Cerebral Palsy and Hypoxic-ischaemic Encephalopathy Flashcards
Define cerebral palsy.
Non-progressive disorder of movement and posture.
Define hypoxic-ischaemic encephalopathy (HIE).
Clinical manifestation of brain injury 48 h after hypoxic event.
Explain the aetiology of cerebral palsy.
Antenatal (80%): Cerebral dysgenesis/malformation, congenital infections (rubella, toxoplasmosis, CMV).
Perinatal (10%): Hypoxic ischaemic encephalopathy, birth trauma.
Postnatal (10%): Meningitis, encephalitis, extradural haemorrhage, IVH, head injury, NAI, hyperbilirubinaemia (kernicterus), prolonged hypoglycaemia.
What is cerebral palsy associated with? What are the risk factors for cerebral palsy?
Associated: Epilepsy, learning difficulties, visual impairment, squints, hearing loss, behavioural disorders.
Risk factors: Preterm delivery, low birthweight.
What are the different types of cerebral palsy?
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Spastic:
- Hemiplegia: damage to middle cerebral artery territory.
- Diplegia: IVH, ventricular dilation or periventricular lesion.
- Quadriplegia: widespread bilateral cerebral lesions.
- Dyskinetic: Abnormality of extrapyramidal pathways (basal ganglia, thalamus).
- Ataxic: Abnormal development of cerebellum.
Explain the aetiology of hypoxic-ischaemic encephalopathy.
Obstructed labour: Malpresentation, cephalopelvic disproportion, multiple births (particularly second twin due to prolapsed cord or malpresentation), postmature neonates.
Hypotension: Maternal haemorrhage (placental abruption, placenta praevia).
Hypertension: Fulminant pregnancy-induced hypertension.
Infants at risk: Preterm infants, infants with CHD.
What is hypoxic-ischaemic encephalopathy?
Other systems affected by inadequate oxygenation and perfusion: persistent pulmonary hypertension of the newborn, meconium aspiration syndrome, acute renal failure, necrotising enterocolitis, hypoglycaemia, disseminated intravascular coagulation, myocardial ischaemia.
Occurs following perinatal events that reduce oxygen and glucose delivery to the brain. The exact pathology is unclear but involves excitatory neurotransmitters (glutamate, glycine), cell death by apoptosis, and an inflammatory reaction.
Summarise the epidemiology of cerebral palsy.
2/1000 live births. Usually presents in infancy.
Summarise the epidemiology of hypoxic-ischaemic encephalopathy.
Moderate–severe HIE in 2–4/1000 live births.
What are the general presenting symptoms for cerebral palsy?
Delayed milestones (see Global Developmental Delay chapter), poor feeding, abnormalities of tone, posture, gait, difficulties with language, impaired social skills.
What are the presenting symptoms of spastic cerebral palsy?
Affected limbs show increased tone (clasp-knife), brisk reflexes, extensor plantar responses:
- Hemiplegia: unilateral, arm > leg, fisting and early hand preference <1-year, characteristic posture of abduction of shoulder, flexion at elbow and wrist, pronation of forearm, and extension of fingers.
- Diplegia: legs > arms, hypertonicity of hip adductors! leg ‘scissoring’.
- Quadriplegia: all 4 limbs affected – arms > legs, poor head control, paucity of movement. Abnormal primitive reflexes and fisting in the first few months.
What are the presenting symptoms of dyskinetic cerebral palsy?
Normal progress until 6–9 months, followed by progressive dystonia of lower limbs, trunk, and mouth exaggerated by involuntary movements; athetoid (writhing) and choreographic movements (jerking).
What are the presenting symptoms of ataxic cerebral palsy?
Hypotonia, ataxia of trunk and limbs, postural imbalance, intention tremor.
What are the presenting symptoms of hypoxic-ischaemic encephalopathy?
Poor APGAR score after 10 minutes.
Neonatal resuscitation was required.
What is stage I hypoxic-ischaemic encephalopathy?
Level of consciousness: Hyper-alert
Muscle tone: Normal
Posture: Normal
DTR/Clonus: Hyperactive
Myoclonus: Present
Moro Reflex: Strong
