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Etiology

• Thrombotic: Atherosclerosis, small vessel lipohyalinosis (lacunar infarcts) → fluctuating symptoms with periods of improvement
• Embolic: Afib, carotid disease, endocarditis, septal defects (PFO) → maximal severity at onset, multiple infarcts in different regions
• Hypoperfusion: Shock → global, nonspecific defects

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Labs to Consider

• STAT fingerstick glucose
• CBC
• Electrolytes including Ca/Mg/Phos
• Liver function tests
• Coagulation studies
  • Generally PT, PTT, fibrinogen
  • Anti-Xa for patients on oral Xa inhibitors (e.g., apiXaban)
• Blood cultures x2 if concern for endocarditis (e.g., fever or history of IV drug use)
• Pregnancy test as appropriate

Diagnosis

CT to rule out hemorrhage (& determine tPA candidacy)

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MRI

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Source localization with duplex US (or CTA/MA), cardiac monitoring, TTE, ambulatory loop recorder

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Stroke Region	Subtype	Clinical Features
Cortical	Anterior Cerebral	Contralateral motor/sensory deficit, with lower extremity predominance; Behavioral changes (abulia, dyspraxia, emotional change)
	Middle Cerebral	Contralateral motor/sensory deficit, with upper extremity and face predominance; Eye deviation towards side of infarction (frontal eye fields)
	Posterior Cerebral	Homonymous hemianopsia; Aphasia (dominant) or neglect (non-dominant); Possible sensory symptoms (from lateral thalamic infarct)
		Contralateral hemianopia with macular sparing
Brainstem	Anterior spinal	Medial Medullary Syndrome: Contralateral upper/lower limb paralysis; Ipsilateral hypoglossal (tongue deviates towards lesion); Loss of proprioception (medial lemniscus)
	PICA	Wallenberg Syndrome (Lateral Medullary): Dysphagia/Hoarseness, Pain/temp from ipsilateral face / contralateral body, Ipsilateral Horner syndrome, Vertigo, nystagmus, ataxia, dysmetria
	AICA	Lateral Pontine Syndrome: Ipsilateral facial paralysis (facial nucleus); Ipsilateral pain/temp from face/contralateral body; Ipsilateral decreased lacrimation/salivation/taste from anterior tongue; Vertigo, nystagmus, ataxia, dysmetria
	Basilar	Medial pons, possible "Locked-In Syndrome": Corticospinal: Unilateral or bilateral paresis; Bulbar: Unilateral or bilateral face weakness, dysarthria, dysphagia, limited jaw movement; Oculomotor: Horizontal gaze palsy, internuclear ophthalmoplegia
Lacunar	Pure Motor	Internal capsule (posterior limb): Unilateral paralysis of face, arm, leg without sensory loss
	Pure Sensory	Thalamus: Unilateral sensory deficit of face, arm, leg without motor loss
	Ataxic Hemiparesis	Internal capsule, basis pontis, or corona radiata: Unilateral weakness and limb ataxia
	Dysarthria-Clumsy Hand	Genu of internal capsule, basal pons: Unilateral face weakness, dysarthria, with hand weakness and clumsiness

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Management

• Thrombolytic: IV Alteplase→ given within 3 - 4.5h (contraindications below)
• BP control (permissive htn): Labetolol, Nicardipine, and Clevidipine
  • < 185/110 if tPA used
  • < 220/120 if no tpa
• Aspirin (or Clopidogrel if allergic): 325mg loading dose within 48h, if tPA used do not start for 24h
• Statin: For all
• Mechanical thrombectomy: being utilized with increased frequency for proximal large vessel occlusions

Contraindications for tPA

Major Exclusion Criteria	Relative Exclusion Criteria
Recent major surgery or trauma	History of stroke or head injury within 3 months
Intracranial hemorrhage or known brain tumor	Active bleeding or bleeding diathesis
Known intracranial structural abnormalities	Severe uncontrolled hypertension
Suspected aortic dissection	Recent use of anticoagulants
Seizure at the onset of stroke	History of gastrointestinal bleeding within 21 days
Rapidly improving or minor stroke symptoms	Platelet count <100,000/mm³
Known severe liver disease or hepatic dysfunction	Blood glucose concentration <50 mg/dL or >400 mg/dL
Current use of direct thrombin inhibitors	Current use of novel oral anticoagulants
Pregnancy or postpartum period (within 14 days)	Dementia or severe cognitive impairment

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Hemorrhagic Transformation

Hemorrhagic transformation may result from the natural evolution of ischemic stroke, usually within the first week

• Petechial hemorrhages: Most hemorrhagic transformations are small, petechial hemorrhages of little clinical significance
• Asymptomatic hematomas: Small hematomas can occur within infarcted brain
• Symptomatic hematomas: Large hematomas may exert mass effect, cause vasogenic edema, and worsen clinical outcomes

Risk factors

• Large infarct size (e.g., hypodensity in more than a third of the MCA territory)
• Coagulopathy (e.g., therapeutic anticoagulation or thrombolysis)
• Older age
• Diabetes mellitus, hyperglycemia
• Uncontrolled hypertension

Treatment

• Stop thrombolytics, reverse any coagulopathies, measure coagulation labs (INR, PTT, fibrinogen, complete blood count, type & cross-match)

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TIA

• TIA is a focal neurologic deficit that resolves within 24h
• Diagnose with MRI or CT
• Source localization: Duplex ultrasound, CT/ MRA, cardiac monitoring, TTE
• Management: Weight loss, smoking cessation, ASA, statin
• Stroke Risk: 8% at 30 days and 10% at 90 days