Strokes and TIAs Flashcards

1
Q

A 68-year-old right-handed woman is brought to the emergency department (ED) 30 minutes after suddenly developing speech difficulty and weakness of the right arm and leg.
Her family members report that she suddenly became mute and slumped down in her chair.
PMH: HTN,angina. Meds: atenolol and amlodipine.
Vitals: Temp is 36.6 °C (98 °F), HR 95 bpm, BP172/86 mm Hg.
Cardiovascular exam: No carotid bruit, + irregularly irregular pulse.
Neurologic exam: Lethargic but arousable patient who is able to follow some simple commands but has severe impairment of word fluency, naming, and repetition. She has a left lateral gaze deviation and right lower facial droop. There is total paralysis of the right upper extremity and, to a lesser degree, weakness of the right lower extremity. The left side displays full antigravity power without drift for 5 seconds.

A

-MCA stroke

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2
Q

cerebral ischemia

A

-Lack of blood flow -> neurons lack glucose -> neurologic symptoms develop -< if lasting for a few minutes can cause infarction (death of brain tissue)
-TIA: If brain flow is rapidly restored, there is no infarction, and symptoms lasts less than 24 hours
-Stroke: Neurological signs/symptoms > 24 hours and demonstrated infarction on imaging

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3
Q

cerebrovascular accident (CVA)

A

-stroke
-abrupt onset of neurologic deficit that is attributable to a focal vascular cause
-2 main types:
-!Ischemic(87%):Occlusion of artery to a region of the brain
-!2/3s are thrombotic
-!1/3s are embolic
-Hemorrhagic(13%) :Bloodvessel in the brainrupturesinto surrounding tissue
-Intracerebral hemorrhage (HTN, AVM) or SAH (aneurysm)

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4
Q

causes of stroke

A

-Thrombosis
-Narrowing of blood vessel due to atherosclerotic plaque -> ↓ blood flow
-Atherosclerotic fibrous cap damage -> platelet aggregation and clotting cascade -> thrombus formation w/ sudden blockage of blood flow

-Embolism
-Cardiac emboli: Afib, rheumatic heart dz, infective endocarditis, myxoma
-Arterial emboli: detachment of blood clot (atherosclerotic plaque) travels and lodges into smaller down stream artery
-Cardiac/aortic emboli: PFO, atheroma in aortic arch, atrial septal aneurysm, calcification of mitral valve annulus
-Cryptogenic: unknown origin

-Lacunar infarct: Narrowing of small blood vessels in the distal vertebral or basilar arteries

-Hypoperfusion: Heart failure with ↓ cardiac output, Watershed regions are the most vulnerable

-Vasculitis: Giant cell arteritis

-Moyamoya disease : Progressive stenosis of cerebral arteries -> ischemia

-Dissection of artery wall

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5
Q

CVA disease epidemiology

A

-Stroke is the 3rd leading cause of death worldwide, 5rd leading cause of death in the USA
-Leading cause of long-term disability
-Risk of first stroke is twice as high for black! > white
-Risk factors: !Age >55yo, HTN!, smoking!, afib!, male, obesity, DM, HLD, cerebral amyloid angiopathy, neoplastic disease, cerebral aneurysms, carotid bruits, drugs (cocaine, OCPs), previous strokes, migraines w/ aura, hematologic disorders (MM, SCD, PCV)

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6
Q

acute cerebrovascular syndromes

A

-stroke- symptoms with infarction
-TSI- transient symptoms with infarction
-TIA- transient ischemic attack WITHOUT infarction

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7
Q

stroke complications

A

-Hemorrhagic transformation
-After ischemic damage there is increased permeability of damaged blood vessels -> bleed
-High risk of transformation: tPA administration, massive stroke, hyperglycemia

-Cerebral edema
-Water accumulation occurs due to defective ATP pumps (sodium) and increased permeability of the blood brain barrier
-Can lead to ↑ ICP and herniation -> MCC DEATH

-Liquefactive necrosis can occur in 3-21 days
-Seizures- Brain injury ↑ irritability of nervous tissue neuronal discharges
-DVT due to immobilization
-Pneumonia due to impaired swallow mechanism / intubation
-Dysphagia occurs if there is damage to structures involving swallowing
-Dementia can occur due to brain damage

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8
Q

early recognition and intervention

A

-Rapid evaluation is essential
-Patients often do not realize something is wrong (anosognosia)
-It is important to teach family and friends about classic signs of a stroke
-TIME IS BRAIN

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9
Q

hemiparesis vs hemiplegia

A

-paresis- weakness
-plegia- paralysis

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10
Q

ataxia

A

-loss of full control of bodily movements

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11
Q

anosognosia

A

-lack of awareness of illness

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12
Q

ischemic penumbra

A

-Tissue surrounding the core region of infarction which is !ischemic but reversibly dysfunctional!
-Maintained by collaterals
-Can be salvaged if re-perfused in time!
-Primary goal of revascularization therapies

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13
Q

common causes of ischemic stroke

A

-Thrombosis:
-Lacunar stroke (small vessel)
-Large-vessel thrombosis
-Dehydration

-Embolic occlusion:

-Artery-to-artery:
-Carotid bifurcation
-Aortic arch
-Arterial dissection

-Cardioembolic:
-Atrial fibrillation
-Mural thrombus
-Myocardial infarction
-Dilated cardiomyopathy
-Valvular lesions
-Mitral stenosis
-Mechanical valve
-Bacterial endocarditis

-Paradoxical embolus:
-Atrial septal defect
-Patent foramen ovale

-Atrial septal aneurysm
-Spontaneous echo contrast
-Stimulant drugs: cocaine, amphetamine

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14
Q

uncommon causes of ischemic stroke (dont need to know)

A

-Hypercoagulable disorders:
-Protein C deficiencya
-Protein S deficiencya
-Antithrombin III deficiencya
-Antiphospholipid syndrome
-Factor V Leiden mutationa
-Prothrombin G20210 mutationa
-Systemic malignancy
-Sickle cell anemia
-β Thalassemia
-Polycythemia vera
-Systemic lupus erythematosus
-Homocysteinemia
-Thrombotic thrombocytopenic purpura
-Disseminated intravascular coagulation
-Dysproteinemiasa
-Nephrotic syndromea
-Inflammatory bowel diseasea
-Oral contraceptives
-COVID-19 infection

-Venous sinus thrombosis

-Fibromuscular dysplasia

-Vasculitis:
-Systemic vasculitis (PAN, granulomatosis with polyangiitis [Wegener’s], Takayasu’s, giant cell arteritis)
-Primary CNS vasculitis
-Meningitis (syphilis, tuberculosis, fungal, bacterial, zoster)

-Noninflammatory vasculopathy
-Reversible vasoconstriction syndrome
-Fabry’s disease
-Angiocentric lymphoma

-Cardiogenic
-Mitral valve calcification
-Atrial myxoma
-Intracardiac tumor
-Marantic endocarditis
-Libman-Sacks endocarditis

-Subarachnoid hemorrhage vasospasm

-Moyamoya disease

-Eclampsia

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15
Q

TOAST classification

A

-Large artery atherosclerosis
-Cardioembolism
-Small-vessel occlusion
-Stroke of other determine etiology
-Stroke of undetermined etiology
-flow reducing carotid stenosis -> if narrow vessel and patient becomes hypotensive -> pressure is not enough to perfuse brain

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16
Q

cardioembolic strokes

A

-~20% of all ischemic strokes are cardioembolic in nature
-Thrombi that detach from heart walls or left sided valves
-Thrombi can fragment or lyse quickly, producing a TIA
-!!Sudden maximum neurologic deficient at onset
-MC blockage in the intracranial carotid artery, MCA, PCA or their branches (less often ACA)
-MCC: Atrial fibrillation!
-Other causes: MI, prosthetic valves, rheumatic heart disease, ischemic cardiomyopathy
-Rare paradoxical embolization can occur when venous thrombi migrate to the arterial circulation
-Patent foramen ovale (PFO)
-Atrial septal defect
-Right-to-left shunting can be demonstrated with bubble-contrast echocardiography !

-Bacterial endocarditis! give rise to septic emboli!, suspect this is multifocal stroke symptoms

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17
Q

artery to artery embolic stroke

A

-Thrombus formations on atherosclerotic plaques can embolize
-MC cause of large vessel occlusion

-Any diseased vessel can be a source:
-Aortic arch
-Common carotid bifurcation
-Internal carotid
-Vertebral artery
-Basilar artery
-cervical artery dissection

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18
Q

artery to artery embolic stroke: cervical artery dissection

A

-cervical artery dissection of the internal carotid or vertebral arteries:
-Artery-to-artery embolic stroke in young patients (<60yo)
-2% of all ischemic strokes
-!Painful dissection preceding stroke by hours/days
-back, back of neck, if carotid -> anterior neck or ipsilateral eye
-High risk: Ehlers-Danlos, Marfans disease, cystic medial necrosis, fibromuscular dysplasia , PCKD
-Trauma (MVA, sports) can cause carotid or vertebral artery dissections
-Spinal manipulative therapy is associated with vertebral artery dissection and stroke

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19
Q

signs and symptoms of strokes

A

-can be obvious or subtle, they include:
-Sudden weakness or numbness to the face, arm, leg. Especially on one side of the body
-Trouble speaking or understanding
-Sudden trouble seeing in one or both eyes
-Sudden trouble walking
-Dizziness or loss of balance or coordination
-Sudden severe headache with no known cause
-Sudden confusion
-Symptoms begin abruptly and correlate with affected brain area
-Symptoms last > 24 hrs
-Symptoms of an ischemic attack are always negative and simultaneous
-Hemiparesis or hemisensory deficits are common -> Contralateral to brain injury

-Thrombotic strokes tend to be gradual ± stepwise, embolic strokes tend to be more abrupt
-Often awake from sleep with neurologic deficits
-May have preceding TIAs

-Embolic strokes occur abruptly over seconds without warning
-Worst deficits present at onset
-MC from heart (embolization), internal carotid, aorta

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20
Q

thrombotic strokes

A

-atherosclerotic plaque rupture
(most common)
-Hypertension
-High cholesterol
-Diabetes
-Blood clotting disorders
-Smoking
-Recreational drug use
-Vessel trauma
-Can be large vessel occlusion!
(LVO) or small vessel occlusion

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21
Q

cardioembolic strokes

A

-~20% of all ischemic strokes are cardioembolic in nature
-Thrombi that detach from heart walls or left sided valves
-Thrombi can fragment or lyse quickly, producing a TIA
-!!Sudden maximum neurologic deficient at onset
-Often embolize into the intracranial carotid artery, MCA, PCA or
their branches (less often ACA)

-MC cause of thrombi: Atrial fibrillation!
-Other causes: MI, prosthetic valves, rheumatic heart disease, ischemic
cardiomyopathy

-Rare paradoxical embolization can occur when venous thrombi
migrate to the arterial circulation
-Patent foramen ovale (PFO)
-Atrial septal defect
-Right-to-left shunting can be demonstrated with bubble-contrast
echocardiography!!!

-Bacterial endocarditis give rise to septic emboli, suspect this
is multifocal stroke symptoms

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22
Q

ACA syndrome

A

-<3% off all strokes are due to ACA occlusion
-ACA supplies:
-Medial and superior frontal and parietal lobes
-Corpus callosum (partial)
-Basal ganglia (partial)

-ACA stroke syndrome:
-!Contralateral hemiplegia- Worse in the legs > arms/hands/face
-Contralateral sensory loss (usually minimal)
-Urinary incontinence
-Frontal lobe dysfunction- personality changes
-Gait apraxia
-Abulia- Absence of willpower or the ability to act decisively, may have a delay in verbal and motor responses

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23
Q

MCA syndrome

A

-MC artery causing stroke
-Proximal MCA = M1 segment

-M1 segment occlusion (total MCA):
-!Contralateral hemiplegia (face/arm > leg)
-!Contralateral hemisensory loss
-Contralateral hemianopsia- blind on the side opposite of the lesion
-Gaze preference to ipsilateral side (towards lesions)
-Dysarthria (d/t face weakness)
-LEFT / Dominant hemisphere: Global aphasia!
-RIGHT: Non-dominant hemisphere: Anosognosia- neglect things they cant see, !constructional apraxia- cant copy drawings, and neglect!

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24
Q

MCA syndromes: Gerstmann syndrome

A

-AFFECTS: Parietal lobe of the dominant side (usually left) ANGULAR GYRUS
-Cause: Stroke (MC), TBI, Tumor

-Signs and symptoms
-Left-right disorientation- cant tell which is which
-Agraphia: Inability to write when you could previously
-Acalculia: Inability to calculate numbers
-Alexia: Inability to read/recognize words you once could read
-Finger agnosia: Impairment in recognizing and naming their own fingers

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25
Q

ICA syndrome

A

-MCA and ACA combined
-Internal carotid artery occlusion
may be asymptomatic
-Symptomatic occlusion similar to
mainstem MCA stroke
-Often preceded by TIAs or
transient monocular blindness due
to ophthalmic artery branch
-amourax fugax

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26
Q

vertebral artery syndrome

A

-symptoms of occlusion are variable
-have plenty of collateral supply
-dissection denoted by pain

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27
Q

Which of the following signs and symptoms would commonly be seen after occlusion of the MCA stem in the left hemisphere (assume that the left hemisphere is dominant for language in this patient). IndicateALLcorrect answers.

A

A. Inability to understand or carry out spoken or written commands!!
B. Inability to speak more than a few stereotyped words!!
C. Lack of response to threatening gestures (visual threat) when they are given on only the left side- neglect is only on right side
D. Paralysis of the right arm!!!
E. Paralysis of the right leg!! (less)
F. Paralysis of the left leg

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28
Q

PCA stroke syndrome

A

-Posterior cerebral artery supplies occipital lobes, inferior temporal lobes, thalamus, midbrain
-Either side:
-!!Contralateral homonymous hemianopia with macular
sparing (lateral geniculate nucleus)
-Contralateral sensory loss (thalamic involvement)

-Dominant side:
-!Alexia without agraphia: CANT read, CAN write -> Affected: Corpus callosum, occipital lobe (typically left)
-!Anomia: difficulty naming objects and colors
-!Visual agnosia: inability to describe what an object is used for

-Non-dominant side
-Prosopagnosia: inability to recognize faces

-Bilateral infarctions: Anton syndrome (cortical blindness)
-RARE
-Affected: bilateral occipital lobes (distal basilar artery or bilateral PCA involvement)
-Cortical blindness, are often unaware they are unable to see

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29
Q

Wallenberg syndrome

A

-lateral medullary infarct
-PICA (off the Vertebral artery)
-Dizziness, nystagmus, N/V, dysarthria,
dysphagia, diplopia, hiccoughs

-!!!!Mixed findings
-Ipsilateral facial numbness (CN V)
-Ipsilateral Horner’s syndrome
(sympathetic)
-Ipsilateral gait ataxia (cerebellum)
-Contralateral loss of pain & temperature
sensation in limbs (spinothalamic)

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30
Q

horner’s syndrome

A

-Damage to the oculosympathetic
pathway of one side of face

-Symptoms will be ipsilateral:
-Ptosis, miosis (small), anhidrosis

-Causes: Idiopathic, brainstem
stroke, carotid dissection,
neoplasm
-Any lesion along the 1st, 2nd, or 3rd
order nerve – there are so many!

-CT or MRI to find underlying
problem

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31
Q

lacunar strokes

A

-Small (2-15mm) non-cortical infarcts (subcortical) caused by occlusion of a single penetrating branch of a large cerebral artery
-Contralateral, mostly motor/sensory defects
-Pure motor stroke: internal capsule lesion- weak
-Pure sensory stroke: thalamic lacunar stroke - numb
-Ataxic hemiparesis
-Dysarthria-clumsy hand syndrome: speech, swallowing difficulties, facial weakness, hand weakness, clumsiness

-pure strokes are subcortical-> just this stuff listed
-dont need to know specifics

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32
Q

basilar strokes

A

-rare <1%
-Supplies the midbrain, the thalamus, and the medial and lateral pons, cerebellum, medial temporal and the occipital lobes.
-Clinical
-Usually sudden collapse and comatose!!!!!
-Consider in any dizziness PLUS neuro deficits
-Proximal basilar occlusion: CN VI palsy, vertical nystagmus,
pinpoint but reactive pupils
-Mid-basilar: Ipsilateral CNVII palsy, contralateral hemiparesis
-!!!!!!Locked in syndrome: Occurs in ventral pons infarction in the
mid-basilar area causing bilateral pontine ischemia. Full body
paralysis except for some vertical eye movement.
-!Top of the basilar syndrome: coma from infarction of the ARAS.
May also have:
-oculomotor disturbances (roving eye movements or eyes looking
downward and inward with inability to reflexly elicit upward movements)
-Hemianopia
-bilateral ptosis
-CN III palsy: pupillary enlargement with preserved reaction to light

-just know locked in syndrome

33
Q

anterior vs posterior circulation

A
34
Q

overview of strokes

A
35
Q

other symptoms that widen differentials

A

-Headache:Presence of headache is often more consistent with other diagnosis (ICH, SAH, CVT) rather than ischemic stroke (rarely some patients may have headaches in the prodromal period before thrombotic strokes).

-Seizure: Usually determined by history from observer. Complex partial seizures without tonic-clonic activity can mimic a stroke. Can also occur in cortical lesions such as SAH, ICH, CVT

-Vomiting:It is more suggestive for elevated intracranial pressure (ICH, SAH, CVT) or may be seen in patients with posterior circulation large artery ischemia.

-Fever:Raise the possibility of endocarditis and embolic stroke.

-Chest pain:Patients with aortic dissection (type A) may develop acute ischemic stroke which is preceded by sudden onset of chest pain. Rarely patients with extensive atherosclerosis may develop ‘AIS’ and acute myocardial infarction simultaneously!

-Neck pain: Think vertebral/carotid arterial dissection.

-Elevated ICP:Global symptoms of elevated ICP include headache, depressed global consciousness and vomiting. Focal symptoms of elevated ICP may be caused by local effects in patients with mass lesions or by herniation syndromes (e.g. subfalcine, central transtentorial, uncal transtentorial, upward cerebellar, cerebellar tonsillar/foramen magnum, and transcalvarial).
-Signs of elevated ICP include CN VI palsies, papilledema.

36
Q

stroke PE

A

-NIHSS is a DIRECTED neuro exam
-Blood pressure- Comparison of blood pressure and pulse on the two sides can reveal
differences related to atherosclerotic disease of the aortic arch or coarctation
of the aorta.
-Ophthalmoscopic examination : embolization in the anterior
circulation
-Neck examination : carotid pulses or the presence of carotid bruits.
-Cardiac examination : arrhythmias or murmurs related to valvular
disease
-Palpation of the temporal arteries : giant cell arteritis (tender,
nodular, or pulseless)
-Distal extremity exam: DVT

37
Q

which is a symptoms of stroke

A

-fever
-diaphoresis
-diarrhea
-sudden trouble seeing!!!!!!!

38
Q

which symptoms belong to which hemispheric stroke

A

Contralateral hemiparesis/hemisensory loss
Contralateral homonymous hemianopia
Dysarthria
Spatial/time deficits!!! (neglect)- ACA
Flat affect- ACA
Impaired judgement- ACA
Impulsivity- ACA
-> RIGHT

Contralateral hemiparesis/hemisensory loss
Contralateral homonymous hemianopia
Dysarthria
Aphasia (90%)
Agraphia
Apraxia
Decreased math comprehension
-> LEFT (dominant)

39
Q

cincinatti prehospital stroke scale (CPSS)

A

-Scoring tool forEMS in the pre-hospital setting

-3 physical examfindings:
-Facial droop
-Arm drift
-Abnormal speech

-<1 minute to perform
-Prescence of 1 finding = 72% chance of stroke

40
Q

stroke flow chart

A
41
Q

door to needle time of <= 60 min

A

-endovascular therapy (from onset for symtpoms)- up to 24 hours for large vessel occlusion -LVO
-admission to monitored bed - within 3 hours
-interfacility transfers- within 1 hour

42
Q

initial evaluation

A

-AIRWAY:Can they clear oral secretions & maintain airway?

-BREATHING:Provide supplemental O2 if oxygen saturation is <94%

-CIRCULATION:Are they hemodynamically stable?
-Hypotensionwith evidence of poor perfusion (shock state) can mimic stroke especially in elderly patients and should be appropriately managed.
-Hypertension:Patients with cerebrovascular accidents frequently have high blood pressure. The approach to blood pressure management in ‘AIS’ is inherently different from the approach in acute hemorrhagic stroke. For this reason, a neuroimaging study (CT or MRI) is critical to help guide blood pressure therapy in patients with acute stroke.
-IV Access:Obtain peripheral intravenous (IV) access andavoid unnecessary lines, and ABGsince minor vascular trauma in patients with ischemic CVA who are deemed to be candidates for thrombolysis may become a real problem.
-Initiate labwork

-DISABILITY:Perform a focused neurological exam and obtain a point-of-care glucose!!
-The focused exam is structured around relevant data gathered during the medical history and is catered to the differential diagnosis. The examiner should be focused on determining whether (1) there is a lesion and (2) where the lesion is localized.

-At the same time, neuro-stroke team should be called, and patient brought to the CT/MRI scanner, an IV is placed as labs are drawn, and pharmacy is alerted that tPA may be needed

43
Q

lab work and others dx

A

-Cardiac monitoring:
-ECG
-Holter

-Chest xray
-Urinalysis
-CBC
-ESR
-BMP and LFTs
-Lipid panel
-Coags (PT/PTT, INR)

-Consider:
-Blood culture - (if suspicious of endocarditis)
-VDRL
-HIV
-Lyme
-ANA
-Anti-phospholipid

44
Q

you and the stroke team

A

-Determine the last seen well (LSW)
-Determine if patient is on anticoagulation
-Determine a NIHSS score
-… wait for neuroimaging, review immediately!

45
Q

stroke scale (NIHSS)

A

-National Institutes of Health Stroke Scale (NIHSS) = evaluates patients with suspected acute stroke and to make decisions about acute treatment.
-Correlates with infarct size, clinical severity, and long term outcome
-≥6 correlates with cortical stroke
-higher the #, worse the stroke
-PCA strokes can have no obvious symptoms

-!!Not all stroke symptoms are captured by the NIHSS
-Good at identifying anterior strokes but its not as reliable for posterior circulation!
-A score of 0 does NOT mean there is no stroke!

-Too time-consuming :(

46
Q

national institutes of health stroke scale (NIHSS)

A
47
Q

stroke imaging modalities: CT

A

-CT head non-contrast** -> NEED TO RULE OUT BLEED -> do not give TPA is there is a bleed
-Acute ischemic stroke vs. hemorrhagic stroke?
-Or another cause for stroke-like symptoms? Is the stroke complete?
-Most acute ischemic stroke are NOT visualized by non-contrast CT in the first 6 hours
-Exclude ICH, abscess, tumor, other stroke mimics
-Often fail to show small cortical infarcts, or, small posterior ischemia strokes

-Early signs of cerebral ischemia that can be seen on CT:
-Small and subtle hypodensity, loss of gray-white!! differentiation, Ventricular compression, Hyperdense MCA sign!!

-CT head non-contrast**
-Side note: IV-tPA is not beneficial in areas of extensive regions of obvious hypodensity, as it is consistent with irreversible injury

48
Q

stroke imaging modalities: MRI brain

A

-Brain MRI with DWI (diffusion weighted imaging)
-Gold standard
-Superior to NCCT for detection of acute infarction
-Areas of decreased water diffusion will appear bright! or hyperintense!
-30% of suspected TIA (due to resolution of sxs) show a rule-in infarct on MRI

-MRI is typically more expensive, more time consuming (15-20 minutes, new protocols as low as 5 minutes), less accessible
-Limited by persons with metal (pacemakers, stents) and those with claustrophobia

49
Q

stroke imaging modalities: CTA or MRA head and neck

A

-Vascular studies
-Usually done immediately after initial CTH
-Detect large vessel occlusions (LVO) which may be amenable to endovascular therapies (EVT)

-Who gets it?
-Qualify for mechanical thrombectomy
-Last seen well within 4.5 hours
-Last seen well within 24 hours + NIHSS≥6 or VAN positive or LVO syndrome

-Does every stroke patient need a CTA? MAYBE.
But remember,the only imaging you need to start thrombolysis is a NCHCT showing no hemorrhage!!!.If the patient is thrombolysis eligible, you can start tPA while obtaining vessel imaging.

50
Q

stroke imaging: cerebral angiography

A

-GOLD STANDARD for identifying and quantifying atherosclerotic stenosis of cerebral arteries
-Characterizes aneurysms, vasospasm, thrombi, AV fistulas, vasculitis, fibromuscular dysplasia
-Risk: arterial damage, hemorrhage, embolic stroke, renal failure from contrast nephropathy

51
Q

stroke imaging: ultrasound

A

-Transcranial dopplers (TCD) can assess MCA, ACA, PCA flow
-Carotid ultrasounds can identify carotid atherosclerosis as source of emobli
-cardiac echo

52
Q

1 goal of AIS: prevent or reverse brain injury

A

-treatments to attain this goal fall within the following categories:
-medical support
-reperfusion therapy: IV thrombolytics (tPA) or endovascular thromboectomy
-antithrombotic tx
-neuroprotection

53
Q

medical management

A

-BP-
-IV labetalol or nicardipine
-Collateral blood flow is blood pressure dependent
-Allow permissive hypertension in the acute phase
-If eligible for tPA and within window, reduce BP if over !>185mmHg SBP or >110mmHg DBP!
-Otherwise reduce if: >220mmHg systolic or >120mmHg diastolic

-Cerebral edema management
-Keep glucose between 60-180 mg/dL
-Give antipyretics if fever present

-Protect airway, prevent aspiration
-HOB elevation 30%, NPO until cleared by specialist

54
Q

stroke management

A

-Determine eligibility for reperfusion therapy
-Goal door-to-needle time ≤60 minutes*

-IV Thrombolytics
-Recombinant Tissue Plasminogen Activator (r-tPA) = tPA = alteplase
-≤ 3 hours from onset1 (some ≤4.5 hrs2)
-Do NOT administer: >3 hours, SBP>185, DBP>110, Bleeding, anticoagulated, hx of recent trauma or surgery or more (see chart)
-No ASA for first 24 hrs after tPA administration

-Important to establish “last seen well” [LSW]
-If patient woke up with stroke symptoms, the onset is defined as when they went to bed

55
Q

tPA for acute ischemic stroke

A

-Administration
-Ensure 2 peripheral IV lines
-rTPA: Administer 0.9 mg/kg IV (max 90mg)
-Give 10% of total dose by initial bolus, remaining 90% over 1 hour
-Frequent BP monitoring

-Avoid urethral catheterization ≥2 hours
-!No other anti-coagulants/platelet for 24 hours
-BP goals after starting: <180 SBP and <105 DBP

-Complications
-Bleeding!!!:
-If decline in neuro status, uncontrolled BP -> stop infusion, give plts/cryoprecipitate and reimage brain emergently
-Angioedema!!!- might need to intubate - famotidine, steroids, benedryl

56
Q

who can and cant get TPA

A
57
Q

what to do in post-tPA bleed

A

-Prevention not cure, make sure you risk-stratified beforehand
-Is it clinically significant?
-Small petechial hemorrhage with no change in NIHSS vs. large hemorrhage with space occupying effect
-Sxs of bleed: Worsening neuro status, seizure, stuttering lacunar infarct, new headache, nausea, vomiting, ↑ BP

-There is no evidence to support any one therapeutic intervention
-!!Stop tPA
-AHA recommends:
-6-8U Platelets
-10U cryoprecipitate

-?Antifibrinolytics: TXA
-? Pro-thrombin complex concentrates (PCCs)

58
Q

Evidence suggests that there is ahigher likelihood of good to excellentfunctional outcome when alteplase is given to adults with an acute ischemic strokewithin what time frame?

A

3 hours!!!!!!!!!
2 hours
90 minutes
60 minutes

59
Q

endovascular revascularization

A

-Large vessels (anterior circulation) often fail to completely open with IV fibrinolytics alone
-Endovascular therapy is recommended for select patients with AIS due to LVO in addition to fibrinolytic therapy

-Mechanical thrombectomy
-Minimally invasive and endovascular procedure
-Performed by neuro-interventionalist radiologist
-!!MT indicated in AIS from LVO in the anterior circulation within 4.5-24 hours of LSW
-As with tPA, clinical benefit is link to time to therapy

-Alternative or adjunctive treatment for those who are ineligible for thrombolytics, or who fail to achieve recanalization with thrombolytics alone

60
Q

mechanical thrombectomy (MT)

A

-General criteria: All patients should meet the general criteria for ‘MT’ which include:
-!!!!‘MT’ can be performed within 24h of the symptom onset at a stroke center with appropriate expertise in the use of stent retrievers
-Vascular imaging (e.g. CTA) shows proximal large artery occlusion in the anterior circulation
-Persistent disabling neurologic deficit
-A small infarct core (i.e. limited signs of early ischemic change) on neuroimaging and absence of hemorrhage

Dont need to know below:
-Specific criteria: For patient selection within a certain time window certain eligibility criteria should be met.
-Within the 6 hours: For patients who can be treated within 6 hours of the symptom onset, the following criteria for ‘MT’ is adapted and modified from MR CLEAN trial:
-Age ≧18 y
-Pre-stroke disability score {modified Rankin Scale (mRS) score of ≤1}
-NIHSS score ≧ 6 or or any persistent neurologic deficit that is potentially disabling
-ASPECTS score ≥6 on noncontrast brain CT or DWI-MRI (figure 16)
-Intracranial arterial occlusion of the distal intracranial ICA, or the M1 or M2 segments of the MCA, or the A1 or A2 segments of ACA, demonstrated with CTA, MRA.

-6 to 24 hours: The DEFUSE and DAWN trials selected patients for treatment beyond 6 hours using imaging-based criteria

61
Q

antiplatelet therapy

A

-Anti-aggregation agents prevent atherothrombotic events (TIA, CVA)
-Inhibits formation of platelet aggregates on disease arteries
-!!Aspirin (ASA), clopidogrel (Plavix), and ticagrelor are the most used agents

-All acute ischemic stroke get !160-300mg! ASA w/i 24-48 hr after onset
-If getting IV-tPA, asa is delayed until 24 hrs after
-Can give rectal ASA if swallowing assessment failed

-Dual antiplatelet therapy (DAPT)
-USUALLY THIS IF NOT TPA
-In patients presenting with !minor non-cardioembolic ischemic stroke (NIHSS score ≤5) who did not receive IV-tPA!; treatment with DAPT started within 24 hours after symptom onset and continued for 21 days is effective in reducing recurrent ischemic stroke for a period of up to 90 days from symptom onset

-Aspirin! (81mg QD) + ticagrelor! (180mg load followed by 90mg BID) for 30 days !
Then continue ASA 81mg daily as monotherapy
Extend DAPT to 3-months if large intracranial atherosclerosis

-Aspirin! (81mg QD) + clopidogrel !(600 mg load, then 75 mg daily) for 30 days!
Then continue ASA 81mg daily as monotherapy
Extend DAPT to 3-months if large intracranial atherosclerosis

62
Q

other therapeutic measures

A

-Start or continue statin therapy: Atorvastatin 80mg daily
-Goal LDL < 70 mg/dL (unless stroke was non-atherothrombotic)

-Prevent complications of bedridden patients:
-DVT prevention with intermittent pneumatic compression devices or subq heparin (delay 24 hrs if getting tPA)
-UTI prevention – no foleys
-Skin protection – frequent turning prevent bed sores
-Pneumonia

-Seizure prophylaxis not recommended, treat seizures if they appear. Seizures often indicate hemorrhagic conversion.

63
Q

complications

A

-Cerebral edema and brain herniation
-Edema peaks on days 2-3 after stroke
-Can cause mass effect ~10 days
-Larger infarct = greater risk for edema
-Can be managed with IV mannitol and water restriction
-Do not allow hypotension
-Special vigilance should be held for cerebellar infarcts
-Cerebellar edema can obstruct CSF flow leading to hydrocephalus and compress directly on the brain stem
-This can cause coma and respiratory arrest

64
Q

which action is not part of the acute stroke pathway

A

Monitoring blood pressure
Seizure prophylaxis!!!!!!
Monitoring temperature
Performing dysphagia screening- Speech language pathologist

65
Q

Identify the systolic blood pressure threshold for withholdingfibrinolytic therapy (TPA) to otherwise eligible patients withacuteischemic stroke

A

177 mm Hg
180 mm Hg
185 mm Hg!!!!!!!!!!!
190 mm Hg

66
Q

adult stroke algorithm

A

-dont need to know?

67
Q

secondary prevention

A

-Initial phase of AIS is medical stabilization + reperfusion therapy (tPA and/or MT)
-Next stage: determine pathophysiology for secondary prevention

-Comprehensive evaluation:
-Cardiac monitoring for occult or paroxysmal afib
-Echocardiography (TEE/TTE) for source of cardio embolism
-Vascular studies (US of neck, CTA/MRA of neck and head arteries)
-Hypercoagulable blood testing - if young

-Afib as cause of cardioembolic infarct: Apixaban 5mg BID daily x lifelong, or Warfarin
-Based on the ARISTOTLE trial (apixaban for reduction in stroke and other thromboembolic events in atrial fibrillation) which showed small superiority for apixaban versus warfarin for major bleeding side effects

-Carotid stenosis: Carotid endarterectomy (CEA) or stenting (CAS)
-NASCET trial showed absolute risk reduction of stroke by 17% in those with carotid stenosis of 70% after surgical procedure
-Also a significant but less robust benefit if pts have 50-70% stenosis
-Harm for patients with <30% stenosis

68
Q

secondary prevention: risk factor modification

A

-Life style modification for secondary prevention:
-Hypertension is the most significant risk factor long term -> Goal <130/80mmHg

-High cholesterol levels
-SPARCL trial = Atorvastatin 80mg daily
-Goal LDL < 70 mg/dL

-Tobacco cessation
-Alcohol reduction / abstinence
-Regular exercise x 40 min / week
-Mediterranean diet
-Weight reduction

69
Q

rehabilitation and recovery

A

-Stroke rehab programs
-Multi-disciplinary approach to recovery
-Early PT, OT, and speech therapy
-Addressing complications and disabilities
-Educating patient and family on prevention of complications of limited mobility
-E.g. pna, dvt, pe, pressure ulcers, muscle contractures

70
Q

A 70-year-old woman presents to the emergency department. Approximately 2 hours ago, she was bending over when she felt her left side go weak and lost vision in her right eye. She was having difficulty talking. Symptoms resolved after 15 minutes, and she reports feeling back to baseline. Her medical history is pertinent for hypertension and hyperlipidemia, for which she currently takes irbesartan 150 mg and lovastatin 20 mg. Her vital signs include a blood pressure of 138/92 mm Hg, heart rate of 88 bpm, respiratory rate of 16 breaths/minute, oxygen saturation of 98%, and temperature of 98.6°F. Physical examination reveals no focal neurologic findings, and no visual field deficit is observed. A CT scan of the brain is without bleed. Which of the following is the most likely diagnosis?

A

Ischemic stroke
Migraine aura
Seizure
Syncope
Transient ischemic attack!!!!!!!

71
Q

transient ischemic stroke

A

-Short lasting neurologic dysfunction due to transient focal ischemia without infarction
-Neuro symptoms = !Minutes to 1 hour! (definition is <=24 hrs)
-Symptoms depend on location, same as stroke!
-Work up the same as a stroke!

-Diagnostic imaging
-CT, MRI, perfusion weight MRI, Carotid ultrasound

-Risk of stroke after a TIA:
-50% in first 24-28 hours if high risk DM/HTN
-10-20% in the first 3 months

72
Q

transient ischemic stroke: risk stratification tool: ABCD2

A

-Predicts likelihood of subsequent stroke in 2 days
-ABCD2 score <4 –> ASA alone
-ABCD2 score≥ 4 –> (dual antiplatelet therapy) DAPT x 21 days

-Prevent strokesby aiming at the cause
-Non-cardioembolic stroke= dual-antiplatelet therapy
-ASA+clopidrogel or ASA+ticagrelor or ASA+dipyridamole (dont worry about the last one)
-Afib = LMWH
-Heart thrombus = DOAC

73
Q

amaurosis fugax

A

-Transient monocular visual loss (2-30 min)
-“Retinal/Ocular TIA”
-Occlusion or stenosis of the ipsilateral internal carotid artery (ICA)
-Thromboembolism from carotid plaque
-Hypoperfusion from stenosis or other cause
-Vasospasms
-Increased plasma viscosity (e.g. MM)
-Atherosclerosis

->50 years old
-Vascular risk factors e.g. HTN, HLD, DM, Smoking, TIA/CVA hx, PVD, cocaine, afib
-Retinoscopy: hollenhorst plaques , pale retina
-ischemia on fundoscopy

74
Q

amaurosis fugax

A

-!Unilateral visual loss, painless, transient
-“Curtain coming down” or “darkening”
-Complete or partial visual field
-!!Spontaneously self resolves
-DDX: giant cell arteritis, central retinal artery occlusion (CRAO), central retinal vein occlusion (CRVO), multiple sclerosis (MS), papilledema, sickle cell anemia

-Harbinger of strokes to come….
-Complete ophtho exam
-Cardiovascular eval: echo, ecg, CTA/MRA/US of the neck
-Neuroimaging: CT/MRI brain
-Labs including inflammatory markers: ESR/CRP

75
Q

Summary:A 68-year-old woman presents with
Thirty minutes of right hemiparesis and aphasia
A history of hypertension and coronary artery disease
Irregularly irregular pulse
BP of 172/86 mm Hg and HR 95 bpm
Most likely diagnosis and part of the brain likely affected: Left middle cerebral
Next diagnostic steps: CT, glucose, neuro exam
Next step in therapy: no bleed -> TPA
Other diagnostic considerations include:
Hypoglycemia, a seizure with postictal Todd paralysis, or a complicated migraine.
If the acuity of onset was less certain, a brain tumor, subdural hematoma, multiple sclerosis, herpes encephalitis, or a brain abscess can mimic a subacute stroke.

A
76
Q

A 74year old manis brought into the hospital by his wife
She statesthat her husband started having sudden left arm weakness and left sided facial paralysis during lunch.
He has a PMHof poorly controlled HTN

Vitals:
HR 92/min
RR 14/min
BP130/86 mmHg
SpO297%
Afib seen on the monitor

A

Monitor for worsening symptoms
Check glucose!
Order emergent CT scanorMRI of the brain!
Active the stroke team!
Complete neurologic screening!
Establish IV access!

What needs to be completed within 10 minutes after hospital arrival?

Neuro assessment!!!!!!!!!
Interpretation of the emergentCT scan or MRI
Administrationof fibrinolytic therapy
Admission to a monitored bed

What are some general questions you need to ask?
When did the symptoms start?!
Has your wife been sick as well?
Do you have any allergies?!
Did you eat anything today?
Do you take any medications?!- blood thinners?
What other symptoms do you have?!

Within 45 minutes theCT suggests an acute ischemic infarction(no signs of hemorrhage ormass lesions). Is this patient acandidate for fibrinolytic therapy?
-YES

You repeat the neuro assessment, and find the patients neurologic function is rapidly improving (without intervention).Is this patient still a candidate for fibrinolytic therapy?
-NO- TIA

77
Q

blood supply

A

-internal carotid arteries (anterior)
-becomes middle cerebral artery
-anterior cerebral artery branches off internal carotid

-vertebrobasilar system (posterior)
-vertebral arteries arise from subclavian arteries
-vertebral arteries join to become basilar artery
-basilar artery becomes the posterior cerebral arteries
-cerebellar arteries arise from vertebral and basilar arteries

-ACA (anterior cerebral artery)
o Origin: Internal carotid artery
o Supplies: Medial frontal and parietal
lobes, anterior limb of the internal
capsule, most of the corpus callosum

  • MCA (middle cerebral artery)
    o Origin: Internal carotid artery
    o Supplies: Lateral frontal and parietal
    lobes, portion of temporal lobes, Genu
    and posterior limb of internal capsule,
    most of the basal ganglia
  • PCA (posterior cerebral artery)
    o Origin: Terminal branches off basilar
    arteries
    o Supplies: Occipital lobe, posteromedial
    temporal lobes, midbrain
78
Q

MCA syndromes: superior and inferior divisons symptoms (NOT ON TEST)

A

Superior division (M3) syndrome:
o Affects: Lateral frontal lobe, superior parietal lobe
o Signs and symptoms:
 Contralateral weakness
* Face/Upper limb > Lower limb
* Lower 1/3 of the face
* Contralateral sensory loss
* Dominant: Expressive aphasia
* If dominant (MC left) affecting Broca’s area
* Non-dominant: Contralateral hemineglect
* If non-dominant hemisphere (MC right)
* Unaware/unresponsive of stimuli on the side contralateral
to the stroke

Inferior division (M3) syndrome:
o AFFECTS: Lateral temporal lobe
o Signs and symptoms
o Contralateral homonymous hemianopia
o More often the upper quadrants because it
supplies the optic radiation fibers
o LEFT/DOMINANT: Receptive aphasia
o Wernicke’s area = speech compression
o Inability to comprehend both written/spoken
language
o RIGHT/NON-DOMINANT: Constructional
apraxia
o Difficulty in motor planning, inability to execute
tasks despite understanding the instructions
and having the physical capability to perform
them

79
Q

posterior circulation strokes

A

-vertigo, ataxia, nausea
-drop to ground
-dreaded Ds- dysarthria, dysphagia, diplopia, dizzy, drowsy, drop attack