Cerebral Palsy and Hypoxic-ischaemic Encephalopathy Flashcards
Define cerebral palsy.
Disorder of movement + posture due to non-progressive lesion of motor pathways in developing brain.
Define hypoxic-ischaemic encephalopathy (HIE).
Clinical manifestation of brain injury 48 h after hypoxic event.
Explain the aetiology of cerebral palsy.
Antenatal (80%): Cerebral malformation, congenital infections (rubella, toxoplasmosis, CMV).
Perinatal (10%): birth asphyxia/ trauma.
Postnatal (10%): Meningitis, IVH, head trauma
What are the risk factors for cerebral palsy?
Maternal infection
Preterm delivery
Low birthweight
What are the different types of cerebral palsy?
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.
Mixed
Explain the aetiology of hypoxic-ischaemic encephalopathy.
Obstructed labour: Malpresentation, cephalopelvic disproportion, multiple births (particularly 2nd twin due to prolapsed cord or malpresentation), postmature neonates.
Hypotension: Maternal haemorrhage (placental abruption, placenta praevia).
HTN: Fulminant pregnancy-induced HTN.
Infants at risk: Preterm infants, infants with CHD.
Which 7 other conditions can arise due to inadequate oxygenation and perfusion in hypoxic-ischaemic encephalopathy?
Persistent pulmonary HTN of the newborn
meconium aspiration syndrome
acute renal failure
NEC
hypoglycaemia
DIC
myocardial ischaemia
Occurs following perinatal events that reduce oxygen + glucose delivery to the brain. Exact pathology is unclear but involves excitatory neurotransmitters (glutamate, glycine), cell death by apoptosis, + an inflammatory reaction.
Summarise the epidemiology of cerebral palsy.
2/1000 live births.
Most common cause of motor impairment.
Clinical manifestations can emerge over time.
Summarise the epidemiology of hypoxic-ischaemic encephalopathy.
Moderate–severe HIE in 2–4/1000 live births.
What causes the increased tone in spastic cerebral palsy?
damage to upper motor neurons
What are 5 general presenting symptoms for cerebral palsy?
Delayed milestones
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 + early hand preference <1y, characteristic posture of abduction of shoulder, flexion at elbow + wrist, pronation of forearm, + 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 + 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, + mouth exaggerated by involuntary movements; athetoid (writhing) + choreographic (jerking).
What are 4 presenting symptoms of ataxic cerebral palsy?
Hypotonia
Ataxia of trunk + limbs
Postural imbalance
Intention tremor.
What are the presenting symptoms of hypoxic-ischaemic encephalopathy?
Poor APGAR score after 10 mins.
Neonatal resuscitation was required.
What is stage I hypoxic-ischaemic encephalopathy?
Level of consciousness
Muscle tone
Posture
DTR/Clonus
Myoclonus
Moro Reflex
Level of consciousness: Hyper-alert
Muscle tone: Normal
Posture: Normal
DTR/Clonus: Hyperactive
Myoclonus: Present
Moro Reflex: Strong
What is stage II hypoxic-ischaemic encephalopathy?
Level of consciousness
Muscle tone
Posture
DTR/Clonus
Myoclonus
Moro Reflex
Level of consciousness: Lethargic
Muscle tone: Hypotonic
Posture: Flexion
DTR/Clonus: Hyperactive
Myoclonus: Present
Moro Reflex: Weak
What is stage III hypoxic-ischaemic encephalopathy?
Level of consciousness
Muscle tone
Posture
DTR/Clonus
Myoclonus
Moro Reflex
Level of consciousness: Stupor/coma
Muscle tone: Flaccid
Posture: Decerebrate
DTR/Clonus: Absent
Myoclonus: Absent
Moro Reflex: Absent
What are the investigations for cerebral palsy and hypoxic-ischaemic encephalopathy?
Assessment of hearing + vision.
EEG if seizure prone.
Bloods: FBCs, U+Es, TFTs, coagualation screen.
Metabolic screen: Inborn errors of metabolism (Galactosemia, glutaric aciduria type 1, PKU, MCADD).
X-ray: If severe deformity.
MRI Brain: Evidence of periventricular leukomalacia, congenital malformations, stroke or haemorrhage.
What is the conservative management for cerebral palsy?
Adaptive equipment
Optimise sleep hygiene
Who is involved in the MDT for management of cerebral palsy and hypoxic-ischaemic encephalopathy?
OT: To suggest adaptive equipment
PTs: improve strength
Nursing care
Dieticians: optimise textures, intake of calcium + vit D for improved BMD
SLT: improve language abilities
Psychology: Counselling support for parents + carers.
Orthopedic surgeons: If severe contractures or bone deformities.
What are some medical managements for cerebral palsy and hypoxic-ischaemic encephalopathy?
Glycopyrronium bromide or transdermal hyoscine hydrobromide: To reduce saliva production.
Anti-convulsant if seizure prone
Monitor serum vitamin D, calcium + phosphate.
May require NG tubes for feeding.
Botulinium toxin to reduce spasticity.
What is the management plan for hypoxic-ischaemic encephalopathy?
Admit to neonatal ICU.
Decrease temperature: THERAPEUTIC COOLING
Treat seizures, infections + correct electrolyte imbalances quickly.
What are 4 complications of cerebral palsy and hypoxic-ischaemic encephalopathy?
Aspiration pneumonia
Failure to thrive
Scoliosis
Dislocated hips
What is the prognosis of cerebral palsy and hypoxic-ischaemic encephalopathy?
Spastic hemiplegia: Delayed but eventually normal gait.
Spastic diplegia: Characteristic gait (knees flexed, toe walking, + adducted hips).
Spastic quadriplegia: Poor prognosis related to feeding disability + immobility. Sufferers often totally dependent + life expectancy significantly reduced. Usually die from chest infections.
Dyskinetic: Usually unable to walk independently, QoL often poor.
Ataxic: Most children walk (though often delayed) with aid of crutches.
Give 6 non-motor problems associated with CP
Learning difficulties 60%
Epilepsy 30%
Squints 30%
Hearing impairment 20%
Visual impairment
Behavioural disorders.
What is the life expectancy for patients with cerebral palsy?
Mild: near normal life expectancy
Difficult to predict due to variety in Sx, severity, + associated conditions
Survival has improved over the years with advances in dx + tx
