Acute Stroke & Intracranial Hemorrhage

Because the primary motor (precentral gyrus) and somatosensory (postcentral gyrus) cortices are organized somatotopically along the cerebral convexity and interhemispheric fissure, the pattern of weakness immediately identifies the occluded cerebral artery: Middle Cerebral Artery (MCA) occlusion infarcts the lateral convexity, causing contralateral face and upper extremity > lower extremity weakness and sensory loss, contralateral homonymous hemianopia (or superior/inferior quadrantanopia), and gaze preference toward the side of the cortical lesion; dominant (left) MCA strokes cause Broca (superior division) or Wernicke (inferior division) aphasia, whereas non-dominant (right) MCA strokes cause contralateral hemispatial neglect and anosognosia. Anterior Cerebral Artery (ACA) occlusion infarcts the medial paracentral lobule, causing contralateral lower extremity > upper extremity weakness/sensory loss, abulia (akinetic mutism), and urinary incontinence. Posterior Cerebral Artery (PCA) occlusion infarcts the occipital cortex, causing contralateral homonymous hemianopia with macular sparing (dual MCA/PCA blood supply to the occipital pole); dominant left PCA splenium extension causes alexia without agraphia. Global hypoperfusion (cardiac arrest, severe hypotension) causes ACA-MCA cortical watershed infarcts presenting with proximal shoulder and hip weakness ('man-in-a-barrel syndrome').

Chronic hypertension and diabetes mellitus induce lipohyalinosis and microatheroma of small deep penetrating arteries (50–400 microns), causing small (<15 mm) subcortical lacunar infarcts characterized by the absence of cortical signs (no aphasia, no neglect, no visual field cut): (1) Posterior limb of the Internal Capsule (lenticulostriate branches of MCA) → Pure Motor Hemiparesis affecting contralateral face, arm, and leg equally; (2) Ventroposterolateral (VPL) Thalamus (thalamoperforating branches of PCA) → Pure Sensory Stroke (followed weeks later by Dejerine-Roussy thalamic pain syndrome); (3) Anterior limb of Internal Capsule / Pons → Ataxic Hemiparesis or Dysarthria-Clumsy Hand Syndrome. In the posterior circulation, brainstem strokes produce 'crossed findings' (ipsilateral cranial nerve palsy + contralateral body tract deficit): Lateral Medullary (Wallenberg) Syndrome (PICA / vertebral artery occlusion) injures the nucleus ambiguus (CN IX/X → hoarseness, dysphagia, loss of gag reflex), vestibular nuclei (vertigo/nystagmus), inferior cerebellar peduncle (ipsilateral ataxia), descending sympathetics (ipsilateral Horner syndrome), spinal trigeminal nucleus (ipsilateral facial pain/temperature loss), and spinothalamic tract (contralateral body pain/temperature loss), while sparing the medial pyramid (no motor weakness).

In any patient presenting with acute focal neurological deficits, the immediate first step is a Non-Contrast Head CT (plus fingerstick blood glucose, as hypoglycemia is the #1 metabolic stroke mimic) to exclude intracerebral or subarachnoid hemorrhage. Once hemorrhage is ruled out, intravenous Alteplase (tPA, 0.9 mg/kg, max 90 mg; 10% bolus over 1 minute, 90% over 60 minutes) or Tenecteplase (TNK, 0.25 mg/kg single bolus) is indicated within 3.0 to 4.5 hours of 'last known normal'. Blood pressure management depends strictly on thrombolytic eligibility: for tPA candidates, BP must be lowered gently with IV Labetalol, Nicardipine, or Clevidipine to <185/110 mmHg before starting tPA and maintained <180/105 mmHg for 24 hours after tPA; for non-tPA candidates, maintain permissive hypertension up to 220/120 mmHg for the first 24–48 hours to preserve collateral perfusion to the ischemic penumbra! Absolute tPA contraindications include prior intracranial hemorrhage, ischemic stroke or severe head trauma within 3 months, active internal bleeding, platelets <100,000/μL, INR >1.7, or therapeutic DOAC use within 48 hours.

Patients with an acute Large Vessel Occlusion (LVO) of the proximal anterior circulation (Internal Carotid Artery or M1/M2 Middle Cerebral Artery) or basilar artery confirmed on CT Angiography (CTA) must be evaluated immediately for Endovascular Mechanical Thrombectomy (stent-retriever or aspiration)—even if they have already received IV tPA (do NOT delay tPA to wait for CTA or thrombectomy!). Within 0 to 6 hours of symptom onset, mechanical thrombectomy is indicated for all eligible anterior LVO patients (NIHSS ≥6, ASPECTS ≥6); between 6 and 24 hours from last known normal (including 'wake-up strokes'), mechanical thrombectomy is indicated when CT Perfusion or Diffusion-Perfusion MRI (DAWN and DEFUSE-3 criteria) demonstrates a small core infarct with a large salvageable ischemic penumbra. Long-term secondary prevention targets the etiology: high-intensity Atorvastatin (80 mg) or Rosuvastatin (20–40 mg), antiplatelet therapy (Aspirin + Clopidogrel dual antiplatelet therapy [DAPT] for 21–90 days after minor stroke [NIHSS ≤3] or high-risk TIA [ABCD² ≥4], followed by monotherapy; note: hold aspirin for 24 hours after IV tPA!), DOAC anticoagulation (apixaban/rivaroxaban) if atrial fibrillation is detected, and Carotid Endarterectomy (CEA) within 2 weeks for symptomatic 70%–99% internal carotid stenosis.

Every brainstem vascular syndrome on COMLEX and USMLE can be solved in seconds using the Brainstem Rule of 4s: (1) There are 4 Cranial Nerves in the Medulla (CN IX, X, XI, XII), 4 in the Pons (CN V, VI, VII, VIII), and 4 above the Pons (CN I, II in forebrain; CN III, IV in midbrain). (2) The 4 Midline (Medial) 'M' structures supplied by paramedian branches (Anterior Spinal Artery in medulla, Basilar paramedian branches in pons, PCA in midbrain) all begin with the letter M: Motor pathway (corticospinal tract → contralateral hemiparesis), Medial Lemniscus (dorsal column pathway → contralateral loss of vibration/proprioception), Medial Longitudinal Fasciculus (MLF → ipsilateral internuclear ophthalmoplegia), and Motor Cranial Nerve nuclei that divide evenly into 12 (CN III, IV, VI, and XII; note that CN V, VII, IX, X, XI are lateral!). (3) The 4 Side (Lateral) 'S' structures supplied by circumferential arteries (PICA, AICA, SCA) all begin with S: Spinocerebellar peduncles (ipsilateral ataxia), Spinothalamic tract (contralateral body pain/temperature loss), Sensory nucleus of CN V (ipsilateral facial pain/temperature loss), and Sympathetic descending pathway (ipsilateral Horner syndrome).

Lacunar strokes are small (< 15 mm) subcortical cavitary infarcts caused by chronic systemic hypertension and diabetes mellitus inducing lipohyalinosis and fibrinoid necrosis of small penetrating arteries (lenticulostriate branches of the MCA, thalamoperforating branches of the PCA, and paramedian branches of the basilar artery). Because the cerebral cortex is completely spared, lacunar strokes NEVER present with aphasia, hemineglect, apraxia, or visual field deficits. Memorize the four classic board syndromes: (1) Posterior Limb of the Internal Capsule (or basis pontis) → Pure Motor Hemiparesis (equal weakness of contralateral face, arm, and leg without sensory or cortical signs; #1 lacunar stroke); (2) Ventral Posterolateral (VPL) / VPM Nucleus of the Thalamus → Pure Sensory Stroke (contralateral hemisensory numbness/paresthesias; may evolve weeks later into excruciating Dejerine-Roussy thalamic pain syndrome); (3) Anterior Limb of Internal Capsule / Pons → Ataxic Hemiparesis or Dysarthria-Clumsy Hand Syndrome; and (4) Subthalamic Nucleus → Contralateral Hemiballismus (wild flinging movements).

Two non-atherothrombotic ischemic stroke mechanisms frequently appear in younger or critically ill patients: (1) Cortical Watershed (Border-Zone) Infarcts occur following severe global cerebral hypoperfusion (cardiac arrest, prolonged septic/hemorrhagic shock, carotid surgery). Infarction develops at the vulnerable distal border zones between the ACA-MCA territories (parasagittal cortex) and MCA-PCA territories, producing 'Man-in-a-Barrel' syndrome—bilateral proximal upper and lower extremity weakness (shoulder/hip girdle) with spared face, hands, and feet. (2) Internal Carotid or Vertebral Artery Dissection is a leading cause of stroke in adults < 45 years old, triggered by minor neck trauma, chiropractic cervical manipulation, yoga, violent coughing/vomiting, or connective tissue disorders (Marfan, Ehlers-Danlos, fibromuscular dysplasia). Internal Carotid Dissection presents with unilateral head/neck pain, ipsilateral partial Horner syndrome (ptosis and miosis WITHOUT anhidrosis, because sweat fibers travel along the external carotid artery), and contralateral MCA ischemia or ipsilateral amaurosis fugax. Confirm with CTA or MRA of the neck ('string sign' or crescentic intramural hematoma) and treat with antiplatelet therapy or anticoagulation.

Although diffusion-weighted MRI (DWI) is the most sensitive imaging modality for detecting hyperacute cerebral ischemia within minutes, Non-Contrast Head CT is the universal first-line emergency test because it can be completed in < 2 minutes and has near-100% sensitivity for excluding acute intracranial hemorrhage. During the first 6 hours of an ischemic stroke, the non-contrast head CT is typically normal (or shows subtle early signs: hyperdense MCA sign from intraluminal thrombus, loss of gray-white differentiation in the basal ganglia/insular ribbon, or sulcal effacement), whereas acute hemorrhage appears immediately bright white (hyperdense). If the CT shows no hemorrhage and the patient is within 4.5 hours of LKN with no contraindications, administer IV Alteplase (0.9 mg/kg, max 90 mg; 10% bolus over 1 min, 90% over 60 min) or a single IV bolus of Tenecteplase (0.25 mg/kg). Strict Rule: Do NOT administer aspirin, clopidogrel, heparin, or DOACs, and avoid placing nasogastric tubes or Foley catheters, for 24 hours after tPA until a 24-hour follow-up head CT rules out hemorrhagic conversion.

Blood pressure management in acute ischemic stroke is one of the most heavily tested board algorithms. Surrounding the irreversibly infarcted core (where cerebral blood flow is < 10 mL/100g/min) lies the ischemic penumbra—viable, stunned tissue perfused by leptomeningeal collaterals whose blood vessels have lost cerebral autoregulation. Because perfusion of the penumbra depends directly on systemic Mean Arterial Pressure (MAP) (Cerebral Perfusion Pressure [CPP] = MAP − ICP), lowering blood pressure precipitously infarcts the penumbra. Therefore: (1) If the patient IS receiving IV tPA/Tenecteplase: Blood pressure MUST be lowered gently to < 185/110 mmHg prior to starting the thrombolytic using IV Labetalol (10–20 mg) or IV Nicardipine infusion, and strictly maintained at < 180/105 mmHg for the first 24 hours after tPA to prevent catastrophic hemorrhagic transformation. (2) If the patient is NOT receiving tPA: Practice Permissive Hypertension—do NOT treat blood pressure unless SBP > 220 mmHg or DBP > 120 mmHg (if > 220/120, lower MAP cautiously by only 15% over the first 24 hours).

IV thrombolytics frequently fail to recanalize large proximal thrombi occluding the distal Internal Carotid Artery (ICA) or proximal M1 segment of the Middle Cerebral Artery. Endovascular Mechanical Thrombectomy (EVT) using a stent-retriever or aspiration catheter is indicated up to 6 hours from LKN for all patients with an anterior circulation Large Vessel Occlusion (LVO) and disabling deficit (NIHSS ≥ 6). Furthermore, based on the landmark DAWN and DEFUSE-3 trials, the window for mechanical thrombectomy is extended from 6 to 24 hours from Last Known Normal (including 'wake-up strokes'!) if CT Perfusion (CTP) or Diffusion/Perfusion MRI demonstrates a favorable core-penumbra mismatch (a small irreversibly infarcted core volume surrounded by a large volume of critically hypoperfused, salvageable penumbra tissue).

The ABCD² score stratifies 48-hour stroke risk after a TIA across 5 clinical variables (total 0–7 points): (1) Age ≥ 60 years (1 pt), (2) Blood pressure ≥ 140/90 mmHg on presentation (1 pt), (3) Clinical features: unilateral motor weakness (2 pts) or speech impairment without weakness (1 pt), (4) Duration: ≥ 60 minutes (2 pts) or 10–59 minutes (1 pt), and (5) Diabetes mellitus (1 pt). Patients with an ABCD² score ≥ 4 (or crescendo TIAs, known carotid stenosis, or atrial fibrillation) require immediate 21-day Dual Antiplatelet Therapy (Aspirin + Clopidogrel) and urgent diagnostic evaluation within 24 hours: (1) Brain MRI with DWI (or CT), (2) Non-invasive Cervical & Intracranial Vascular Imaging (Carotid Duplex Ultrasound, CTA, or MRA), (3) 12-lead ECG and continuous cardiac telemetry / 30-day ambulatory Holter monitor (to detect occult paroxysmal atrial fibrillation), (4) Transthoracic Echocardiogram (TTE) (or TEE if young/cryptogenic), and (5) Fasting lipid panel and HbA_1c.

Based on the landmark NASCET trial, surgical Carotid Endarterectomy (CEA)—performed ideally within 2 weeks of an ipsilateral hemispheric TIA, non-disabling stroke, or retinal amaurosis fugax—dramatically reduces 5-year stroke risk in patients with 70% to 99% symptomatic internal carotid artery stenosis (and offers moderate benefit in 50–69% symptomatic stenosis, particularly in men). CEA is not indicated for < 50% stenosis and is strictly contraindicated in 100% complete carotid occlusion. For asymptomatic carotid stenosis (≥ 70–80%), intensive medical therapy (aspirin, atorvastatin 80 mg, BP control) is primary, though CEA may be considered if perioperative stroke/death risk is < 3%. Board exams frequently test iatrogenic cranial nerve injuries during CEA dissection in the carotid triangle: (1) Hypoglossal nerve (CN XII — #1 most commonly injured nerve) → tongue deviates ipsilaterally toward the side of surgery; (2) Vagus / Recurrent Laryngeal nerve (CN X) → hoarse voice/vocal cord paralysis; (3) Marginal Mandibular branch of Facial nerve (CN VII) → asymmetric smile (drooping ipsilateral lower lip); and (4) Glossopharyngeal nerve (CN IX) / Carotid Sinus nerve of Hering → labile postoperative blood pressure.

Students frequently confuse coronary antiplatelet rules (where DAPT is given for 12 months) with cerebrovascular rules. In non-cardioembolic ischemic stroke or TIA, short-term DAPT (Aspirin 81 mg + Clopidogrel 75 mg) is given for ONLY 21 days in patients presenting within 24–72 hours of a minor stroke (NIHSS ≤ 3) or high-risk TIA (ABCD² ≥ 4) (or for 90 days in severe 70–99% intracranial large-artery atherosclerosis). Beyond 21 to 90 days, continuing DAPT long-term (MATCH, CHARISMA, SPS3 trials) does NOT further reduce recurrent stroke and significantly increases fatal intracranial hemorrhage! After completing the 21-day DAPT course, step down to lifelong single antiplatelet monotherapy (either Clopidogrel 75 mg daily, Aspirin 81–325 mg daily, or Aspirin + Extended-Release Dipyridamole). Furthermore, if a patient has Atrial Fibrillation, antiplatelet therapy is grossly inadequate—they require lifelong oral anticoagulation with a DOAC (apixaban, rivaroxaban, dabigatran) or Warfarin.

Board vignettes allow pinpoint localization of hypertensive intraparenchymal hemorrhages based on eye movements and motor signs: (1) Putamen / External Capsule (#1 most common site, 50% — lenticulostriate arteries): compresses the adjacent posterior limb of the internal capsule, causing contralateral hemiplegia, hemisensory loss, and conjugate gaze deviation TOWARD the side of the hemorrhage; (2) Thalamus (thalamoperforating arteries): causes profound contralateral hemisensory loss, hemiparesis, and vertical gaze palsy with eyes forced downward and inward ('peering at the tip of the nose') and small nonreactive pupils; (3) Pons (basilar paramedian perforators): causes rapid deep coma within minutes, quadriplegia/decerebrate posturing, absent horizontal doll's eyes, and classic 'pinpoint' (1 mm) reactive pupils (destruction of descending sympathetic tracts with intact midbrain Edinger-Westphal); and (4) Cerebellum (superior/anterior/posterior inferior cerebellar arteries): presents with sudden occipital headache, repeated vomiting, vertigo, truncal/limb ataxia, and inability to stand or walk (initially WITHOUT hemiparesis!). Because a cerebellar hematoma sits in the tight posterior fossa, it rapidly compresses the 4th ventricle (causing acute obstructive hydrocephalus) and brainstem (tonsillar herniation)—making emergent surgical suboccipital decompression mandatory for cerebellar hemorrhage > 3 cm.

After surviving the initial rupture of a saccular berry aneurysm, patients with Subarachnoid Hemorrhage face three time-specific inpatient complications: (1) Rebleeding (peaks within the first 24 hours) carries a > 50% mortality and is prevented by lowering SBP < 160 mmHg (with IV nicardipine or labetalol) and performing early endovascular coiling or surgical microclipping within 24–72 hours; (2) Delayed Cerebral Ischemia / Arterial Vasospasm (occurs between Days 3 and 14, peaking at Days 7–10) is triggered by oxyhemoglobin and inflammatory breakdown products of subarachnoid blood irritating the exterior of Circle of Willis arteries, presenting with new focal deficits or decline in mentation (detected by Transcranial Doppler ultrasound showing elevated MCA velocities > 120–200 cm/s). Prevent vasospasm in ALL SAH patients by starting Oral Nimodipine (60 mg q4h for 21 days) on day 1; if symptomatic vasospasm develops after aneurysm securing, treat with induced hypertension (norepinephrine/phenylephrine) and euvolemia; and (3) Hyponatremia from either SIADH (euvolemic → fluid restriction) or Cerebral Salt Wasting (hypovolemic from BNP release → isotonic/hypertonic saline volume replacement; never restrict fluids in SAH as hypovolemia precipitates vasospasm!).

Compare the two extra-axial traumatic hematomas: Epidural Hematoma (EDH) results from a skull fracture across the thin pterion (junction of frontal, parietal, temporal, and sphenoid bones) lacerating the high-pressure Middle Meningeal Artery. Arterial blood strips the periosteal layer of the dura away from the inner table of the calvarium, forming a biconvex (lens-shaped) hyperdensity that cannot cross suture lines where the periosteal dura is tightly anchored. Expanding temporal mass effect pushes the medial temporal lobe (uncus) across the tentorial incisura (uncal herniation), compressing the ipsilateral Oculomotor nerve (CN III → blown dilated pupil first, then 'down and out' palsy), the ipsilateral cerebral peduncle (contralateral hemiparesis), and the Posterior Cerebral Artery (contralateral homonymous hemianopsia) before Duret brainstem hemorrhages occur. Subdural Hematoma (SDH) results from venous bleeding of cortical bridging veins into the potential space beneath the meningeal dura, forming a crescent-shaped hematoma that freely crosses suture lines along the entire hemisphere (stopping only at the midline falx cerebri).