# Cerebral Palsy

> Cerebral palsy for FMGE Paediatrics: spastic diplegia in preterms, kernicterus dyskinesia, GMFCS, botulinum toxin and baclofen therapy.

- Canonical URL: https://prepelephant.com/topics/fmge/paediatrics/cerebral-palsy-fmge
- Exam / course: FMGE · Subject: Paediatrics
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-02
- Last updated: 2026-10-02
- How to cite: "Cerebral Palsy", PrepElephant, https://prepelephant.com/topics/fmge/paediatrics/cerebral-palsy-fmge

## Direct answer

Cerebral palsy describes a permanent, non-progressive disorder of posture and movement caused by an insult to the developing fetal or infant brain, with a prevalence near 2-3 per 1000 live births; the motor lesion is fixed but its orthopaedic consequences (contractures, bony torsion) progress, and up to half of affected children carry additional epilepsy, intellectual disability, visual, hearing or feeding problems. Spastic types dominate — hemiplegia, diplegia (the preterm pattern, legs worse than arms) and quadriplegia (most severe, highest rate of comorbidity); dyskinetic cerebral palsy with choreoathetosis is the classic kernicterus legacy in India. Management is multidisciplinary: physiotherapy from diagnosis, botulinum toxin for focal spasticity, oral or intrathecal baclofen for generalised tone, orthopaedic surgery for contractures, and GMFCS grading to frame realistic mobility goals.

## What you must remember

- **Types:** spastic diplegia follows prematurity and periventricular leukomalacia (legs strikingly more than arms, scissoring); spastic quadriplegia carries the worst prognosis and the highest seizure and dysphagia burden; dyskinetic (athetoid) points to kernicterus or severe asphyxia; ataxic is rarest.
- **Cause timeline:** antenatal (malformations, congenital infections, TORCH), perinatal (prematurity is the strongest single risk factor; asphyxia explains only a minority), and postnatal (neonatal meningitis, kernicterus, head injury) — roughly a third remain unexplained despite MRI.
- **Examination hallmarks:** increased tone that is velocity-dependent (clasp-knife), hyperreflexia, extensor plantars, persistent primitive reflexes, scissoring or toe-walking, and delayed motor milestones with hand preference before one year in hemiplegia (early hand preference is itself a red flag).
- **Associations to actively hunt:** epilepsy in about a third, intellectual disability, squint and refractive error, hearing loss (kernicterus sensorineural), drooling and gastro-oesophageal reflux, osteopenia, undernutrition from feeding difficulty.
- **GMFCS I-V:** grades walking without limitation through to wheelchair transport; level at age two predicts adult mobility closely enough to guide surgical ambition.
- **Tone ladder:** physiotherapy and casting are the base; botulinum toxin A (focal, effect about three to six months) into gastrocnemius or adductors; oral baclofen, diazepam or tizanidine for generalised spasticity; intrathecal baclofen pumps and selective dorsal rhizotomy for selected severe cases; tendon-lengthening surgery timed after age four to six years in most centres.
- **Kernicterus thread:** an unconjugated bilirubin overshoot in a G6PD-deficient or late-discharged newborn producing deafness, upward gaze palsy and athetosis is a specifically Indian exam stem — the auditory neuropathy means normal OAE may mislead; order BERA.

## Working through a "late walker"

A 14-month-old boy born at 30 weeks stands on tiptoes, legs crossing when held upright, hands fisted but socially engaging and babbling. Reason it in layers. First, is this cerebral palsy or something else? Progressive weakness would show a positive Gowers sign or calf pseudohypertrophy (creatinine kinase for Duchenne, which is X-linked and rare in ex-preterms); metabolic disease declares itself with regression. Second, topography: legs more than arms, plus the preterm history, equals spastic diplegia — order MRI to document periventricular leukomalacia although it rarely changes management. Third, comorbidity sweep: ophthalmology for retinopathy of prematurity and squint, audiology, feeding and growth review, and watch for epilepsy. Fourth, therapy economics: in India, the family needs a sustainable home programme — positioning, stretching, aided standing — more than monthly hospital visits; botulinum toxin to gastrosoleus can be considered when focal spasticity blocks gait training, and a single multilevel surgical plan beats repeated piecemeal operations. Fifth, school and support: a GMFCS II child may mainstream; enrol in early intervention now, because outcome tracks stimulation intensity more than any drug.

## How the FMGE frames it

Expect three stem patterns. One gives tone and topography — "legs affected more than arms in a preterm" — and asks the type (diplegia). Two attaches mechanism to type — athetosis plus sensorineural deafness after neonatal jaundice (kernicterus); asymmetry with early hand preference (hemiplegia). Three tests management order: physiotherapy is the cornerstone answer, botulinum toxin is for focal spasticity, and the drug examined most often is baclofen. A favourite distractor: "cerebral palsy is a progressive disease" — false; the brain lesion is fixed, and worsening comes from contractures, with true progression suggesting an alternative diagnosis.

## Frequently asked questions

### Which type of cerebral palsy is typical of a preterm infant?

Spastic diplegia, from periventricular leukomalacia affecting the corticospinal tracts to the legs; diparesis with scissoring and toe-walking is the picture.

### What distinguishes dyskinetic cerebral palsy?

Involuntary choreoathetoid or dystonic movements from basal ganglia damage, classically after kernicterus or severe perinatal asphyxia, frequently with sensorineural hearing loss and upward gaze palsy.

### What is the GMFCS?

The Gross Motor Function Classification System, a five-level scale from independent walking (I) to full wheelchair dependence (V) that predicts long-term mobility and guides intervention intensity.

### When is botulinum toxin used in cerebral palsy?

For focal, dynamic spasticity — most often gastrocnemius or hip adductor overactivity — to create a therapy window; the effect lasts roughly three to six months and is combined with casting and physiotherapy.

### Which associated problems must be screened at every visit?

Epilepsy, visual and hearing impairment, intellectual disability, feeding difficulty and undernutrition, drooling, constipation and hip displacement (surveillance hip X-rays in non-ambulators).