

Thalamus

A
  • contra hemiparesis and hemisensory loss
  • nonreactive miotic pupils
  • upgaze palsy
  • eyes deviate toward hemiparesis
81
Q

central lobe

A
  • contra hemiparesis (Frontal lobe)
  • contra hemisensory loss (parietal lobe)
  • homonymous hemianopsia (occipital lobe)
  • eyes deviate away from hemiparesis
  • high incidence of seizures
82
Q

pons

A
  • deep coma and total paralysis within minutes

- pinpoint reactive pupils

83
Q

anterior cord syndrome

A
  • 2/2 injury to the anterior spinal artery affecting ant 2/3 of the spinal cord
  • neurological findings:
  • –b/l hemiparesis: lateral corticospinal tract at level of cord injury and below
  • –diminished b/l pain and temp sensation (1-2 levels below cord injury)
  • –intact b/l proprioception, vibe sense, and light touch (dorsal column gets blood from post spinal arteries)
84
Q

parietal lobar hemorrhage

A

-amyloid angiopathy is most common cause of spontaneous lobar hemorrhage, especially in pts >60

85
Q

what should be done before thrombolytic therapy (iv alteplase) is given

A

-noncontrast head CT to rule out hemorrhagic stroke and screen for other contraindications to therapy

86
Q

nontraumatic SAH

A
  • most commonly d/t ruptured saccular berry aneurysm
  • CT without contrast shows acute hemorrhage surrounding brainstem and basal cisterns
  • negative head CT? undergo LP-high opening pressure and xanthochromia
87
Q

what should be done with pts with a confirmed diagnosis

A

-further evaluate with cerebral angiography and tx with craniotomy with aneurysm clipping OR endovascular methods (coiling/stenting of aneurysm)

88
Q

spontaneous deep intracerebral hemorrhage

A
  • typically caused by hypertensive vasculopathy involving penetrating branches of the major cerebral arteries
  • chronic HTN leads to formation of charcot-bouchard aneurysms which may rupture and bleed within the deep brain structures
  • common locations include: basal ganglia (putamen), cerebellar nuclei, thalamus, pons
89
Q

putaminal hemorrhage

A
  • contra hemiparesis

- contra sensory loss d/t injury of the adjacent internal capsule

90
Q

central retinal artery occlusion

A
  • monocular painless acute vision loss
  • most commonly caused by an embolized atherosclerotic plaque form the ipsi carotid artery
  • w/u includes noninvasive imaging of the carotids to evaluate for stenosis
91
Q

diabetic ophthalmoplegia

A
  • most common cause of CN3 palsy in adults is ischemic neuropathy d/t poorly controlled DM
  • paralysis of levator muscle and 4EOMs with preserved pupillary response
  • cp: ptosis, down and out gaze, diplopia, nml pupillary resp
92
Q

neurologic complications of infective endocarditis

A
  • embolic stroke
  • cerebral hemorrhage
  • brain abscess
  • acute encephalopathy or meningoencephalitis
93
Q

lesion of posterior limb of internal capsule (lacunar infarct)

A
  • acute unilat motor impairment (pure motor hemiparesis)
  • no sensory or cortical deficits
  • no visual field abnormalities
  • assoc most commonly with chronic HTN which leads to arteriolar sclerosis and occlusion of deep penetrating branches of major cerebral arteries
94
Q

MCA occlusion lesion

A
  • contra somatosensory and motor deficit (face, arm, leg)
  • conjugate eye deviation toward side of infarct
  • homonymous hemianopia
  • aphasia (dominant hemisphere)
  • hemineglect (nondominant hemisphere)
95
Q

ACA occlusion lesion

A
  • contra somtosensory and motor deficit, predominantly in LE
  • abulia (lack of will or initiative)
  • dyspraxia, emotional disturbances, urinary incontinence
96
Q

Vertebrobasilar system lesion (supplying the brainstem)

A
  • alternate syndrome with contra hemiplegia and ipsi CN involvement
  • possible ataxia

NEURO (21 decks)

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