Last edited: 8/20/2021

1. ACUTE ISCHEMIC STROKE

Acute Ischemic Stroke: Etiology, Pathophysiology, Clinical Medical Editor: Adara Garcia Maestu
Features, Diagnostics, Treatment

Embolic causes most commonly affect the MCA, PCA or

OUTLINE smaller cortical vessels

I) EPIDEMIOLOGY
II) PATHOPHYSIOLOGY
III) STROKE SYNDROMES / SYMPTOMS BY
VASCULAR TERRITORY
IV) DIAGNOSIS
V) TREATMENT
VI) COMPLICATIONS
VII) REVIEW QUESTIONS
VIII) REFERENCES

EPIDEMIOLOGY Figure 1 Diagram demonstrating the origin of paradoxical and

cardiac emboli
Risk Factors
Non-modifiable (things you can’t fix) THROMBOTIC CAUSES
o Age ≥ 65
o Males > Females Large Vessel Atherosclerosis
o African American or Hispanic ethnicity Caused by above risk factors
o Family History of cardiovascular/cerebrovascular o Esp. HTN, DM, HLD, smoking and age
disease
Pathophysiology:
Modifiable (things you can fix) 1) Plaque in vessel wall ruptures
o Hypertension (HTN) 2) Thrombus develops over plaque decreasing lumen
o Diabetes Mellitus (DM) 3) Decreased blood flow beyond thrombus
o Atherosclerosis or Hyperlipidemia (HDL) 4) Ischemia → Infarction
o Obesity
o Tobacco, drug and alcohol abuse Most common sites:
o ICA after bifurcation of common carotid artery
 Due to carotid stenosis
I) PATHOPHYSIOLOGY o Vertebrobasilar System
o Stem of the MCA or just prior to its first bifurcation
EMBOLIC CAUSES
Cardiac Emboli
Atrial Fibrillation
Left ventricular thrombus Figure 2 Rupture of a plaque
CHF with low ejection fraction Small Vessel Atherosclerosis
o This increases stasis of blood flow and risk of clots
forming Same causes and pathophysiology as large vessel
atherosclerosis (see above)
Septic emboli from infective endocarditis vegetations on
Most common sites:
mitral or aortic valve
o Lenticulostriate vessels:
o Could be tricuspid in intravenous drug users
 These supply basal ganglia, internal capsule and
Fibrinous material on mitral or aortic valves from corona radiata
rheumatic heart disease o Small pontine penetrating vessels
Mechanical heart valve (highly thrombogenic)
Arterial Emboli GLOBAL CEREBRAL ISCHEMIA
From plaque on Aortic or Internal Carotid Artery Systemic Hypoperfusion
Plaque or piece of it is dislodged
Embolus gets stuck in downstream cerebral vessel Due to cardiogenic, obstructive or septic shock
Decreased blood flow beyond embolism 1) Decrease in Mean Arterial Pressure (MAP)
Ischemia → Infarction 2) ↓ cerebral perfusion and oxygen delivery (ischemia)
3) Infarction of watershed areas
Paradoxical Emboli
Watershed areas refers to regions of the brain
From DVT in patients with Patent Foramen Ovale (PFO)
situated furthest away from supplying blood vessels.
or Atrial Septal Aneurysm
Because of this, they are the most susceptible to
Thrombus dislodges and enters RA via IVC
infarction due to low blood pressure!
Moves to LA/PFO or septal aneurysm
Enters LV, then aorta and ICA
Risk is increased in the setting of concomitant carotid
Embolus gets stuck in downstream cerebral vessel
stenosis (further reduces cerebral flow)
Decreased blood flow beyond embolism
Ischemia → Infarction

Acute ischemic stroke NEURO PATHOLOGY: Note #1. 1 of 7

Severe and Prolonged Hypoxia II) STROKE SYNDROMES / SYMPTOMS BY VASCULAR
Occurs in acute respiratory failure TERRITORY
1) Decreased oxygen content in blood due to
ventilation-perfusion (V/Q) mismatch
2) ↓ oxygen delivery to the brain despite adequate (A) ANTERIOR CIRCULATION STROKES
perfusion These account for roughly 70% of strokes
3) Infarction of watershed areas
Middle Cerebral Artery (MCA) stroke
In a cardiopulmonary arrest, a mixture of hypoperfusion This is the most common type of stroke
(heart is not pumping) and hypoxia (lungs aren’t drawing in The MCA supplies:
air) results in very likely infarction and stroke if not o Lateral portions of frontal and parietal lobes
corrected o Superior part of the temporal lobe
o Basal Ganglia
OTHER CAUSES
Hypercoagulable States Superior division infarct
Diseases that cause clots to form (usually venous) May damage the following structures:
Inherited thrombophilias o Primary Motor Cortex (lateral portion)
o Factor V Leiden  Contralateral weakness or paralysis of upper
o Antithrombin III deficiency limbs, face and upper trunk
o Protein C and S deficiency o Primary somatosensory cortex (lateral portion)
o Prothrombin gene mutation  Contralateral sensory loss of upper limbs, face
and upper trunk
Acquired thrombophilias o Frontal eye field
o Antiphospholipid Syndrome  Ipsilateral gaze deviation
o Heparin induced Thrombocytopenia (HIT) o Broca’s area
Polycythemia  Broca’s (Expressive) aphasia (can understand but
not speak)
Vasculitis
Causes Inferior division infarct
o Autoimmune May damage the following structures:
 Giant Cell Arteritis o Wernicke’s area
 Takayasu’s Arteritis  Wernicke’s (Receptive) aphasia (can speak but
o Infectious not understand)
 Tuberculosis o Optic radiations
 Syphilis  Contralateral homonymous hemianopia or
 Varicella Zoster Virus quadrantanopia without macular sparing
o Primary CNS Vasculitis
Infarct of the MCA on the non-dominant side
Pathophysiology
1) Inflammation of the lining of blood vessels causes (Usually right side) can result in damage to the following
endothelial dysfunction structures:
2) Dysregulation of clotting system leads to o Right parietal and temporal lobe
increased risk of clots  Apraxia → Difficulty performing voluntary actions
3) Ischemia → Infarction despite intact motor function and desire to
OR perform movement
1) Inflammation of the lining of blood vessels causes  Hemieglect → Unaware of visual or somatic
narrowing of the lumen sensations on contralateral side of the body
2) Decreased blood flow in cerebral vessels
Anterior Cerebral Artery (ACA) stroke
(ischemia)
3) Infarction The ACA supplies:
o Medial portions of frontal and parietal lobes
Arterial Dissection
o Basal Ganglia
Causes An infarct may damage the following structures:
o Trauma
o Fibromuscular Dysplasia (i) Primary motor cortex (medial portion)
o Connective tissue diseases
o Contralateral weakness or paralysis of lower limbs
 Marfan’s Syndrome
and lower trunk
 Ehlers Danlos Syndrome
Pathophysiology (ii) Primary somatosensory cortex (medial portion)
1) Tear within the vessel wall (tunica intima) o Contralateral sensory loss of lower limbs and trunk
2) Blood moves in between tunica intima and tunica
media dissecting them (iii) Paracentral lobule of parietal lobe
3) Collection of blood bulges into the lumen, o Urinary incontinence
narrowing it o Fecal incontinence
4) Ischemia → Infarction
(iv) Prefrontal cortex and anterior cingulate cortex
o Abulia→ Decreased motivation to perform tasks
o Akinetic mutism
 Occurs in bilateral frontal lobe infarcts
 Severe decreased motivation to perform tasks
Figure 1 Arterial Dissection  No response to pain

2 of 7 NEURO PATHOLOGY: Note #1. Acute ischemic stroke

  Catatonic Vertebral Artery + PICA

(v) Anterior/superior frontal lobe Vertebral Artery gives off:

o Anterior Spinal Artery (ASA)
o Transcortical motor aphasia→ Similar to Broca’s  Supplies medial medulla
aphasia but maintain the ability to repeat phrases o Posterior Inferior Cerebellar Artery (PICA)
Internal Carotid Artery (ICA) stroke  Supplies lateral medulla and posterior inferior
cerebellum
The ICA supplies both the MCA and ACA, therefore a
mixture of both these stroke syndromes’ symptoms can
be seen with a severe ICA infarct Infarct of vertebral artery/ASA
In 5% of patients it ICA infarct can cause PCA stroke
May damage the following structures:
syndrome due to fetal variant
o CN XII nucleus
ICA also supplies the retina and infarct may cause:
 Ipsilateral tongue deviation
o Amaurosis Fugax→ Transient ipsilateral mono-ocular
o Medial Lemniscus
vision loss that may become permanent if not treated  Contralateral sensory loss of whole side
• Proprioception
Lenticulostriate Arteries • Fine touch
• Vibrations
Small arterial branches off the MCA that supply
o Corticospinal tracts in pyramids before decussation
subcortical and brainstem structures
 Contralateral weakness or paralysis of whole side
An infarct damages the posterior limb of the internal
capsule and other basal ganglia resulting in various
lacunar stroke syndromes: Infarct of PICA (Wallenburg Syndrome)
Pure Motor Stroke May damage the following structures:
o Contralateral weakness of whole side o Inferior cerebellar peduncles
Sensorimotor Stroke  Ipsilateral ataxia→ Impaired co-ordination and
o Contralateral weakness of whole side balance
o Contralateral sensory loss/paresthesia of whole side o Nucleus Ambiguus (CN IX, X, XI)
Ataxic Hemiparesis  Dysphagia
o Ipsilateral weakness and ataxia  Hoarseness
 Vocal cord paralysis (dysphonia)
Dysarthria (clumsy hand syndrome)  Diminished cough and gag reflexes
o Contralateral weakness of face and hand  Contralateral uvular deviation
o Dysarthria o Vestibular nuclei
Pure Sensory Stroke  Nausea and Vomiting
o Contralateral sensory loss/paresthesia of whole side  Vertigo
 Nystagmus
o Descending Sympathetic Tracts
III) POSTERIOR CIRCULATION STROKES  Ipsilateral Horner’s syndrome (Ptosis, Miosis,
Anhidrosis)
These account for roughly 30% of strokes
o Spinal Trigeminal Nucleus (CN V)
Posterior cerebral artery (PCA)  Ipsilateral sensory loss of face
• Pain
The PCA supplies:
• Temperature
o Midbrain
o Spinothalamic Tract
o Occipital lobes
 Contralateral sensory loss of the whole side
o Posteromedial region of temporal lobe
o Thalamus • Pain
• Temperature
An infarct may damage the following structures:

(i) Occipital lobe Basilar artery + AICA

o Homonymous Hemianopia with macular sparing Basilar artery gives off:
o Paramedian branches
(ii) Thalamus
 Supply medial pons
o Variable/contralateral sensory loss or paresthesia of o Superior Cerebellar Artery
whole side o Anterior Inferior Cerebellar Artery (AICA)
o Visual field cut (damage to lateral geniculate nucleus)  Supply lateral pons
o Decreased arousal or coma

(iii) Midbrain Infarct of paramedian arteries

o Weber Syndrome May cause damage to the following structures:
 Ipsilateral CN III palsy o CN VI (Abducens) nucleus
 Contralateral hemiplegia  Ipsilateral loss of eye abduction
o Claude Syndrome  Medial gaze deviation
 Ipsilateral CN III palsy o Medial Longitudinal Fasciculus (MLF)
 Contralateral ataxia  Internuclear ophthalmoplegia→ Inability to co-
o Benedikt Syndrome ordinate eye movements
 Combination of Weber and Claude syndromes o Paramedian Pontine Reticular Formation (PPRF)
 Loss of ipsilateral gaze
o Medial Lemniscus

Acute ischemic stroke NEURO PATHOLOGY: Note #1. 3 of 7

  Contralateral loss of fine touch, proprioception and
vibration
o Corticospinal tract
 Contralateral weakness
Infarct of AICA
May cause damage to the following structures:
o Middle Cerebellar Peduncles
 Ipsilateral Ataxia→ Impaired co-ordination and
balance
o Vestibular Nucleus
 Vertigo
 Nausea and Vomiting
 Nystagmus
o Cochlear Nuclei
 Decreased hearing
 Tinnitus
o Descending Sympathetic tracts
 Horner’s Syndrome (Ptosis, Anhidrosis, Miosis)
o CN V (trigeminal) nucleus + tract
 Ipsilateral loss of sensation to face
 Loss of ipsilateral corneal reflex
 Ipsilateral mastication muscle weakness
o Spinothalamic Tracts
 Contralateral loss of pain and temperature on
whole side
o CN VII (facial) nucleus
 Ipsilateral facial weakness (usually lower part)
WATERSHED INFARCTS
Infarcts of watershed areas→ Regions of the brain
situated furthest away from supplying blood vessels
o Found where two vascular territories anastamose
Most susceptible to infarction during low perfusion states
(↓ BP)
MCA / ACA watershed zone infarct
Contralateral weakness/paralysis and sensory loss of
upper and lower extremities
Also known as “Man in a Barrel” Syndrome
MCA / PCA watershed zone infarct
Visual dysfunctions
o Prosopagnosia→ Patient sees objects/people but
can’t make out what/who they are
o Homonymous Hemianopia
o Balint’s Syndrome (rare)
 Simultanagnosia→ Inability to perceive more than
one object at a time Eg. Patient will see individual
trees but is unable to recognize the forest
 Optic ataxia→ Lack of co-ordination between
visual input and hand movements Eg. Patient
touches their own nose but struggles to touch the
physician’s finger
 Oculomotor apraxia→ Inability to shift gaze
voluntarily despite desire to do so and intact
function of extraocular muscles
IV) DIAGNOSIS
ACUTE WORKUP
Imaging
STAT non-contrast CT of the head
o Rule out intra-cranial hemorrhage (ICH) and sub-
arachnoid hemorrhage (SAH)
o Analyze for early ischemic changes:
 Hyperdense MCA / Basilar artery where the clot is
 Hypodensity of brain tissue (infarction) within 3
hours of stroke
4 of 7 NEURO PATHOLOGY: Note #1.
CT angiogram of head and neck
o Filling defects
o Vessel cutoffs
o Large vessel occlusions
12 lead ECG
o To assess for any acute MI or arrythmias
(AFib/Aflutter) as potential causes
Labs
o POC glucose
 Rule out hypoglycemia as stroke mimic
o Don’t delay treatment to obtain the following unless
there is concern or your institution requires it per
protocol:
 CBC
• Asses for severe anemia, suggestive of
bleeding which can contraindicate TPA
• Assess for severe thrombocytopenia (<100k)
which may affect TPA administration
• Polycythemia as possible cause for occlusion
 Coagulation Studies
• INR > 1.7
o Check if they take Warfarin or have liver
failure which can contraindicate TPA
Etiology/Risk factors workup
Transthoracic/Transesophageal echocardiogram
o Assess for atrial or ventricular thrombi
o Assess for valve vegetations or mechanical valve
o Assess for low EF or wall motion abnormalities
o Assess for PFO or atrial defect
 Can further evaluate with TCD bubble study
 Check if bubbles cross atria and float up to
cerebral circulation
CT angiogram, MR angiogram or Carotid Doppler
o Assess aortic and carotid circulation for stenosis or
dissections
o Assess for intracranial atherosclerosis
MRI
o Assess stroke burden and rule out other etiology
 Diffusion-weighted imaging (DWI) shows up bright
when infarction present
 Apparent Diffusion Coefficient (ADC) shows up
dark when infarction present
 T2 flair shows cytotoxic edema when infarction
present
Holter Monitor
o Assess for any paroxysmal atrial fibrillation or flutter
Labs
o Lipid panel to assess for hyperlipidemia
o Hemoglobin A1c to assess for DM
o TSH with reflex to assess for hyperthyroidism which
can cause AFib
o Hypercoagulable workup if patient young with history
of DVT and no apparent etiology
 Factor V
 Protein C and S
 Antithrombin III activity
 Prothrombin activity
 Antiphospholipid antibodies
• Cardiolipin, lupus anticoagulant and beta
glycoprotein
 PF4 antibodies + serotonin release assay if
suspect HIT
o ESR, CRP, ANA panel, ANCA to assess for vasculitis
(low on differential
o VDRL, RPR to rule out syphilis and PCR for VZV as
causes of infectious vasculitis (low on differential)
NIHSS Assessment
Tool to assess stroke severity and predict outcomes
Acute ischemic stroke
 11 categories with scores ranging from 0 to 42
No strict cutoff for IV TPA although some research
suggests NIHSS >4
Don’t memorize- Use MD calc or other Tool Kits
V) TREATMENT
ACUTE TREATMENT OF STROKE
o DOACs preferred by patients because there is no
need to monitor INR weekly
Hold anticoagulation if:
o Infective endocarditis is a cardioembolic cause
o In large hemispheric stroke infarcts for 2-4 weeks
after stroke due to high risk of hemorrhagic
transformation

Intravenous TPA Antiplatelet Therapy

Mechanism of action: Indications:

o TPA→ ↑ plasmin formation→ ↑ fibrin degradation o Post stroke
o History of coronary artery disease with stents
from clot→ Breakdown of clot
Aspirin or clopidogrel used for non-embolic strokes 24-
Indications:
48hrs after stroke
o Acute neurological deficit
o Last known well < 3hrs Percutaneous closure of PFO/atrial defect
OR
If <60 y/o with cryptogenic strokes
o Last known well < 4.5hrs if:
 Patient is 18 or older Carotid Revascularization Procedures
 NIHSS is lower than 25
Carotid Endarterectomy (CEA)
 There is no history of DM or previous stroke
o Indications:
 Affected area on scan is < 1/3 of MCA territory
 Symptomatic Carotid Stenosis >70%
o No ICH or SAH on CT
 Symptomatic Carotid Stenosis <70% if older male
o No active bleeding
o No recent anticoagulation Carotid Artery Stenting
o Preferred over CEA when high risk of periprocedural
Dosage:
complications
o 0.9mg/kg
o 10% given as a bolus Risk Factor Modifications
o Remaining given over the next hour
Hypertension
Monitoring post IV-TPA: o Antihypertensives optimized or started
o Blood pressure <185/110 for 24hrs
 Lower BP with nicardipine or labetalol Diabetes
o Neuro checks o Insulin / oral antidiabetic medications optimized or
 Every 15 mins for 1st hour started
 Every 30 mins for next 6 hours Hyperlipidemmia
 Every hour for 24hrs o Statins optimized or started
o CT scan 24hrs after administration Smoking cessation
 Assess any hemorrhagic transformation Weight loss in obese patients
 Evaluate any evolution of infarct
 Give the okay to start anticoagulation if needed VI) COMPLICATIONS
Mechanical Thrombectomy
Cerebral Edema/Elevated ICP
Interventional radiology procedure using real time
Usually peaks 3-5 days post infarct of large MCA territory
imaging to thread a catheter or stent retriever into
o Infarct→ cytotoxic edema→ Midline shift→ ↑ ICP→
affected vessel and remove clot
Herniation risk
Indications:
o Large vessel occlusion Treatment Options:
 Proximal MCA o Decompressive Hemicraniectomy
 ICA terminus o ICP supportive measures:
 Vertebral and Basilar arteries  Keep neck midline
o Last known well between 6-24hrs (earlier preferred)  Elevate head of bed 30 degrees
o Salvageable penumbra  Reduce agitation and pain
 Use CT or MR perfusion studies to identify o Sedation and intubation if ICP not controlled with
 CT aspects score > 6 supportive measures
• Determines benefit of procedure  Propofol drip (decreases basal metabolic rate and
cerebral blood flow leading to reduced ICP)
TREATMENT FOR PREVENTION o Hypertonic Agents
Anticoagulation  23.4% hypertonic saline with emergent ICP crisis if
central line is present
Indications:  25% mannitol with emergent ICP if peripheral IV
o Atrial Fibrillation  Prophylaxis of cerebral edema with continuous
o LV or LA thrombus infusion of 3% hypertonic saline to a goal of 150-
o Mechanical heart valve 155
o CHF with reduced EF
o Cerebral venous sinus thrombosis with venous infarct
o Hypercoagulable disorder
Heparin drip or lovenox as a bridge to warfarin or DOACs
for long term control
o Heparin is easy to titrate while in hospital
o Warfarin superior to DOACs with mechanical valves
and AFib secondary to mitral stenosis

Acute ischemic stroke NEURO PATHOLOGY: Note #1. 5 of 7

Post TPA complications Ischemic strokes also carry risk of causing nonconvulsive
status epilepticus
Hemorrhagic Conversion
o Can only be proven by continuous EEG
o Suspect with acute neuro change
o Obtain CT to confirm Treatment options:
o Treatment options: o Levetiracetam
 Stop TPA if still running o Valproate
 Reverse TPA if <12-24hrs after infusion o Phenytoin or fosphenytoin
• Tranexamic Acid (TXA)
Aspiration Pneumonia
• Cryoprecipitate
• Platelet transfusion if needed Stroke→ Dysphagia→ Inability to clear secretions
properly→ aspiration→ ↑Risk of pneumonia
Requires proper speech evaluation to determine if patient
can eat/drink or requires a feeding tube
If pneumonia develops:
o Antibiotics against pathogen from sputum cultures

Angioedema
o TPA can cause allergic reaction of lips and larynx
o Treatment options:
 Antihistamines
 IV steroids
 Low threshold for intubation
Seizures
Ischemic infarcts can become a focus of epileptogenic
potential leading to focal seizures with risk of generalizing

VII) SUMMARY TABLE

Table 1-1 Stroke Syndromes Summary Table

Vessel Symptoms Vessel Symptoms

Contralateral weakness/paralysis and sensory Ataxia

loss of upper limbs, face and upper trunk Dysphagia, Dysphonia, ↓ gag and cough
Ipsilateral gaze deviation PICA reflexes
MCA Aphasia (expressive, receptive or both) (Lateral Contralateral uvular deviation
Contralateral Homonymous hemianopia Medulla) Vertigo, N/V, Nystagmus
without macular sparing Ipsilateral Horner’s Syndrome
Apraxia + Hemineglect if infarct on non- Loss of pain and temperature on ipsilateral
dominant hemisphere face and contralateral whole side
Contralateral weakness/paralysis and sensory
loss of lower limbs and lower trunk Vertebral Contralateral weakness/paralysis and sensory
Urinary and fecal incontinence Artery/ASA loss (fine touch, vibration + proprioception) of
ACA
Abulia or Akinetic mutism (Medial whole side
Transcortical motor aphasia (able to repeat Medulla) Ipsilateral tongue deviation
phrases)

Ataxia
Vertigo, N/V, Nystagmus
Hearing loss + tinnitus
Mixture of MCA and ACA symptoms AICA Ipsilateral Horner’s Syndrome
ICA May have PCA symptoms if fetal variant (Lateral Ipsilateral loss of sensation to face, loss of
present Pons) corneal reflex and weakness of mastication
Amaurosis Fugax
and facial muscles
Contralateral loss of pain and temperature on
whole side

Homonymous Hemianopia with macular

Basilar Contralateral weakness and loss of fine touch,
sparing
Artery proprioception and vibration
PCA Variable or contralateral sensory
(Medial Ipsilateral loss of eye abduction→ Medial gaze
loss/paresthesia of whole side (thalamus)
Pons) deviation
Weber, Claude or Benedikt Syndromes
Intranuclear ophthalmoplegia
(midbrain)

6 of 7 NEURO PATHOLOGY: Note #1. Acute ischemic stroke

 VIII) REVIEW QUESTIONS IX) REFERENCES
● Parvathaneni A, M Das J. Balint Syndrome. [Updated 2021 Jun
1) Which is the most important modifiable risk factor
30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls
for strokes? Publishing; 2021 Jan-. Available from:
a. High BMI https://www.ncbi.nlm.nih.gov/books/NBK544347/
b. Low exercise levels ● Bickley LS, Szilagyi PG, Hoffman RM, Soriano RP, Bates B.
Bates' Guide to Physical Examination and History Taking.
c. Hypertension Philadelphia: Wolters Kluwer; 2021.
d. Cigarette smoking ● Longmore JM. Mini Oxford Handbook of Clinical Medicine.
Oxford: Oxford University Press; 2015.
2) Which of the following is a stroke symptom? ● Sabatine MS. Pocket Medicine: the Massachusetts General
a. Sudden confusion Hospital Handbook of Internal Medicine. Philadelphia: Wolters
b. Sudden weakness in an arm or leg Kluwer; 2020.
● Williams DA. Pance Prep Pearls. Middletown, DE: Kindle Direct
c. Sudden severe headache with no cause Publishing Platform; 2020.
d. Sudden trouble seeing ● Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
e. All of the above Loscalzo J. Harrison's Principles of Internal Medicine. New York
etc.: McGraw-Hill Education; 2018.
3) Which of the following is characteristic of an ACA ● Cucchiara BL, Messé SR. Antiplatelet therapy for secondary
prevention of stroke. In: Post TW, ed. UpToDate .
stroke?
● Schur PH, Kaplan AA. Treatment of antiphospholipid syndrome.
a. Ataxia In: Post TW, ed. UpToDate
b. Intranuclear ophthalmoplegia ● The Pocket Guide to Neurocritical Care: A Concise Reference
c. Ipsilateral tongue deviation for the Evaluation and Management of Neurologic Emergencies.
Chicago, IL: Neurocritical Care Society; 2017.
d. All of the above ● Westover MB, DeCroos EC, Awad KM, Bianchi MT. Pocket
Neurology. Philadelphia: Wolters Kluwer; 2016.
4) Damage to which of these structures is associated ● Lee K. The NeuroICU Book. New York: McGraw-Hill Education;
with urinary incontinence? 2018.
a. Paracentral lobule of parietal lobe ● Louis R Caplan. Overview of the Evaluation of Stroke. In: Post
b. Midbrain TW, ed. UpToDate.
● Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the
c. Anterior/Superior frontal lobe Early Management of Patients With Acute Ischemic Stroke: 2019
d. None of the above Update to the 2018 Guidelines for the Early Management of Acute
Ischemic Stroke: A Guideline for Healthcare Professionals From the
5) Patients suffering from Wernicke’s Aphasia can American Heart Association/American Stroke Association. Stroke
understand what it is said to them. .2019; 50(12).
● Le T, Bhushan V, Skelley N. First Aid for the USMLE Step 2 CK.
a. True McGraw-Hill Education; 2012
b. False ● Kleindorfer DO, Towfighi A, Chaturvedi S, et al. 2021 Guideline
c. Depends on the patient for the Prevention of Stroke in Patients With Stroke and Transient
Ischemic Attack: A Guideline From the American Heart
6) Which of the following is the most appropriate first Association/American Stroke Association. Stroke .2021
test for a query stroke? ● Caplan LR, Kasner SE, Dashe JF. Etiology, Classification, and
Epidemiology of Stroke. In: Post TW, ed. UpToDate .
a. 12-lead ECG
b. Head and neck MRI
c. Non-contrast head CT
d. Coagulation studies

CHECK YOUR ANSWERS

Acute ischemic stroke NEURO PATHOLOGY: Note #1. 7 of 7