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Child with Hemiplegia

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Etiopathogenesis

1. Definition Acute onset hemiplegia is the sudden development of weakness on one side of the body. It is a neurological emergency caused by the disruption of the Corticospinal (Pyramidal) pathways.

2. Pathophysiology The mechanism of weakness depends on the underlying etiology:

  • Ischemia/Infarction: Energy failure leading to cytotoxic edema (Stroke).
  • Post-ictal Inhibition: Exhaustion of neurons following a seizure (Todd’s Paresis).
  • Inflammation/Demyelination: Interruption of conduction (ADEM).
  • Cortical Spreading Depression: Wave of depolarization followed by suppression (Hemiplegic Migraine).

3. Etiology (Classification) Causes are broadly divided into Vascular (Stroke) and Non-Vascular (Mimics).

A. Vascular Causes (Stroke) - Most Common

  • Arterial Ischemic Stroke (AIS):
    • Arteriopathies: Focal Cerebral Arteriopathy (Post-Varicella), Moyamoya disease, Dissection (Trauma).
    • Hematologic: Sickle Cell Disease, Prothrombotic states (Protein C/S deficiency).
    • Cardiac: Congenital Heart Disease (R-L shunts), Endocarditis.
  • Cerebral Sinovenous Thrombosis (CSVT): Complication of mastoiditis, dehydration, or nephrotic syndrome.
  • Hemorrhagic Stroke: Rupture of AVM or Cavernoma.

B. Infectious and Inflammatory

  • ADEM (Acute Disseminated Encephalomyelitis): Post-viral/vaccine immune response affecting white matter.
  • Intracranial Abscess: Pyogenic or Tuberculoma (Mass effect).
  • Meningitis: Bacterial meningitis causing vasculitis/infarction.
  • Encephalitis: HSV (typically causes focal temporal lobe necrosis).

C. Functional and Paroxysmal (Common Mimics)

  • Todd’s Paresis: Post-ictal weakness following a focal seizure. Lasts minutes to 48 hours.
  • Hemiplegic Migraine: Headache preceded/accompanied by reversible hemiplegia. Strong family history.

D. Metabolic / Toxic

  • Hypoglycemia: Can present with focal signs (stroke mimic).
  • MELAS: Mitochondrial stroke-like episodes.

Management

1. Acute Stabilization (The “ABC” Approach)

  • Airway/Breathing: Protect airway if GCS is low. Maintain oxygen saturation > 94%.
  • Circulation: Maintain normotension. Avoid hypotension (worsens perfusion).
  • Glucose: Check Bedside Glucose immediately. Correct hypoglycemia.
  • Seizure Control: Stop active seizures with Benzodiazepines (Midazolam/Lorazepam).

2. Diagnostic Evaluation The goal is to differentiate Stroke from Mimics.

  • Neuroimaging (Stat):
    • MRI Brain with DWI (Gold Standard):
      • Restricted Diffusion: Confirms Ischemic Stroke.
      • T2 Hyperintensities: Suggests ADEM or Encephalitis.
      • Ring Enhancement: Suggests Abscess.
    • CT Head: Used if MRI unavailable or to rule out acute hemorrhage/mass effect.
  • Laboratory Workup:
    • CBC, Platelets, Coagulation profile (PT/APTT).
    • Inflammatory markers (CRP, ESR) for ADEM/Infection.
    • Sickling test (if relevant).
  • EEG: If non-convulsive status or Todd’s paresis is suspected.

3. Specific Treatment (Etiology Driven)

  • A. If Vascular (Stroke):

    • Neuroprotection: Maintain Normothermia, Normoglycemia, Normotension.
    • Aspirin: 3–5 mg/kg/day (First-line for non-cardioembolic AIS).
    • Anticoagulation (LMWH): Indicated for Arterial Dissection or CSVT.
    • Sickle Cell: Exchange transfusion to lower HbS < 30%.

  • B. If Inflammatory (ADEM):

    • High-dose IV Methylprednisolone (30 mg/kg/day for 3–5 days).
    • IVIG if steroid-unresponsive.

  • C. If Infectious:

    • Abscess: IV Antibiotics + Neurosurgical drainage.
    • HSV Encephalitis: IV Acyclovir.

  • D. If Todd’s Paresis:

    • Optimization of anti-epileptic drugs; observation (weakness resolves spontaneously).

4. Rehabilitation

  • Early initiation of Physiotherapy (constraint-induced movement therapy) and Occupational Therapy to prevent contractures and utilize neuroplasticity.

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