Makindo Medical Notes

✨ Cerebral Palsy (CP) & Hypoxic-Ischaemic Encephalopathy (HIE) CP is the most common cause of long-term childhood physical disability. It results from a non-progressive insult to the developing brain, usually before age 2. ✨ A major perinatal cause is HIE – brain injury due to reduced oxygen and blood flow around birth. Motor impairment is the hallmark, but associated cognitive, sensory, and communication difficulties are frequent. 👉 Understanding CP & HIE is essential for exam revision, neonatal practice, and family counselling.

📌 Definition

• Cerebral Palsy: umbrella term for permanent movement & posture disorders caused by non-progressive brain injury or abnormal development before, during, or shortly after birth.
• HIE: neonatal encephalopathy caused by reduced cerebral oxygenation/perfusion ➝ neuronal death, seizures, encephalopathy, and long-term risk of CP.
• Both conditions often overlap: moderate–severe HIE is a leading cause of CP worldwide.

📊 Epidemiology

• CP prevalence: ~2–3 per 1000 live births in the UK.
• HIE occurs in ~1.5 per 1000 term births; risk is higher with intrapartum complications.
• ↑ risk in premature & low birthweight infants.
• Slight male predominance (~1.3:1).
• NICU advances = ↑ survival of preterm & HIE infants ➝ CP prevalence relatively stable.

⚠️ Aetiology

• Any insult damaging the immature brain (up to 2 years) may lead to CP. ✨ HIE is a key perinatal insult, often due to birth asphyxia, placental abruption, cord prolapse, or prolonged labour.

Stage	Examples
📌 Prenatal	Intrauterine infection (CMV, rubella, toxoplasmosis), genetic abnormalities, maternal alcohol/drug use, placental insufficiency, IUGR.
📌 Perinatal	HIE (birth asphyxia, prolonged/obstructed labour, cord accidents), prematurity (<28w), kernicterus (jaundice), neonatal hypoglycaemia.
📌 Postnatal	Meningitis, encephalitis, trauma, intraventricular haemorrhage, hypoxia, cerebral venous thrombosis.

🧩 Pathophysiology

• HIE triggers energy failure (↓ ATP), excitotoxicity, and free radical damage ➝ selective neuronal necrosis.
• Damage to motor cortex / pyramidal tracts → spastic CP.
• Damage to basal ganglia (common in HIE) → dyskinetic CP.
• Damage to cerebellum → ataxic CP.
• Prematurity & hypoxia-ischaemia are key mechanisms; periventricular leukomalacia in preterms is a classic substrate.

🧪 Investigations

• Clinical diagnosis (Hx + exam for CP; perinatal distress + seizures for HIE).
• 🧲 MRI brain = gold standard. - HIE: watershed cortical and deep grey matter injury. - CP: periventricular leukomalacia, old bleeds, malformations.
• Metabolic/genetic testing if atypical/progressive.
• Developmental assessments & MDT review.

⚕️ Management

• HIE (neonatal): therapeutic hypothermia (cooling within 6h of birth) reduces CP risk, seizure management, intensive NICU support.
• CP (long-term): multidisciplinary rehab (PT/OT/SALT), spasticity drugs (baclofen, botulinum toxin), surgery, orthoses, educational and family support.

📉 Prognosis

• HIE: outcome depends on severity; severe HIE ➝ high CP and mortality risk.
• CP: prognosis depends on type/severity/comorbidities. Mild cases ➝ independent living; severe quadriplegia ➝ shortened lifespan, respiratory complications.

🧠 Exam Pearls

• ✨ Moderate–severe HIE is the single most important perinatal cause of CP.
• Spastic diplegia → think prematurity (PVL).
• Jaundice/kernicterus → dyskinetic CP (basal ganglia).
• HIE with basal ganglia damage → dystonic/athetoid CP.