Child with Hemiplegia

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.