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Cerebral Palsy

High EvidenceUpdated: 2025-12-24

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Red Flags

  • Regression of milestones (NOT CP — investigate for metabolic/genetic causes)
  • Progressive deterioration of function
  • Acquired symptoms after age 2 years
  • Microcephaly at birth with normal head growth
  • Family history of progressive neurological disease
  • Seizures in absence of other CP features
Overview

Cerebral Palsy

1. Clinical Overview

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]


2. Epidemiology

Incidence & Prevalence

ParameterData
Prevalence2-3 per 1,000 live births
UK births affected~1,800 new cases per year
Total UK population with CP~30,000-40,000
TrendStable; increased preterm survival offsets improved care

Demographics

FactorDetails
SexMales slightly more affected (1.3:1)
Gestational ageStrong inverse relationship — highest in very preterm
BirthweightInverse relationship — highest in very low birthweight
SocioeconomicHigher rates in lower socioeconomic groups

Risk Factors

FactorRelative RiskNotes
Prematurity (<28 weeks)50-100xMajor risk factor
Very low birthweight (<1500 g)25-50xRelated to prematurity
Multiple pregnancy5xTwins; higher if one twin dies in utero
Hypoxic-ischaemic encephalopathy10-20xTerm infants with perinatal asphyxia
Intrauterine infection5xChorioamnionitis, TORCH
Neonatal encephalopathyHighClinical syndrome associated with HIE
KernicterusHighSevere unconjugated hyperbilirubinaemia
Intrauterine growth restriction2-3xPlacental insufficiency
Maternal infectionsVariableUTI, sepsis, TORCH
Birth asphyxia10xAbnormal fetal heart rate, low Apgar

Timing of Brain Injury

TimingProportionCommon 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

3. Pathophysiology

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

TypeProportionBrain Region AffectedClinical Features
Spastic70-80%Pyramidal (motor cortex, corticospinal tracts)Increased tone (velocity-dependent), hyperreflexia, clonus, Babinski positive
Dyskinetic10-15%Extrapyramidal (basal ganglia, thalamus)Involuntary movements: athetosis (writhing), dystonia (sustained twisting), chorea
Ataxic5%CerebellumHypotonia, intention tremor, dysmetria, broad-based gait
MixedVariableMultiple regionsCombination of above

Classification by Distribution

DistributionDescriptionCommon Cause
HemiplegiaOne side affected (arm usually > leg)Stroke, unilateral lesion
DiplegiaBoth legs affected > armsPeriventricular leukomalacia (preterm)
QuadriplegiaAll four limbs, trunk, oromotor involvementSevere bilateral injury (term asphyxia)
MonoplegiaSingle limb (rare)Localised lesion

4. Clinical Presentation

Early Signs (Infants)

SignDescription
Motor delayNot meeting motor milestones (sitting, rolling, crawling)
Abnormal toneHypotonia initially; spasticity develops later
Persistence of primitive reflexesMoro, ATNR persisting beyond normal age
Hand preference before 1 yearEarly hand dominance suggests hemiplegia
Asymmetric movementsOne side used less than the other
Feeding difficultiesWeak suck, choking, prolonged feeds
FistingPersistent thumb adduction

Signs by CP Type

TypeSigns
Spastic hemiplegiaUnilateral weakness, arm flexed/pronated, leg extended, circumduction gait, neglect of affected hand
Spastic diplegiaScissoring gait, toe-walking, legs stiff, crouch gait (older child), relatively preserved arm function
Spastic quadriplegiaAll limbs affected, poor head control, oromotor dysfunction, often severe intellectual disability, epilepsy common
DyskineticInvoluntary movements (athetosis/dystonia), variable tone, drooling, speech difficulty, intelligence often preserved
AtaxicHypotonia, intention tremor, dysmetria, wide-based gait, nystagmus

Associated Conditions

ConditionPrevalence in CPNotes
Epilepsy25-50%More common in hemiplegic and quadriplegic CP
Intellectual disability30-50%Ranges from mild to profound
Speech and language disorder40-60%Dysarthria, expressive difficulties
Visual impairment10-15%Cortical visual impairment; strabismus
Hearing impairment5-10%Especially with kernicterus history
Feeding difficulties30-40%Dysphagia, aspiration risk
Behavioural problems25%ADHD, autism spectrum traits
Sleep disordersCommonPain, 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

5. Clinical Examination

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

TestTechniqueSignificance
Catch (Modified Ashworth)Rapid passive stretchVelocity-dependent catch = spasticity
Sustained clonusRapid dorsiflexion>5 beats = upper motor neurone lesion
Babinski signPlantar strokeUpgoing toe = pyramidal tract lesion
ATNR persistenceTurn head → fencing postureAbnormal if persists >6 months
Gower's signRise from floorProximal weakness (not typical CP)

Functional Classification (GMFCS)

LevelDescription
IWalks without limitations; may have difficulty with advanced skills
IIWalks with limitations; difficulty with uneven surfaces, inclines
IIIWalks with hand-held mobility device (walker)
IVSelf-mobility with limitations; may use powered mobility
VTransported in manual wheelchair; severe limitations

6. Investigations

First-Line Investigations

InvestigationRationaleExpected Findings
MRI BrainIdentify structural abnormalityPVL (preterm), watershed injury, basal ganglia lesion, stroke, malformation
Developmental assessmentBaseline functionMotor delay, cognitive assessment
Vision and hearing screenAssociated impairmentsCortical visual impairment, sensorineural hearing loss

MRI Findings by CP Type

CP TypeTypical MRI Findings
Spastic diplegiaPeriventricular leukomalacia (PVL); dilated ventricles; reduced white matter
Spastic quadriplegiaExtensive white matter loss; deep grey matter injury; cystic encephalomalacia
Spastic hemiplegiaFocal infarct (MCA territory); porencephalic cyst; unilateral lesion
DyskineticBasal ganglia/thalamic lesions (bilateral); often from acute profound asphyxia or kernicterus
AtaxicCerebellar hypoplasia; sometimes normal imaging; consider genetic causes

Additional Investigations

InvestigationIndication
Metabolic screenAtypical features, regression, consanguinity, family history
Genetic testingAtaxic CP, family history, no clear aetiology, dysmorphism
EEGClinical seizures or suspected subclinical epilepsy
Hip surveillance X-rayAll children with CP (hip dysplasia screening)
Video swallow studyFeeding difficulties, recurrent chest infections

7. Management

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

SeverityApproach
Mild, localisedPhysiotherapy, stretching, orthoses
Moderate, focalBotulinum toxin A injections + physio
Moderate, generalisedOral baclofen or diazepam
Severe, generalisedIntrathecal baclofen (ITB) pump
Fixed contracturesOrthopaedic surgery
Selected ambulant childrenSelective Dorsal Rhizotomy (SDR)

Pharmacological Treatments

DrugMechanismIndicationDose
Baclofen (oral)GABA-B agonistGeneralised spasticity5-20 mg TDS (titrate slowly)
DiazepamGABA-A agonistSpasticity, spasms0.1-0.3 mg/kg/day
TizanidineAlpha-2 agonistSpasticity2-24 mg/day
Botulinum toxin ABlocks acetylcholine releaseFocal spasticity4-6 U/kg per muscle (max 20 U/kg)
Intrathecal baclofenDirect spinal deliverySevere generalisedProgrammable pump

8. Complications

Musculoskeletal Complications

ComplicationIncidencePrevention/Management
Hip dysplasia/dislocation35% (up to 90% in GMFCS V)Surveillance X-rays; brace; reconstructive surgery
Scoliosis20-60%Seating; bracing; spinal fusion
ContracturesVery commonStretching; splinting; surgery
OsteoporosisCommonWeight-bearing; vitamin D; bisphosphonates
FracturesIncreased riskFall prevention; bone health optimisation

Medical Complications

ComplicationManagement
EpilepsyAntiepileptic drugs
Aspiration/pneumoniaThickened feeds; gastrostomy; chest physio
MalnutritionDietetics; gastrostomy if needed
ConstipationLaxatives; adequate fluids
PainOften underrecognised; multimodal analgesia
Sleep disturbanceSleep hygiene; melatonin
Urinary dysfunctionBladder training; catheterisation

9. Prognosis & Outcomes

Ambulatory Prognosis

GMFCS LevelMotor Prognosis
IIndependent walking; minimal limitations
IIWalking with some difficulty; may need aids outdoors
IIIWalking with aids indoors; wheelchair for longer distances
IVSelf-mobility limited; powered wheelchair
VDependent for all mobility; high care needs

Life Expectancy

SeverityLife ExpectancyNotes
Mild (GMFCS I-II)Near-normalSimilar to general population
Moderate (GMFCS III)ReducedDepends on comorbidities
Severe (GMFCS IV-V)Significantly reducedRespiratory complications; nutrition

Prognostic Factors

Good PrognosisPoor Prognosis
Hemiplegia or mild diplegiaQuadriplegia
Independent sitting by 2 yearsUnable to sit independently
GMFCS I-IIGMFCS IV-V
Preserved cognitionSevere intellectual disability
No epilepsyRefractory epilepsy
Good nutritionFailure to thrive

10. Evidence & Guidelines

Key Guidelines

GuidelineOrganisationYearKey Points
Cerebral Palsy in Under 25s (NG62)NICE2017Early recognition, assessment, and management
Hip Surveillance ProgrammeAACPDMUpdated regularlyRegular X-rays for hip dysplasia
Spasticity ManagementNICE2012Stepwise 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

InterventionLevelEvidence
Botulinum toxin for focal spasticity1aRCTs, meta-analyses
Intrathecal baclofen for severe spasticity1bRCTs
SDR for selected ambulant children1bRCTs
Hip surveillance2aPopulation studies

11. Patient/Layperson Explanation

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

12. References

Guidelines

  1. National Institute for Health and Care Excellence (NICE). Cerebral palsy in under 25s: assessment and management (NG62). 2017. nice.org.uk/guidance/ng62

  2. NICE. Spasticity in under 19s: management (CG145). 2012. nice.org.uk/guidance/cg145

Key Studies

  1. 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

  2. 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

  3. 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

  1. 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

  2. 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

  1. Scope. Cerebral palsy information. scope.org.uk

  2. Cerebral Palsy Scotland. cerebralpalsyscotland.org.uk


13. Examination Focus

High-Yield Exam Topics

TopicKey Points
ClassificationSpastic (70-80%), Dyskinetic, Ataxic; Hemiplegia, Diplegia, Quadriplegia
Key pathologyPVL (preterm, diplegia); Basal ganglia (term asphyxia, dyskinetic); Stroke (hemiplegia)
GMFCS5-level motor function classification (I = walks without limitations; V = wheelchair)
Non-progressiveBrain injury is static; regression = NOT CP
ComorbiditiesEpilepsy, intellectual disability, visual/hearing impairment
Spasticity managementPhysio → 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

ErrorCorrect Approach
Saying CP is caused by birth asphyxiaOnly 10-20% perinatal; 70-80% prenatal causes
Describing CP as progressiveBrain injury is STATIC; musculoskeletal problems progress
Not recognising regression as a red flagRegression of milestones = NOT CP; investigate
Forgetting hip surveillanceAll children with CP need regular hip X-rays
Missing associated conditionsAlways 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.

Last updated: 2025-12-24

At a Glance

EvidenceHigh
Last Updated2025-12-24

Red Flags

  • Regression of milestones (NOT CP — investigate for metabolic/genetic causes)
  • Progressive deterioration of function
  • Acquired symptoms after age 2 years
  • Microcephaly at birth with normal head growth
  • Family history of progressive neurological disease
  • Seizures in absence of other CP features

Clinical Pearls

  • arms), Quadriplegia (all four limbs)
  • **"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.
  • leg) | Stroke, unilateral lesion |
  • arms | Periventricular leukomalacia (preterm) |

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines