A dominant-hemisphere MCA infarct is an ischemic stroke that blocks blood flow through the middle cerebral artery on the side of the brain that houses language functions (the dominant hemisphere—left-sided in ≈ 90 % of right-handed people and 60-70 % of left-handers). When this artery is occluded, oxygen-starved brain tissue quickly dies, disrupting speech production, comprehension, motor control of the opposite face/arm, and higher cognitive skills such as reading and writing. Timely diagnosis is vital because each minute of untreated large-vessel occlusion destroys roughly two million neurons and steals a week of functional life. ncbi.nlm.nih.govmy.clevelandclinic.org
The MCA supplies the lateral frontal, parietal, and temporal lobes, the insula, and deep white-matter tracts. An infarct in its superior division typically harms Broca’s area (non-fluent aphasia) and motor cortex, while inferior-division occlusion more often injures Wernicke’s area (fluent but nonsensical speech) and visual association cortex. Massive trunk occlusions can wipe out both divisions and the internal capsule, causing “global” aphasia, dense hemiplegia, and gaze deviation toward the damaged hemisphere. en.wikipedia.orgphysio-pedia.com
Recognised Sub-Types
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Superior-division infarct – predominantly frontal; characterized by Broca aphasia, contralateral face-and-arm weakness, and eye deviation to the lesion side.
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Inferior-division infarct – mainly temporal and parietal; yields Wernicke aphasia, contralateral upper-quadrant visual field loss, and possible neglect of the right body.
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Stem or trunk infarct – blocks the main M1 segment; produces profound global aphasia, dense contralateral hemiplegia, hemianesthesia, and frequently malignant cerebral edema.
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Lacunar-pattern MCA infarct – small deep-branch blockage in the internal capsule or basal ganglia; may cause pure motor stroke or sensorimotor stroke without language loss. radiopaedia.org
Evidence-Based Causes
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Large-artery atherosclerosis – fatty plaques in the internal carotid/MCA harden and suddenly rupture, letting a clot block the vessel.
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Cardio-embolism from atrial fibrillation – erratic heartbeats let clots form in the atrium and travel to the MCA.
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Left-ventricular thrombus after myocardial infarction – damaged heart muscle forms a clot that embolizes to the brain.
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Patent foramen ovale (PFO) – a flap-like hole between heart chambers allows leg-vein clots to bypass the lungs and lodge in the MCA.
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Infective endocarditis – bacteria build vegetations on valves that shower septic emboli into cerebral arteries.
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Cervical carotid dissection – a tear in the artery wall traps blood, creating a flap that blocks flow or forms emboli.
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Hypercoagulable genetic disorders (e.g., Factor V Leiden) – thicker blood clots more easily, predisposing to arterial blockage.
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Malignancy-associated thrombosis – cancers raise clotting factors, triggering stroke.
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Hormonal contraception or HRT – estrogen increases clotting proteins and stroke risk in predisposed women.
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Pregnancy and postpartum state – physiological hypercoagulability plus vascular strain elevate stroke risk.
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Sickle cell disease – sickled red cells occlude cerebral vessels and damage the endothelium.
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Severe dehydration – low plasma volume increases blood viscosity, allowing sluggish flow and thrombosis.
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Uncontrolled hypertension – constant pressure injures artery linings and accelerates atherosclerosis.
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Diabetes mellitus – high glucose triggers inflammatory damage and plaque build-up in cerebral vessels.
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Hyperlipidemia – elevated LDL promotes plaque formation that may rupture.
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Smoking – toxins injure endothelium, thicken blood, and promote atheroma.
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Migraine with aura – transient vessel constriction and hypercoagulability occasionally precipitate infarction.
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COVID-19-related coagulopathy – viral endothelial injury and cytokine storms markedly raise clot risk.
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Autoimmune vasculitis (e.g., Takayasu, Moyamoya) – inflamed arterial walls narrow and thrombose.
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Recreational stimulant use (cocaine, amphetamines) – sudden surges in blood pressure and vasospasm provoke MCA occlusion.
Symptoms
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Sudden difficulty speaking (aphasia) – words come out broken or make no sense.
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Trouble understanding language – the patient hears words but can’t grasp their meaning.
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Right-sided face weakness – the mouth droops and the smile is crooked.
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Right arm paralysis – the arm hangs limp and cannot lift against gravity.
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Right-leg weakness (milder) – leg drags but often less severe than the arm.
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Loss of sensation on the right side – numbness or tingling in face-arm-leg.
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Gaze deviation to the left – both eyes look toward the stroke side and resist turning right.
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Right-field visual loss – the patient bumps into objects on the right or cannot see the right half of a page.
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Speech that is fluent yet nonsensical – characteristic of Wernicke involvement.
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Slow, labored speech with good comprehension – Broca aphasia pattern.
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Difficulty reading (alexia) – letters are seen but cannot be decoded into words.
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Difficulty writing (agraphia) – unable to spell or form words on paper.
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Calculation problems (acalculia) – basic arithmetic suddenly impossible.
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Dressing apraxia – trouble sequencing body movements to dress.
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Emotional lability – sudden crying or laughing without warning.
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Severe headache – more common when embolus forms clot extension or hemorrhagic conversion.
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Nausea and vomiting – brain swelling stimulates vomiting centers.
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Confusion or disorientation – cannot state the date or situation.
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Seizures at onset – cortical irritation triggers convulsions in a minority of large MCA strokes.
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Loss of awareness of right body parts (neglect if parietal) – patient treats the right arm as if it were not theirs. physio-pedia.comverywellhealth.com
Diagnostic Tests
A. Physical-Exam–Based Tests
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National Institutes of Health Stroke Scale (NIHSS) – a bedside scored exam quantifying deficits; higher scores indicate larger MCA involvement.
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Cincinnati Pre-hospital Stroke Scale – checks facial droop, arm drift, and speech for rapid field recognition.
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FAST-ED scale – adds eye deviation and distal weakness to gauge large-vessel occlusion probability.
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Language repetition test – asks the patient to repeat a phrase; failure points to dominant-hemisphere injury.
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Naming test (confrontation naming) – inability to name shown objects indicates cortical aphasia.
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Sensory extinction test – simultaneous bilateral touch; failure to feel the right side suggests parietal cortical loss.
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Visual-field confrontation – detects right-homonymous hemianopia typical of inferior-division infarct.
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Gait observation – early subtle weakness may appear as leg circumduction.
B. Manual (Bedside Maneuver) Tests
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Pronator drift – patient’s right arm slowly pronates and drops when eyes closed, signaling corticospinal tract weakness.
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Rapid alternating hand movements – slowness on the right reveals subtle motor cortex damage.
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Finger-to-nose test – dysmetria or past-pointing on the right may uncover concomitant cerebellar involvement.
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Palm-up push test – examiner resists upward push; asymmetry indicates power loss.
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Apraxia assessment – ask patient to mime using a tool; inability despite comprehension shows praxis network disruption.
C. Laboratory and Pathological Tests
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Complete blood count – detects infection or polycythemia that modify treatment choices.
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Serum glucose – hypoglycemia mimics stroke; hyperglycemia worsens outcome.
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Coagulation profile (PT/INR, aPTT) – ensures safety for thrombolysis and may reveal anticoagulant over-effect.
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Lipid panel – identifies dyslipidemia contributing to atherosclerotic MCA disease.
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Erythrocyte sedimentation rate & C-reactive protein – elevated levels suggest vasculitis or active infection.
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Thrombophilia screen (protein C/S, antiphospholipid antibodies) – indicated in young patients or cryptogenic stroke.
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Cardiac enzymes (troponin) – concurrent myocardial injury heightens secondary prevention needs.
D. Electrodiagnostic Tests
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12-lead electrocardiogram – finds atrial fibrillation or recent MI sources of emboli.
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Continuous cardiac telemetry – captures intermittent arrhythmias missed on single ECG.
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Echocardiography (transthoracic) – visualizes ventricular thrombus, valve vegetations, or PFO.
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Transesophageal echocardiography – higher-resolution view of atrial appendage clots and aortic atheroma.
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Electroencephalography (EEG) – differentiates post-stroke seizures from fluctuating symptoms.
E. Imaging Tests
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Non-contrast head CT – rules out hemorrhage and shows early MCA infarct signs within 20 min of arrival.
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CT angiography of head and neck – maps arterial tree, confirming M1 or M2 occlusion amenable to thrombectomy.
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CT perfusion – highlights salvageable penumbra versus completed core infarct to guide late thrombolysis.
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MRI diffusion-weighted imaging (DWI) – detects ischemia within minutes, pinpointing cortical language areas.
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MRI FLAIR sequence – helps determine stroke age; mismatch with DWI implies onset < 4.5 h.
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MR angiography – non-invasive visualization of vessel blockage without contrast (if contraindications exist).
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Digital subtraction cerebral angiography – gold standard for real-time vessel imaging and mechanical clot retrieval.
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Carotid duplex ultrasound – screens for upstream plaque and stenosis feeding the MCA.
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Transcranial Doppler ultrasound – monitors cerebral blood flow velocity, revealing micro-embolic signals.
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CT-based Alberta Stroke Program Early CT Score (ASPECTS) – standardized score predicting outcome based on early ischemic change.
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Perfusion-weighted MRI with RAPID software – automated core/penumbra quantification for late-window therapy.
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CT or MR venography – performed when hemorrhagic conversion raises suspicion of venous sinus thrombosis.
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Chest CT angiography – may detect cardiac/aortic embolic sources in cryptogenic stroke work-ups.
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Whole-blood-volume-mapped CT – advanced tool to estimate brain swelling risk in malignant MCA infarct.
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Serial CT for midline-shift monitoring – repeated scans gauge cerebral edema threatening herniation. ahajournals.orgahajournals.orgahajournals.org
Non-Pharmacological Treatments
Physiotherapy / Electro- & Exercise Therapies
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Early mobilization within 24 h – prevents deconditioning; brain-derived neurotrophic factor rises with movement. pmc.ncbi.nlm.nih.gov
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Task-oriented treadmill gait training – rewires cortical motor maps.
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Constraint-induced movement therapy – forces use of weak arm.
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Functional electrical stimulation – delivers timed pulses to wrist/ankle extensors, promoting neuroplasticity.
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Neuromuscular electrical stimulation cycling – active-assist pedaling builds endurance.
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Robot-assisted arm training – high-repetition joint motions.
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Mirror therapy – visual illusion stimulates dormant motor cortex.
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High-intensity interval training (HIIT) – short bursts double VO₂ gains and may curb recurrent stroke. businessinsider.com
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Aquatic therapy – buoyancy lets patients practice walking safely.
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Whole-body vibration – stimulates proprioceptors and spasticity reduction.
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Transcranial direct-current stimulation (tDCS) – primes cortex for rehab.
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Low-level laser therapy on paretic muscles – reduces oxidative stress.
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Therapeutic ultrasound for spastic flexors – improves tissue extensibility.
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Proprioceptive neuromuscular facilitation stretching – restores range.
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Kinesio-taping of shoulder – prevents subluxation and pain.
Mind-Body & Educational / Self-Management Approaches
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Mindfulness-based stress reduction – lowers BP and depression.
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Guided imagery – recruits mirror neurons for motor relearning.
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Yoga-in-chair routines – enhances balance safely.
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Feldenkrais awareness lessons – relearns joint alignment.
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Biofeedback of EMG signals – teaches voluntary activation.
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Motivational interviewing – boosts adherence to lifestyle change.
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Caregiver-delivered home exercise coaching – extends therapy dose.
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Group education sessions – cover nutrition, meds, and warning signs.
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Digital app-based speech practice – 1 000 + repetitions daily.
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Community-based cardiac rehab programs – supervised aerobic plan.
Dietary Molecular Supplements
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1. Omega-3 fish oil 1–2 g/day – anti-inflammatory membrane repair; watch bleeding risk.
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2. Curcumin 500 mg twice daily with pepperine – antioxidant; early trial shows smaller infarcts. flintrehab.compmc.ncbi.nlm.nih.gov
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3. Coenzyme Q10 200 mg/day – mitochondrial support; meta-analysis hints at functional gains.
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4. Vitamin D3 2 000 IU/day – modulates neurotrophic factors.
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5. Magnesium citrate 300 mg/day – supports synaptic plasticity.
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6. Alpha-lipoic acid 600 mg/day – scavenges free radicals and improves glucose control.
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7. Resveratrol 250 mg/day – activates sirtuins and cerebral blood flow.
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8. N-acetyl-cysteine 600 mg TID – boosts glutathione pools.
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9. B-complex with folate – lowers homocysteine.
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10. Probiotic blend (Lactobacillus + Bifidobacterium 10 billion CFU) – gut-brain axis anti-inflammation.
Always discuss with a physician; evidence is supportive but not conclusive. health.com
Key Drugs for Dominant-Hemisphere MCA Stroke
(Each paragraph gives plain-English purpose, class, dosage, timing window, key side effects)
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Alteplase (tPA) – Thrombolytic. Dose = 0.9 mg/kg (max 90 mg): 10 % IV bolus, rest over 60 min within 4.5 h of onset. Risk = bleeding. ahajournals.org
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Tenecteplase – Single IV push 0.25 mg/kg (max 25 mg) within 4.5 h; easier administration, similar bleed risk. tnkase.comdhhs.ne.gov
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Aspirin 160–325 mg once after 24 h CT-clear, then 81 mg daily. Antiplatelet; watch stomach upset.
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Clopidogrel 300 mg load then 75 mg/d – when combined with aspirin for 21 days in minor stroke to reduce recurrence; bleeding/bruising. jamanetwork.comahajournals.org
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Atorvastatin 80 mg nightly – high-intensity statin; lowers LDL and stabilizes plaques; watch muscle pain. ahajournals.org
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Rosuvastatin 40 mg nightly – alternative high-intensity statin.
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Apixaban 5 mg BID – DOAC anticoagulant for AF-related stroke once hemorrhage is ruled out; risk = bleeding. jacc.org
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Rivaroxaban 20 mg daily – similar to apixaban; renal dose adjust.
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Lisinopril 10–40 mg daily – ACE inhibitor to keep BP < 140/90 after acute phase; can cause cough. ahajournals.orgpcna.net
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Amlodipine 5–10 mg daily – calcium-channel blocker; controls BP without fatigue.
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Empagliflozin 10 mg daily – SGLT2 inhibitor for diabetics; lowers vascular risk but watch dehydration.
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Semaglutide 0.5 mg weekly – GLP-1 agonist that cuts stroke risk in diabetics; GI side effects. verywellhealth.com
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Levetiracetam 500 mg BID – antiepileptic for post-stroke seizures; fatigue and mood changes possible.
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Metoprolol 25–100 mg BID – rate control in AF; avoid bradycardia.
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Ezetimibe 10 mg daily – add-on to statin to reach LDL < 70 mg/dL. stroke.org
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Nicardipine IV infusion – titrated to keep BP < 180/105 mm Hg during first 24 h; converts to oral later.
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Mannitol 0.25–1 g/kg IV – reduces cerebral edema in malignant infarct; monitor osmolar gap.
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Dexamethasone 4 mg Q6h – anti-edema adjunct when herniation threatened (controversial).
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Fluoxetine 20 mg daily – improves post-stroke mood and may enhance motor recovery; monitor for GI upset.
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Vitamin K1 10 mg IV – reverses warfarin pre-thrombolysis if INR > 1.7.
Special Drugs (Bisphosphonates, Regenerative, Viscous, Stem-Cell-Related)
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Alendronate 70 mg weekly – bisphosphonate preventing immobilization-related osteoporosis post-stroke.
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Zoledronic acid 5 mg IV yearly – potent fracture risk reducer.
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Teriparatide 20 µg SC daily – regenerative bone anabolic for hemiplegic hip.
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Hyaluronic-acid injection 40 mg into hemiparetic shoulder – viscosupplement easing painful glenohumeral arthritis from subluxation.
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Platelet-rich plasma 3 mL into spastic flexor forearm – regenerative soft-tissue healing.
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Mesenchymal stem-cell IV infusion 1 × 10⁶ cells/kg once – experimental neuro-regeneration; research setting only. pubmed.ncbi.nlm.nih.gov
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Allogeneic MultiStem (phase III) – up-to-24-h window IV to dampen inflammation. jamanetwork.com
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3K3A-activated protein C 540 µg/kg IV – cytoprotective; trial stage.
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Nerinetide (NA-1) 2.6 mg/kg IV – PSD-95 inhibitor reducing penumbral death in EVT patients.
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Edaravone dexborneol 30 mg IV BID – free-radical scavenger approved in parts of Asia.
Note: Items 6-10 remain experimental or region-restricted and should only be used in clinical trials.
Surgical / Endovascular Procedures
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Mechanical thrombectomy – stent-retriever or aspiration within 24 h for large-vessel occlusion; restores flow and cuts disability. ahajournals.org
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Decompressive hemicraniectomy – removes a skull flap to relieve pressure in malignant edema; halves mortality. pmc.ncbi.nlm.nih.gov
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Carotid endarterectomy – plaque removal prevents future stroke when ipsilateral stenosis ≥ 70 %. strokebestpractices.ca
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Carotid artery stenting – option for high-surgical-risk patients. esvs.org
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Extracranial-intracranial bypass – vein graft supplies distal MCA in rare moyamoya or athero-occlusion.
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Ventriculoperitoneal shunt – treats hydrocephalus from infarct-related bleed.
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Botulinum-toxin chemodenervation (office procedure) – reduces spasticity improving range.
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Deep-brain stimulation of thalamus – experimental for post-stroke tremor.
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Orthopedic tendon-lengthening – releases severe ankle equinus contracture preventing ulcers.
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Shoulder arthroscopy with capsular release – relieves painful frozen shoulder hindering rehab.
Prevention Tips
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Keep blood pressure below 130/80 mm Hg.
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Take prescribed high-intensity statin every night.
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If you have AF, stay on anticoagulation.
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Walk briskly 30 min a day or do HIIT equivalents.
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Eat a Mediterranean-style diet rich in fruits, veggies, fish, and olive oil.
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Quit smoking completely; even a few cigarettes raise risk.
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Limit alcohol to ≤ 1 drink/day women or ≤ 2 men.
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Maintain healthy waist circumference; lose ≥ 5 % body weight if overweight.
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Screen and treat sleep apnea; CPAP lowers recurrent stroke.
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Keep fasting LDL < 70 mg/dL and HbA1c < 7 % if diabetic. ahajournals.orgverywellhealth.com
When to See a Doctor Urgently
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FAST signs – Face droop, Arm weakness, Speech difficulty, Time to call emergency.
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Sudden severe headache with vomiting.
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New seizures or collapse.
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Worsening weakness or swelling days after the first stroke (signals malignant edema).
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Sudden vision loss or new atrial fibrillation fluttering.
Call emergency services immediately; “time is brain.”
Things To Do and 10 Things To Avoid
Do
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Take medicines exactly as prescribed.
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Use a daily pill box and alarms.
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Keep a blood-pressure log.
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Attend physiotherapy consistently.
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Eat plenty of colorful plants.
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Stay hydrated.
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Wear compression socks on weak leg if advised.
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Practice speech drills daily.
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Join a stroke-survivor support group.
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Get annual flu and pneumonia shots.
Avoid
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Stopping antiplatelets without approval.
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Ignoring sudden numbness or dizziness.
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Sitting for > 60 minutes without leg movement.
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Excess salt and ultra-processed snacks.
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Binge drinking.
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Crash dieting that loses muscle.
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Heavy lifting in the first month post-stroke.
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Over-the-counter decongestants that raise BP.
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Smoking or vaping nicotine.
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“Dr. Google” self-medication without professional input.
Frequently Asked Questions
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Can speech return fully? – Many regain conversational speech within 3–6 months with intensive therapy; younger brains recover better.
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Is thrombectomy painful? – Performed under conscious sedation; most feel only groin pressure.
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What is the golden time for tPA? – Ideally < 3 h, still benefits up to 4.5 h.
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Can I fly after stroke? – Usually safe after 2 weeks if stable; discuss DVT precautions.
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Do statins cause memory loss? – High-quality studies show no link; benefits outweigh anecdotal concerns.
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Will I need lifelong anticoagulation? – Only if a permanent source like AF exists.
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Are stem-cell therapies approved? – Not yet; only within clinical trials.
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What exercises are safe? – Walking, stationary cycling, supervised resistance bands; avoid high-impact until strength returns.
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Will depression go away? – Post-stroke depression is common; SSRIs plus counseling are effective.
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Can supplements replace medication? – No; they may help recovery but never substitute proven drugs.
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Is shoulder pain normal? – Yes, due to subluxation; early positioning and taping help.
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Why is my arm spastic? – Spinal reflexes over-fire after brain injury; stretching and botulinum toxin improve it.
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Does weather affect recovery? – Hot, humid conditions may worsen fatigue; hydrate and cool environment.
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Can a second stroke be prevented? – Up to 80 % reduction is possible with strict risk-factor control.
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Are women’s risks different? – Pregnancy, hormone therapy, and migraine raise risk; guidelines now tailor prevention for women. verywellhealth.com
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: July 04, 2025.