# Seminar 02: Stroke and Cerebrovascular Disease ## Year 3: Neurology Clerkship --- ## Learning Objectives By the end of this seminar, students will be able to: 1. Classify stroke by mechanism (ischemic vs hemorrhagic) 2. Recognize stroke syndromes by vascular territory 3. Apply acute stroke evaluation and management protocols 4. Identify candidates for thrombolysis and thrombectomy 5. Manage secondary stroke prevention 6. Recognize stroke mimics and transient ischemic attacks --- ## Seminar Outline ### I. Stroke Overview Stroke represents a leading cause of death and disability worldwide, with profound implications for patients, families, and healthcare systems. In the United States, stroke ranks as the fifth leading cause of death, with approximately 795,000 strokes occurring annually. The vast majority of strokes, comprising roughly 87 percent, are ischemic in nature and result from arterial occlusion, while the remaining 13 percent are hemorrhagic, divided between intracerebral hemorrhage and subarachnoid hemorrhage. Stroke remains the leading cause of long-term disability in adults, emphasizing the critical importance of prevention, rapid recognition, and effective acute treatment to minimize lasting neurological impairment. Risk factor identification and modification form the cornerstone of primary stroke prevention. Hypertension stands as the single most important modifiable risk factor, with blood pressure control dramatically reducing stroke incidence. Diabetes mellitus increases stroke risk through accelerated atherosclerosis and small vessel disease, while hyperlipidemia contributes to large artery atherosclerosis. Atrial fibrillation represents a potent risk factor for cardioembolic stroke, with anticoagulation providing substantial risk reduction. Smoking cessation, weight management, regular physical activity, and moderation of alcohol intake all contribute to stroke prevention. Non-modifiable risk factors include advancing age, male sex, African American race, family history of stroke, and personal history of prior stroke or transient ischemic attack. Ischemic stroke classification by mechanism guides both acute treatment and secondary prevention strategies. Large vessel atherosclerosis from stenosis greater than 50 percent or unstable plaque accounts for a significant proportion of strokes and may warrant carotid revascularization. Cardioembolism from atrial fibrillation, valvular heart disease, or recent myocardial infarction with wall motion abnormality requires anticoagulation for prevention. Small vessel occlusion or lacunar stroke results from lipohyalinosis of penetrating arteries and produces characteristic clinical syndromes. Other determined etiologies include arterial dissection, hypercoagulable states, and vasculitis. Cryptogenic stroke, where the mechanism remains unknown despite thorough evaluation, comprises a substantial proportion of cases and increasingly prompts extended cardiac monitoring to detect occult atrial fibrillation. The concept of "time is brain" encapsulates the urgency of acute stroke treatment and drives modern stroke care systems. The ischemic penumbra represents potentially salvageable brain tissue surrounding the irreversibly damaged core, and this tissue remains viable only for a limited time window. Studies demonstrate that approximately 1.9 million neurons are lost per minute during acute ischemic stroke, emphasizing the critical importance of minimizing time to treatment. This biological reality drives the development of stroke systems of care designed to rapidly identify stroke patients, transport them to capable facilities, and deliver time-sensitive treatments. Every minute saved in the stroke treatment chain translates to improved outcomes and reduced disability. Panel A: Stroke epidemiology showing incidence, mortality rates, and proportion of ischemic versus hemorrhagic types. Panel B: Modifiable and non-modifiable risk factors with relative risk contributions and prevention strategies. Panel C: Ischemic stroke classification by mechanism with TOAST criteria and implications for management. Panel D: Time is brain concept illustrating penumbra evolution, neuronal loss per minute, and treatment time windows. --- ### II. Stroke Syndromes by Vascular Territory Anterior circulation strokes arise from occlusion of the internal carotid artery or its branches and produce characteristic clinical syndromes based on the affected territory. Anterior cerebral artery strokes cause contralateral leg weakness greater than arm weakness due to the medial motor homunculus distribution, along with abulia, urinary incontinence from frontal lobe involvement, and alien limb phenomenon when the corpus callosum is affected. Superior division middle cerebral artery strokes produce contralateral face and arm weakness greater than leg, with Broca aphasia in dominant hemisphere lesions manifesting as nonfluent speech with preserved comprehension. Inferior division middle cerebral artery strokes cause Wernicke aphasia in dominant hemisphere lesions with fluent but meaningless speech and impaired comprehension, while non-dominant lesions produce hemispatial neglect. Complete middle cerebral artery occlusion produces devastating deficits including hemiplegia, hemianesthesia, homonymous hemianopia, gaze preference toward the lesion, and global aphasia or profound neglect. Posterior circulation strokes involve the vertebrobasilar system and produce syndromes reflecting brainstem, cerebellar, and occipital lobe dysfunction. Posterior cerebral artery strokes cause contralateral homonymous hemianopia from occipital lobe infarction, often with macular sparing due to dual blood supply, and may produce memory impairment from hippocampal involvement. Top of the basilar syndrome results from rostral brainstem and thalamic ischemia, causing visual symptoms, behavioral changes, and somnolence. Complete basilar artery occlusion is catastrophic, potentially causing quadriplegia, cranial nerve palsies, coma, and death, though locked-in syndrome with preserved consciousness but only vertical eye movement may occur. Cerebellar strokes cause vertigo, nausea, ataxia, and nystagmus, and carry significant risk of posterior fossa swelling with brainstem compression requiring close monitoring. Lacunar syndromes result from small vessel disease affecting penetrating arteries and produce distinctive clinical patterns without cortical signs. Pure motor hemiparesis causes weakness of face, arm, and leg without sensory loss, typically localizing to the posterior limb of the internal capsule or basis pontis. Pure sensory stroke produces hemisensory loss without motor deficits, indicating thalamic lacunar infarction. Ataxic hemiparesis combines weakness with ipsilateral ataxia out of proportion to weakness, often from pontine or internal capsule lacunes. Dysarthria-clumsy hand syndrome causes slurred speech and impaired hand coordination, typically from pontine lesions. Sensorimotor stroke affecting both motor and sensory function suggests thalamocapsular location. The absence of cortical signs such as aphasia, neglect, and visual field deficits characterizes these syndromes. Brainstem stroke syndromes produce classic patterns of crossed findings with ipsilateral cranial nerve deficits and contralateral body weakness or sensory loss. Wallenberg syndrome, or lateral medullary syndrome from posterior inferior cerebellar artery territory infarction, causes ipsilateral facial pain and temperature loss, Horner syndrome, cerebellar ataxia, and dysphagia with contralateral body pain and temperature loss. Medial medullary syndrome produces ipsilateral tongue weakness with contralateral hemiparesis from pyramidal tract involvement. Weber syndrome from midbrain infarction causes ipsilateral third nerve palsy with contralateral hemiparesis. Locked-in syndrome from ventral pontine infarction produces quadriplegia and anarthria with preserved consciousness, allowing communication only through vertical eye movements and blinking, and must be distinguished from coma. Panel A: Anterior circulation territories with ACA, MCA superior and inferior divisions, and corresponding clinical syndromes. Panel B: Posterior circulation anatomy showing PCA, basilar artery, and cerebellar arteries with associated stroke syndromes. Panel C: Lacunar syndrome classification with lesion locations, clinical features, and absence of cortical signs. Panel D: Classic brainstem syndromes including Wallenberg, medial medullary, Weber, and locked-in syndrome with anatomic correlations. --- ### III. Acute Stroke Assessment Rapid and systematic evaluation is essential when a patient presents with suspected stroke, as treatment options are time-limited. Initial assessment follows the ABC paradigm to ensure airway patency, adequate breathing, and circulatory stability before proceeding with neurological evaluation. Glucose must be checked immediately, as hypoglycemia can mimic stroke and is readily correctable, while hyperglycemia worsens stroke outcomes and requires management. Establishing the last known well time is critical for determining eligibility for time-sensitive therapies. The NIH Stroke Scale provides a standardized, reproducible measure of stroke severity that guides treatment decisions and predicts outcomes. Emergent non-contrast CT of the head is the first imaging priority to exclude hemorrhage before thrombolysis. The NIH Stroke Scale quantifies stroke severity across multiple domains and ranges from 0 to 42 points. Level of consciousness is assessed through responsiveness, orientation questions, and command following. Gaze evaluates horizontal eye movements, while visual fields are tested by confrontation. Facial palsy, motor strength in arms and legs, limb ataxia, and sensory function are systematically assessed. Language evaluation includes naming, comprehension, and description of a picture. Dysarthria is graded based on speech clarity, and extinction and inattention are tested through simultaneous bilateral stimulation. Each component receives a score, with the total providing a severity measure where higher scores indicate more severe strokes. An NIHSS of 0-4 indicates minor stroke, 5-15 moderate stroke, 16-20 moderate to severe, and greater than 20 severe stroke. Imaging plays a central role in acute stroke evaluation, with different modalities providing complementary information. Non-contrast CT is obtained first to exclude hemorrhage, which is an absolute contraindication to thrombolysis, and may show early ischemic changes such as loss of gray-white differentiation or sulcal effacement. CT angiography identifies large vessel occlusions amenable to mechanical thrombectomy and assesses the intracranial and extracranial circulation. CT perfusion evaluates the ischemic core versus penumbra mismatch, which is particularly valuable for extended time window thrombectomy decisions. MRI with diffusion-weighted imaging is the most sensitive modality for detecting acute ischemia, showing restricted diffusion within minutes of onset. MR angiography provides vessel imaging without contrast, and MR perfusion can assess tissue at risk. Stroke mimics account for a significant proportion of patients presenting with stroke-like symptoms and must be considered in the differential diagnosis. Hypoglycemia causes focal neurological deficits that resolve with glucose correction and should always be excluded early. Postictal Todd paralysis following seizure produces transient focal weakness that typically resolves within hours. Migraine with aura can cause neurological symptoms including hemiparesis and visual disturbance, typically with headache and gradual symptom evolution. Conversion disorder produces neurologically inconsistent findings and may be suggested by variable weakness, give-way quality, and intact reflexes. Brain tumors cause subacute progressive deficits rather than acute onset and do not follow vascular territories. Recognition of mimics prevents unnecessary thrombolysis while ensuring true strokes receive timely treatment. Panel A: Acute stroke assessment protocol with ABCs, glucose check, last known well time, and NIHSS components. Panel B: NIH Stroke Scale scoring breakdown by domain with severity classifications and prognostic implications. Panel C: Stroke imaging algorithm showing CT, CTA, CT perfusion, and MRI roles with timing and indications. Panel D: Common stroke mimics with distinguishing clinical features and evaluation approach. --- ### IV. Acute Ischemic Stroke Treatment Intravenous thrombolysis with alteplase or tenecteplase remains the cornerstone of acute ischemic stroke treatment when administered within the appropriate time window to eligible patients. Alteplase is dosed at 0.9 mg per kilogram with a maximum of 90 mg, with 10 percent given as a bolus and the remainder infused over 60 minutes. Tenecteplase offers the advantage of single bolus dosing and is increasingly used. Treatment must be initiated within 4.5 hours of the last known well time, with earlier treatment associated with better outcomes. Blood pressure must be below 185/110 mmHg before thrombolysis and maintained below 180/105 mmHg for the subsequent 24 hours. The clinical deficit should be measurable on the NIH Stroke Scale, as thrombolysis carries risk that must be balanced against expected benefit. Numerous contraindications to thrombolysis must be considered before treatment. Absolute contraindications include hemorrhage on CT, recent major surgery within 14 days, prior intracranial hemorrhage, intracranial neoplasm or arteriovenous malformation, active internal bleeding, and severe uncontrolled hypertension despite treatment. Relative contraindications include minor or rapidly improving symptoms, though rapidly improving symptoms that remain disabling warrant treatment. Recent gastrointestinal or genitourinary bleeding, pregnancy, seizure at stroke onset, recent lumbar puncture or arterial puncture, international normalized ratio greater than 1.7, platelet count below 100,000, or recent use of direct oral anticoagulants require careful consideration and may preclude treatment in certain circumstances. Mechanical thrombectomy has revolutionized treatment of acute ischemic stroke from large vessel occlusion, with multiple randomized trials demonstrating dramatic benefit. The treatment window extends to 24 hours in selected patients based on imaging evidence of salvageable tissue. Eligible patients typically have large vessel occlusion of the internal carotid artery terminus or proximal middle cerebral artery, NIHSS score of 6 or greater, and favorable imaging profile with small core and large penumbra on CT perfusion. The DAWN and DEFUSE 3 trials established the benefit of thrombectomy in the extended time window for patients with clinical-core mismatch. Thrombectomy should be pursued in addition to rather than instead of intravenous thrombolysis when both are indicated, as combined therapy offers the best outcomes. Post-thrombolysis care requires intensive monitoring to detect complications and optimize outcomes. Neurological examination should be repeated every 15 minutes for the first 2 hours, then every 30 minutes for the next 6 hours, and then hourly for the remainder of the first 24 hours. Blood pressure must be maintained below 180/105 mmHg, with treatment for elevation and avoidance of excessive reduction. Anticoagulation and antiplatelet therapy are held for 24 hours post-thrombolysis. A follow-up CT should be obtained at 24 hours or sooner if clinical deterioration occurs. Symptomatic intracranial hemorrhage complicates approximately 6 percent of cases and requires immediate cessation of thrombolysis infusion, emergent CT imaging, reversal of fibrinolysis, and supportive care. Panel A: Intravenous thrombolysis protocol with alteplase and tenecteplase dosing, time windows, and blood pressure targets. Panel B: Absolute and relative contraindications to thrombolysis organized by system with clinical decision considerations. Panel C: Mechanical thrombectomy eligibility criteria including imaging features, NIHSS thresholds, and extended window selection. Panel D: Post-thrombolysis monitoring schedule with nursing assessments, blood pressure management, and hemorrhage recognition. --- ### V. Hemorrhagic Stroke Intracerebral hemorrhage accounts for approximately 10-15 percent of all strokes and carries higher mortality and morbidity than ischemic stroke. Hypertension is the most common cause, with characteristic locations in the basal ganglia, thalamus, pons, and cerebellum where penetrating arteries are subject to lipohyalinosis. Cerebral amyloid angiopathy primarily affects elderly patients and causes lobar hemorrhages that may recur, with MRI showing evidence of prior microhemorrhages. Arteriovenous malformations present with hemorrhage in younger patients and require specialized vascular evaluation. Anticoagulation-associated hemorrhage may occur at any location and requires urgent reversal. Underlying tumors may bleed and should be considered, particularly with atypical locations or surrounding edema disproportionate to hemorrhage age. Management of intracerebral hemorrhage focuses on preventing hematoma expansion, managing intracranial pressure, and preventing complications. Blood pressure reduction is a key intervention, with a target systolic pressure below 140 mmHg if the patient presents with systolic pressure below 220 mmHg, though aggressive reduction should be avoided if intracranial pressure is elevated. Anticoagulation must be rapidly reversed using vitamin K and prothrombin complex concentrate for warfarin or specific reversal agents for direct oral anticoagulants including idarucizumab for dabigatran and andexanet alfa for factor Xa inhibitors. Intracranial pressure management includes head elevation, osmotic therapy, and consideration of surgical decompression. Fever, hyperglycemia, and seizures should be treated aggressively to prevent secondary injury. Subarachnoid hemorrhage results most commonly from rupture of an intracranial aneurysm and presents with sudden severe headache described as the worst of the patient's life. The headache reaches maximum intensity within minutes and is often accompanied by nausea, vomiting, photophobia, and neck stiffness from meningeal irritation. Altered consciousness occurs in severe cases. CT sensitivity for subarachnoid hemorrhage is approximately 95 percent in the first 6 hours but decreases over time, making lumbar puncture necessary to exclude the diagnosis when CT is negative but clinical suspicion remains high. Xanthochromia, the yellowish discoloration of cerebrospinal fluid from hemoglobin breakdown, indicates subarachnoid blood and distinguishes true hemorrhage from traumatic tap. The Hunt-Hess scale grades clinical severity and predicts prognosis. Subarachnoid hemorrhage complications require intensive monitoring and management in the days to weeks following the initial event. Rebleeding is the most immediate concern and carries high mortality, making early aneurysm securing through surgical clipping or endovascular coiling the treatment priority. Vasospasm develops between days 3 and 14 and causes delayed cerebral ischemia manifesting as new focal deficits or declining consciousness; nimodipine is administered prophylactically, and euvolemia is maintained. Hydrocephalus may develop acutely requiring external ventricular drainage or later requiring permanent ventriculoperitoneal shunting. Hyponatremia occurs commonly from syndrome of inappropriate antidiuretic hormone secretion or cerebral salt wasting and requires careful differentiation to guide fluid management. Seizures may occur and may warrant prophylaxis, though routine long-term prophylaxis is not indicated. Panel A: Intracerebral hemorrhage locations and causes including hypertensive, amyloid angiopathy, AVM, and anticoagulation-associated. Panel B: ICH management algorithm with blood pressure targets, anticoagulation reversal agents, and ICP interventions. Panel C: Subarachnoid hemorrhage presentation with thunderclap headache, CT sensitivity over time, and lumbar puncture interpretation. Panel D: SAH complications timeline showing rebleeding, vasospasm window, hydrocephalus, and hyponatremia with management strategies. --- ### VI. Transient Ischemic Attack Transient ischemic attack represents a medical emergency that demands urgent evaluation and treatment to prevent completed stroke. The classic definition of TIA as focal neurological deficit lasting less than 24 hours has been supplanted by a tissue-based definition requiring absence of infarction on imaging, as many brief symptoms cause permanent ischemic changes. The mechanism of TIA is identical to ischemic stroke, involving transient arterial occlusion from embolism or in situ thrombosis that resolves spontaneously. The significance of TIA lies in its role as a warning of impending stroke, with risk highest in the hours and days immediately following the event. This creates a critical window for intervention to prevent permanent disability. The ABCD2 score provides a validated tool for stratifying stroke risk following TIA and guiding triage decisions. Age 60 or older contributes one point, blood pressure 140/90 mmHg or higher at presentation contributes one point, and clinical features of unilateral weakness add two points while speech disturbance without weakness adds one point. Symptom duration of 60 minutes or longer adds two points, while duration of 10 to 59 minutes adds one point. Diabetes adds one point. The total score ranges from 0 to 7, with higher scores indicating higher short-term stroke risk. However, even low-risk scores do not eliminate the need for urgent evaluation, as treatable etiologies such as high-grade carotid stenosis may be present regardless of score. Evaluation of TIA requires comprehensive assessment to identify the mechanism and guide prevention. MRI with diffusion-weighted imaging should be obtained to determine whether infarction has occurred, reclassifying events with positive imaging as stroke regardless of symptom duration. Vessel imaging with CT angiography or MR angiography evaluates the carotid and intracranial arteries for stenosis or dissection. Cardiac evaluation includes electrocardiogram to detect atrial fibrillation, telemetry monitoring for at least 24 hours, and echocardiography to evaluate for cardiac sources of embolism. Extended cardiac monitoring with implantable loop recorders increases detection of paroxysmal atrial fibrillation. Laboratory evaluation includes lipid panel and hemoglobin A1c to identify treatable risk factors. Management of TIA focuses on immediate risk reduction and long-term prevention. Dual antiplatelet therapy with aspirin and clopidogrel for 21 days provides greater early protection than aspirin alone for high-risk TIA and minor stroke, followed by single antiplatelet therapy. High-intensity statin therapy should be initiated regardless of baseline LDL, as statins provide benefit through pleiotropic effects beyond lipid lowering. Blood pressure control with a target below 130/80 mmHg should be established. Symptomatic carotid stenosis of 70 percent or greater warrants revascularization with endarterectomy or stenting, ideally within 2 weeks of the event when benefit is greatest. Stenosis of 50-69 percent may benefit from revascularization in selected patients. Panel A: TIA definition evolution from time-based to tissue-based criteria with clinical implications. Panel B: ABCD2 score components with point values and risk stratification for 2-day and 7-day stroke risk. Panel C: TIA evaluation protocol including imaging, cardiac workup, and laboratory studies with timing. Panel D: TIA management strategy with antiplatelet selection, statin therapy, blood pressure targets, and carotid revascularization indications. --- ### VII. Secondary Prevention Antiplatelet therapy forms the foundation of secondary prevention for non-cardioembolic ischemic stroke and TIA. Aspirin at doses of 81 to 325 mg daily is the most commonly used first-line agent with proven efficacy. Clopidogrel at 75 mg daily provides an alternative for patients who cannot tolerate aspirin or who have experienced stroke while on aspirin. The combination of aspirin and clopidogrel for 21 days following high-risk TIA or minor stroke provides enhanced early protection, after which therapy should convert to single antiplatelet therapy to minimize bleeding risk. Aspirin combined with extended-release dipyridamole offers another alternative, though gastrointestinal tolerability may be limiting. Antiplatelet selection should consider individual patient factors including prior gastrointestinal bleeding, drug interactions, and cost. Anticoagulation is indicated for secondary prevention when atrial fibrillation or another high-risk cardiac source of embolism is identified. Direct oral anticoagulants including dabigatran, rivaroxaban, apixaban, and edoxaban are preferred over warfarin for non-valvular atrial fibrillation due to superior efficacy, safety, and convenience. Warfarin remains necessary for patients with mechanical heart valves. Left ventricular thrombus may be treated with warfarin or a direct oral anticoagulant depending on clinical context. The timing of anticoagulation initiation after acute stroke requires balancing hemorrhagic transformation risk against recurrent embolism risk, with most guidelines suggesting waiting 2 to 14 days depending on stroke size and hemorrhagic transformation status. Risk factor modification addresses the underlying conditions that promote atherosclerosis and cardiovascular disease. Blood pressure control with a target below 130/80 mmHg significantly reduces recurrent stroke risk, with multiple antihypertensive classes acceptable. Lipid management with high-intensity statin therapy targets LDL cholesterol below 70 mg/dL, with additional agents such as ezetimibe or PCSK9 inhibitors for patients not achieving goal. Diabetes management with target hemoglobin A1c below 7 percent reduces microvascular complications, though cardiovascular benefit is less clearly established. Smoking cessation is essential and reduces stroke risk within years of quitting. Regular physical activity, healthy diet, and weight management provide additional benefit. Carotid revascularization offers substantial benefit for symptomatic high-grade carotid stenosis. Carotid endarterectomy or carotid artery stenting should be performed for symptomatic stenosis of 70 percent or greater, with surgery traditionally preferred when surgical risk is acceptable. Symptomatic stenosis of 50-69 percent may benefit from revascularization in selected patients, with the number needed to treat being higher than for severe stenosis. Timing of intervention is critical, with maximum benefit achieved when revascularization is performed within 2 weeks of the index event; waiting longer diminishes the preventive value as early recurrence risk declines. Asymptomatic carotid stenosis of 70 percent or greater may warrant revascularization if surgical risk is low, though the benefit is smaller than for symptomatic disease. Panel A: Antiplatelet therapy options with dosing, indications for aspirin, clopidogrel, combination therapy, and dipyridamole. Panel B: Anticoagulation selection for cardioembolic stroke showing DOAC versus warfarin indications and timing after stroke. Panel C: Risk factor targets for blood pressure, LDL cholesterol, hemoglobin A1c, and lifestyle modifications with evidence levels. Panel D: Carotid revascularization decision algorithm based on symptom status, stenosis degree, and timing from event. --- ### VIII. Special Stroke Considerations Stroke in young patients requires expanded etiological investigation beyond the typical workup for older patients. Arterial dissection of the carotid or vertebral arteries may result from trauma, neck manipulation, or occur spontaneously, and is detected by MRA with fat saturation sequences or CTA showing intramural hematoma. Patent foramen ovale with paradoxical embolism should be evaluated with bubble echocardiography. Hypercoagulable states including factor V Leiden mutation, protein C or S deficiency, and antiphospholipid syndrome require testing when no other etiology is found. Drug use, particularly cocaine and amphetamines, causes vasospasm and accelerated atherosclerosis. Vasculitis affecting cerebral vessels may be inflammatory or infectious and may require conventional angiography for diagnosis. The finding of cryptogenic stroke in a young patient mandates thorough investigation. Posterior circulation stroke poses unique diagnostic challenges and must be recognized to avoid catastrophic outcomes. Symptoms of vertigo, diplopia, ataxia, and visual disturbance may be attributed to peripheral causes, delaying diagnosis. The HINTS examination distinguishes central from peripheral causes of acute vestibular syndrome, with a central pattern indicating stroke. Horizontal head impulse that is normal rather than abnormal, direction-changing nystagmus, and skew deviation indicate central pathology. Basilar artery occlusion represents a neurological emergency with high mortality, presenting with bilateral motor deficits, bulbar dysfunction, altered consciousness, and pupillary abnormalities. Emergent CTA and consideration of endovascular therapy are warranted when basilar occlusion is suspected. Cerebellar stroke requires vigilant monitoring for posterior fossa swelling and hydrocephalus. The cerebellum is confined within the posterior fossa, and edema following stroke can compress the brainstem, causing rapid clinical deterioration. Patients may present with vertigo, nausea, ataxia, and headache, symptoms that can seem benign initially. Progressive obtundation, new brainstem signs, or respiratory irregularity should prompt immediate imaging and neurosurgical consultation. Decompressive suboccipital craniectomy can be life-saving and should be performed before irreversible brainstem injury occurs. All patients with significant cerebellar stroke warrant ICU-level monitoring during the period of maximum edema risk. Malignant middle cerebral artery syndrome occurs when large MCA territory infarction produces mass effect sufficient to cause herniation. Patients at highest risk are younger with less cerebral atrophy to accommodate swelling, typically with complete MCA occlusion. Edema peaks at 3-5 days post-stroke, during which time close monitoring for declining consciousness and pupillary changes is essential. Hemicraniectomy performed within 48 hours in patients younger than 60 significantly reduces mortality, though survivors may have substantial residual deficits. The decision to proceed with surgery should involve discussions with family about expected outcomes and quality of life considerations, recognizing that survival with disability may or may not align with patient values. Panel A: Young stroke etiologies including dissection, PFO, hypercoagulable states, and drug use with specific testing approaches. Panel B: Posterior circulation stroke recognition with HINTS examination technique and basilar occlusion warning signs. Panel C: Cerebellar stroke monitoring protocol with decompression indications and timing for surgical intervention. Panel D: Malignant MCA syndrome timeline showing edema progression, herniation signs, and hemicraniectomy decision factors. --- ### IX. Stroke Rehabilitation Rehabilitation represents an essential component of comprehensive stroke care that begins in the acute setting and continues throughout recovery. The goals of rehabilitation include maximizing functional independence, preventing secondary complications, and facilitating return to community participation. Physical impairments addressed include hemiparesis through strengthening and motor relearning, spasticity through stretching and pharmacotherapy, and balance and gait dysfunction. Cognitive impairments require evaluation and targeted interventions. Speech and language therapy addresses aphasia through compensatory strategies and restorative approaches. Depression is common following stroke and impairs rehabilitation participation, requiring screening and treatment. The intensity and setting of rehabilitation should match patient needs and tolerance. Multiple therapy disciplines contribute to comprehensive stroke rehabilitation. Physical therapy focuses on mobility, strength, balance, and gait training, helping patients regain the ability to transfer, walk, and navigate their environment safely. Occupational therapy addresses activities of daily living such as dressing, bathing, and toileting, along with upper extremity function and use of adaptive equipment. Speech-language pathology targets not only language impairments but also cognitive-communication disorders and swallowing dysfunction. Cognitive therapy addresses attention, memory, and executive function deficits that interfere with daily functioning and safety. Vocational rehabilitation helps appropriate patients return to work through evaluation and workplace modifications. Medical complications following stroke require prevention and management to optimize rehabilitation outcomes. Deep venous thrombosis and pulmonary embolism risk is elevated due to immobility and hemiparesis, necessitating prophylaxis with compression devices and anticoagulation when not contraindicated. Aspiration pneumonia results from dysphagia and requires swallowing evaluation before oral intake and aspiration precautions. Depression affects approximately one-third of stroke survivors and requires screening with tools such as the PHQ-9 and treatment with antidepressants and psychotherapy. Spasticity may interfere with function and positioning, managed with stretching, oral medications such as baclofen and tizanidine, and botulinum toxin injections for focal spasticity. Falls prevention requires ongoing attention to environmental modification and supervision. Stroke prognosis depends on multiple factors that inform goal-setting and discharge planning. Initial stroke severity as measured by the NIHSS is the strongest predictor of functional outcome. Younger age is associated with better recovery, though elderly patients also benefit from rehabilitation. Hemorrhagic transformation worsens prognosis. The intensity and quality of rehabilitation influence outcomes, with more intensive therapy generally producing better results. Most motor recovery occurs within the first 3 months, though gains can continue for a year or longer. Early improvement in the first weeks predicts better ultimate outcomes. Prognostic counseling should balance honesty about likely outcomes with recognition of individual variability and maintenance of hope. Panel A: Stroke rehabilitation goals spanning physical independence, complication prevention, and community reintegration. Panel B: Interdisciplinary therapy team with PT, OT, SLP, cognitive therapy, and vocational rehabilitation roles. Panel C: Post-stroke medical complications including DVT prophylaxis, aspiration prevention, depression screening, and spasticity management. Panel D: Prognostic factors for stroke recovery including NIHSS, age, timing of improvement, and rehabilitation intensity effects. --- ### X. Stroke Systems of Care Organized stroke systems of care ensure that patients have access to appropriate treatment regardless of where symptoms develop. Comprehensive stroke centers provide 24/7 availability of mechanical thrombectomy, neurosurgical intervention, and neurointensive care, and serve as referral centers for complex cases. Primary stroke centers offer continuous capability for intravenous thrombolysis and dedicated stroke units but transfer patients requiring thrombectomy or neurosurgery. Acute stroke ready hospitals provide initial assessment, thrombolysis when appropriate, and expeditious transfer to higher levels of care. This tiered system allows treatment initiation close to home while ensuring access to advanced interventions. Pre-hospital care plays a critical role in minimizing time to treatment. Public education campaigns teach recognition of stroke symptoms using the FAST mnemonic: Face drooping, Arm weakness, Speech difficulty, and Time to call 911. Emergency medical services protocols include stroke screening, pre-notification of receiving hospitals, and bypass of closer facilities to transport directly to stroke centers when appropriate. Mobile stroke units equipped with CT scanners and telemedicine capability can deliver thrombolysis in the field, dramatically reducing time to treatment. Pre-hospital triage tools identify patients likely to have large vessel occlusion who should be transported directly to thrombectomy-capable centers. Quality metrics drive continuous improvement in stroke care delivery. Door-to-needle time for thrombolysis should be below 60 minutes, with benchmarks pushing toward 45 minutes or less. Door-to-groin puncture time for thrombectomy should be below 90 minutes. All stroke patients should receive dysphagia screening before any oral intake. DVT prophylaxis should be initiated within 48 hours of admission. Statin therapy and appropriate antithrombotic therapy should be prescribed at discharge for ischemic stroke. Stroke education covering warning signs, risk factors, and medication adherence should be provided to patients and families. These metrics are tracked, reported, and used to identify opportunities for improvement. Patient education prepares stroke survivors and their families for the challenges of recovery and prevention of recurrence. Warning signs of stroke should be reviewed so that patients and family members can recognize recurrent events and respond immediately. Modifiable risk factors should be explained along with specific steps for management. Medication adherence must be emphasized, as secondary prevention drugs are only effective when taken consistently. Follow-up appointments with neurology, primary care, and rehabilitation providers should be scheduled before discharge. Community resources including stroke support groups and caregiver support services can assist with adjustment and provide ongoing education and emotional support. Panel A: Stroke center certification levels with comprehensive, primary, and acute stroke ready capabilities and transfer relationships. Panel B: Pre-hospital stroke care including FAST public education, EMS protocols, pre-notification, and mobile stroke units. Panel C: Quality metrics dashboard showing door-to-needle time, door-to-groin time, dysphagia screening, and discharge measures. Panel D: Patient education components covering warning signs, risk factor modification, medication adherence, and follow-up planning. --- ## Summary - Stroke classification divides events into 87 percent ischemic and 13 percent hemorrhagic, with the principle that time is brain driving urgent treatment - Hypertension is the most important modifiable risk factor for stroke, with atrial fibrillation, diabetes, and smoking also contributing significantly - NIH Stroke Scale quantifies stroke severity from 0 to 42 and guides treatment decisions and prognostication - Intravenous thrombolysis with alteplase is dosed at 0.9 mg/kg with maximum 90 mg, initiated within 4.5 hours of last known well - Mechanical thrombectomy for large vessel occlusion can be performed up to 24 hours with favorable imaging and extends benefit beyond thrombolysis alone - Lacunar syndromes include pure motor hemiparesis, pure sensory stroke, and ataxic hemiparesis without cortical signs - Wallenberg syndrome from lateral medullary infarction causes ipsilateral facial sensory loss and Horner syndrome with contralateral body sensory loss - TIA demands urgent evaluation with the ABCD2 score stratifying risk and dual antiplatelet therapy providing enhanced early protection - Subarachnoid hemorrhage presents with worst headache of life and complications include vasospasm between days 3 and 14 - Secondary stroke prevention includes antiplatelet or anticoagulant therapy, statin treatment, and blood pressure control below 130/80 mmHg --- ## Key Terms | Term | Definition | |------|------------| | Penumbra | Ischemic but potentially salvageable brain tissue surrounding the infarct core | | Thrombolysis | Pharmacological dissolution of arterial clot using tissue plasminogen activator | | Thrombectomy | Mechanical retrieval of arterial clot using endovascular devices | | Lacunar infarct | Small subcortical infarct resulting from occlusion of a single penetrating artery | | Large vessel occlusion | Blockage of a major cerebral artery such as the internal carotid or proximal middle cerebral artery | | Vasospasm | Arterial narrowing following subarachnoid hemorrhage causing delayed cerebral ischemia | | CHA2DS2-VASc | Risk stratification score for stroke in patients with atrial fibrillation | | NIHSS | National Institutes of Health Stroke Scale quantifying neurological deficit severity | --- *This content is subject to the [MIT License](https://opensource.org/licenses/MIT). © 2024–2026 Hibbert School of Medicine.*