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Neuro > CNS Hemorrhagic stroke and Ischemia > Flashcards

CNS Hemorrhagic stroke and Ischemia Flashcards

1
Q

What’s up with an epidural hematoma?

A
  • Occurs between the skull and dura
    • TYPICALLY the middle meningeal artery (classic presentation)
    • Collect in a convex, or lemon/lens shaped hematoma (on imaging)
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2
Q

What is up with hemorrhagic transformation

A
  • An an ischemic stroke bed, you can get a large vessel to bust and “tranform” into a hemorrhage
    • Mostly with large vessel cortical strokes
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3
Q

What is meant by intra-parenchymal hemorrhages?

A
  • Formed blood clots which dissect into the brain

* Can be anywhere and have lots of causes

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4
Q

What are subarachnoid hemorrhages?

A
  • Right next to brain, underneath arachnoid layer
    • Trauma is most common cause
    • Can be AVM (aneurisms) can be a non-traumatic cause
    • RARE - cortical subarachnoid hemorrhage can show up with vasospasm, migraine, ischemia or without obvious cause
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5
Q

What’s up with a subdural hemorrhage?

A
  • Between dura and thin arachnoid covering brain
    • Typically from torn or ruptured bridging vein between dura and cortex
    • Layers like a banana (on imaging)
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6
Q

What is usually the cause of intraperenchymal hemorrhages?

A
  • HTN and age
    • Usually occur in the basal ganglia (putamen), thalamus, pons and cerebellar deep grey matter
    • If you see a hemorrhage in one of these areas in a HTN patient, no need to look further
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7
Q

What’s up with amyloid angiopathy?

A
  • A specific entity in which patients get recurrent lobar hemorrhages that lead to progressive dementia and disability
    • Amyloid deposition is found in the vessels (intramural)
    • Different from systemic amyloidosis or to alzheimer’s amyolid plaques
    • Can be found, however, in conjunction with alzheimers
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8
Q

Is a subdural hemorrhage usually trauma related?

A
  • Not like the epidural ones
    • In older patients brain atrophy makes it easier to tear bridging veins
    • They can happen and not present clinically at all
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9
Q

Where do non-traumatic subarachnoid hemorrhages come from?

A
  • 80% aneurysmal rupture
    • 15% ateriovenous malformation
    • Remember the rare occurance of the cortical SAH, which is more “leaky” than an arterial rupture and bleed
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10
Q

What is the typical presentation of hemorrhage?

A
  • Think of what mass effect and herniation might entail
    • Usually sudden onstet of neurological deficiets
    • Typically have associated headache, nausea, vomiting along with depressed level of consciousness
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11
Q

What is the typical presentation of hemorrhage?

A
  • Think of what mass effect and herniation might entail
    • Usually sudden onstet of neurological deficiets
    • Typically have associated headache, nausea, vomiting along with depressed level of consciousness
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12
Q

What type of hemorrhage is HTN NOT a risk factor for?

A

• Subarachnoid hemorrhage (SAH)

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13
Q

What might be the patients complaint in the situation of non-traumatic subarachnoid hemorrhage?

A
  • Onset is “cataclysmic”
    • “firecracker” or explosion in the head
    • (very sincere headage)
    • Sudden death in 1/3 from either acute hydrocephalus OR from sympathetic surge and cardiac arrhythia
    • CNIII palsy can be a presenting sign
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14
Q

What is the hunt and hess classification of subarachnoid hemorrhage

A
  • Grade 1 - asymptomatic or minimal headache; slight nuchal rigidity
    • Grade 2 - moderate to severe headache, nuchal rigidity, no neurological deficit (apart from cranial nerve palsy)
    • Grade 3 - drowsiness, confusion, or mild focal deficit
    • Grade 4 - stupor, moderate to severe hemiparesis, possible early decerebrate posturing
    • Grade 5 - deep coma, decerebrate posturing moribund
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15
Q

What is the course of an intraparenchymal hematoma?

A
  • Begin with a mild headache, deficit, nausea
    • Progress over a few minutes to hours into decreased levels of consciousness
    • Often can look like a hemiparesis steadily progressing into hemiplagia
    • Remember this problem is seen more with increased age and HTN
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16
Q

If you see amyloid crystals with a birefringence lens what CNS hemorrhagic disease are you looking at?

A
  • Cerebral amyloid angiopathy
    • Disease of the aged characterized by recurrent lobar hemorrhages that are often curiously well tolerated
    • No primary therapy
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17
Q

Why would platelet and anti-coag theraphy help with future hemorrhage after an initial ischemic event?

A
  • Ischemia can end up resulting in hemorrhagic transformation
    • Thus, if you can prevent the ischemia (by thomboses) then you can prevent the transformation and hemorrhage
    • Important in smoking patients
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18
Q

How does intracranial hemorrhage cause damage to the brain?

A
  • Mass effect
    • Focal and secondary ischemia (shutting off cerebral vasculature because of such a high pressure)
    • Effects of irritating blood (induction of vasospasm)
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19
Q

What is the formula for cerebral perfusion pressure?

A
  • CPP = MAP - ICP

* Systolic BP above 160 is associated with a higher risk of recurrent hemorrhage

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20
Q

What is the treatment paradigm of SAH in terms of blood pressure?

A
  • SAH = subarachnoid hemorrhage
    • These problems are often surgically treated, so part of medical management is preparation for surgery
    • Benefit by sedation and relative hypotension reduces the risk of re-bleeding before surgical intervention
    • Treatment with nimodipine and statins help reduce the amount of ischemic damage from vasospasm
    • After surgery, you really need to keep the BP normal or even higher than normal to reduce vasospasm
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21
Q

What can Nimodipine and Statin pharmacologic therapy be helpful with?

A
  • Subarachnoid hemorrhage
    • Can reduce amount of ischemic damage from vasospasm
    • Caused by irritation of blood vessels by the blood in the subarachnoid space
    • After surgery, you really need to keep the BP normal or even higher than normal to reduce vasospasm
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22
Q

What diagnostic procedure must be done in the case of SAH?

A
  • Subarachnoid hemorrhage requires an angiogram to determine the cause of the bleeding
    • Can also determine potential efficacy of surgery or if surgery is even indicated
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23
Q

In general, what does stroke or cerebrovascular disease mean?

A
  • Any vascular injury to the brain

* Hemorrhage or ischemic

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24
Q

What is meant by transient Ischemic Attack?

A
  • Aka - TIA
    • Ischemic neurological deficits that have completely resolved by 24 hours regardless of their severity or relative duration
    • Depth and duration of ischemia can vary so there is no exact time agreed upon as “transient”
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25
Q

What is the overall general clinical presentation of a stroke?

A
  • The severity of the stroke will depend on the size of the vessel (and thus the area of ischemia) involved
    • Focal neurological deficits come on rapidly with no warning
    • Headache
    • Rapid change in consciousness
    • Onset is most severe with farily quick improvement over seconds, minutes, hours, days, weeks
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26
Q

What is the overall general clinical presentation of a stroke?

A
  • The severity of the stroke will depend on the size of the vessel (and thus the area of ischemia) involved
    • Focal neurological deficits come on rapidly with no warning
    • Headache
    • Rapid change in consciousness
    • Onset is most severe with farily quick improvement over seconds, minutes, hours, days, weeks
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27
Q

What will a typical patient with a large vessel (middle cerebral artery) stroke present with?

A
  • Hemiparesis,
    • hemi-sensory loss
    • Homonymous hemi-anopsia (lack of sight) contralateral to the ischemic side of the brain
    • To get this you need a large vessel stroke mechanism or major artery occlusion
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28
Q

Compare and contrast a large vessel and small vessel stroke.

A

• Large vessel, large area of dysfunction, many actions and sensory deficits
○ Can look like a full hemiparesis
• Small vessel, isolated motor or isolated sensory deficit on one side of the body
○ Caused by occlusion of the small penetrating vessels that arise from larger arteries deep in the brain
○ Produce lacunar infarctions
○ Can contribute to multi-infarct dementia from multiple lacunar strokes that can accumulate over many years

29
Q

What are the risk factors associated with atherosclerosis and why does this matter for ischemic stroke?

A
  • Matters because atherosclerotic plaques can break off and occlude cerebral arteries
    • Internal carotid can be occluded like coronary arteries
    • Age
    • Men
    • Race
    • Hypertension
    • Lipid disorders
    • Insulin resistance
    • Homocysteine elevation
    • Smoking
    • Obesity
    • Physical inactivity
    • Diabetes
    • Alcohol abuse
30
Q

What’s the confusing thing about alcohol being an atherosclerosis risk factor?

A
  • 1-2 drinks a day can decrease your risk, but once you get into 6-pack a day or just plain alcoholic, it increases your risk
    • Both of these risks are evidence supported
31
Q

What can happen in the heart that could cause an ischemic stroke?

A
  • Atrial fibrillation, congestive heart failure and valvular disorders
    • Rarely, atrial septal defect
    • These structural problems allow for clots to form and emboli to be ejected into blood stream
    • Emboli can occlude major or minor cerebral vasculature
32
Q

An IV drug user would be at higher risk for what specific type of stroke?

A

• Infected embolic stroke
• Can also create a mycotic aneurysm
○ Infected aneurysm, or seat of infection on a vessel that destroys the wall
○ The loss of structural integrity might lead to dissection, or just a base for throwing extra small clots into the brain

33
Q

What neoplastic condition (and it’s relation to stroke) seems to be over-represented on board exams?

A
  • Atrial myxoma and other intravascular or cardiac tumors
    • They can cause stroke as well
    • Throw little tumor-bits that can end up occluding vessels
34
Q

A young patient free of risk factors gets a stroke. Your differential changes to include what?

A
  • Vasculopathies
    • Hematological disorders
    • Inflammatory mechansims
    • Venous infarction
    • Vasospasm
35
Q

What are the particular vasculopathies we talked about that can increase the risk of “young stroke”?

A

• FMD = fibromuscular dysplasia
○ Mostly women, hypertrophy of arterial media, surgical dilatation is treatment
○ HSV-1 virus is candidate cause
• Moya-moya
○ Epstein barr virus is associated
○ Intimal hyperlasia and secular aneurysms and dissection
○ Children, more common in asian and african descent
• Spontaneous arterial dissection
○ Tear in endothelium, blood pooling between layers
○ Can throw clots, therapy is anticoag
○ HSV-1 also candidate

36
Q

What hematological disorders should you be concerned about causing ischemic strokes?

A
  • Familial/genetic disorders in preventing thrombosis
    • Factor V leiden, prothrombin gene deletion, deficiencies in protein C, protein S, antithrombin
    • If the body can’t bust up clots well AND there is a PFO or ASD…you could have paradoxical embolization
37
Q

What is paradoxical embolization?

A

• A thrombosis of venous origin that somehow manages to cross through a cardiac defect to get into arterial circulation and cause problems

38
Q

Why is Sickle Cell anemia a concern in ischemic strokes?

A

• Sickle cell crises can create thromboses that can occlude small and medium vessels in the brain

39
Q

What does the state of malignancy have to do with ischemic strokes?

A
  • Malignancies can cause a hypercoagulable state

* If there is stroke history and blood tests show coag, search for malignancy

40
Q

What risk factor for ischemic stroke is present in menopausal women as well as young women?

A
  • Oral contraceptive pill and hormonal therapy
    • Implicated in stroke and venous thrombosis
    • 25X increased risk if there is the triad of migrane-smoker-OCP
41
Q

What autoantibodies, when present, can lead to spontaneous miscarriage AND risk of ischemic stroke?

A
  • Antiphospholipid antibodies

* Therapies range but often look like antithrombotics or anticoag (warfarin)

42
Q

Does a vasculitis have to be a systemic disease to affect the CNS?

A
  • Nope. While the vasculidities CAN secondarily affect CNS
    • There are cases of isolated CNS vasculitis
    • Traditionally auto-immune, but infections causes are candidates now too
    • VZV is increasingly a candidate
43
Q

How can migraine and stroke be related?

A
  • Migraine is common, the link to stoke is pretty uncommon
    • Vasospasm (sterile serotonin mediated intramural inflammation)
    • Increased platelet aggregation that clogs the microcirculation leading to permanent cellular injury
    • Treatment is antiplatelet therapy
44
Q

What venous stroke -related problems should you be aware of?

A
  • Post partum sagittal sinus thrombosis (3-5 days)
    • Non-traumatic venous infarction from dehydration, CNS infections and hypercoag states
    • The most common cause is major head trauma
45
Q

Sympathetic drugs, severe HTN and primary vessel irritation can all help cause what?

A

• Vasospasm. Can result in ischemic brain damage

46
Q

What pharmacological agents are shown to reduce the long term risk of recurrent ischemic stroke?

A
  • Aspirin
    • Thienopyridines (clopidogrel, prasurgrel, ticlopidine)
    • Anticoagulants
47
Q

Should you use combo therapy for stroke risk reduction?

A
  • It could help after catheter-invasive procedures or after a major ischemic event.
    • HOWEVER, long term benefit??? Not really supported
    • Common combos are aspirin and clopidogrel OR aspirin-warfarin
48
Q

What are the aspirin recommendations for reducing stroke risk?

A
  • Single coated aspirin a day either 81mg, or 325mg
    • GI catastrophes do occur
    • Cost of aspirin therapy can be increased if an H2 blocker or proton pump inhibitor is required on a regular basis (to block the GI complications)
49
Q

Atrial fibrillation should be first treated with?

A
  • Warfarin is highly effective in primary prevention of stroke in afib
    • Relative risk of stroke is reduced by 70%
    • The other situation for warfarin is mechanical heart valves
50
Q

What are the class of newer, alternative oral anticoagulants called?

A
  • DTIs or direct thrombin inhibitors
    • Include dabigatran, rivaroxiban, apixaban
    • Most of their benefits are in lower risk populations
    • NOT mechanical valves situations
51
Q

What are the hospital used injected/IV anticoags?

A
  • Drug (target)
    • Heparin (ATIII, thrombin)
    • LMW heparins (ATIII, Thrombin, Xa)
    • Argatroban (thrombin)
52
Q

Whats the CHADS score?

A
  • A risk score grading atrial fribrillations as a risk for causing stroke
    • Points for age, HTN, CHF, DM, previous stroke
    • This is for weighing the risk of hemorrhage in geriatric population with benefit of stroke reduction
53
Q

What is an endarterectomy?

A

• Carotidendarterectomy(CEA) is a surgical procedure used to reduce the risk of stroke, by correcting stenosis (narrowing) in the common carotid artery or internal carotid artery.Endarterectomyis the removal of material on the inside (end(o)-) of an artery.

54
Q

When do you refer for an endarterectomy?

A
  • 70-90% stenosis

* Not effective before that

55
Q

Ischemic stroke resuscitation…can it be done?

A
  • Yes, with TPA (tissue plasminogen activator)
    • But it must be IV or IA and within 4.5 hours of stroke
    • Keep fluids up, maximize cardiac output, don’t lower BP
56
Q

The two most important/common mistakes you can make in stroke care that minimize long term outcome are…?

A

• Delaying the treatment of dehydration (by being afraid to administer saline b/c of CHF for example)
○ Do treat the dehydration
• Inducing hypotension (treating the HTN associated with stroke for about a week)
○ Resist lowering blood pressure

57
Q

When do you use glucose supplementation in a stroke patient?

A
  • In the RARE hypoglycemic stroke patient, glucose can really help with hemiplegic deficits (even abolish them)
    • However, in non-hypoglycemic patients, glucose admin can really mess them up (through breaking of atherosclerotic plaque)
    • The risk is too much in normal people so use glucose or insulin only in bad cases of hypoglycemia or unstable glucose
58
Q

Can there be a stroke without a visualized problem by both MRI and CT?

A

• Clinical symptoms don’t lie, so yes, there are silent strokes (in terms of silent on imaging)

59
Q

In what cases would a lumbar puncture be a particularly helpful diagnostic procedure?

A

• Exclude neurosyphilis
• Vasculitis
• Inflammatory conditions
• RARELY, stroke mimic
• Subarachnoid hemorrhage (when other imaging doesn’t find it)
○ been going on for a while before the CT that missed it
○ Spinal or brainstem source that is not in the region of scanning
○ See xanthochromia indicating blood staining the CSF in the recent weeks

60
Q

What is the CHADS2 score?

A
  • (points) letter- risk factor
    • (1)C - congestive heart failure
    • (1)H - HTM, consistently above 140/90 mmHg (or consistently treated with pharm.)
    • (1)A - age (over 75 years)
    • (1)D - diabetes melitus
    • (2)S2 - prior stroke or TIA
61
Q

What does the CHADS2 score mean?

A
  • It tells you the evidence based risk of stroke given the score of the metric
    • 0 - 1.9%
    • 1 - 2.8%
    • 2 - 4%
    • 3 - 5.9%
    • 4 - 8.5%
    • 5 - 12.5%
    • 6 - 18.2%
62
Q

What is the general mode of treatment depending on CHADS2 score?

A
  • 0 - aspirin if any coags and start them on daily aspirin
    • 1 - can use warfarin or aspirin for anticoag, and start them on aspirin daily or raise INR to 2.0-3.0
    • 2 or greater - warfarin is your anticoag and you raise INR to 2.0-3.0 (unless other contraindication)
63
Q

Where are the common ICH locations?

A
  • ICH - intracranial hemorrhage
    • Cerebral lobes
    • Basal ganglia
    • Thalamus
    • Pons
    • cerebellum
64
Q

Where in the cerebral vasculature do you more often see saccular (berry) aneurysms?

A
  • 40% - anterior cerebral artery just before the anterior communicating artery shoots off
    • 34% - middle cerebral artery
    • 20% - internal carotid, before bifurcation into middle and anterior cerebral arteries
    • 4% - basilar artery
65
Q

There is a vessel malformation that is an important source of bleeds in colorado. What is it?

A

• Cavernous angioma

66
Q

What does the presence of an acute hemorrhagic infarction imply?

A
  • Reperfusion of dead tissue
    • A clot is lodged proximally in the vessel (we were given a middle cerebral artery picture)
    • As the clot busts (natural course or b/c of anti-coags) it showers other vessels with smaller chunks AND moves more distally in the vessel
    • Reprofusion of the proximal offshoots is the result, which will leak out of the damaged vessels into surrounding parenchyma
67
Q

Where will you see more reprofusion leakage, the grey or the white matter?

A
  • Grey, which is more perfused with more vessels anywhay

* Therea re more small foci of hemorrhage in the necrotic gray matter than in white matter

68
Q

How big is an infarction to be classified as a lacunar infarction?

A
  • = 1cm

* Associated symptoms often hemiparesis or hemisensory loss

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