Cerebral Palsy
Summary
Cerebral palsy (CP) is a group of permanent disorders of movement and posture, attributed to non-progressive disturbances in the developing fetal or infant brain. It is the most common cause of physical disability in childhood, affecting approximately 2-3 per 1,000 live births. The motor disorders are often accompanied by disturbances of sensation, perception, cognition, communication, behaviour, and epilepsy. CP is classified by motor type (spastic, dyskinetic, ataxic, mixed), anatomical distribution (hemiplegia, diplegia, quadriplegia), and functional severity (GMFCS levels I-V). The underlying brain lesion is non-progressive, but secondary musculoskeletal complications develop over time. Management is multidisciplinary, focusing on maximising function, preventing complications, and improving quality of life.
Key Facts
- Prevalence: 2-3 per 1,000 live births; stable despite improved neonatal care (improved preterm survival)
- Causes: Prematurity (major risk factor), hypoxic-ischaemic encephalopathy (HIE), intrauterine infection, kernicterus
- Key pathology: Periventricular leukomalacia (PVL) in preterm; watershed infarcts in term
- Classification: Spastic (70-80%), Dyskinetic (10-15%), Ataxic (5%), Mixed
- Distribution: Hemiplegia (one side), Diplegia (legs > arms), Quadriplegia (all four limbs)
- Functional classification: GMFCS levels I (walks without limitations) to V (severe limitations, wheelchair)
- Non-progressive brain injury: But secondary musculoskeletal problems develop over time
- Comorbidities: Epilepsy (25-50%), intellectual disability, visual/hearing impairment, feeding difficulties
- Life expectancy: Varies by severity; many live into adulthood
Clinical Pearls
"Non-progressive Brain, Progressive Musculoskeletal": The brain injury in CP is static, but the musculoskeletal consequences (contractures, scoliosis, hip dysplasia) are progressive. This distinction is essential for prognosis discussions.
"Regression = Not CP": If a child loses previously acquired skills, this is NOT CP. Investigate for metabolic or degenerative neurological conditions. CP is characterised by motor delay, not regression.
"Premature + White Matter = PVL": Periventricular leukomalacia (injury to white matter around ventricles) is the classic lesion in preterm infants, leading to spastic diplegia (legs affected more than arms).
"The Stiff Baby Becomes Floppy First": Some children with spastic CP initially present with hypotonia before spasticity develops. The motor pattern may not be fully apparent until 12-24 months.
"Scissoring Gait = Spastic Diplegia": The classic scissoring gait (knees crossing midline) with toe-walking is pathognomonic of spastic diplegia from bilateral periventricular injury.
Why This Matters Clinically
Cerebral palsy is the most common childhood physical disability and requires lifelong multidisciplinary care. Early recognition enables timely intervention, which improves developmental outcomes. Understanding the classification helps predict functional trajectory and guide management. Distinguishing CP from progressive neurological conditions is critical — regression of milestones mandates urgent investigation.[1,2]
Incidence & Prevalence
| Parameter | Data |
|---|---|
| Prevalence | 2-3 per 1,000 live births |
| UK births affected | ~1,800 new cases per year |
| Total UK population with CP | ~30,000-40,000 |
| Trend | Stable; increased preterm survival offsets improved care |
Demographics
| Factor | Details |
|---|---|
| Sex | Males slightly more affected (1.3:1) |
| Gestational age | Strong inverse relationship — highest in very preterm |
| Birthweight | Inverse relationship — highest in very low birthweight |
| Socioeconomic | Higher rates in lower socioeconomic groups |
Risk Factors
| Factor | Relative Risk | Notes |
|---|---|---|
| Prematurity (<28 weeks) | 50-100x | Major risk factor |
| Very low birthweight (<1500 g) | 25-50x | Related to prematurity |
| Multiple pregnancy | 5x | Twins; higher if one twin dies in utero |
| Hypoxic-ischaemic encephalopathy | 10-20x | Term infants with perinatal asphyxia |
| Intrauterine infection | 5x | Chorioamnionitis, TORCH |
| Neonatal encephalopathy | High | Clinical syndrome associated with HIE |
| Kernicterus | High | Severe unconjugated hyperbilirubinaemia |
| Intrauterine growth restriction | 2-3x | Placental insufficiency |
| Maternal infections | Variable | UTI, sepsis, TORCH |
| Birth asphyxia | 10x | Abnormal fetal heart rate, low Apgar |
Timing of Brain Injury
| Timing | Proportion | Common Causes |
|---|---|---|
| Prenatal (before labour) | 70-80% | Prematurity, PVL, intrauterine infection, genetic |
| Perinatal (during birth) | 10-20% | HIE, acute intrapartum events |
| Postnatal (<2 years) | 5-10% | Meningitis, head injury, stroke, near-drowning |
Mechanisms of Brain Injury
Step 1: Vulnerability of Developing Brain
- Immature brain is susceptible to hypoxia, ischaemia, and inflammation
- Oligodendrocyte precursors (myelinating cells) are particularly vulnerable
- Timing of insult determines pattern of injury
Step 2: Preterm Brain Injury (Periventricular Leukomalacia)
- Premature infants vulnerable to white matter injury
- Periventricular region has watershed blood supply
- Hypoxia-ischaemia damages oligodendrocyte precursors
- Results in cystic or diffuse white matter injury
- Motor fibres to legs run close to ventricles → spastic diplegia
Step 3: Term Brain Injury (Watershed/Basal Ganglia)
- Term infants susceptible to grey matter injury
- Watershed zones (between vascular territories) vulnerable
- Basal ganglia and thalamus affected in acute severe asphyxia
- Results in spastic quadriplegia or dyskinetic CP
Step 4: Vascular Injury
- Intrauterine stroke → hemiplegic CP
- Middle cerebral artery territory most common
- May affect one hemisphere → contralateral hemiplegia
Step 5: Secondary Musculoskeletal Changes
- Imbalanced muscle activation → contractures
- Abnormal forces on growing skeleton → hip dysplasia, scoliosis
- Spasticity gradually worsens muscle shortening
- Bone density reduced due to immobility
Classification by Motor Type
| Type | Proportion | Brain Region Affected | Clinical Features |
|---|---|---|---|
| Spastic | 70-80% | Pyramidal (motor cortex, corticospinal tracts) | Increased tone (velocity-dependent), hyperreflexia, clonus, Babinski positive |
| Dyskinetic | 10-15% | Extrapyramidal (basal ganglia, thalamus) | Involuntary movements: athetosis (writhing), dystonia (sustained twisting), chorea |
| Ataxic | 5% | Cerebellum | Hypotonia, intention tremor, dysmetria, broad-based gait |
| Mixed | Variable | Multiple regions | Combination of above |
Classification by Distribution
| Distribution | Description | Common Cause |
|---|---|---|
| Hemiplegia | One side affected (arm usually > leg) | Stroke, unilateral lesion |
| Diplegia | Both legs affected > arms | Periventricular leukomalacia (preterm) |
| Quadriplegia | All four limbs, trunk, oromotor involvement | Severe bilateral injury (term asphyxia) |
| Monoplegia | Single limb (rare) | Localised lesion |
Early Signs (Infants)
| Sign | Description |
|---|---|
| Motor delay | Not meeting motor milestones (sitting, rolling, crawling) |
| Abnormal tone | Hypotonia initially; spasticity develops later |
| Persistence of primitive reflexes | Moro, ATNR persisting beyond normal age |
| Hand preference before 1 year | Early hand dominance suggests hemiplegia |
| Asymmetric movements | One side used less than the other |
| Feeding difficulties | Weak suck, choking, prolonged feeds |
| Fisting | Persistent thumb adduction |
Signs by CP Type
| Type | Signs |
|---|---|
| Spastic hemiplegia | Unilateral weakness, arm flexed/pronated, leg extended, circumduction gait, neglect of affected hand |
| Spastic diplegia | Scissoring gait, toe-walking, legs stiff, crouch gait (older child), relatively preserved arm function |
| Spastic quadriplegia | All limbs affected, poor head control, oromotor dysfunction, often severe intellectual disability, epilepsy common |
| Dyskinetic | Involuntary movements (athetosis/dystonia), variable tone, drooling, speech difficulty, intelligence often preserved |
| Ataxic | Hypotonia, intention tremor, dysmetria, wide-based gait, nystagmus |
Associated Conditions
| Condition | Prevalence in CP | Notes |
|---|---|---|
| Epilepsy | 25-50% | More common in hemiplegic and quadriplegic CP |
| Intellectual disability | 30-50% | Ranges from mild to profound |
| Speech and language disorder | 40-60% | Dysarthria, expressive difficulties |
| Visual impairment | 10-15% | Cortical visual impairment; strabismus |
| Hearing impairment | 5-10% | Especially with kernicterus history |
| Feeding difficulties | 30-40% | Dysphagia, aspiration risk |
| Behavioural problems | 25% | ADHD, autism spectrum traits |
| Sleep disorders | Common | Pain, spasticity, epilepsy contribute |
Red Flags
[!CAUTION] Red Flags — Consider Alternative Diagnosis:
- Developmental REGRESSION — loss of previously acquired skills (NOT CP)
- Progressive deterioration of motor function
- Normal early development followed by late-onset symptoms
- Family history of neurological disease
- Dysmorphic features suggesting genetic syndrome
- No identified risk factors for CP
- MRI normal or shows unexpected findings
Structured Examination
General Observation:
- Posture at rest
- Spontaneous movement pattern
- Asymmetry
- Involuntary movements
- Alertness and interaction
Motor Examination:
- Tone: Spasticity (velocity-dependent), rigidity, hypotonia
- Power: Weakness pattern (pyramidal = extensors in arms, flexors in legs)
- Reflexes: Hyperreflexia, clonus, Babinski sign
- Primitive reflexes: Persistence of Moro, ATNR, grasp
Gait Assessment:
- Scissoring (spastic diplegia)
- Circumduction (hemiplegia)
- Toe-walking
- Crouch gait (hip and knee flexion in older children)
- Ataxic gait (wide-based, unsteady)
Oromotor Assessment:
- Drooling
- Jaw thrust
- Tongue thrust
- Swallowing coordination
Special Tests
| Test | Technique | Significance |
|---|---|---|
| Catch (Modified Ashworth) | Rapid passive stretch | Velocity-dependent catch = spasticity |
| Sustained clonus | Rapid dorsiflexion | >5 beats = upper motor neurone lesion |
| Babinski sign | Plantar stroke | Upgoing toe = pyramidal tract lesion |
| ATNR persistence | Turn head → fencing posture | Abnormal if persists >6 months |
| Gower's sign | Rise from floor | Proximal weakness (not typical CP) |
Functional Classification (GMFCS)
| Level | Description |
|---|---|
| I | Walks without limitations; may have difficulty with advanced skills |
| II | Walks with limitations; difficulty with uneven surfaces, inclines |
| III | Walks with hand-held mobility device (walker) |
| IV | Self-mobility with limitations; may use powered mobility |
| V | Transported in manual wheelchair; severe limitations |
First-Line Investigations
| Investigation | Rationale | Expected Findings |
|---|---|---|
| MRI Brain | Identify structural abnormality | PVL (preterm), watershed injury, basal ganglia lesion, stroke, malformation |
| Developmental assessment | Baseline function | Motor delay, cognitive assessment |
| Vision and hearing screen | Associated impairments | Cortical visual impairment, sensorineural hearing loss |
MRI Findings by CP Type
| CP Type | Typical MRI Findings |
|---|---|
| Spastic diplegia | Periventricular leukomalacia (PVL); dilated ventricles; reduced white matter |
| Spastic quadriplegia | Extensive white matter loss; deep grey matter injury; cystic encephalomalacia |
| Spastic hemiplegia | Focal infarct (MCA territory); porencephalic cyst; unilateral lesion |
| Dyskinetic | Basal ganglia/thalamic lesions (bilateral); often from acute profound asphyxia or kernicterus |
| Ataxic | Cerebellar hypoplasia; sometimes normal imaging; consider genetic causes |
Additional Investigations
| Investigation | Indication |
|---|---|
| Metabolic screen | Atypical features, regression, consanguinity, family history |
| Genetic testing | Ataxic CP, family history, no clear aetiology, dysmorphism |
| EEG | Clinical seizures or suspected subclinical epilepsy |
| Hip surveillance X-ray | All children with CP (hip dysplasia screening) |
| Video swallow study | Feeding difficulties, recurrent chest infections |
Management Algorithm
CEREBRAL PALSY MANAGEMENT
↓
┌───────────────────────────────────────────────────────────────┐
│ DIAGNOSIS & CLASSIFICATION │
├───────────────────────────────────────────────────────────────┤
│ ➤ MRI brain to identify lesion │
│ ➤ Classify: Motor type (spastic, dyskinetic, ataxic) │
│ ➤ Classify: Distribution (hemiplegia, diplegia, quadriplegia)│
│ ➤ Classify: GMFCS level (I-V) │
│ ➤ Screen for comorbidities (epilepsy, vision, hearing) │
└───────────────────────────────────────────────────────────────┘
↓
┌───────────────────────────────────────────────────────────────┐
│ MULTIDISCIPLINARY TEAM (MDT) │
├───────────────────────────────────────────────────────────────┤
│ ➤ Paediatrician/Neurologist — Coordination, seizures, meds │
│ ➤ Physiotherapy — Motor function, strength, mobility │
│ ➤ Occupational Therapy — Fine motor, ADLs, equipment │
│ ➤ Speech & Language Therapy — Communication, swallowing │
│ ➤ Orthopaedics — Hip surveillance, contractures, surgery │
│ ➤ Rehabilitation — Comprehensive care │
│ ➤ Social services — Support, respite, benefits │
│ ➤ Education — Special educational needs support │
│ ➤ Psychology — Behavioural, emotional support │
└───────────────────────────────────────────────────────────────┘
↓
┌───────────────────────────────────────────────────────────────┐
│ SPASTICITY MANAGEMENT │
├───────────────────────────────────────────────────────────────┤
│ CONSERVATIVE: │
│ ➤ Physiotherapy — Stretching, strengthening │
│ ➤ Orthoses — AFOs, splints │
│ ➤ Positioning — Standing frames, seating │
│ │
│ PHARMACOLOGICAL: │
│ ➤ Oral: Baclofen, diazepam, tizanidine │
│ ➤ Focal: Botulinum toxin A injections (key muscles) │
│ ➤ Intrathecal: Baclofen pump (severe generalised spasticity) │
│ │
│ SURGICAL: │
│ ➤ Selective Dorsal Rhizotomy (SDR) — Selected GMFCS II-III │
│ ➤ Orthopaedic surgery — Tendon lengthening, osteotomies │
│ ➤ Hip reconstruction — For subluxation/dislocation │
└───────────────────────────────────────────────────────────────┘
↓
┌───────────────────────────────────────────────────────────────┐
│ COMORBIDITY MANAGEMENT │
├───────────────────────────────────────────────────────────────┤
│ ➤ Epilepsy — Antiepileptic drugs (LEV, VPA, etc.) │
│ ➤ Feeding — Gastrostomy if unsafe oral feeding │
│ ➤ Drooling — Anticholinergics, botox to salivary glands │
│ ➤ Constipation — Laxatives, dietary management │
│ ➤ Pain — Often undertreated; multimodal approach │
│ ➤ Sleep — Sleep hygiene, melatonin │
│ ➤ Behaviour — ADHD meds, psychology input │
└───────────────────────────────────────────────────────────────┘
Spasticity Management Algorithm
| Severity | Approach |
|---|---|
| Mild, localised | Physiotherapy, stretching, orthoses |
| Moderate, focal | Botulinum toxin A injections + physio |
| Moderate, generalised | Oral baclofen or diazepam |
| Severe, generalised | Intrathecal baclofen (ITB) pump |
| Fixed contractures | Orthopaedic surgery |
| Selected ambulant children | Selective Dorsal Rhizotomy (SDR) |
Pharmacological Treatments
| Drug | Mechanism | Indication | Dose |
|---|---|---|---|
| Baclofen (oral) | GABA-B agonist | Generalised spasticity | 5-20 mg TDS (titrate slowly) |
| Diazepam | GABA-A agonist | Spasticity, spasms | 0.1-0.3 mg/kg/day |
| Tizanidine | Alpha-2 agonist | Spasticity | 2-24 mg/day |
| Botulinum toxin A | Blocks acetylcholine release | Focal spasticity | 4-6 U/kg per muscle (max 20 U/kg) |
| Intrathecal baclofen | Direct spinal delivery | Severe generalised | Programmable pump |
Musculoskeletal Complications
| Complication | Incidence | Prevention/Management |
|---|---|---|
| Hip dysplasia/dislocation | 35% (up to 90% in GMFCS V) | Surveillance X-rays; brace; reconstructive surgery |
| Scoliosis | 20-60% | Seating; bracing; spinal fusion |
| Contractures | Very common | Stretching; splinting; surgery |
| Osteoporosis | Common | Weight-bearing; vitamin D; bisphosphonates |
| Fractures | Increased risk | Fall prevention; bone health optimisation |
Medical Complications
| Complication | Management |
|---|---|
| Epilepsy | Antiepileptic drugs |
| Aspiration/pneumonia | Thickened feeds; gastrostomy; chest physio |
| Malnutrition | Dietetics; gastrostomy if needed |
| Constipation | Laxatives; adequate fluids |
| Pain | Often underrecognised; multimodal analgesia |
| Sleep disturbance | Sleep hygiene; melatonin |
| Urinary dysfunction | Bladder training; catheterisation |
Ambulatory Prognosis
| GMFCS Level | Motor Prognosis |
|---|---|
| I | Independent walking; minimal limitations |
| II | Walking with some difficulty; may need aids outdoors |
| III | Walking with aids indoors; wheelchair for longer distances |
| IV | Self-mobility limited; powered wheelchair |
| V | Dependent for all mobility; high care needs |
Life Expectancy
| Severity | Life Expectancy | Notes |
|---|---|---|
| Mild (GMFCS I-II) | Near-normal | Similar to general population |
| Moderate (GMFCS III) | Reduced | Depends on comorbidities |
| Severe (GMFCS IV-V) | Significantly reduced | Respiratory complications; nutrition |
Prognostic Factors
| Good Prognosis | Poor Prognosis |
|---|---|
| Hemiplegia or mild diplegia | Quadriplegia |
| Independent sitting by 2 years | Unable to sit independently |
| GMFCS I-II | GMFCS IV-V |
| Preserved cognition | Severe intellectual disability |
| No epilepsy | Refractory epilepsy |
| Good nutrition | Failure to thrive |
Key Guidelines
| Guideline | Organisation | Year | Key Points |
|---|---|---|---|
| Cerebral Palsy in Under 25s (NG62) | NICE | 2017 | Early recognition, assessment, and management |
| Hip Surveillance Programme | AACPDM | Updated regularly | Regular X-rays for hip dysplasia |
| Spasticity Management | NICE | 2012 | Stepwise approach to spasticity |
Landmark Studies
GMFCS Development (Palisano et al. 1997)
- Developed 5-level classification system
- Validated, reliable, widely used globally
- Predicts motor prognosis
- PMID: 9161656
SDR Evidence (McLaughlin et al. 2002)
- RCT of Selective Dorsal Rhizotomy
- Showed improvements in spasticity and function in selected children
- PMID: 11872903
Swedish Hip Surveillance Programme
- Population-based hip surveillance reduced dislocation rate from 8% to <0.5%
- Model for preventive orthopaedic care
- PMID: 15580352
Evidence Strength
| Intervention | Level | Evidence |
|---|---|---|
| Botulinum toxin for focal spasticity | 1a | RCTs, meta-analyses |
| Intrathecal baclofen for severe spasticity | 1b | RCTs |
| SDR for selected ambulant children | 1b | RCTs |
| Hip surveillance | 2a | Population studies |
What is Cerebral Palsy?
Cerebral palsy (CP) is a condition that affects movement and posture. It is caused by damage to the developing brain, usually before or around birth. "Cerebral" refers to the brain, and "palsy" means problems with movement.
Why does it happen?
The brain injury that causes CP can happen:
- Before birth (most common) — often related to premature birth
- During birth — lack of oxygen (rare)
- After birth — infections like meningitis, or head injury (rare)
In many cases, the exact cause is not known.
What are the symptoms?
CP affects children differently. Some have mild difficulties, while others have more significant challenges:
- Stiff or floppy muscles
- Difficulty with walking, balance, or coordination
- Problems with fine movements (writing, dressing)
- Speech difficulties
- Some children may also have learning difficulties, epilepsy, or vision problems
How is it treated?
There is no cure for CP, but many treatments help:
- Physiotherapy — to improve movement and prevent stiffness
- Occupational therapy — to help with everyday tasks
- Speech therapy — to improve communication and swallowing
- Medicines — to reduce muscle stiffness (spasticity)
- Botox injections — to relax specific muscles
- Surgery — sometimes needed for tight muscles or hip problems
What to expect?
CP is a lifelong condition, but it is NOT progressive — the brain injury does not get worse. Many children with CP live happy, fulfilling lives. Early intervention and ongoing support make a big difference.
When to seek help
See a doctor if you notice:
- Your child losing skills they previously had (this is NOT typical of CP)
- Worsening seizures
- Difficulty breathing or frequent chest infections
- Signs of hip pain or worsening walking
Guidelines
-
National Institute for Health and Care Excellence (NICE). Cerebral palsy in under 25s: assessment and management (NG62). 2017. nice.org.uk/guidance/ng62
-
NICE. Spasticity in under 19s: management (CG145). 2012. nice.org.uk/guidance/cg145
Key Studies
-
Palisano R, Rosenbaum P, Walter S, et al. Development and reliability of a system to classify gross motor function in children with cerebral palsy. Dev Med Child Neurol. 1997;39(4):214-223. PMID: 9161656
-
McLaughlin J, Bjornson K, Temkin N, et al. Selective dorsal rhizotomy: meta-analysis of three randomized controlled trials. Dev Med Child Neurol. 2002;44(1):17-25. PMID: 11811645
-
Hägglund G, Andersson S, Düppe H, et al. Prevention of dislocation of the hip in children with cerebral palsy. J Bone Joint Surg Br. 2005;87(1):95-101. PMID: 15686244
Reviews
-
Rosenbaum P, Paneth N, Leviton A, et al. A report: the definition and classification of cerebral palsy April 2006. Dev Med Child Neurol Suppl. 2007;109:8-14. PMID: 17370477
-
Novak I, Morgan C, Adde L, et al. Early, Accurate Diagnosis and Early Intervention in Cerebral Palsy: Advances in Diagnosis and Treatment. JAMA Pediatr. 2017;171(9):897-907. PMID: 28715518
Patient Resources
-
Scope. Cerebral palsy information. scope.org.uk
-
Cerebral Palsy Scotland. cerebralpalsyscotland.org.uk
High-Yield Exam Topics
| Topic | Key Points |
|---|---|
| Classification | Spastic (70-80%), Dyskinetic, Ataxic; Hemiplegia, Diplegia, Quadriplegia |
| Key pathology | PVL (preterm, diplegia); Basal ganglia (term asphyxia, dyskinetic); Stroke (hemiplegia) |
| GMFCS | 5-level motor function classification (I = walks without limitations; V = wheelchair) |
| Non-progressive | Brain injury is static; regression = NOT CP |
| Comorbidities | Epilepsy, intellectual disability, visual/hearing impairment |
| Spasticity management | Physio → Botox → Oral baclofen → ITB pump → SDR/surgery |
Sample Viva Questions
Q1: A 2-year-old presents with motor delay, spasticity, and scissoring gait. What is the likely diagnosis and what investigations would you perform?
Model Answer: The presentation suggests spastic diplegic cerebral palsy. I would take a detailed history including pregnancy, prematurity, neonatal course, and developmental history. Key investigation is MRI brain, which would likely show periventricular leukomalacia (PVL) in a previously preterm infant. I would also screen for associated conditions: vision and hearing assessment, developmental assessment. I would classify using GMFCS and establish multidisciplinary follow-up with physiotherapy, orthopaedics (hip surveillance), and speech therapy.
Q2: Why is it important to distinguish CP from progressive neurological conditions?
Model Answer: CP is characterised by a non-progressive brain injury. The clinical presentation may evolve as the child develops, but there should be no regression of skills. If a child loses previously acquired skills or shows progressive deterioration, this suggests a different diagnosis such as:
- Metabolic disorders (leukodystrophies, mitochondrial diseases)
- Neurodegenerative conditions (Rett syndrome, Batten disease)
- Structural lesions (tumours)
This distinction is critical because progressive conditions require specific investigation (metabolic screen, genetic testing) and may have different treatments or implications for prognosis and genetic counselling.
Q3: What is the evidence for Selective Dorsal Rhizotomy (SDR)?
Model Answer: SDR is a neurosurgical procedure that selectively cuts sensory nerve rootlets in the lumbar spine to reduce spasticity. Evidence supports its use in carefully selected ambulant children with spastic diplegia (typically GMFCS II-III). McLaughlin et al.'s meta-analysis of three RCTs showed improvements in spasticity and gross motor function. Selection criteria include: pure spasticity (not dystonia), adequate strength, reasonable cognition for rehab, and clear evidence of spasticity limiting function. SDR requires intensive post-operative rehabilitation. It is not suitable for all children and requires specialist assessment.
Common Exam Errors
| Error | Correct Approach |
|---|---|
| Saying CP is caused by birth asphyxia | Only 10-20% perinatal; 70-80% prenatal causes |
| Describing CP as progressive | Brain injury is STATIC; musculoskeletal problems progress |
| Not recognising regression as a red flag | Regression of milestones = NOT CP; investigate |
| Forgetting hip surveillance | All children with CP need regular hip X-rays |
| Missing associated conditions | Always screen for epilepsy, vision, hearing, cognition |
Last Reviewed: 2025-12-24 | MedVellum Editorial Team
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.