Stroke Syndromes

• Definition: A stroke syndrome is the stereotyped constellation of deficits produced when a specific arterial territory or perforator loses perfusion; the deficit map is a bedside angiogram, letting you localize the lesion before imaging returns.
• Why it matters: Localization drives triage. A cortical syndrome (aphasia, neglect, gaze deviation) suggests large vessel occlusion and therefore thrombectomy candidacy, while a pure motor hemiparesis suggests a perforator lacune managed medically. Time-dependent reperfusion means the syndrome you recognize in the first minutes determines disability at 90 days.
• Burden: Stroke is a leading cause of death in the United States and the leading cause of long-term adult disability; the American Heart Association reports on the order of 795,000 strokes annually, roughly three-quarters of them first events.

Who examiners put in the stem

• Age: Risk approximately doubles each decade after 55; most strokes occur in patients over 65.
• Race/ethnicity: Black Americans have substantially higher incidence and earlier age of onset, driven largely by hypertension and diabetes prevalence; intracranial atherosclerosis is disproportionately common in Black, Hispanic, and East Asian patients.
• Sex: Men have higher age-adjusted incidence, but because women live longer they account for more absolute strokes and worse outcomes.
• Young patients (<50): Think dissection, patent foramen ovale with paradoxical embolism, hypercoagulable states, sickle cell disease, vasculitis, and stimulant use rather than atherosclerosis.

Framework worth memorizing

• Anterior circulation (ICA → ACA/MCA): cortical signs, aphasia, neglect, contralateral weakness.
• Posterior circulation (vertebrobasilar → PCA): crossed findings, diplopia, vertigo, ataxia, visual field loss.
• Small vessel: lacunar syndromes without cortical signs.
• Watershed: border-zone infarction from global hypoperfusion rather than focal occlusion.

Mechanistic categories (TOAST classification)

• Large-artery atherosclerosis: Plaque at the carotid bifurcation, ICA siphon, or vertebrobasilar origin causes artery-to-artery embolism or in-situ thrombosis. Suspect when the stem mentions a carotid bruit or stuttering, repetitive deficits in one territory.
• Cardioembolism: Atrial fibrillation is the archetype; also recent MI with akinetic segment or LV thrombus, dilated cardiomyopathy, mechanical valves, infective endocarditis, and atrial myxoma. Emboli favor the MCA and often produce abrupt, maximal-at-onset deficits and multiterritory infarcts.
• Small-vessel (lacunar) disease: Chronic hypertension and diabetes drive lipohyalinosis and microatheroma of lenticulostriate, thalamoperforator, and basilar penetrators.
• Hypoperfusion/watershed: Cardiac arrest, sepsis, or over-aggressive antihypertensive therapy in a patient with fixed carotid stenosis.
• Other determined cause: Cervical artery dissection (neck manipulation, trauma, fibromuscular dysplasia, connective tissue disease), paradoxical embolism through a PFO, vasculitis, sickle cell disease, antiphospholipid syndrome, hyperhomocysteinemia, cocaine or amphetamine use, and postpartum states.

Non-modifiable risk factors

• Age, male sex, Black or Hispanic ethnicity, family history, and prior stroke/TIA — prior TIA is the single strongest short-term predictor of imminent stroke.

Modifiable risk factors (the ones examiners expect you to treat)

• Hypertension: the dominant modifiable risk factor for both ischemic and hemorrhagic stroke; the ACC/AHA 2017 hypertension guideline treats it as the highest-yield target.
• Atrial fibrillation: risk stratified by CHA₂DS₂-VASc, with anticoagulation recommended per ACC/AHA/HRS.
• Diabetes, dyslipidemia, cigarette smoking, obesity, physical inactivity, obstructive sleep apnea, heavy alcohol use.
• Estrogen-containing contraceptives in a smoker over 35, and in migraine with aura — a classic stem pairing.
• Asymptomatic carotid stenosis: the USPSTF recommends against screening the general adult population.

• Flow thresholds: Normal cerebral blood flow is roughly 50 mL/100 g/min. Below about 20 mL/100 g/min electrical failure occurs and neurons go silent — this is the symptomatic but viable penumbra. Below roughly 10 mL/100 g/min, membrane pumps fail and the core infarcts within minutes. The clinical deficit reflects core plus penumbra; reperfusion recovers only the penumbra, which is why time and collaterals govern outcome.
• Ischemic cascade: ATP depletion halts Na⁺/K⁺-ATPase → anoxic depolarization → cytotoxic edema (water shifts intracellularly, producing restricted diffusion on MRI within minutes). Depolarization releases glutamate, which floods NMDA/AMPA receptors → calcium influx → activation of phospholipases, proteases, and nitric oxide synthase → free radical injury, mitochondrial permeability transition, and both necrosis (core) and apoptosis (penumbra).
• Reperfusion injury: Restored flow through an infarcted, matrix-metalloproteinase-degraded blood–brain barrier delivers oxygen radicals and neutrophils, producing vasogenic edema and hemorrhagic transformation — the mechanistic reason thrombolysis carries bleeding risk and why large completed infarcts are excluded.
• Why syndromes are stereotyped: Perfusion territories map onto functional anatomy. The MCA's superior division supplies the lateral motor/sensory strip for face and arm plus Broca's area; the ACA supplies the paracentral lobule serving the leg; the PCA supplies the calcarine cortex and thalamus. Deep lenticulostriate perforators are end arteries with no collateral supply, so occlusion produces a discrete lacune in the internal capsule — dense contralateral hemiparesis with no cortical signs because the cortex is spared.
• Brainstem crossed syndromes: Long tracts (corticospinal, spinothalamic) have already or not yet decussated while cranial nerve nuclei act ipsilaterally, yielding ipsilateral cranial nerve deficits with contralateral body deficits.
• Watershed physiology: Border zones between ACA/MCA and MCA/PCA sit at the distal end of two arterial trees; global hypotension starves them first, producing bilateral proximal arm weakness (man in a barrel) or transcortical aphasia.

• The universal feature: Sudden, focal, negative neurologic deficit that is maximal at or near onset and conforms to a vascular territory. Gradual onset, positive phenomena (tingling marching up a limb, scintillations), or non-anatomic findings argue for mimic — migraine aura, seizure with Todd paralysis, hypoglycemia, or conversion disorder.

Territory-specific findings and their mechanism

• MCA superior division: Face/arm-predominant weakness (lateral homunculus) with Broca aphasia — effortful, non-fluent speech, intact comprehension, patient frustrated.
• MCA inferior division: Wernicke aphasia — fluent but meaningless speech with impaired comprehension, no weakness; often mistaken for delirium or psychosis.
• Right MCA: Hemispatial neglect, anosognosia, and eyes deviated toward the lesion from unopposed contralateral frontal eye field drive.
• ACA: Leg-predominant weakness plus abulia, grasp reflex, and urinary incontinence from medial frontal and paracentral involvement.
• PCA: Homonymous hemianopia with macular sparing (occipital pole collateral from MCA); thalamic involvement gives contralateral sensory loss and later Dejerine-Roussy central pain. Bilateral occipital infarction with denial of blindness is Anton syndrome.
• **Lateral medullary (Wallenberg, PICA/vertebral)**: Ipsilateral facial pain/temperature loss, Horner syndrome, hoarseness and dysphagia, ataxia, vertigo, with contralateral body pain/temperature loss and sparing of strength.
• Medial medullary: Contralateral arm/leg weakness, contralateral vibration/proprioception loss, ipsilateral tongue deviation (CN XII).
• Basilar: Quadriparesis with preserved vertical gaze and consciousness (locked-in syndrome), or coma with pinpoint pons pupils.
• Lacunar syndromes: Pure motor hemiparesis (posterior limb internal capsule), pure sensory (VPL thalamus), ataxic hemiparesis, dysarthria–clumsy hand — never aphasia, neglect, or visual field cut.

Immediate (parallel, not sequential)

• Fingerstick glucose: The one lab that must precede thrombolysis; hypoglycemia is the classic stroke mimic and the AHA/ASA 2019 acute stroke guideline permits treatment decisions without waiting for other labs in most patients.
• NIHSS: Quantifies severity (0–42) and predicts LVO; scores in the higher range with cortical signs should trigger vessel imaging. Establish last known well, not "time symptoms were noticed."
• Non-contrast head CT: First imaging test. Its job is to exclude hemorrhage, not to confirm infarct. Early ischemic signs — loss of gray-white differentiation, insular ribbon sign, sulcal effacement, hyperdense MCA sign — appear before frank hypodensity. ASPECTS grades early MCA-territory change out of 10 and informs thrombectomy selection.

Vessel and tissue imaging

• CT angiography head and neck: Identifies large vessel occlusion, dissection, and carotid stenosis; obtained without waiting for creatinine in most protocols.
• CT perfusion or MRI DWI/PWI: Defines core versus penumbra for late-window thrombectomy selection, following the DAWN and DEFUSE 3 trial paradigms embedded in AHA/ASA recommendations.
• MRI with DWI: Most sensitive confirmatory test — restricted diffusion with low ADC within minutes; the gold standard for small brainstem and lacunar infarcts that CT misses.

Etiologic workup (do not delay reperfusion for it)

• ECG and telemetry ≥24 hours, with prolonged ambulatory monitoring when the source remains cryptogenic, to capture paroxysmal atrial fibrillation.
• Echocardiography for thrombus, vegetation, or right-to-left shunt (agitated saline study for PFO).
• Carotid duplex or CTA/MRA, lipid panel, hemoglobin A1c; hypercoagulable and vasculitis testing reserved for young or otherwise unexplained cases.
• ABCD2 score stratifies short-term stroke risk after TIA and, with imaging, guides urgent versus expedited evaluation.

Stabilize first

• Airway, breathing, circulation; treat hypoglycemia, keep oxygen saturation above 94% but do not give supplemental oxygen to non-hypoxic patients (AHA/ASA 2019). Head of bed positioning and NPO status pending a bedside dysphagia screen before any oral intake.

Reperfusion — the first decision

• IV thrombolysis: Alteplase within 4.5 hours of last known well; tenecteplase is an accepted alternative in AHA/ASA recommendations, given as a single bolus. Blood pressure must be lowered to below 185/110 mmHg before the bolus — labetalol or nicardipine IV — and maintained below 180/105 mmHg for 24 hours afterward.
• Mechanical thrombectomy: For anterior circulation large vessel occlusion, performed even if the patient received thrombolytics; late-window treatment requires perfusion or DWI mismatch selection.

Antithrombotics

• Aspirin within 24–48 hours, but delayed 24 hours after thrombolysis and only after repeat imaging excludes hemorrhage.
• Short-course dual antiplatelet therapy (aspirin plus clopidogrel) for minor non-cardioembolic stroke or high-risk TIA, started early and continued approximately 21 days before dropping to monotherapy (AHA/ASA 2021, reflecting CHANCE and POINT). Prolonged DAPT increases bleeding without benefit.
• Anticoagulation for atrial fibrillation — a direct oral anticoagulant such as apixaban preferred over warfarin except with mechanical valves or moderate-to-severe mitral stenosis; timing of initiation is individualized against infarct size and hemorrhagic transformation risk.

Secondary prevention and definitive procedures

• High-intensity statin (atorvastatin), intensive blood pressure control after the acute period, glycemic control, and smoking cessation.
• Carotid endarterectomy for symptomatic high-grade ipsilateral stenosis, ideally within two weeks; stenting for poor surgical candidates.

Contraindicated or avoided

• Thrombolysis with intracranial hemorrhage, recent intracranial surgery, or the exclusions already listed; aggressive lowering of permissive hypertension in non-thrombolysed patients, which extends the penumbra into the core; and routine prophylactic antiepileptics or corticosteroids for ischemic edema.

Neurologic emergencies

• Hemorrhagic transformation: Reperfusion into infarcted, BBB-disrupted tissue; highest risk with large infarcts, cardioembolism, and thrombolysis. Signaled by acute neurologic decline, new headache, vomiting, or an abrupt blood pressure surge — stop any thrombolytic/anticoagulant, obtain emergent non-contrast CT, and reverse coagulopathy with cryoprecipitate or antifibrinolytics per AHA/ASA guidance.
• Malignant cerebral edema: Cytotoxic then vasogenic edema in a complete MCA or large cerebellar infarct, peaking around days 2–5. Declining consciousness with pupillary asymmetry or midline shift means impending herniation; decompressive hemicraniectomy (or suboccipital craniectomy with ventriculostomy for cerebellar infarction) is life-saving, with greatest mortality benefit in younger patients.
• Orolingual angioedema after alteplase, particularly in patients on ACE inhibitors — a bradykinin-mediated airway emergency requiring immediate airway assessment.
• Seizures: Cortical infarcts irritate perilesional cortex; treat recurrent seizures, but AHA/ASA does not endorse prophylaxis.

Systemic and subacute

• Aspiration pneumonia: Dysphagia plus depressed cough; the reason for a formal swallow screen before oral intake. Fever with new infiltrate signals it.
• Venous thromboembolism: Immobility and paretic limb stasis; intermittent pneumatic compression is recommended, with pharmacologic prophylaxis added once hemorrhage risk allows.
• Cardiac injury: Insular cortex infarction drives catecholamine surge producing arrhythmia, troponin elevation, and neurogenic stunned myocardium.
• Hyponatremia from SIADH or cerebral salt wasting; distinguish by volume status.
• Post-stroke depression, cognitive impairment, and vascular dementia — screen routinely, as depression independently worsens rehabilitation outcomes.
• Spasticity, contractures, hemiplegic shoulder subluxation, and pressure ulcers from immobility.
• Central post-stroke pain (Dejerine-Roussy) after thalamic infarction: delayed burning contralateral pain and allodynia, treated with agents such as gabapentinoids or tricyclics rather than opioids.

• Check the glucose before anything else. Hypoglycemia perfectly mimics a hemispheric stroke and is the fastest correctable mimic; after that, non-contrast CT to exclude hemorrhage is the single best next step in essentially every acute stem.
• Cortical signs separate big vessel from small vessel. Aphasia, neglect, or a visual field cut means cortex and therefore a large vessel — get CT angiography and consider thrombectomy. A dense pure motor hemiparesis with no aphasia or neglect is a lacune in the posterior limb of the internal capsule; thrombectomy has no role.
• Face and arm > leg is MCA; leg > arm is ACA. The homunculus explains it — the medial paracentral lobule is ACA territory.
• ***Wallenberg* is the classic crossed syndrome: ipsilateral facial sensory loss, Horner syndrome, hoarseness, ataxia; contralateral body pain/temperature loss; strength is preserved**. Weakness in a "lateral medullary" answer choice is the distractor.
• Homonymous hemianopia with macular sparing = PCA, spared because the occipital pole receives MCA collateral flow.
• Watershed infarcts follow hypotension, not embolism — bilateral proximal arm weakness (man in a barrel) after cardiac arrest or major hemorrhage.
• Eyes deviate toward the lesion in a hemispheric stroke and away from the lesion in a seizure focus — a favorite discriminator.
• TIA is a diagnosis of urgency, not reassurance. AHA/ASA recommends expedited evaluation with vessel imaging plus short-course dual antiplatelet therapy for high-risk TIA and minor stroke, dropped to monotherapy after roughly three weeks — indefinite DAPT is the trap.
• Common distractor: giving antihypertensives to normalize blood pressure in an untreated ischemic stroke. Permissive hypertension maintains penumbral perfusion; aggressive lowering converts penumbra into core.

• Ischemic stroke (85%) vs hemorrhagic stroke (15%); ischemic further divided into thrombotic and embolic
• "Time is brain": thrombolysis window is 4.5 hours (IV tPA) and 24 hours (mechanical thrombectomy)
• NIH Stroke Scale (NIHSS) is primary severity/outcome predictor; score >25 = high mortality risk
• Stroke syndromes follow vascular territories: MCA, ACA, PCA, vertebrobasilar
• Transient ischemic attack (TIA) = stroke symptoms that resolve <24 hours (typically minutes to hours)

1. 1.Assuming all strokes need immediate imaging before tPA: CT head rules out hemorrhage, but do NOT delay thrombolytics—door-to-needle goal is <60 minutes. Minor symptoms or improving deficits are NOT absolute contraindications.
2. 2.Confusing TIA with stroke: TIA has identical presentation but complete resolution <24 hours; carries high recurrence risk (10% within 90 days) and requires urgent workup and antiplatelet therapy; do NOT delay imaging/carotid studies.
3. 3.Missing contraindications to thrombolytics: Recent surgery, active bleeding, INR >1.7, platelet count <100k, severe hyperglycemia (>400), and symptom onset >4.5 hrs are key exclusions; also exclude hemorrhagic stroke before giving tPA.

Ischemic Stroke

• IV thrombolysis: Alteplase (tPA) 0.9 mg/kg IV bolus within 4.5 hours (0.9 mg/kg, max 90 mg)
• Mechanical thrombectomy: For large vessel occlusion (MCA, ICA, basilar) up to 24 hours if appropriate imaging selection criteria met
• Dual antiplatelet therapy (aspirin + clopidogrel) OR anticoagulation (if cardioembolic)
• Blood pressure management: Permissive hypertension (keep SBP <220 mmHg unless on thrombolytics)

Hemorrhagic Stroke

• Aggressive BP control: Target SBP 140 mmHg (reverse coagulopathy if needed)
• Reverse anticoagulation: FFP/PCC for warfarin; idarucizumab for dabigatran
• Supportive care: Airway protection, ICU monitoring, DVT