Types of Superior-Division Infarct Stroke neurologists informally subdivide this syndrome to guide prognosis and therapy: Complete trunk occlusion – The whole superior M2 stem is blocked, producing dense faciobrachial paralysis and, in the dominant hemisphere, a classic Broca aphasia with reading and writing impairment. Partial (branch‐selective) infarct – Only one frontal or parietal cortical branch is obstructed; deficits are focal (e.g., isolated hand weakness or apraxia). Border-zone (watershed) extension – Hypoperfusion spreads into the ACA–MCA watershed, adding leg weakness and, occasionally, abulia. Dominant-hemisphere infarct – Broca aphasia, agrammatism, dysarthria, impaired repetition, with preserved comprehension; emotional frustration is common. Non-dominant-hemisphere infarct – Severe left-sided neglect, anosognosia, constructional apraxia, and sometimes forced-gaze deviation toward the right. Combined cortical-subcortical pattern – When clot fragments shower lenticulostriate perforators, deep motor fibres in the posterior limb of the internal capsule die, amplifying weakness. Early-reperfusion (“spectacular shrinking deficit”) – Rapid thrombolysis or spontaneous lysis rescues penumbral tissue, and dramatic recovery occurs within hours. Malignant frontal infarct – A large proximal clot causes massive oedema, raised intracranial pressure, and early herniation; decompressive hemicraniectomy may be lifesaving. Stepwise (lacuno-cortical) progression – Successive emboli or in-situ thrombosis enlarge the lesion over 24–48 h, producing a stuttering course. Silent cortical infarct – Tiny branch occlusions may remain asymptomatic or present only with subtle executive slowing, detectable on MRI during work-up for another reason. Causes Atherosclerotic plaque rupture in the internal carotid artery – Cholesterol-rich plaque cracks, a clot forms, and bits of thrombus break off and sail into the superior trunk.ncbi.nlm.nih.gov Cardio-embolic atrial fibrillation – An irregular heartbeat lets blood pool in the left atrium, a clot forms and shoots up the carotid. Patent foramen ovale with paradoxical embolus – A leg-vein clot sneaks through the heart’s flap valve and lodges in the MCA.ncbi.nlm.nih.gov Endocarditis (infected heart valve) – Septic debris or platelet–fibrin clumps peel off the valve. Prosthetic-valve thrombosis – Mechanical valves sometimes generate platelet-rich clots despite anticoagulation. Carotid-artery dissection – A tear in the arterial wall traps blood; the false lumen spawns emboli. Moyamoya or twig-like MCA anomaly – Fragile, narrowed collateral channels thrombose during hypotension. Hypercoagulable genetic states (e.g., Factor V Leiden) – Blood clots too readily, encouraging in-situ thrombosis. Antiphospholipid antibody syndrome – Auto-antibodies activate clotting cascades. Sickle-cell disease – Rigid red cells block arterioles and damage endothelium. COVID-19-associated coagulopathy – Viral inflammation and platelet activation thicken the blood. Hypertension-driven lipohyalinosis of small branches – Vessel walls scar, narrow, and ultimately occlude—especially in penetrating arterioles that feed the superior trunk. Severe hyperlipidaemia – High LDL accelerates plaque growth in proximal MCA. Smoking-induced endothelial dysfunction – Tobacco toxins injure the vessel lining and promote thrombosis. Cocaine or amphetamine use – Sudden surges in blood pressure trigger vasospasm and clot. Giant-cell (temporal) arteritis – Granulomatous inflammation narrows cerebral branches. Radiation-induced vasculopathy after head-neck cancer therapy – Intimal fibrosis appears years later and occludes the trunk. Post-partum cerebral angiopathy – Hormonal and haemodynamic shifts provoke reversible vasoconstriction and clot. Malignancy-related non-bacterial thrombotic endocarditis – Mucin-rich tumours generate sterile vegetations that embolise. Iatrogenic embolus during cardiac catheterisation – A dislodged aortic‐arch plaque travels upward. Common Symptoms Sudden weakness of the right (or left) face and arm – The opposite side of the body droops or feels heavy.ncbi.nlm.nih.govmy.clevelandclinic.orgen.wikipedia.org Clumsy hand or fingers – Fine motor tasks like buttoning a shirt become impossible. Slurred speech (dysarthria) – Mouth muscles are weak or poorly coordinated.my.clevelandclinic.org Non-fluent or “telegraphic” speech (Broca aphasia) – Words come out laboriously, but understanding is intact.ncbi.nlm.nih.gov Difficulty naming objects (anomia) – The word is “on the tip of the tongue.” Grammatical errors (agrammatism) – Sentences lack small connecting words. Reading and writing trouble (alexia/agraphia) – Letters appear jumbled or writing is effortful. Forced gaze toward the stroke side – Eye-movement centres in frontal cortex misfire, so both eyes look rightward in a left hemiparesis. Mild numbness of face or arm – Pins-and-needles, usually less severe than weakness.ncbi.nlm.nih.gov Pronounced neglect of the opposite side – In non-dominant strokes, the person ignores the left body and space. Apraxia (motor planning failure) – Can’t sequence movements to brush teeth despite having strength. Difficulty with complex hand tasks (ideomotor apraxia) – Gesturing “wave goodbye” is clumsy. Arm-drop drift – The raised arm drifts down involuntarily during testing. Emotional frustration or depression – Insightful patients with Broca aphasia often cry easily. Headache on stroke onset – Less common than in hemorrhage but may accompany large emboli. Seizure (focal-to-generalised) – Irritated cortex fires abnormally, especially in younger patients. Visual field “cut” (upper quadrantopia) – Superior division lesions rarely extend far enough posteriorly, but partial visual loss can occur when oedema spreads. Impaired attention and working memory – Frontal cortex is offline, so the patient is distractible. Primitive reflexes (grasp, pout) – Release signs emerge weeks later during recovery. Muscle stiffness and spasticity – UMN signs appear as early flaccidity resolves. Diagnostic Tests A. Physical-Exam Assessments NIH Stroke Scale (NIHSS) – A structured bedside score that quantifies stroke severity and predicts outcomes; items target language, motor power, gaze, neglect, and sensation. Vital-sign survey – Blood pressure, pulse, oxygen saturation, temperature guide acute management. Cranial-nerve examination – Detects facial droop, gaze palsy, dysarthria, and swallowing risk. Motor strength grading – 0-to-5 scale identifies hemiparesis distribution and follow-up recovery. Sensory testing (light-touch, pin, proprioception) – Delineates cortical from subcortical deficits. Deep-tendon reflexes – Brisk reflexes and an upgoing plantar indicate upper-motor-neuron injury. Coordination checks (finger-to-nose, rapid alternation) – Reveal cerebellar mimicry or true cortical dysfunction. Gait observation – Identifies circumduction and foot-drop once ambulatory. Assessment of neglect (line cancellation during exam) – Quick bedside screening in non-dominant strokes. Swallow screen – Protects the airway by detecting dysphagia before oral intake. B. Manual (Bedside-Provocation) Tests Pronator-drift test – Supinated arm drifts downward/medially within 10 s, signalling corticospinal weakness. Rapid finger-tapping – Slowed rate reflects fine-motor impairment in the MCA hand knob. Limb-activation test – Examiner moves the weak arm; lack of spontaneous use suggests motor neglect. Clock-drawing task – Visuospatial neglect and planning errors become obvious; quick cognitive screen. Picture-description (Cookie-Theft) test – Elicits expressive language deficits or neglect in speech. Apraxia screening (gesture imitation) – Patient copies symbolic gestures; difficulty = frontal-parietal damage. Line-bisection task – Horizontal line is bisected too far to the right in left-neglect. Frontal-release sign elicitation (grasp reflex) – Persistent grasping indicates extensive frontal injury. C. Laboratory & Pathological Tests Complete blood count (CBC) – Looks for anaemia and thrombocytopenia that influence thrombolysis safety. Serum electrolytes and creatinine – Detect derangements that mimic stroke (e.g., hyponatraemia) and calculate contrast dose. Random blood glucose – Hypoglycaemia or hyperglycaemia can present with focal deficits and worsens outcome. Coagulation profile (PT/INR, aPTT) – Guides tPA eligibility and screens for coagulopathies. Lipid profile – Identifies dyslipidaemia for secondary prevention. HbA1c – Gauges chronic glycaemic control, a stroke risk modifier. High-sensitivity CRP and ESR – Inflammatory markers hint at vasculitis or giant-cell arteritis. Cardiac troponin – Detects concurrent myocardial injury from cardio-embolic sources. D-dimer – Elevated in hypercoagulable or cancer-related strokes; prompts search for occult malignancy. Thrombophilia panel (protein C, S, antithrombin, antiphospholipid antibodies) – Selectively ordered in young or cryptogenic cases. D. Electro-Diagnostic Tests 12-lead electrocardiogram (ECG) – Identifies atrial fibrillation, flutter, or acute MI as embolic sources.my.clevelandclinic.org Continuous cardiac telemetry or Holter monitor – Catches paroxysmal arrhythmias missed on a single ECG. Transcranial Doppler ultrasound (TCD) – Detects real-time micro-embolic signals and monitors recanalisation. Carotid and vertebral duplex ultrasound (extra-cranial) – Measures stenosis that may require endarterectomy. EEG (electroencephalography) – Rules out post-stroke seizures or non-convulsive status mimicking deficit. Somatosensory evoked potentials (SSEP) – Estimates cortical sensory pathway integrity when patient is sedated. Brainstem auditory evoked responses (BAER) – Adds prognostic data in comatose patients with suspected large-hemispheric infarcts. Surface electromyography (EMG) during recovery – Quantifies spasticity and guides rehab strategies. E. Imaging Investigations Non-contrast CT head – Fast first-line test; rules out haemorrhage and may show early ischaemic change.my.clevelandclinic.org CT angiography (CTA) of head and neck – Visualises the clot in the superior M2 trunk, collateral flow, carotid stenosis. CT perfusion – Maps salvageable penumbra to support endovascular therapy up to 24 h. MRI brain with diffusion-weighted imaging (DWI) – Highly sensitive for acute cortical infarction within minutes. MR angiography (MRA) – Alternative to CTA when iodinated contrast is contraindicated. Digital subtraction angiography (DSA) – Gold-standard vascular roadmap and portal for thrombectomy. High-resolution vessel-wall MRI – Detects dissection flaps or vasculitis in the MCA trunk. Gradient-echo (GRE) or susceptibility-weighted imaging (SWI) – Finds micro-haemorrhage that alters anticoagulation plans. Positron-emission tomography (PET) cerebral blood-flow study – Research tool predicting infarct growth. Repeat CT or MRI 24 h post-lysis – Confirms reperfusion and screens for haemorrhagic transformation. Non-pharmacological treatments Physiotherapy & electrotherapy Constraint-Induced Movement Therapy (CIMT) – intensive, repetitive tasks with the affected limb while restraining the good limb; drives cortical re-mapping. Evidence: improves upper-limb function by ~25 % at 90 days. pubmed.ncbi.nlm.nih.gov Task-Oriented Repetitive Practice – reach-grasp-release circuits, 300–400 reps/day to boost synaptic plasticity. Mirror Therapy – reflecting healthy limb tricks mirror neurons; increases motor-evoked potentials. Functional Electrical Stimulation (FES) – 20–50 mA pulses recruit dormant motor units, reducing shoulder subluxation. Neuromuscular Electrical Stimulation cycling – pedals while stimulating quads/gluteals; improves gait speed. Transcranial Magnetic Stimulation (rTMS) – 1 Hz inhibitory over contralesional M1 to unmask ipsilesional cortex. Transcranial Direct Current Stimulation (tDCS) – 2 mA anodal boost on affected hemisphere for 20 min/day. Robot-assisted arm exoskeleton training – precise trajectory guidance, accelerates arm-hand recovery. Body-Weight-Supported Treadmill Training – harness unloads 30 % body weight to practice symmetric gait. Aquatic Therapy – buoyancy allows early standing and reduces spasticity through warmth. Whole-body Vibration Therapy – 30 Hz plate stimulates proprioceptors, reduces ankle clonus. Virtual-Reality Gaming – Kinect®-based reach & balance games heighten motivation and neuroplasticity. Thermal Contrast Therapy – alternating hot/cold packs dampen pain and swelling. Orthotic Bracing & functional splints – positions wrist and thumb to prevent contracture. Low-level Laser Therapy (photobiomodulation) – emerging; may up-regulate mitochondrial cytochrome-c oxidase. Exercise, mind-body & education Progressive Resistance Training – 2–3 sets, 8–12 reps at 60–80 % 1-RM, twice weekly to rebuild motor units. Aerobic Cycling or Nu-Step® 150 min/week – elevates BDNF, improves VO₂-peak. Static and dynamic stretching – 30-second holds, three reps, prevents contractures. Balance-board & perturbation training – strengthens ankle strategies. Gait-speed interval walks – short bursts at 110 % preferred speed enhance stride symmetry. Yoga (Hatha) – slow poses plus diaphragmatic breathing calm sympathetic tone, cut BP ~5 mm Hg. Tai Chi / Qigong – slow choreographed shifts improve proprioception and postural sway. Pilates core stabilization – bridges and pelvic tilts reduce trunk lean. Mindfulness-Based Stress Reduction – 45-minute guided meditation reduces depression and fatigue. Music Therapy / Rhythmic Auditory Stimulation – metronome-paced stepping entrains cadence. Art Therapy – fine-motor brush strokes stimulate hand dexterity and self-expression. Biofeedback (surface EMG) – visualizes firing patterns; patients learn to dampen spastic co-contraction. Cognitive-Behavioral Therapy for post-stroke fatigue – targets maladaptive beliefs. Patient & Caregiver Goal-Setting Workshops – SMART goals align rehab tasks. Peer-led Self-Management Education – teaches BP, glucose logging, medication adherence. key drugs Alteplase 0.9 mg/kg IV (max 90 mg) | fibrinolytic | within 4.5 h | bleeding, angio-edema. ncbi.nlm.nih.gov Tenecteplase 0.25 mg/kg IV push | fibrinolytic | alternative, especially with planned thrombectomy | bleeding. ahajournals.org Aspirin 160–325 mg load → 81 mg daily | antiplatelet | start 24 h after alteplase | gastric upset, bleeding. Clopidogrel 300 mg load, then 75 mg/d | P2Y12 blocker | combine with aspirin 21 days in minor stroke | rash, neutropenia. Dual antiplatelet (ASA + Clopidogrel) | combo | NIHSS ≤ 3 small infarct | ↑bleeding versus monotherapy. Atorvastatin 80 mg nightly | high-intensity statin | start day 1 | myalgia, transaminitis. Rosuvastatin 40 mg nightly | statin | statin‐intolerant alternatives | same. Apixaban 5 mg twice daily | DOAC | non-valvular AF after 3–14 days | bruising, GI bleed. Rivaroxaban 20 mg nightly with food | DOAC | non-valvular AF | bleeding. Warfarin INR 2-3 | VKA | valvular AF/mechanical valve | lab checks, drug-food interactions. Lisinopril 10–40 mg/d | ACE inhibitor | secondary prevention BP goal 5 mm saves life in

Question

Types of Superior-Division Infarct
Stroke neurologists informally subdivide this syndrome to guide prognosis and therapy:


 	
Complete trunk occlusion – The whole superior M2 stem is blocked, producing dense faciobrachial paralysis and, in the dominant hemisphere, a classic Broca aphasia with reading and writing impairment.

 	
Partial (branch‐selective) infarct – Only one frontal or parietal cortical branch is obstructed; deficits are focal (e.g., isolated hand weakness or apraxia).

 	
Border-zone (watershed) extension – Hypoperfusion spreads into the ACA–MCA watershed, adding leg weakness and, occasionally, abulia.

 	
Dominant-hemisphere infarct – Broca aphasia, agrammatism, dysarthria, impaired repetition, with preserved comprehension; emotional frustration is common.

 	
Non-dominant-hemisphere infarct – Severe left-sided neglect, anosognosia, constructional apraxia, and sometimes forced-gaze deviation toward the right.

 	
Combined cortical-subcortical pattern – When clot fragments shower lenticulostriate perforators, deep motor fibres in the posterior limb of the internal capsule die, amplifying weakness.

 	
Early-reperfusion (“spectacular shrinking deficit”) – Rapid thrombolysis or spontaneous lysis rescues penumbral tissue, and dramatic recovery occurs within hours.

 	
Malignant frontal infarct – A large proximal clot causes massive oedema, raised intracranial pressure, and early herniation; decompressive hemicraniectomy may be lifesaving.

 	
Stepwise (lacuno-cortical) progression – Successive emboli or in-situ thrombosis enlarge the lesion over 24–48 h, producing a stuttering course.

 	
Silent cortical infarct – Tiny branch occlusions may remain asymptomatic or present only with subtle executive slowing, detectable on MRI during work-up for another reason.





Causes

 	
Atherosclerotic plaque rupture in the internal carotid artery – Cholesterol-rich plaque cracks, a clot forms, and bits of thrombus break off and sail into the superior trunk.ncbi.nlm.nih.gov

 	
Cardio-embolic atrial fibrillation – An irregular heartbeat lets blood pool in the left atrium, a clot forms and shoots up the carotid.

 	
Patent foramen ovale with paradoxical embolus – A leg-vein clot sneaks through the heart’s flap valve and lodges in the MCA.ncbi.nlm.nih.gov

 	
Endocarditis (infected heart valve) – Septic debris or platelet–fibrin clumps peel off the valve.

 	
Prosthetic-valve thrombosis – Mechanical valves sometimes generate platelet-rich clots despite anticoagulation.

 	
Carotid-artery dissection – A tear in the arterial wall traps blood; the false lumen spawns emboli.

 	
Moyamoya or twig-like MCA anomaly – Fragile, narrowed collateral channels thrombose during hypotension.

 	
Hypercoagulable genetic states (e.g., Factor V Leiden) – Blood clots too readily, encouraging in-situ thrombosis.

 	
Antiphospholipid antibody syndrome – Auto-antibodies activate clotting cascades.

 	
Sickle-cell disease – Rigid red cells block arterioles and damage endothelium.

 	
COVID-19-associated coagulopathy – Viral inflammation and platelet activation thicken the blood.

 	
Hypertension-driven lipohyalinosis of small branches – Vessel walls scar, narrow, and ultimately occlude—especially in penetrating arterioles that feed the superior trunk.

 	
Severe hyperlipidaemia – High LDL accelerates plaque growth in proximal MCA.

 	
Smoking-induced endothelial dysfunction – Tobacco toxins injure the vessel lining and promote thrombosis.

 	
Cocaine or amphetamine use – Sudden surges in blood pressure trigger vasospasm and clot.

 	
Giant-cell (temporal) arteritis – Granulomatous inflammation narrows cerebral branches.

 	
Radiation-induced vasculopathy after head-neck cancer therapy – Intimal fibrosis appears years later and occludes the trunk.

 	
Post-partum cerebral angiopathy – Hormonal and haemodynamic shifts provoke reversible vasoconstriction and clot.

 	
Malignancy-related non-bacterial thrombotic endocarditis – Mucin-rich tumours generate sterile vegetations that embolise.

 	
Iatrogenic embolus during cardiac catheterisation – A dislodged aortic‐arch plaque travels upward.





Common Symptoms

 	
Sudden weakness of the right (or left) face and arm – The opposite side of the body droops or feels heavy.ncbi.nlm.nih.govmy.clevelandclinic.orgen.wikipedia.org

 	
Clumsy hand or fingers – Fine motor tasks like buttoning a shirt become impossible.

 	
Slurred speech (dysarthria) – Mouth muscles are weak or poorly coordinated.my.clevelandclinic.org

 	
Non-fluent or “telegraphic” speech (Broca aphasia) – Words come out laboriously, but understanding is intact.ncbi.nlm.nih.gov

 	
Difficulty naming objects (anomia) – The word is “on the tip of the tongue.”

 	
Grammatical errors (agrammatism) – Sentences lack small connecting words.

 	
Reading and writing trouble (alexia/agraphia) – Letters appear jumbled or writing is effortful.

 	
Forced gaze toward the stroke side – Eye-movement centres in frontal cortex misfire, so both eyes look rightward in a left hemiparesis.

 	
Mild numbness of face or arm – Pins-and-needles, usually less severe than weakness.ncbi.nlm.nih.gov

 	
Pronounced neglect of the opposite side – In non-dominant strokes, the person ignores the left body and space.

 	
Apraxia (motor planning failure) – Can’t sequence movements to brush teeth despite having strength.

 	
Difficulty with complex hand tasks (ideomotor apraxia) – Gesturing “wave goodbye” is clumsy.

 	
Arm-drop drift – The raised arm drifts down involuntarily during testing.

 	
Emotional frustration or depression – Insightful patients with Broca aphasia often cry easily.

 	
Headache on stroke onset – Less common than in hemorrhage but may accompany large emboli.

 	
Seizure (focal-to-generalised) – Irritated cortex fires abnormally, especially in younger patients.

 	
Visual field “cut” (upper quadrantopia) – Superior division lesions rarely extend far enough posteriorly, but partial visual loss can occur when oedema spreads.

 	
Impaired attention and working memory – Frontal cortex is offline, so the patient is distractible.

 	
Primitive reflexes (grasp, pout) – Release signs emerge weeks later during recovery.

 	
Muscle stiffness and spasticity – UMN signs appear as early flaccidity resolves.





Diagnostic Tests
A. Physical-Exam Assessments

 	
NIH Stroke Scale (NIHSS) – A structured bedside score that quantifies stroke severity and predicts outcomes; items target language, motor power, gaze, neglect, and sensation.

 	
Vital-sign survey – Blood pressure, pulse, oxygen saturation, temperature guide acute management.

 	
Cranial-nerve examination – Detects facial droop, gaze palsy, dysarthria, and swallowing risk.

 	
Motor strength grading – 0-to-5 scale identifies hemiparesis distribution and follow-up recovery.

 	
Sensory testing (light-touch, pin, proprioception) – Delineates cortical from subcortical deficits.

 	
Deep-tendon reflexes – Brisk reflexes and an upgoing plantar indicate upper-motor-neuron injury.

 	
Coordination checks (finger-to-nose, rapid alternation) – Reveal cerebellar mimicry or true cortical dysfunction.

 	
Gait observation – Identifies circumduction and foot-drop once ambulatory.

 	
Assessment of neglect (line cancellation during exam) – Quick bedside screening in non-dominant strokes.

 	
Swallow screen – Protects the airway by detecting dysphagia before oral intake.


B. Manual (Bedside-Provocation) Tests

 	
Pronator-drift test – Supinated arm drifts downward/medially within 10 s, signalling corticospinal weakness.

 	
Rapid finger-tapping – Slowed rate reflects fine-motor impairment in the MCA hand knob.

 	
Limb-activation test – Examiner moves the weak arm; lack of spontaneous use suggests motor neglect.

 	
Clock-drawing task – Visuospatial neglect and planning errors become obvious; quick cognitive screen.

 	
Picture-description (Cookie-Theft) test – Elicits expressive language deficits or neglect in speech.

 	
Apraxia screening (gesture imitation) – Patient copies symbolic gestures; difficulty = frontal-parietal damage.

 	
Line-bisection task – Horizontal line is bisected too far to the right in left-neglect.

 	
Frontal-release sign elicitation (grasp reflex) – Persistent grasping indicates extensive frontal injury.


C. Laboratory & Pathological Tests

 	
Complete blood count (CBC) – Looks for anaemia and thrombocytopenia that influence thrombolysis safety.

 	
Serum electrolytes and creatinine – Detect derangements that mimic stroke (e.g., hyponatraemia) and calculate contrast dose.

 	
Random blood glucose – Hypoglycaemia or hyperglycaemia can present with focal deficits and worsens outcome.

 	
Coagulation profile (PT/INR, aPTT) – Guides tPA eligibility and screens for coagulopathies.

 	
Lipid profile – Identifies dyslipidaemia for secondary prevention.

 	
HbA1c – Gauges chronic glycaemic control, a stroke risk modifier.

 	
High-sensitivity CRP and ESR – Inflammatory markers hint at vasculitis or giant-cell arteritis.

 	
Cardiac troponin – Detects concurrent myocardial injury from cardio-embolic sources.

 	
D-dimer – Elevated in hypercoagulable or cancer-related strokes; prompts search for occult malignancy.

 	
Thrombophilia panel (protein C, S, antithrombin, antiphospholipid antibodies) – Selectively ordered in young or cryptogenic cases.


D. Electro-Diagnostic Tests

 	
12-lead electrocardiogram (ECG) – Identifies atrial fibrillation, flutter, or acute MI as embolic sources.my.clevelandclinic.org

 	
Continuous cardiac telemetry or Holter monitor – Catches paroxysmal arrhythmias missed on a single ECG.

 	
Transcranial Doppler ultrasound (TCD) – Detects real-time micro-embolic signals and monitors recanalisation.

 	
Carotid and vertebral duplex ultrasound (extra-cranial) – Measures stenosis that may require endarterectomy.

 	
EEG (electroencephalography) – Rules out post-stroke seizures or non-convulsive status mimicking deficit.

 	
Somatosensory evoked potentials (SSEP) – Estimates cortical sensory pathway integrity when patient is sedated.

 	
Brainstem auditory evoked responses (BAER) – Adds prognostic data in comatose patients with suspected large-hemispheric infarcts.

 	
Surface electromyography (EMG) during recovery – Quantifies spasticity and guides rehab strategies.


E. Imaging Investigations

 	
Non-contrast CT head – Fast first-line test; rules out haemorrhage and may show early ischaemic change.my.clevelandclinic.org

 	
CT angiography (CTA) of head and neck – Visualises the clot in the superior M2 trunk, collateral flow, carotid stenosis.

 	
CT perfusion – Maps salvageable penumbra to support endovascular therapy up to 24 h.

 	
MRI brain with diffusion-weighted imaging (DWI) – Highly sensitive for acute cortical infarction within minutes.

 	
MR angiography (MRA) – Alternative to CTA when iodinated contrast is contraindicated.

 	
Digital subtraction angiography (DSA) – Gold-standard vascular roadmap and portal for thrombectomy.

 	
High-resolution vessel-wall MRI – Detects dissection flaps or vasculitis in the MCA trunk.

 	
Gradient-echo (GRE) or susceptibility-weighted imaging (SWI) – Finds micro-haemorrhage that alters anticoagulation plans.

 	
Positron-emission tomography (PET) cerebral blood-flow study – Research tool predicting infarct growth.

 	
Repeat CT or MRI 24 h post-lysis – Confirms reperfusion and screens for haemorrhagic transformation.


Non-pharmacological treatments
Physiotherapy & electrotherapy

 	
Constraint-Induced Movement Therapy (CIMT) – intensive, repetitive tasks with the affected limb while restraining the good limb; drives cortical re-mapping. Evidence: improves upper-limb function by ~25 % at 90 days. pubmed.ncbi.nlm.nih.gov

 	
Task-Oriented Repetitive Practice – reach-grasp-release circuits, 300–400 reps/day to boost synaptic plasticity.

 	
Mirror Therapy – reflecting healthy limb tricks mirror neurons; increases motor-evoked potentials.

 	
Functional Electrical Stimulation (FES) – 20–50 mA pulses recruit dormant motor units, reducing shoulder subluxation.

 	
Neuromuscular Electrical Stimulation cycling – pedals while stimulating quads/gluteals; improves gait speed.

 	
Transcranial Magnetic Stimulation (rTMS) – 1 Hz inhibitory over contralesional M1 to unmask ipsilesional cortex.

 	
Transcranial Direct Current Stimulation (tDCS) – 2 mA anodal boost on affected hemisphere for 20 min/day.

 	
Robot-assisted arm exoskeleton training – precise trajectory guidance, accelerates arm-hand recovery.

 	
Body-Weight-Supported Treadmill Training – harness unloads 30 % body weight to practice symmetric gait.

 	
Aquatic Therapy – buoyancy allows early standing and reduces spasticity through warmth.

 	
Whole-body Vibration Therapy – 30 Hz plate stimulates proprioceptors, reduces ankle clonus.

 	
Virtual-Reality Gaming – Kinect®-based reach & balance games heighten motivation and neuroplasticity.

 	
Thermal Contrast Therapy – alternating hot/cold packs dampen pain and swelling.

 	
Orthotic Bracing & functional splints – positions wrist and thumb to prevent contracture.

 	
Low-level Laser Therapy (photobiomodulation) – emerging; may up-regulate mitochondrial cytochrome-c oxidase.


Exercise, mind-body & education

 	
Progressive Resistance Training – 2–3 sets, 8–12 reps at 60–80 % 1-RM, twice weekly to rebuild motor units.

 	
Aerobic Cycling or Nu-Step® 150 min/week – elevates BDNF, improves VO₂-peak.

 	
Static and dynamic stretching – 30-second holds, three reps, prevents contractures.

 	
Balance-board & perturbation training – strengthens ankle strategies.

 	
Gait-speed interval walks – short bursts at 110 % preferred speed enhance stride symmetry.

 	
Yoga (Hatha) – slow poses plus diaphragmatic breathing calm sympathetic tone, cut BP ~5 mm Hg.

 	
Tai Chi / Qigong – slow choreographed shifts improve proprioception and postural sway.

 	
Pilates core stabilization – bridges and pelvic tilts reduce trunk lean.

 	
Mindfulness-Based Stress Reduction – 45-minute guided meditation reduces depression and fatigue.

 	
Music Therapy / Rhythmic Auditory Stimulation – metronome-paced stepping entrains cadence.

 	
Art Therapy – fine-motor brush strokes stimulate hand dexterity and self-expression.

 	
Biofeedback (surface EMG) – visualizes firing patterns; patients learn to dampen spastic co-contraction.

 	
Cognitive-Behavioral Therapy for post-stroke fatigue – targets maladaptive beliefs.

 	
Patient & Caregiver Goal-Setting Workshops – SMART goals align rehab tasks.

 	
Peer-led Self-Management Education – teaches BP, glucose logging, medication adherence.





key drugs

 	
Alteplase 0.9 mg/kg IV (max 90 mg) | fibrinolytic | within 4.5 h | bleeding, angio-edema. ncbi.nlm.nih.gov

 	
Tenecteplase 0.25 mg/kg IV push | fibrinolytic | alternative, especially with planned thrombectomy | bleeding. ahajournals.org

 	
Aspirin 160–325 mg load → 81 mg daily | antiplatelet | start 24 h after alteplase | gastric upset, bleeding.

 	
Clopidogrel 300 mg load, then 75 mg/d | P2Y12 blocker | combine with aspirin 21 days in minor stroke | rash, neutropenia.

 	
Dual antiplatelet (ASA + Clopidogrel) | combo | NIHSS ≤ 3 small infarct | ↑bleeding versus monotherapy.

 	
Atorvastatin 80 mg nightly | high-intensity statin | start day 1 | myalgia, transaminitis.

 	
Rosuvastatin 40 mg nightly | statin | statin‐intolerant alternatives | same.

 	
Apixaban 5 mg twice daily | DOAC | non-valvular AF after 3–14 days | bruising, GI bleed.

 	
Rivaroxaban 20 mg nightly with food | DOAC | non-valvular AF | bleeding.

 	
Warfarin INR 2-3 | VKA | valvular AF/mechanical valve | lab checks, drug-food interactions.

 	
Lisinopril 10–40 mg/d | ACE inhibitor | secondary prevention BP goal <130/80 | cough, hyper-K⁺.

 	
Amlodipine 5–10 mg/d | calcium-channel blocker | alt. BP agent | ankle edema.

 	
Hydrochlorothiazide 25 mg/d | thiazide diuretic | add-on for BP | hypo-K⁺, photosensitivity.

 	
Empagliflozin 10 mg/d | SGLT2 inhibitor | diabetic stroke survivor | genital infections.

 	
Metformin 500–2000 mg/d | biguanide | insulin-sensitizer | lactic acidosis (rare).

 	
Fluoxetine 20 mg/d | SSRI | enhances motor recovery in select patients | GI upset, hyponatremia.

 	
Citicoline 500–1000 mg BID | neuro-protective nucleotide | improves attentional network | insomnia.

 	
Edaravone 60 mg IV daily ×14 d | free-radical scavenger | early neuroprotection (Japan) | renal issues.

 	
Piracetam 1.6 g TID | nootropic | adjunct cognitive recovery | nervousness.

 	
Nimodipine 60 mg q4h | cerebral vasospasm prophylaxis if subarachnoid hemorrhage complicates | hypotension.





Dietary molecular supplements

 	
Vitamin D₃ 1,000–2,000 IU/d – lowers inflammatory cytokines; meta-analysis shows up to 17 % stroke-risk drop. eatingwell.com

 	
Omega-3 DHA/EPA 1 g/d – competes with arachidonic acid; forms pro-resolving mediators. en.wikipedia.org

 	
Coenzyme Q10 100 mg BID – bolsters mitochondrial ATP; antioxidant.

 	
Curcumin 500 mg BID (with piperine) – NF-κB inhibition, reduces post-stroke edema.

 	
Resveratrol 150 mg/d – SIRT-1 activation, endothelial nitric-oxide boost.

 	
Magnesium citrate 300 mg elemental/d – vasodilator, lowers BP.

 	
Potassium (dietary 3.4 g/d) – smooth-muscle hyper-polarization; BP control.

 	
Alpha-lipoic acid 600 mg/d – regenerates vitamin C/E, chelates metals.

 	
L-Arginine 3 g/d – substrate for nitric-oxide synthase; improves flow-mediated dilation.

 	
Methyl-folate+B₆+B₁₂ combo (400 µg/ 25 mg/ 1 mg) – drops homocysteine.





Drugs (bisphosphonates, regenerative, viscosupplement, stem-cell based)

 	
Alendronate 70 mg once weekly | bisphosphonate | preserves bone in hemiplegia; watch reflux. pubmed.ncbi.nlm.nih.gov

 	
Risedronate 35 mg weekly – similar.

 	
Zoledronic acid 5 mg IV yearly – potent anti-resorptive, infusion flu-like syndrome.

 	
Cerebrolysin 30 mL IV over 15 min ×10 days | regenerative peptide mixture | may enhance neurogenesis.

 	
Granulocyte-colony stimulating factor 250 µg/d SC ×5 – mobilizes endogenous stem cells; investigational.

 	
Hyaluronic-acid 20 mg intra-articular weekly ×3 | viscosupplement | eases hemiplegic shoulder arthropathy.

 	
Umbilical cord-derived MSC 1 × 10⁶ cells/kg IV – shows best composite neurological recovery. pubmed.ncbi.nlm.nih.gov

 	
Bone-marrow mononuclear cells 10⁸ intra-arterial one-time – improves Fugl-Meyer scores.

 	
Teriparatide 20 µg SC daily | anabolic bone agent | counters disuse osteoporosis.

 	
Autologous peripheral-blood CD34⁺ stem infusion 5 × 10⁷ cells – early-phase trials.



Note: Items 4–10 remain experimental; enroll only in regulated trials.




Surgeries & procedures

 	
Mechanical thrombectomy (stent-retriever or aspiration) – within 24 h for LVO; raises odds of mRS 0–2 by 30 %. pubmed.ncbi.nlm.nih.gov

 	
Direct aspiration first-pass technique (ADAPT) – minimalist catheter suction.

 	
Carotid endarterectomy – ≥70 % ipsilateral stenosis after index stroke.

 	
Carotid artery stenting – high-risk surgical candidates.

 	
Decompressive hemicraniectomy – malignant edema with midline shift >5 mm saves life in <60 y.o.

 	
Extracranial–intracranial (STA-MCA) bypass – rare, for flow-limiting stenosis unamenable to stent.

 	
Endoscopic third ventriculostomy / EVD – relieves hydrocephalus.

 	
Tendon-transfer surgery (pronator→extensor) – restores hand opening in dense spasticity.

 	
Achilles-tendon lengthening – corrects equinus foot preventing brace fit.

 	
Implantable cortical neuro-prosthesis trial – brain-computer interfaces for hand grasp.





Prevention strategies

 	
Keep systolic BP < 130 mm Hg through lifestyle + meds.

 	
Stop smoking—nicotine triples re-stroke risk.

 	
Adopt a Mediterranean-style diet rich in olive oil & greens.

 	
Exercise 150 min/week brisk walking or cycling.

 	
Limit alcohol ≤ 1 drink/day (women) or 2 (men).

 	
Tighten diabetes control (target HbA1c < 7 %).

 	
Drive LDL-C to < 70 mg/dL with high-intensity statin.

 	
Anticoagulate atrial fibrillation promptly.

 	
Treat sleep apnea with CPAP to cut nocturnal BP spikes.

 	
Schedule annual carotid/vascular check-ups if high-risk.





When should you see a doctor—or call emergency services?

Accepted Answer

Immediately (call EMS) if speech suddenly slurs, one side of face droops, or an arm won’t rise—every minute equals ~2 million dying neurons. Within 24 h of any new numbness, vision dimming, or brief TIA-like spell. Every 3–6 months during the first year for medication review, BP and lipid monitoring, and rehab goal resets. Sooner if dizziness, palpitations, calf swelling, or sudden headache appear—possible new embolus or hemorrhagic conversion.

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