Supratentorial Ipsilateral Hemiplegia

Types
Causes
Symptoms
Diagnostic Tests
Non-Pharmacological Treatments
Pharmacological Treatments
Dietary Molecular Supplements
Regenerative & Specialty Drugs
Surgical Interventions
Prevention Strategies
When to See a Doctor
“What to Do” & “What to Avoid”
Frequently Asked Questions
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Supratentorial Ipsilateral Hemiplegia is a rare neurological condition in which paralysis of one side of the body occurs on the same side as a lesion located above the tentorium cerebelli (the supratentorial compartment of the brain). Under normal circumstances, damage to the motor pathways in one cerebral hemisphere causes weakness or paralysis on the opposite side of the body. In supratentorial ipsilateral hemiplegia, however, a mass lesion or hemorrhage in one hemisphere pushes the brain downward through the tentorial notch, compressing the opposite cerebral peduncle against the rigid tentorial edge. This “notch” damages motor fibers before they cross, producing a paradoxical weakness on the same side as the original lesion.

Supratentorial ipsilateral hemiplegia is a rare neurologic phenomenon in which a lesion above the tentorium cerebelli (supratentorial region) paradoxically produces weakness of the same-side body (hemiplegia), most often via Kernohan’s notch phenomenon. In this scenario, an expanding mass (e.g., epidural hematoma, tumor) on one cerebral hemisphere herniates under the tentorial edge, compressing the contralateral cerebral peduncle. The result is a “false localizing sign” of weakness on the same side as the primary lesion.

The phenomenon was first described by Kernohan and Woltman in 1929, and is often called the Kernohan–Woltman notch phenomenon. It represents a “false localizing sign,” because the clinical findings misleadingly suggest damage in the hemisphere ipsilateral to the weakness. Patients typically present with acute or subacute onset of limb paralysis on the same side as a supratentorial mass, accompanied by signs of increased intracranial pressure such as headache, nausea, or altered consciousness. Recognizing this condition is critical to avoid surgical missteps and to plan appropriate treatment to relieve the mass effect and preserve neurological function.

Types

Acute Traumatic Kernohan’s Notch Phenomenon
Occurring after severe head injury, acute traumatic Kernohan’s notch involves rapid accumulation of blood—often from an epidural or subdural hematoma—causing transtentorial herniation. The resulting compression of the contralateral cerebral peduncle produces sudden ipsilateral paralysis.
Chronic Subdural Hematoma–Induced Notch
In chronic subdural collections, slower venous bleeding allows gradual brain shift. Over weeks or months, this may indent the peduncle, leading to progressive ipsilateral limb weakness that can fluctuate with changes in intracranial pressure.
Neoplastic Mass–Related Notch
Large tumors—primary or metastatic—above the tentorium may slowly expand. As they grow, they displace brain tissue and compress the opposite peduncle. Symptoms develop insidiously, often in tandem with signs of focal cortical irritation like seizures.
Vascular Lesion–Caused Notch
Space-occupying vascular malformations (such as arteriovenous malformations or hemorrhagic strokes) can precipitate herniation. When bleeding is brisk, clinical presentation mimics that of traumatic herniation; when gradual, it resembles the neoplastic variety.
Infectious or Inflammatory Mass Effect
Brain abscesses, tuberculomas, or granulomas may behave like tumors, exerting mass effect. These lesions often present subacutely, with systemic signs of infection accompanying the paradoxical ipsilateral weakness.
Iatrogenic Postoperative Notch
Occasionally seen after neurosurgical procedures, residual or recurrent hematoma, contusion, or brain swelling adjacent to the resection cavity can push tissue across the tentorial notch, triggering ipsilateral hemiplegia.
Edema from Large Infarcts
Massive ischemic strokes in one hemisphere can lead to cytotoxic and vasogenic edema. If unchecked, the swelling may herniate the brain downward, creating a Kernohan’s notch and resulting in same-side motor deficits.
Cerebral Venous Sinus Thrombosis
Extensive venous outflow obstruction can cause hemorrhagic infarction and raised intracranial pressure. In rare cases, the pressure gradient produces peduncle indentation and ipsilateral weakness.

Causes

Epidural Hematoma
Rapid arterial bleeding between skull and dura creates high-pressure mass, leading to acute transtentorial herniation and peduncular compression.
Acute Subdural Hematoma
Venous bleeding beneath the dura accumulates quickly in trauma, causing midline shift and contralateral peduncle indentation.
Chronic Subdural Hematoma
Slow venous ooze builds over weeks, producing a gradually enlarging mass and unpredictable shifts with changes in intracranial pressure.
Intracerebral Hemorrhage
Bleeding into brain parenchyma, especially in the temporal or parietal lobes, may directly compress adjacent structures and shift the midline.
Glioblastoma Multiforme
Aggressive primary brain tumor expands rapidly, often outstripping blood supply, causing edema and mass effect.
Meningioma
Typically benign and slow-growing, meningiomas on the cerebral convexities can reach large sizes before producing symptoms.
Metastatic Carcinoma
Secondary brain tumors—commonly from lung or breast primaries—can be multiple and hemorrhagic, accelerating intracranial pressure rise.
Brain Abscess
Focal infection with pus formation creates a ring-enhancing lesion that may mimic tumor, often with fever and elevated inflammatory markers.
Arteriovenous Malformation (AVM)
Abnormal high-flow vessels can rupture, leading to hemorrhage or chronic mass effect from nidus.
Cavernous Malformation
Low-flow vascular lesions that may bleed repeatedly, causing mixed-density lesions on imaging and subtle mass shifts.
Primary CNS Lymphoma
In immunocompromised patients, lymphoma can behave like a rapidly growing mass, with both peritumoral edema and mass effect.
Tuberculoma
Mycobacterial granuloma in the brain is common in endemic areas; patients present with subacute headaches and focal deficits.
Neurosarcoidosis
Granulomatous inflammation creates mass lesions that can mimic tumors or abscesses, sometimes with cranial nerve involvement.
Traumatic Contusion
Brain bruises from coup-contrecoup injuries may hemorrhage and swell, causing localized mass effect and shift.
Hemorrhagic Conversion of Ischemic Stroke
Large infarcts may bleed into necrotic tissue, creating a space-occupying lesion in the first week after stroke.
Postoperative Hematoma
Bleeding at the surgical site can accumulate rapidly, especially in anticoagulated patients, leading to acute herniation syndromes.
Spontaneous Subarachnoid Hemorrhage with Clot Formation
Though primarily in the subarachnoid space, large clots can lodge in sulci and fissures, promoting focal edema and pressure.
Idiopathic Intracranial Hypertension with Asymmetric Edema
Rarely, idiopathic pressure elevation can cause focal bulging of one hemisphere against the tentorium.
Cryptococcal Granuloma
Fungal infections in immunosuppressed patients can form mass-like lesions with surrounding edema.
Parasitic Cyst (Neurocysticercosis)
Larval cysts of Taenia solium provoke inflammatory edema and may coalesce into large masses in endemic regions.

Symptoms

Ipsilateral Limb Weakness
The hallmark sign is paralysis or severe weakness of arm and leg on the same side as the brain lesion.
Spasticity
Increased muscle tone with resistance to passive movement often develops days after injury, indicating upper motor neuron involvement.
Hyperreflexia
Exaggerated deep tendon reflexes occur due to loss of inhibitory signals from the damaged motor pathways.
Positive Babinski Sign
Stroking the sole elicits an upward big toe response, a classic indicator of corticospinal tract disruption.
Altered Consciousness
Ranging from drowsiness to coma, altered mental status reflects raised intracranial pressure and brainstem compression.
Headache
Often severe and throbbing, headache results from stretching of pain-sensitive dura and increased intracranial pressure.
Nausea and Vomiting
Pressure on the medullary vomiting centers produces nausea, retching, and projectile vomiting.
Ipsilateral Oculomotor Nerve Palsy
Compression near the edge of the tentorium can involve cranial nerve III, causing eyelid droop and pupil dilation on the same side.
Pupillary Asymmetry
Unequal pupil sizes (anisocoria) arise when one oculomotor nerve is compressed.
Visual Field Defects
Displacement of optic radiations may cause homonymous hemianopia or quadrantanopia.
Seizures
Irritation of cortical tissue by mass or hemorrhage can produce focal or generalized seizures.
Aphasia
When the dominant hemisphere is involved, patients may struggle to speak or understand language.
Dysarthria
Slurred or slow speech can result from motor control disruption in facial and tongue muscles.
Ataxia
Loss of coordination occurs if the mass effect impinges on cerebellar pathways above the tentorium.
Sensory Changes
Numbness, tingling, or decreased sensation may accompany motor deficits on the affected side.
Neck Stiffness
Particularly in infectious causes, meningeal irritation produces resistance to neck flexion.
Fever
Suggestive of abscess or other infectious etiologies coexisting with mass effect.
Cognitive Dysfunction
Memory problems, confusion, or personality changes can arise from frontal lobe involvement.
Hydrocephalus Signs
Enlarged ventricles from obstructive effects may produce gait disturbance and urinary incontinence.
Posturing
Decorticate or decerebrate postures reflect severe brainstem compression in late stages.

Diagnostic Tests

Physical Exam Tests

Manual Muscle Testing (MRC Scale)
Grading muscle strength on a 0–5 scale helps quantify the degree of limb weakness and monitor recovery over time.
Deep Tendon Reflex Assessment
Eliciting reflexes at the biceps, triceps, patella, and Achilles provides insight into upper motor neuron involvement.
Tone Evaluation
Passive flexion and extension of limbs reveal spasticity versus flaccidity, guiding therapy choices.
Babinski Reflex Check
Stroking the lateral sole and observing toe movement confirms corticospinal tract disruption when positive.
Cranial Nerve Examination
Testing eye movements, facial symmetry, and swallowing functions identifies accompanying nerve palsies.
Sensation Testing
Using light touch, pinprick, and vibration modalities maps out sensory deficits in the affected limbs.
Coordination Tests
Finger-to-nose and heel-to-shin tests assess cerebellar function and coordination, which may be secondarily involved.
Gait Observation
Watching the patient walk (if able) can reveal spastic gait patterns, circumduction, or ataxia.

Manual Tests

Ashworth Scale for Spasticity
Grading resistance during passive movement quantifies spasticity severity for treatment planning.
Clonus Elicitation
Rapid dorsiflexion of the foot checks for rhythmic muscle contractions, a sign of hyperactive reflexes.
Hoffmann’s Sign
Flicking the distal phalanx of the middle finger can reveal upper motor neuron lesions if other fingers flex.
Pronator Drift Test
With arms outstretched and eyes closed, subtle downward rotation of one forearm indicates pyramidal tract damage.
Hoover’s Test
Differentiates true weakness from non-organic causes by assessing involuntary extension of the contralateral hip.
Lhermitte’s Sign
Neck flexion causing electric-shock sensations down the spine suggests cervical involvement or lesions.
Doll’s Eye (Oculocephalic) Maneuver
Passive head rotation to observe eye movements gauges brainstem integrity in comatose patients.
Pupillary Light Reflex Test
Shining light into each eye checks for equal constriction, indicating oculomotor nerve function.

Laboratory and Pathological Tests

Complete Blood Count (CBC)
Evaluates for infection or anemia, which may accompany abscesses or chronic disease.
Coagulation Profile (PT/INR, aPTT)
Assesses bleeding risk and guides management in hemorrhagic causes.
Comprehensive Metabolic Panel
Checks electrolytes, liver, and kidney function, since metabolic derangements can mimic neurological deficits.
Inflammatory Markers (ESR, CRP)
Elevated levels suggest infection or inflammatory masses such as abscess or neurosarcoidosis.
Blood Cultures
When infection is suspected, cultures help tailor antibiotic therapy.
Tumor Markers (e.g., CEA, AFP)
May be elevated in metastatic disease, assisting in identifying the primary cancer source.
Cerebrospinal Fluid Analysis
Obtained via lumbar puncture to detect infection, malignancy, or inflammatory changes.
Biopsy of Lesion
Stereotactic or open biopsy provides definitive histopathological diagnosis in neoplastic or infectious cases.

Electrodiagnostic Tests

Electromyography (EMG)
Measures electrical activity of muscles, distinguishing between nerve and muscle pathology.
Nerve Conduction Studies
Evaluate the speed and amplitude of peripheral nerve signals to rule out peripheral neuropathy.
Somatosensory Evoked Potentials (SSEPs)
Assess dorsal column and sensory pathway integrity from limbs to cortex.
Transcranial Magnetic Stimulation (TMS)
Stimulates cortical motor areas to evaluate corticospinal tract conduction and map functional reserve.
Motor Evoked Potentials (MEPs)
Similar to TMS but recorded from muscles, they quantify central motor conduction times.
Electroencephalography (EEG)
Records cortical electrical activity, useful when seizures accompany mass lesions.
Brainstem Auditory Evoked Potentials (BAEPs)
Test integrity of auditory pathways and brainstem function, aiding in prognosis.
Visual Evoked Potentials (VEPs)
Assess optic pathway function, especially when visual field defects are reported.

Imaging Tests

Noncontrast Head CT Scan
First-line in trauma or hemorrhage to detect blood, mass effect, and midline shift quickly.
Contrast-Enhanced CT Scan
Highlights tumors, abscess capsules, and disrupted blood–brain barrier.
Magnetic Resonance Imaging (MRI) Brain
Gold standard for detailed soft tissue resolution, differentiating edema, tumor, and infarction.
T1-, T2-, and FLAIR Sequences on MRI
Define lesion characteristics: T1 for anatomy, T2/FLAIR for edema and non-enhancing components.
Diffusion-Weighted Imaging (DWI)
Identifies acute ischemic strokes within minutes of onset, helping to detect early infarcts with mass effect.
Magnetic Resonance Angiography (MRA)
Visualizes cerebral arteries, detecting aneurysms or vascular malformations contributing to bleeding.
Magnetic Resonance Venography (MRV)
Assesses venous sinuses, diagnosing thrombosis that may lead to hemorrhagic infarction.
Digital Subtraction Angiography (DSA)
Invasive but definitive for vascular lesion characterization when noninvasive imaging is equivocal.

Non-Pharmacological Treatments

A. Physiotherapy & Electrotherapy Therapies

Transcutaneous Electrical Nerve Stimulation (TENS)
Description: Low-voltage electrical current delivered via skin electrodes.
Purpose: Pain relief and spasticity reduction.
Mechanism: Activates Aβ fibers to inhibit nociceptive signals in the dorsal horn.
Neuromuscular Electrical Stimulation (NMES)
Description: Electrical pulses that evoke muscle contractions.
Purpose: Prevent muscle atrophy and improve voluntary control.
Mechanism: Stimulates alpha-motor neurons to strengthen muscle fibers.
Functional Electrical Stimulation (FES)
Description: Timed electrical stimulation during functional tasks (e.g., gait).
Purpose: Restore task-specific movement patterns.
Mechanism: Coordinates muscle activation to mimic physiological motor sequences.
Repetitive Transcranial Magnetic Stimulation (rTMS)
Description: Magnetic pulses over motor cortex.
Purpose: Modulate cortical excitability, reduce spasticity.
Mechanism: Induces long-term potentiation or depression in targeted neural circuits.
Ultrasound Therapy
Description: High-frequency sound waves applied to tissues.
Purpose: Promote tissue healing, reduce inflammation.
Mechanism: Enhances microcirculation and fibroblast activity via mechanical acoustic streaming.
Low-Level Laser Therapy (LLLT)
Description: Near-infrared light delivered to injured tissues.
Purpose: Accelerate nerve regeneration, reduce edema.
Mechanism: Photobiomodulation increases ATP production and cell proliferation.
Interferential Current Therapy
Description: Crossing medium-frequency currents.
Purpose: Deep pain control and muscle relaxation.
Mechanism: Beats at low frequency create analgesic effects via gate control.
Galvanic Stimulation
Description: Continuous direct current.
Purpose: Sensory retraining and pain modulation.
Mechanism: Alters nerve membrane potentials, promoting desensitization.
Diathermy (Shortwave/Microwave)
Description: Deep heating using electromagnetic waves.
Purpose: Increase tissue extensibility, decrease joint stiffness.
Mechanism: Thermal effects increase circulation and collagen flexibility.
Cryotherapy
Description: Application of cold packs or vapocoolant sprays.
Purpose: Control acute pain and spasticity.
Mechanism: Lowers nerve conduction velocity and local metabolism.
Thermotherapy
Description: Heat application via packs or infrared lamps.
Purpose: Relax muscles, improve range of motion.
Mechanism: Vasodilation increases nutrient delivery and waste removal.
Pulsed Electromagnetic Field Therapy (PEMF)
Description: Low-frequency electromagnetic pulses.
Purpose: Enhance nerve repair and pain relief.
Mechanism: Influences calcium ion flux and nitric oxide synthesis in neurons.
Photobiomodulation Therapy
Description: Light in red/near-infrared range applied to nerve pathways.
Purpose: Promote neuroprotection and reduce oxidative stress.
Mechanism: Activates cytochrome C oxidase in mitochondria, boosting ATP.
Vibration Therapy
Description: Local or whole-body mechanical vibration.
Purpose: Improve muscle tone, proprioception.
Mechanism: Stimulates muscle spindles, enhancing motor neuron firing patterns.
Electromyographic Biofeedback
Description: Real-time EMG signals displayed to patient.
Purpose: Foster active muscle control and reduce co-contraction.
Mechanism: Visual/auditory feedback enhances neuroplasticity through motor learning.

B. Exercise Therapies

Strengthening Exercises
Focused resistance training for weakened muscle groups to restore functional capacity.
Stretching & Range-of-Motion
Regular passive and active stretches to maintain joint mobility and prevent contractures.
Task-Specific Training
Practicing everyday activities (e.g., reaching, grasping) to reinforce neural pathways.
Balance & Proprioception Training
Use of unstable surfaces and weight shifts to improve postural control.
Gait Training
Assisted walking practice—overground or treadmill—to normalize walking patterns.
Constraint-Induced Movement Therapy
Restricting the unaffected limb to encourage use of the affected side and cortical remapping.

C. Mind-Body Therapies

Yoga
Combines gentle postures and breathing to enhance body awareness and reduce spasticity.
Tai Chi
Slow, flowing movements improve balance, coordination, and mind–body connection.
Guided Imagery & Relaxation
Visualization techniques to lower muscle tone and anxiety.
Mindfulness Meditation
Focused attention practices that decrease stress hormones and improve motor control.

D. Educational & Self-Management Strategies

Patient Education Programs
Structured teaching on condition, prognosis, and self-care to empower active involvement.
Home Exercise Diaries
Written logs to track adherence, progress, and setbacks in rehabilitation exercises.
Goal-Setting & Action Planning
Collaborative SMART goals (Specific, Measurable, Achievable, Relevant, Timely) for motivation.
Pain-Coping Skills Training
Cognitive-behavioral techniques to reinterpret pain and reduce catastrophizing.
Caregiver Training & Support
Instruction for family members on safe transfers, positioning, and emotional support.

Pharmacological Treatments

Aspirin (Antiplatelet)
– Dosage: 75–325 mg once daily in acute stroke prevention.
– Timing: With food in the morning.
– Side Effects: Gastrointestinal upset, bleeding risk.
Clopidogrel (Antiplatelet)
– Dosage: 75 mg once daily.
– Timing: Morning, with or without food.
– Side Effects: Thrombocytopenia, rash, bleeding.
Warfarin (Anticoagulant)
– Dosage: 2–5 mg daily, adjusted to INR 2–3.
– Timing: Evening, consistent timing.
– Side Effects: Bleeding, skin necrosis, teratogenicity.
Heparin (Low-Molecular-Weight) (Anticoagulant)
– Dosage: 40 mg subcutaneously once daily.
– Timing: At the same time each day.
– Side Effects: Heparin-induced thrombocytopenia, bleeding.
Atorvastatin (Statin)
– Dosage: 10–80 mg once daily.
– Timing: Evening to align with hepatic cholesterol synthesis.
– Side Effects: Myalgia, elevated liver enzymes.
Lisinopril (ACE Inhibitor)
– Dosage: 5–20 mg once daily.
– Timing: Morning.
– Side Effects: Cough, hyperkalemia, hypotension.
Nimodipine (Calcium-Channel Blocker)
– Dosage: 60 mg every 4 hours for 21 days (subarachnoid hemorrhage).
– Timing: Evenly spaced doses.
– Side Effects: Hypotension, headache.
Mannitol (Osmotic Agent)
– Dosage: 0.25–1 g/kg IV every 6 hours.
– Timing: Acute intracranial pressure spikes.
– Side Effects: Electrolyte imbalance, dehydration.
Phenytoin (Antiepileptic)
– Dosage: 100 mg three times daily (maintenance).
– Timing: With meals.
– Side Effects: Gingival hyperplasia, ataxia, rash.
Gabapentin (Antineuropathic)
– Dosage: 300 mg three times daily, titrate to 1,200 mg/day.
– Timing: Morning, noon, evening.
– Side Effects: Dizziness, somnolence.
Baclofen (Antispasticity)
– Dosage: 5 mg three times daily, up to 80 mg/day.
– Timing: Titrate gradually.
– Side Effects: Weakness, sedation.
Tizanidine (Antispasticity)
– Dosage: 2 mg every 6–8 hours, max 36 mg/day.
– Timing: With or without food.
– Side Effects: Hypotension, dry mouth.
Dantrolene (Antispasticity)
– Dosage: 25 mg once daily, titrate to 100 mg four times daily.
– Timing: With meals.
– Side Effects: Hepatotoxicity, muscle weakness.
Diazepam (Benzodiazepine)
– Dosage: 2–10 mg two to four times daily as needed.
– Timing: Bedtime if sedation is an issue.
– Side Effects: Sedation, dependence.
Morphine (Opioid Analgesic)
– Dosage: 2.5–10 mg IV/SC every 2–4 hours PRN.
– Timing: As needed for severe pain.
– Side Effects: Respiratory depression, constipation.
Ibuprofen (NSAID)
– Dosage: 200–400 mg every 4–6 hours PRN.
– Timing: With food.
– Side Effects: GI bleeding, renal impairment.
Acetaminophen (Analgesic)
– Dosage: 500–1,000 mg every 4–6 hours, max 4 g/day.
– Timing: Evenly spaced.
– Side Effects: Hepatotoxicity at high doses.
Edaravone (Neuroprotective)
– Dosage: 30 mg IV twice daily for 14 days.
– Timing: Acute ischemic stroke.
– Side Effects: Contusion, gait disturbance.
Citicoline (Nootropic)
– Dosage: 500–2,000 mg/day orally.
– Timing: Divided doses.
– Side Effects: Insomnia, digestive upset.
Rivaroxaban (Direct Oral Anticoagulant)
– Dosage: 20 mg once daily with evening meal.
– Timing: Evening.
– Side Effects: Bleeding, anemia.

Dietary Molecular Supplements

Omega-3 Fatty Acids (Fish Oil)
– Dosage: 1,000 mg omega-3 daily.
– Function:** Anti-inflammatory and neuroprotective.
– Mechanism:** Modulates membrane fluidity and reduces cytokine production.
Vitamin B12 (Cobalamin)
– Dosage: 1,000 µg IM weekly (deficiency) or 500 µg PO daily.
– Function:** Myelin synthesis and repair.
– Mechanism:** Cofactor for methylation reactions in CNS.
Folic Acid
– Dosage: 400–800 µg daily.
– Function:** Neurogenesis support.
– Mechanism:** DNA synthesis and repair in neurons.
Vitamin D₃ (Cholecalciferol)
– Dosage: 1,000–2,000 IU daily.
– Function:** Modulates neuroinflammation.
– Mechanism:** Binds CNS vitamin D receptors, regulating neurotrophic factors.
Magnesium
– Dosage: 200–400 mg daily.
– Function:** Neurotransmission and spasm reduction.
– Mechanism:** NMDA receptor antagonism, stabilizing neuronal membranes.
Coenzyme Q₁₀
– Dosage: 100–300 mg daily.
– Function:** Mitochondrial energy support.
– Mechanism:** Electron carrier in oxidative phosphorylation, reducing oxidative stress.
Curcumin
– Dosage: 500 mg twice daily with piperine.
– Function:** Anti-inflammatory and antioxidant.
– Mechanism:** Inhibits NF-κB pathway and scavenges free radicals.
Resveratrol
– Dosage: 150–500 mg daily.
– Function:** Neuroprotection via SIRT1 activation.
– Mechanism:** Enhances mitochondrial biogenesis and anti-apoptotic signaling.
Acetyl-L-Carnitine
– Dosage: 1,000–2,000 mg daily.
– Function:** Supports neuronal energy metabolism.
– Mechanism:** Transports fatty acids into mitochondria for ATP generation.
Ginkgo Biloba Extract
– Dosage: 120–240 mg daily.
– Function:** Improves cerebral blood flow and cognition.
– Mechanism:** Vasodilation via nitric oxide and antioxidant effects.

Regenerative & Specialty Drugs

Bisphosphonates

Alendronate
– Dosage: 70 mg once weekly.
– Function:** Prevents osteoporosis in immobilized patients.
– Mechanism:** Inhibits osteoclast-mediated bone resorption.
Zoledronic Acid
– Dosage: 5 mg IV once yearly.
– Function:** Long-term bone density support.
– Mechanism:** Binds hydroxyapatite, inducing osteoclast apoptosis.

Regenerative Growth Factors

Erythropoietin (EPO)
– Dosage: 30,000 IU SC weekly (stroke trials).
– Function:** Neuroprotection and angiogenesis.
– Mechanism:** Activates anti-apoptotic pathways in neurons.
Granulocyte Colony-Stimulating Factor (G-CSF)
– Dosage: 5 µg/kg SC daily for 5 days.
– Function:** Mobilizes stem cells, supports repair.
– Mechanism:** Promotes bone marrow progenitor migration to injury sites.
Intravenous IGF-1
– Dosage: Experimental.
– Function:** Promotes neuronal survival and synaptic plasticity.
– Mechanism:** Activates PI3K/Akt signaling in CNS.

Viscosupplementation

Hyaluronic Acid Injection
– Dosage: 20 mg intra-articular weekly ×3 (for osteoarthritis post-immobilization).
– Function:** Joint lubrication and cartilage support.
– Mechanism:** Restores viscoelasticity in synovial fluid.
Cross-Linked Sodium Hyaluronate
– Dosage: 60 mg single injection.
– Function:** Long-lasting joint cushioning.
– Mechanism:** Resists enzymatic degradation for >6 months.
Polyacrylamide Hydrogel
– Dosage: 2 mL intra-articular.
– Function:** Soft tissue augmentation in atrophied muscles.
– Mechanism:** Provides mechanical scaffold for tissue regrowth.

Stem-Cell Based Therapies

Autologous Mesenchymal Stem Cells (MSCs)
– Dosage: 10–50 million cells intrathecal or IV.
– Function:** Promote neurorepair and immunomodulation.
– Mechanism:** Secrete trophic factors and differentiate into neural lineages.
Allogeneic Umbilical Cord-Derived MSCs
– Dosage: 1–2 million cells/kg IV infusion.
– Function:** Enhance functional recovery.
– Mechanism:** Paracrine signaling to reduce inflammation and apoptosis.

Surgical Interventions

Decompressive Craniectomy
– Procedure:** Remove skull flap to lower intracranial pressure.
– Benefit:** Reduces herniation risk and secondary injury.
Hematoma Evacuation
– Procedure:** Burr hole or craniotomy to remove intracerebral/extradural bleed.
– Benefit:** Immediate pressure relief, improved perfusion.
Tumor Resection
– Procedure:** Microsurgical excision of supratentorial mass.
– Benefit:** Resolves mass effect causing hemiplegia.
Endoscopic Third Ventriculostomy
– Procedure:** Create CSF bypass in obstructive hydrocephalus.
– Benefit:** Normalizes pressure without permanent shunt.
Carotid Endarterectomy
– Procedure:** Remove plaque from internal carotid artery.
– Benefit:** Reduces stroke risk in ipsilateral hemisphere.
Mechanical Thrombectomy
– Procedure:** Catheter-based clot retrieval in acute ischemic stroke.
– Benefit:** Rapid reperfusion, better motor outcomes.
Microvascular Decompression
– Procedure:** Relieve vascular compression on cranial nerves (if coexistent neuropathy).
– Benefit:** Alleviates secondary motor deficits.
Selective Dorsal Rhizotomy
– Procedure:** Section sensory nerve roots to reduce spasticity.
– Benefit:** Long-term spasticity control in chronic hemiplegia.
Tendon Transfer Surgery
– Procedure:** Re-anchor tendons from functioning muscles to restore balance.
– Benefit:** Improves hand and foot function.
Intrathecal Baclofen Pump
– Procedure:** Implant pump to deliver baclofen directly to spinal CSF.
– Benefit:** Targeted spasticity management with fewer systemic side effects.

Prevention Strategies

Blood Pressure Control
Maintaining target BP (< 130/80 mmHg) to reduce stroke risk.
Lipid Management
Statin therapy to achieve LDL < 70 mg/dL.
Diabetes Management
HbA1c < 7% via diet, medications.
Smoking Cessation
Eliminates vasculotoxic effects of tobacco.
Healthy Diet
DASH or Mediterranean diet rich in fruits, vegetables, whole grains.
Regular Exercise
≥ 150 minutes/week moderate aerobic activity.
Weight Management
BMI 18.5–24.9 kg/m² to lower vascular risk.
Moderate Alcohol
≤ 1 drink/day women, ≤ 2 drinks/day men.
Stress Reduction
Mindfulness, counseling to control cortisol spikes.
Antiplatelet Prophylaxis
Low-dose aspirin for high cardiovascular risk patients.

When to See a Doctor

Sudden Onset of Weakness: Any abrupt limb or facial droop.
Severe Headache: “Worst headache of life” with neurological signs.
Altered Consciousness: Confusion, drowsiness, or coma.
Seizures: New-onset convulsions.
Vision Changes: Sudden vision loss or double vision.
Balance Problems: Acute dizziness or inability to stand.
Speech Difficulties: Slurred or garbled speech.
New Numbness/Tingling: Especially unilateral.
Severe Neck Stiffness: May indicate hemorrhage or infection.
Rapid Deterioration: Any fast decline in function or cognition.

“What to Do” & “What to Avoid”

What to Do:

Adhere strictly to rehabilitation plan.
Maintain hydration and balanced nutrition.
Practice safe transfers with assistance.
Monitor blood pressure daily.
Use assistive devices as prescribed.
Keep a symptom diary for fluctuations.
Engage in social support groups.
Follow medication schedule precisely.
Rest between exercise sessions.
Attend all follow-up appointments.

What to Avoid:

Skipping rehab exercises.
Overexertion or sudden heavy lifting.
Smoking or secondhand smoke.
Excessive alcohol consumption.
Ignoring new symptoms.
Driving without medical clearance.
Unsupervised electrical therapies at home.
High-salt or high-fat diets.
Irregular medication timings.
Isolating—avoid emotional stress alone.

Frequently Asked Questions

What exactly is supratentorial ipsilateral hemiplegia?
It’s a false localizing sign where a mass above the tentorium causes same-side paralysis via compression of the opposite cerebral peduncle.
How common is this condition?
Very rare—most supratentorial lesions cause opposite-side weakness. Kernohan’s notch accounts for only 1–2% of herniation cases.
What are the main causes?
Epidural hematoma, subdural hematoma, intracerebral hemorrhage, space-occupying tumors, or rapid cerebral edema.
Can it be reversed?
Prompt surgical decompression can restore motor function in many patients; delays increase permanent deficit risk.
What is the typical recovery time?
Early motor improvements occur within weeks; full functional gains may take 6–12 months of rehab.
Are there specific imaging tests?
CT or MRI head scans detect mass effect; diffusion tensor imaging can assess corticospinal tract integrity.
Is physical therapy enough?
Therapy is essential but often combined with electrical modalities and medications for optimal recovery.
What medications help spasticity?
Baclofen, tizanidine, and intrathecal baclofen—tailored dosing minimizes side effects.
Should patients take supplements?
Omega-3s, B-vitamins, and antioxidants support neurorepair—but consult a neurologist first.
What lifestyle changes are key?
Strict blood pressure control, cholesterol management, smoking cessation, and regular exercise.
Is surgery always required?
Not always—small, stable lesions may be managed conservatively; expanding masses usually need decompression.
When is physical therapy started?
As soon as medically stable—often within 24–48 hours post-injury or surgery.
Can mental exercises help?
Yes—mirror therapy and motor imagery promote cortical reorganization.
What are long-term outcomes?
Vary widely: some regain near-normal function, others have permanent weakness or disability.
How do I prevent recurrence?
Strict management of vascular risk factors and regular follow-up imaging for tumor surveillance.

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: June 29, 2025.

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Supratentorial Ipsilateral Hemiplegia

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