Alexandrov - Stroke Flashcards

1
Q

What is stroke?

A
  • Injury to the brain caused by:
    1. Interruption of its BF (ischemic) or
    2. Bleeding (hemorrhagic) into or around brain
  • Clinically, the loss of blood supply to the brain produces abrupt onset of focal neuro deficits that frequently result in permanent disability or death
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2
Q

What is TIA?

A
  • Transient ischemic attack
  • Abrupt onset of focal neuro deficits that resolve in <1hr
  • Important WARNING SIGN for future stroke
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3
Q

What are silent strokes?

A
  • Acute focal neuro symptoms and signs that resolve completely, but take longer than 1 hr to do so
    1. Invariably associated with detectable injury on MRI brain scans
  • May also be called resolving ischemic neuro deficits (RIND’s) -> although clinically detectable neuro deficit may appear to have resolved, MRI brain scan will show evidence of focal brain injury
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4
Q

What are the 2 “flavors” of stroke? How common are they, and what are some causes?

A
  • HEMORRHAGIC: 20%, and may be caused by bleeding into brain parenchyma (intracerebral hem) or bleeding around surface of brain (subarachnoid hem), which occur in roughly equal portions
  • ISCHEMIC: majority (80%), and can occur as result of atherosclerotic occlusion of intra-or extracerebral blood vessel, embolus to brain from heart of cerebral blood vessel, or disease of lumen of small arterioles (lacunar infarcts)
    1. Sizable proportion of these are CRYPTOGENIC
  • IMAGES: IC hem on top L (bright white blood in basal ganglia), subarachnoid hem in lower L (star-shaped silhouette of basilar cistern)
    1. Upper right digital subtraction arteriogram of atherosclerotic plaque in ICA (red arrow)
    2. Coronal section through pons showing lacunar infarct in mid-pons (yellow arrow)
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5
Q

What is the epi of stroke?

A
  • 3rd leading COD in the US, and leading cause of adult disability
  • Death rate fell 13.9% from 1987-97, but # of strokes each year has INC
  • Risk of having stroke and dying from one INC w/age, but significant # of strokes in ppl <65
    1. Very high mortality rate in the SE: TN #3
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6
Q

What are the non-modifiable risk factors for stroke?

A
  • AGE: doubles each decade >55
  • GENDER: male 1.5x risk of F
  • RACE: AA at 2x risk of European Americans
  • FAMILY HX: other genetic factors
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7
Q

What are the modifiable risk factors for stroke?

A
  • HTN
  • Diabetes
  • Hyperlipidemia
  • Smoking
  • Carotid artery stenosis
  • Atrial fibrillation
  • Obesity
  • Physical inactivity
  • NOTE: each of these is amenable to change via Rx tx, sx, or alteration of lifestyle
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8
Q

What is the #1 risk factor for stroke? List some other things with high relative risk.

A
  • HTN is #1 risk factor for stroke: based on combo of relative risk (3-5x) and prevalence (>30%)
  • RR for afib 5-17x, but low prevalence (<5%)
  • Other risk factors around 2x RR and prevalence b/t 20-30% (except carotid artery stenosis = <10% prev)
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9
Q

What is the pathological consequence of focal brain ischemia?

A
  • Cerebral infarct, where infarction is defined as focal necrosis of all cellular elements of brain, i.e., neurons, glia, and other supporting brain cells
  • NOTE: brain utilization in conscious man attached
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10
Q

What is selective ischemic necrosis? When are you most likely to see it?

A
  • ONLY brain neurons are injured (instead of the focal necrosis of all cellular elements of the brain seen with cerebral infarction)
    1. Affects only specific pops of highly vulnerable neurons, like CA1 pyramidals of hippocampus and Purkinje cells of cerebellum
  • Encountered most commonly in pts suffering transient global brain ischemia from CARDIAC ARREST and successful cardiac resuscitation
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11
Q

What happens to an ischemic neuron vs. a normal neuron?

A
  • NORMAL: metabolizes glu delivered by blood almost exclusively via aerobic metabolism; mito generate adequate ATP and PCr to sustain membrane ion pumping mechs that maintain fluctuating membrane ion gradients and membrane potential associated with depolarization and repolarization
  • ISCHEMIC: w/in mins of loss of blood supply, brain energy stores depleted via metabolism of glu via glycolytic pathways w/accumulation of lactic acid -> if not rapidly reversed, catabolic mechs triggered and cell will die
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12
Q

How do hyperglycemia and hyperthermia affect stroke brain injury? Implications?

A
  • They accelerate it, and exacerbate stroke brain injury
  • Elevated brain glu/glycogen stores or elevated circulating glu will provide further fuel for glycolysis, resulting in higher concentrations of lactic acid
  • A GOAL for acute stroke intervention is to normalize elevated body temp and rapidly treat hyperglycemia
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13
Q

What is the difference b/t core and penumbral ischemia? Implications?

A
  • Reduction of BF NOT uniform
  • CORE: severe ischemia, and tissue dies (or suffers irreversible injury) in <1hr (area most remote from blood vessels that may provide collateral BF)
  • PENUMBRA: moderate ischemia, and tissue dies in 4-6hrs -> acute intervention that restores blood supply to this territory has potential for salvaging brain tissue otherwise destined to die
    1. Basis for acute stroke intervention having a therapeutic window of 4-6 hours
  • NOTE: image shows L hemisphere w/pre-rolandic branch of MCA occluded by embolus
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14
Q

How does CBF autoregulation change in pts with chronic HTN? Implications?

A
  • NORMAL: CBF relatively constant (independent of MAP) b/t MAP of 55 - 155 mm Hg -> this is important bc MAP can fluctuate rapidly and widely w/changing position, but CBF does NOT fluctuate w/body position changes in normal folk
    1. MAP < 55 = severe hypoTN, reduced CBF, and syncope
    2. MAP > 155 = hypertensive encephalopathy
  • CHRONIC HTN: curve shifted to the R, so less severe hypotension or even BP levels considered normal can now result in DEC CBF
    1. Majority of stroke pts are HTNsive, so must be careful not to acutely lower BP bc risk of further reducing CBF to already ischemic vascular bed
    a. Loss of auto-regulation in penumbra and core, so depend on MAP -> lowering BP may cross infarction threshold in penumbral zone, INC extent of cerebral infarct
    2. Recommendation NOT to lower BP in pts who aren’t candidates for thrombolytic therapy unless systolic >220 or diastolic >120
    a. Lower BP only by 10-15% in first 24hrs if above these #’s
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15
Q

What is the equation for CBF? Approximate measure in normal folk/threshold for infarction?

A
  • CBF = MAP/CVR where MAP = mean arterial pressure and CVR = cerebral vascular resistance
  • About 55mL/100gm brain/min in normal ppl
    1. Threshold for infarction = 20
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16
Q

What are the neuro signs and symptoms of stroke?

A
  • Common neuro deficits include:
    1. Weakness or paralysis (acute onset on 1 side of body)
    2. Loss of sensation in 1 limb or on 1 side of body
    3. Loss of vision in one eye (amaurosis fugax: painless, transient monocular vision loss) or field
    4. Difficulty talking/understanding what is being said
    5. Difficulty w/organization or perception (cognitive abilities)
    6. Clumsiness of lack of balance
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17
Q

What are the ischemic stroke categories/subtypes?

A
  • CIRCULATION:
    1. Anterior: ICA, MCA, ACA, any of their branches
    2. Posterior: PCA, VA, SCA, AICA, PICA, branches
  • VESSEL SIZE:
    1. Large: ICA, MCA, ACA, PCA, VA, SCA, AICA, PICA
    2. Small: long and short penetrating branches of these aa
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18
Q

Briefly describe the cerebral circulation (image).

A
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19
Q

What functional areas of the brain are supplied by the MCA (image)?

A
  • Motor/sensory cortical regions
  • FEF
  • Broca’s
  • Wernicke’s
  • Optic radiations
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20
Q

What parts of the cortical homunculus are supplied by the ACA vs. the PCA? What do the lenticulostriate aa supply?

A
  • ACA: lower limb + trunk, shoulders
  • MCA: upper limbs and face
    1. Lenticulostriate: pyramidal tract axons to cortex + putamen, globus pallidus, and caudate
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21
Q

What structures are supplied by the ACA vs. the PCA (midsagittal view)?

A
  • ACA: medial frontal lobe, corpus callosum, motor + sensory to lower limbs/trunk
  • PCA: temporal lobe and hippocampal formation, optic radiations, deep perforating branches to thalamus and hypothalamus
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22
Q

Describe the Circle of Willis. What is it for?

A
  • Functions to provide collateral BF in instances of proximal occlusions (closer to heart) of cerebral blood vessels
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23
Q

Describe the blood supply to the brainstem (image).

A
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24
Q

What is medullary stroke syndrome (Wallenberg’s; image)?

A
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25
Q

What is pontine stroke syndrome (image)?

A
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26
Q

What is midbrain stroke syndrome (Benedikt; image)?

A
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27
Q

What are the signs/symptoms of an anterior circulation stroke? Potentially affected vessels?

A
  • ICA, MCA, ACA, or any of their branches
  • Ipsilateral blindness or contralateral inferior quadrantanopsia
  • Contralateral gaze paresis
  • Contralateral mono/hemiparesis and/or mono/hemi-sensory deficit
  • Aphasia in dominant hemisphere or neglect in nondominant hemisphere
  • Any combo of the above
  • EX: occlusion of parietal-temporal branches of left MCA would produce R-sided inferior quadrantanopsia
  • NOTE: image shows signs/symptoms 2o to occluded aa in graphic (ICA, ophthalmic, central retinal) -> clot + emboli
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28
Q

Why is it important to be able to distinguish b/t anterior and posterior circulation strokes?

A

Bc these 2 vascular territories carry slightly different prognoses and tx options

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29
Q

What are the signs/symptoms of a posterior circulation stroke? Potentially affected vessels?

A
  • PCA, VA, SCA, AICA, PICA, or any of their branches
  • Unilateral, bilateral, or crossed (face/body) weakness or sensory deficits
  • Contralateral homonymous hemianopsia or superior quadrantanopsia
  • Vertigo, N/V, gait ataxia, diplopia, dysphagia, Horner’s syndrome
  • Altered consciousness and amnesia
  • Any combo of the above
  • EX: L PCA occlusion will cause homonymous hemi-anopsia of R visual field (visual field loss on same side of both eyes bc left 1/2 of brain has visual pathways for R hemifield of both eyes, and vice versa)
  • NOTE: crossed extremity signs, while possible, are very rarely caused by lesion above foramen magnum (not unusual to have crossed motor or sensory signs involving ipsilateral face and contralateral limbs)
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30
Q

What are lacunar strokes? What are the 4 classic syndromes?

A
  • Small areas of ischemic necrosis caused by occlusion of small, penetrating arteries
  • SYNDROMES:
    1. Pure hemiparesis: can occur at any of several locations along corticospinal/spinothalamic tracts, but most common sites are INTERNAL CAPSULE and PONS
    2. Pure hemisensory deficit: same as above + lacunes involving VPL nucleus of THALAMUS
    3. Ataxia hemiparesis (pontine stroke syndrome)
    4. Dysarthria: clumsy hand syndrome (medullary stroke syndrome = Wallenberg)
  • IMAGE: left arrows pointing to 2 of several lacunar infarcts; right arrows pointing to bilateral thalamic lacunes
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31
Q

What should be on your DDx for ischemic stroke?

A
  • PT WITH ACUTE ONSET OF FOCAL NEURO SIGNS AND SYMPTOMS:
    1. Hemorrhagic stroke
    2. Subdural hematoma
    3. Syncope/near syncope
    4. Radiculopathy
    5. Bell’s palsy
    6. Multiple sclerosis
    7. Brain tumor
    8. Migraine
    9. Seizure
    10. Hypo/hyperglycemia
    11. Hypoxia
32
Q

What are some of the etiologic diagnoses for a pt with ischemic stroke?

A
  • Atherothrombosis/atheroemboli
  • Lipohyalinosis and fibrinoid necrosis (small vessels causing lacunar strokes)
  • Cardiogenic emboli
  • Vasculitis
  • Hematologic disorders
  • Drug related
  • Others
33
Q

How can atherothrombosis/atheroemboli cause ischemic stroke?

A
  • Gradual buildup of atheromatous plaque (in walls of common carotid and bifurcation of internal/external carotid aa in attached image)
  • Ulcerative process leading to PLT deposition and formation of red clot that may enlarge with time to totally occlude vessel or fragment and send small PLT and/or thromboemboli to distal cerebral blood vessels
34
Q

What are some common sites of atherothrombosis/atheroemboli in the brain?

A
  • Origins of carotid/vertebral aa
  • Bifurcations of common carotid aa
  • ICA’s at carotid siphon (in cavernous sinus) and branch points of MCA and ACA
  • M1 segment of MCA: horizontal segment proximal to Sylvian fissure
  • Basilar artery (vertebrobasilar aa)
35
Q

What is this?

A

Plaque in basilar artery

36
Q

What happened here?

A

Plaque in carotid bifurcation

37
Q

What is the pathogenesis of lacunar stroke?

A
  • Microatheroma: analogous to atherothrombosis in large cerebral vessels
  • Microemboli: from more proximal blood vessels or heart
  • Lipohyalinosis & fibrinoid necrosis MOST COMMON
    1. Histo transformation that occurs in smooth mm and intima of small penetrating cerebral vessels as a consequence of chronic HTN
38
Q

What are the common causes of cardiogenic emboli?

A
  • Arrhythmia (afib): MCC
  • Valvular heart disease: mitral stenosis, bacterial endocarditis, prosthetic heart valves
  • Mural thrombus: MI (i.e., from CAD)
  • NOTE: brain receives 20% of CO, so it is a common target for embolic material released from the heart
39
Q

What are some uncommon causes of cardiogenic emboli?

A
  • Atrial myxoma (heart tumor)
  • Valvular heart disease: mitral valve prolapse, non-bac (marantic) endocarditis via cancer or SLE (Libman-Sacks emboli)
  • Mural thrombus via cardiomyopathy
  • Paradoxical embolus: right-left shunt -> arise from deep venous circulation and bypass being filtered out by lungs as they move from R ventricle to L via patent foramen ovale of VSD
40
Q

What do you see here?

A

Embolus in basilar artery (traveled from heart via vertebral artery to occlude basilar apex)

41
Q

What is going on here? Neuro presentation?

A
  • CNS VASCULITIS: inflammation of CNS vessels producing segmental narrowing and multifocal occlusions (appearance on cerebral arteriogram; CAG)
  • NEURO PRESENTATION is multifocal, reflecting multiple small- and medium-sized vessel occlusions
    1. Different presentation than “garden variety” ischemic strokes
42
Q

What are some of the causes of CNS vasculitis?

A
  • Collagen vascular diseases: SLE (MCC)
  • Giant cell arteritis: pts >55, and responds well to steroid Rx (unilateral headaches over temporal artery)
    1. Untreated, can cause strokes and lead to blindness -> early dx important
  • Infectious vasculitis: syphilis, lyme, AIDS, zoster, hep B, bacterial, fungal, TB
  • Hypersensitivity vasculitis
  • Wegener’s granulomatosis
  • Behcet’s disease: rare immune-mediated small-vessel systemic vasculitis that often presents with mucous membrane ulceration and ocular problems
  • Primary CNS vasculitis
43
Q

What are some heme disorders that can precipitate ischemic stroke?

A
  • Hyperviscosity syndromes: polycythemia, multiple myeloma -> sludging within capillaries
  • Hypercoagulable conditions: antiphospholipid or anti-cardiolipin syn, protein C and S def, cancer, pregnancy, factor V leiden def, thrombocytosis
  • Hemoglobinopathies: sickle cell
44
Q

What are some drug-related causes of ischemic stroke?

A
  • Street drugs: cocaine (most common offender; crack), LSD, amphetamines, phencyclidine, methylphenidate, sympathomimetics
  • Ethanol in excess leads to dehydration and sludging of blood cells that may cause stroke
  • Oral contraceptives: high-dose estrogen carries greater risk, but no prep is entirely safe
45
Q

What are some “other” causes of ischemic stroke?

A
  • Fibromuscular dysplasia: abnormal proliferation of tissue in blood vessel walls, and uncommon cause of stroke
  • Carotid or vertebral artery dissection: spontaneous or traumatic
  • Homocystinemia: elevated levels can cause strokes via blood vessel inflammation and enhancing blood coagulation
  • Other emboli: fat, air, bone marrow
  • Vasospasm: subarachnoid hemorrhage
  • Migraine: uncommon, but INC in women with migraines who smoke and/or take OC’s
46
Q

What are the 4 distinct types of cerebral hemorrhage? What would their imaging look like?

A
  • SUBARACHNOID (SAH): arrows pointing to blood filling sulci overlying L neocortex
  • INTRACEREBRAL (ICH): blood in basal ganglia
  • EPIDURAL (EDH): blood b/t inner plate of skull bone and dura -> characteristic convex, or lens shape
  • SUBDURAL (SDH): over L cerebral hemisphere -> 2 hemorrhages separated by several wks or more bc layer of bright white blood outer most and beneath it is second less dense layer containing 2 distinct densities bc RBC’s lyse and release contents over time
  • NOTE: recall you are looking at brain slice from bottom up and less dense = darker
47
Q

What are the 2 anatomic diagnoses of hemorrhagic stroke?

A
  • SUBARACHNOID hemorrhage: bleeding into subarachnoid space accounts for about 50% of cerebral hemorrhages
  • PARENCHYMAL (aka, intracerebral): bleeding into substance of brain accounts for about 50% of cerebral hemorrhages
48
Q

What are some of the etiologic diagnoses for hemorrhagic stroke?

A
  • Berry aneurysm
  • Vascular malformation
  • Traumatic
  • Mycotic aneurysm
  • HTN
  • Tumor
  • Bleeding diatheses
  • Anticoagulant complication
  • Congophilic angiopathy
  • Vasculitis
  • Ilicit drug use
49
Q

What is aneurysmal SAH?

A
  • 80% (MCC) of SAH a rupture of berry or saccular aneurysm (berry aneurysm classically at branch pt b/t circle of willis and cerebral artery)
    1. Most common locations in attached image: anterior much more common (ACOM, PCOM, MCA) than posterior
  • Berry aneurysms common: 20% w/aneurysm <2mm (rarely bleed), 5% w/aneurysm 2-5mm (occasionally bleed), aneurysm >5mm bleed at rate of 1-3%/yr
    1. Reflect devo defects in blood vessel wall that tend to enlarge w/time
  • Best treated surgically or via intravascular coils
50
Q

What are the risk factors for SAH?

A
  • Tobacco use
  • Ethanol abuse
  • HTN
  • Oral contraceptives
  • Stimulant drugs: cocaine, etc.
  • Low cholesterol
  • Genetics: polycystic kidneys, Marfan’s syndrome
51
Q

What is the prognosis for SAH?

A
  • 10-15% die prior to ER
  • 25% die in next 3 months
  • About 40% of survivors have neuro sequelae
52
Q

What are the symptoms of SAH?

A
  • Sudden, severe headache -> “worst headache of my life
  • Rapid LOC in some (2o to large pulse pressure change delivered to brainstem as a result of arterial blood entering subarachnoid space), but not all, pts
  • Neck stiffness/pain, photophobia, phonophobia (w/in hours of rupture of berry aneurysm) -> reflect irritation and inflammation of meninges 2o to breakdown products of RBC lysis
  • N/V
  • Focal neuro signs frequently minimal or absent: helps distinguish this type of stroke from ischemic stroke
53
Q

What are the signs of SAH?

A
  • Abnormal vital signs: elevated BP, arrhythmias (due to RBC breakdown products that irritate brainstem centers regulating HR)
  • Focal neuro signs subtle or absent (but can help locate aa site of aneurysm):
    1. CN III paresis: dilated pupil + opthalmoparesis (ICA/PCOM junction)
    2. Paraparesis: bilateral leg weakness (ACA)
    3. Hemiparesis: MCA
  • Meningeal signs: usually present, but may be subtle or delayed for several hours after aneurysm rupture and onset of headache
  • Retinal hemorrhages
54
Q

What is the most important noninvasive diagnostic test to reveal SAH? What will you see? What if you don’t see anything?

A
  • Non-contrast CT: can reveal blood in subarachnoid space or brain -> location and amount of blood helps localize site of ruptured aneurysm + predict likelihood of delayed complication called vasospasm
    1. May be (-) if bleeding is slight or CT delayed for several days
  • If (-) and you suspect SAH, perform LP to rule out bleeding -> ONLY 100% method to rule out subarachnoid bleed
55
Q

When should you do an LP in pt with suspected SAH? What might you find?

A
  • If CT (-) for blood and SAH suspected, do LP -> delay for about 4 hours after symptom (headache) onset
    1. Allows time for some RBC’s in subarachnoid space to lyse and release Hb into spinal fluid -> presence of Hb or its breakdown products in spinal fluid will help distinguish bt appearance of blood in spinal fluid from nicked vein vs. blood from rupture of berry aneurysm
  • If CSF appears bloody or discolored, immediately centrifuge it and examine for xanthochromia
    1. RBC’s from nicked vein during tap will remain intact and spun down during centrifugation, leaving supernatant clear (like normal CSF)
    2. Red tinge or discoloration after centrifuging means Hb dissolved in spinal fluid from RBC’s that have been in spinal fluid for hours (i.e., from ruptured aneurysm)
56
Q

Briefly summarize SAH presentation and LP results.

A
  • PRESENTATION: severe headache, may have LOC, may demonstrate (+) Kerning’s or Brudzinski signs (of meningeal irritation)
  • LP: bloody spinal fluid that doesn’t clear after collecting several tubes = ruptured berry aneurysm or yellow tubes (xanthochromia) indicating breakdown of Hb = ruptured aneurysm (yellow discoloration takes a day to or more after rupture of aneurysm to develop)
57
Q

What neuroradiology exams will you do post-CT/LP if dx of SAH confirmed?

A
  • Need to ID site of ruptured blood vessel:
    1. Magnetic resonance arteriography (MRA) will reveal larger (>5mm) aneurysms
    2. GOLD STANDARD: 4-vessel digital subtraction arteriography (DSA) for demonstrating 1 or more aneurysms (may be multiple, esp. with PCKD)
58
Q

What is the tx for SAH?

A
  • Definitive tx for berry aneurysm is combo (or one or the other) of interventional radiology to:
    1. Coil some aneurysms: placement of small coils w/in aneurysm via intra-arterial catheter -> cause aneurysm to clot and seal itself
    2. +/- surgical clipping: at neck of aneurysm
59
Q

What is the sx approach to basilar artery aneurysm?

A
60
Q

What happened here?

A
  • Digitial subtraction arteriography (DSA) of basilar tip aneurysm (yellow arrow) before placement of coils in lumen of aneurysm (left)
  • After placement of coils (right): note that after coil placement, aneurysm has clotted off & arteriographic dye cannot enter aneurysm
61
Q

What is parenchymal hemorrhage? Causes? Most common sites?

A
  • Hemorrhage into substance of the brain
  • MCC: trauma, HTN, arteriovenous malformations (in DEC freq)
    1. Chronic HTN causes microaneurysms called Charcot Bouchard aneurysms in small, penetrating microvessels that eventually rupture
    2. Hypertensive bleeds occur most frequently in basal ganglia, thalamus, cerebellum, and pons (see attached image)
62
Q

What are the common locations of parenchymal hemorrhages in the brain?

A
  • B, C, D, E reflect hemorrhage of microaneurysms 2o to chronic HTN
  • A is NOT 1 of the areas that harbors small penetrating arterioles that are the site of Charcot Bouchard aneurysms, so etiology of these cortical, polar (poles of the brain) hemorrhages NOT usually related to HTN
63
Q

What is an AVM?

A
  • Arteriovenous malformation: occur in several varieties with greater or lesser tendencies to rupture and bleed
  • Attached image shows typical AVM w/its appearance on DSA and CT scans
64
Q

What is the tx for parenchymal hemorrhage due to AVM?

A
  • Intravascular occlusion of ACM with coils, followed by sx removal or gamma knife obliteration of AVM
65
Q

What are the txs for hypertensive/traumatic hemorrhage?

A
  • Correct any bleeding problem (Vit K, FFP, rFVIIa, prothrombin complex concentrate)
  • Reduce BP to <160/100 or MAP <130 mm Hg
  • Monitor for and tx elevated intracranial pressure
  • If signs of herniation develop, hyperventilate, osmotic Rx, neurosurgical Rx are required
    1. Maintain CPP b/t 60-80 mm Hg
66
Q

How does stroke present? What are the first steps in dx and mgmt?

A
  • PRESENTATION: abrupt onset of focal neuro signs and symptoms
  • 1st, check and stabilize all vital signs (BP, HR, vent, T)
  • Collect hx of event with special attention to time of symptom onset, which is best determined by asking pt or family when pt was last observed to be “normal”
    1. Ask about symptom progression, whether headache is present, and how severe
  • Formulate anatomical dx (brain region, vascular supply -> neuro exam will help with this)
  • PMHx: stroke risk factors, meds + FHx: vascular disease, HTN, hyperlipidemia + SHx: tobacco, EtOH, illicit drugs
67
Q

What are you particularly interested in doing in the physical exam for stroke (excluding neuro)?

A
  • HR and rhythm
  • BP in both arms
  • Presence of absence of carotid bruits
  • Peripheral vascular exam
  • NOTE: at this point, you should be asking yourself if this is a stroke or a stroke mimic -> if it is a stroke, is it ischemic or hemorrhagic?
68
Q

What are the standard labs for suspected stroke?

A
  • EKG with rhythm strip
  • CXR to evaluate heart size
  • CBC w/differential and PLT count
  • Chemistry profile: glu, BUN, electrolytes, lipid profile
  • Clotting times: INR, aPTT
  • Head CT w/o contrast
  • NOTE: additional lab tests you may consider ordering are attached
69
Q

What are some tests you may order for radiologic eval of stroke?

A
  • Echocardiogram
  • Carotid artery ultrasound
  • Head MRI
  • Head and neck MRA
  • CT arteriogram
  • Digital subtraction arteriogram
  • NOTE: selection of tests will depend on pt presentation
70
Q

When does CT scan begin to pick-up an evolving infarct? What is this type of imaging best used for?

A
  • Head CT begins to detect evolving infarcts w/in about 6-12hrs -> CT scan is NOT a good imaging tool to detect an early ischemic stroke
  • CT scan is HIGHLY SENSITIVE to hemorrhage, so it is indicated in all pts presenting with stroke symptoms to rule out hemorrhagic stroke (see attached image)
71
Q

What type of imaging is best to detect early ischemic infarct?

A
  • Attached scans were obtained b/t 1-2 hours after symptom onset:
    1. CT scan appears entirely normal (neither this nor MRI flair able to detect full extent of stroke evolving during early hrs after symptom onset)
    2. MRI FLAIR shows only small area of L parietal lobe w/early hyperintensity
    3. MRI DIW reveals large area of hyperintensity: very sensitive to early ischemic changes in tissue
72
Q

How might stroke look on ultrasound?

A
  • Ultrasound images of carotid aa attached: note narrowing at origin of ICA on DSA and similar narrowing on B-mode images
  • NOTE: doppler image below records wave of blood moving through carotid artery
73
Q

What type of imaging is this?

A
  • Magnetic resonance arteriogram of intracranial vasculature
74
Q

What happened here?

A
  • Absence of MCA vessels due to occlusion in L figure before alteplase (aka, tissue plasminogen activator or tPA)
  • Presence of vessels after lysis of the clot in the R figure (post-alteplase)
  • NOTE: DSA (digital subtraction arteriogram) imaging
75
Q

What are the 2 techniques for angiography of cervical and cerebral vessels?

A
  • Catheter placement via femoral artery + injection of contrast dye to create DSA images of extra- and intracranial blood vessels
  • Can also do IV placement (see attached image)
76
Q

What is the acute tx for stroke?

A
  • Tx with IV tPA if <4.5hr from symptom onset and pt meets other strict criteria
  • Tx with intraarterial tPA if <6hr from symptom onset and pt meets other strict criteria
  • Retrieve clot w/intra-arterial retrieving device if <8hr from symptom onset and pt meets other strict criteria
77
Q

What is the prophylactic tx for stroke?

A
  • Vascular stenting or endarterectomy for stenosis >70% of lumen diameter
  • Anti-HTN Rx, anti-lipid Rx
  • Anti-PLT’s (ASA) Rx for atherothrombotic stroke (reduces recurrence of ischemic stroke)
  • Anti-coagulants (Warfarin) for cardioembolic (reduces recurrence of ischemic stroke)
  • Anti-diabetic Rx
  • Stop smoking
  • Physical exercise
  • NOTE: prophylaxis most effective method for dealing with stroke