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Cerebral Palsy - Comprehensive Neurology Notes

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1. DEFINITION

1. A disorder of movement and posture (weakness, spasticity, dystonia, ataxia, or choreoathetosis) with onset prior to age 1-2 years
2. Reliable evidence that the disorder is due to a disturbance in the fetal or infant brain
3. No evidence of progression or worsening over time
4. Significant functional limitation in the performance of desired activities
5. Reasonable expectation that the disorder will persist throughout life

Despite the nonprogressive nature of the underlying lesion (historically called "static encephalopathy"), the clinical expression changes dynamically with growth, maturation, and aging. CP is therefore better understood as a dynamic, evolving disorder rather than a fixed static condition. - Bradley and Daroff's Neurology in Clinical Practice

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2. EPIDEMIOLOGY

• Most common neuromotor disorder of childhood
• Overall incidence: approximately 2 per 1000 live births
• Prevalence inversely proportional to gestational age:
  • Term births: 1-2 per 1000
  • Very premature infants: 40-60 per 1000
• Life expectancy is strongly linked to severity:
  • Ambulatory, self-feeding 15-year-olds: projected additional 55 years
  • Immobile, tube-fed 15-year-olds: projected additional 13 years
• Dyskinetic CP carries the highest mortality among subtypes
• Factors increasing mortality: female sex, cognitive impairment, epilepsy
• Common causes of death: aspiration pneumonia, urinary tract infections, sepsis, seizures, fractures

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3. ETIOLOGY AND RISK FACTORS

Prenatal Causes

• Congenital brain malformations
• Intrauterine infections (TORCH: Toxoplasma, Rubella, CMV, Herpes)
• Genetic/chromosomal abnormalities
• Maternal trauma, toxin exposure
• Placental insufficiency

Perinatal Causes

• Periventricular leukomalacia (PVL) - most common cause in preterm infants; white matter injury from ischemia or infection
• Hypoxic-ischemic encephalopathy (HIE) - most common cause in term infants
• Intraventricular hemorrhage (IVH)
• Neonatal stroke
• Kernicterus (bilirubin toxicity to basal ganglia - classic cause of dyskinetic CP)
• Neonatal sepsis/meningitis

Postnatal Causes (first 2 years)

• Meningitis/encephalitis
• Traumatic brain injury (including non-accidental injury)
• Stroke
• Anoxia/near-drowning

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4. NEUROPATHOLOGY AND NEUROANATOMY

Pathophysiology of Spasticity (Upper Motor Neuron Syndrome)

• Increased tendon reflexes with radiation
• Clonus
• Positive Babinski sign
• Involuntary activation of remote muscles
• Spasticity
• Extensor and flexor spasms

• Muscle weakness
• Loss of dexterity
• Fatigability
• Loss of selective control of muscle and limb segments
• Nonmotor changes: cognition, communication, behavioral, sleep disturbance

"Positive features are more amenable to active intervention but of less relevance to overall disability. Negative features, characterized by a reduction in motor activity, are more causative to disability." - Bradley and Daroff's Neurology in Clinical Practice

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5. CLASSIFICATION

A. By Type of Motor Involvement

I. Spastic CP (80% of all cases)

• Upper motor neuron lesion; pyramidal tracts involved
• Velocity-dependent increased tone (clasp-knife), clonus, hyperreflexia, Babinski sign
• Further classified by topographic distribution:

II. Dyskinetic CP (15% of extrapyramidal cases)

• Extrapyramidal lesion (basal ganglia/thalamus)
• Lead-pipe or candle-wax rigidity; variable tone; clonus may be absent or present
• Subtypes:
  • Dystonic: Involuntary sustained/repetitive twisting movements and postures; often painful; reflects basal ganglia pathology
  • Choreoathetoid: Irregular, writhing, purposeless movements (chorea + athetosis combined); classic in kernicterus
  • Athetoid: Slow, writhing distal movements

III. Ataxic CP (~5%)

• Cerebellar origin
• Hypotonia, intention tremor, wide-based gait, dysmetria, dysdiadochokinesia
• Impaired balance and coordination

IV. Hypotonic CP

• Axial, appendicular, or generalized hypotonia
• Often reflects diffuse, severe cerebral and/or cerebellar cortical dysfunction
• Many evolve into spastic or dyskinetic subtypes with age

V. Mixed CP

• Combination of features, most commonly spastic + dyskinetic

B. Functional Classification - GMFCS

• GMFCS has been shown to be predictive of hip dislocation risk
• GMFCS IV/V: ~50% risk of developing scoliosis
• Remains stable and reliable as a prognostic tool after age 2

C. Manual Abilities Classification System (MACS)

• Five-level system assessing how a child uses hands in activities of daily living
• Ages 4-18 years; validated with good-to-excellent interrater reliability
• Mirrors GMFCS concept but applied to upper limb function

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6. CLINICAL FEATURES AND ASSOCIATED CONDITIONS

Motor Features

• Abnormal tone (spastic, dystonic, hypotonic, or mixed)
• Abnormal movement patterns and primitive reflexes persisting beyond expected age
• Contractures and musculoskeletal deformities (hip dislocation, equinus foot, scoliosis)
• Gait abnormalities

Common Gait Patterns in Spastic CP

• Equinus gait (toe-walking): plantarflexion deformity, gastrocnemius spasticity
• Crouch gait: hip and knee flexion, excessive ankle dorsiflexion
• Scissor gait: hip adductor spasticity causing legs to cross midline
• Stiff-knee gait: failure of knee flexion in swing due to rectus femoris spasticity
• Trendelenburg gait: hip abductor weakness

Associated Conditions (Comorbidities)

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7. DIAGNOSIS

Clinical Criteria

Key History Points

• Perinatal history: prematurity, birth complications, APGAR scores, need for resuscitation
• Developmental milestones: delayed or abnormal motor milestones
• Family history to exclude hereditary spastic paraplegias
• History of infection, trauma, or anoxia in the first 2 years

Clinical Examination Findings

• Primitive reflex persistence beyond expected age: Moro, ATNR (asymmetric tonic neck reflex), palmar grasp
• Absent protective/equilibrium reactions past expected age
• Hyperreflexia, clonus, Babinski sign (in spastic types)
• Abnormal tone patterns
• Hand preference before 18 months strongly suggests hemiplegia

Investigations

• MRI brain: abnormal in 70-90% of individuals with CP; identifies white matter injury, cortical malformations, basal ganglia lesions
• EEG: if seizures suspected
• Metabolic screen: rule out inborn errors of metabolism (especially if atypical features)
• Genetic testing: chromosome microarray, whole exome sequencing if etiology unexplained
• Hearing evaluation, visual assessment, ophthalmology review
• Swallowing assessment (videofluoroscopic swallow study)

Once a diagnosis of CP is suspected, classification follows based on the predominant movement abnormality: spastic, dyskinetic, or hypotonic-ataxic, and then further by topographic distribution. - Bradley and Daroff's Neurology in Clinical Practice

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8. PHYSIOTHERAPY ASSESSMENT

8A. Assessment Principles

• Body structure/function (tone, strength, ROM, reflexes)
• Activity (functional motor abilities)
• Participation (school, community, home roles)
• Contextual factors (environment, assistive devices)

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8B. Subjective Assessment

• Chief complaint and primary functional goals
• Birth history, neonatal course, diagnosis timeline
• Current medications (especially antispasmodics)
• Feeding method (oral vs. gastrostomy)
• Seizure history and control
• Pain: location, triggers, character, impact on function
• Mobility aids currently in use
• School placement and participation level
• Sleep patterns

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8C. Objective Assessment Tools

1. Tone Assessment

• Modified Ashworth Scale (MAS): Grades spasticity 0-4 based on resistance during passive movement
• Modified Tardieu Scale (MTS): Preferred over MAS; distinguishes spasticity (velocity-dependent) from contracture (velocity-independent); measures R1 (reflex catch angle) and R2 (full passive ROM)
  • Spasticity angle = R2 - R1; larger angle = more spasticity
• Hypertonia Assessment Tool (HAT): Differentiates spasticity, dystonia, and rigidity

2. Gross Motor Function

• Gross Motor Function Measure (GMFM-88 and GMFM-66): Gold standard for measuring gross motor ability; 5 dimensions: Lying/Rolling, Sitting, Crawling/Kneeling, Standing, Walking/Running/Jumping
• GMFCS (as above): functional classification/prognosis

3. Selective Motor Control

• Selective Control Assessment of the Lower Extremity (SCALE): Tests selective voluntary movement at hip, knee, ankle, subtalar, toes
• Each joint graded: Normal (2), Impaired (1), Unable (0)

4. Muscle Strength

• Manual Muscle Testing (MMT) - modified for pediatric use
• Hand-held dynamometry for quantitative measurement

5. Range of Motion

• Goniometry for all key joints
• Key measurements in CP:
  • Hip: flexion, extension (Thomas test for hip flexion contracture), abduction, internal/external rotation
  • Knee: flexion contracture, popliteal angle (hamstring tightness)
  • Ankle: dorsiflexion with knee extended (gastrocnemius) and knee flexed (soleus)
  • Silverskiold test: differentiates gastrocnemius from soleus tightness

6. Gait Analysis

• Observational Gait Scale (OGS): Standardized visual gait analysis tool
• Edinburgh Visual Gait Scale (EVGS): Systematic video-based gait analysis
• 3D Instrumented Gait Analysis (IGA): Gold standard; provides kinematics, kinetics, and EMG data to guide surgical and therapeutic decisions
• Timed Up and Go (TUG): Functional mobility and fall risk
• 10-Meter Walk Test (10MWT): Walking speed

7. Balance Assessment

• Pediatric Balance Scale (PBS): Adapted from Berg Balance Scale for children
• Functional Reach Test
• Balance Error Scoring System (BESS)

8. Activity and Function Scales

• Pediatric Evaluation of Disability Inventory (PEDI): Self-care, mobility, social function
• Functional Mobility Scale (FMS): Rates walking ability over 5m, 50m, 500m distances
• Goal Attainment Scaling (GAS): Individualized goal setting and outcome measurement

9. Quality of Life

• Cerebral Palsy Quality of Life Questionnaire (CP QOL-Child)
• KIDSCREEN

10. Pain Assessment

• Wong-Baker FACES Pain Scale (for children)
• Non-Communicating Children's Pain Checklist (NCCPC): for non-verbal children
• Comfort scale for children who cannot self-report

11. Hip Surveillance

• Reimer's Migration Percentage (MP) on X-ray: the proportion of femoral head uncovered by the acetabulum
  • MP > 40%: indicated for intervention
  • Frequency of surveillance guided by GMFCS level (higher GMFCS = more frequent X-rays)

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9. PHYSIOTHERAPY MANAGEMENT

9A. Overarching Goals

1. Maximize functional independence and mobility
2. Prevent/minimize secondary complications (contractures, deformity, pain)
3. Optimize participation in home, school, and community
4. Support caregiver education and home program adherence
5. Coordinate with the multidisciplinary team (physiatry, orthopaedics, neurology, OT, SLT)

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9B. Stretching and Range of Motion

• Passive stretching: Daily stretching of spastic muscles (gastrocnemius, hamstrings, hip adductors, hip flexors, wrist/finger flexors)
• Prolonged low-load stretch (>30 minutes) more effective than brief stretching for preventing contracture
• Evidence suggests passive stretching alone has limited long-term benefit for tone reduction but does maintain ROM and reduce contracture risk

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9C. Strengthening

• Progressive resistance training: Safely effective in CP; targets weak antagonist muscles
• Addresses the negative features of UMN syndrome (weakness, loss of dexterity)
• Focus muscles: hip extensors and abductors, knee extensors, ankle dorsiflexors
• Does NOT worsen spasticity (evidence-based reassurance)

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9D. Neurodevelopmental Treatment (NDT / Bobath Approach)

• Aims to inhibit abnormal movement patterns and facilitate normal movement patterns
• Hands-on facilitation through key points of control
• Focus on achieving normal postural reactions and selective movement
• Widely used but evidence base is moderate; best as part of broader intensive therapy

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9E. Task-Specific and Functional Training

• Intensive task-specific training: High repetition of functional tasks (standing, stepping, reaching) drives neuroplasticity
• Constraint-Induced Movement Therapy (CIMT): For hemiplegic CP; constrains the unaffected hand to force use of the affected hand; strong evidence for upper limb function improvement
• Treadmill training / Partial body-weight supported treadmill training (PBWSTT): Improves gait speed and endurance, especially in ambulatory CP

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9F. Postural Management

• 24-hour postural management: Addressing posture across all positions (lying, sitting, standing) throughout the day and night
• Positioning equipment: Specialist seating systems, standing frames, sleep systems
• Spinal management: Seating modifications and TLSO bracing for scoliosis management (especially GMFCS IV-V)

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9G. Orthotics

• Ankle-Foot Orthoses (AFOs): Most commonly prescribed
  • Solid AFO: controls equinus in low activity, prevents plantarflexion
  • Hinged/articulated AFO: allows dorsiflexion, used in crouch gait
  • Ground Reaction AFO (GRAFO): resists crouch gait with anterior shell
  • Supramalleolar Orthosis (SMO): addresses subtalar instability
• Knee-Ankle-Foot Orthoses (KAFO): For knee instability
• Hip abduction orthoses: To maintain hip range and reduce dislocation risk
• Thumb and wrist splints: For upper limb management in hemiplegia

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9H. Hydrotherapy

• Warm water reduces muscle tone
• Buoyancy facilitates movement and reduces fear
• Cardiovascular fitness, balance, and gait training
• Particularly beneficial for GMFCS III-V who struggle with land-based therapy

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9I. Electrical Stimulation

• Neuromuscular Electrical Stimulation (NMES): Stimulates weakened muscles (e.g., ankle dorsiflexors, quadriceps) to improve strength and function
• Transcutaneous Electrical Nerve Stimulation (TENS): Pain management
• Functional Electrical Stimulation (FES): Applied during gait for drop foot correction

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9J. Hippotherapy and Equine-Assisted Therapy

• Rhythmic movement of horse approximates pelvic motion in human gait
• Improves trunk control, balance, postural tone, and motor function
• Good evidence for GMFCS I-III

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10. PHARMACOLOGICAL MANAGEMENT OF SPASTICITY

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11. SURGICAL MANAGEMENT

Soft Tissue Procedures

• Heel cord lengthening (TAL): For equinus deformity
• Hamstring lengthening: For crouch gait with knee flexion contracture
• Hip adductor release: Prevents/treats hip dislocation
• Rectus femoris transfer: For stiff-knee gait
• Split anterior tibial tendon transfer (SPLATT): For varus foot deformity

Bony Procedures

• Femoral varus derotation osteotomy (VDRO): For hip subluxation/dislocation
• Periacetabular/Dega osteotomy: Improves acetabular coverage
• Subtalar fusion / Calcaneal lengthening: For planovalgus foot

Neurological Procedures

• Selective Dorsal Rhizotomy (SDR): Surgical sectioning of sensory rootlets (L1-S2) to reduce spasticity; best evidence for ambulatory diplegia (GMFCS II-III); irreversible; requires intensive post-op physiotherapy
• Deep Brain Stimulation (DBS): For dystonic CP; growing evidence base; targets globus pallidus internus (GPi)

Spinal Surgery

• Posterior spinal fusion for scoliosis (GMFCS IV-V with curves >50 degrees)
• Complications reported in up to 81% of CP cases (including 15-19% infection rate)

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12. PROGNOSIS AND LONG-TERM OUTCOMES

• CP is a lifelong condition but with modern management, most individuals survive into adulthood
• Ambulatory potential largely determined by GMFCS level and presence of sitting balance by age 2
• Rule of 2s for ambulation prediction:
  • If independent sitting by age 2 → likely independent ambulation
  • If not sitting by age 4 → ambulation unlikely
• Adults with CP face accelerated aging, increased musculoskeletal pain, fatigue, and risk of secondary conditions
• Regular surveillance and transition to adult services is essential

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13. MULTIDISCIPLINARY TEAM

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• Bradley and Daroff's Neurology in Clinical Practice - Chapter 111 (Cerebral Palsy)
• Campbell's Operative Orthopaedics 15th Ed 2026 - Chapter 35 (Cerebral Palsy)
• Miller's Review of Orthopaedics 9th Edition
• The Harriet Lane Handbook 23rd Edition - Chapter 9 (Table 9.9)
• Creasy & Resnik's Maternal-Fetal Medicine

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Cerebral Palsy - Investigations in Detail

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OVERVIEW

1. Identify the underlying etiology of the brain injury or malformation
2. Exclude progressive neurological conditions that may mimic CP (CP mimics)
3. Identify treatable causes (certain metabolic/genetic disorders)
4. Screen for and monitor comorbidities (epilepsy, visual, hearing, cognitive, nutritional, orthopedic)

"Although CP is a clinical diagnosis, all children should undergo investigations to identify the underlying cause and exclude progressive conditions." - Royal Children's Hospital Clinical Practice Guidelines

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I. NEUROIMAGING

A. Magnetic Resonance Imaging (MRI) Brain

• Abnormal in 70-90% of individuals with CP
• Provides information on type, severity, and timing of brain injury
• In approximately 15-18% of cases, MRI is normal or nonspecific - this should raise suspicion for an underlying genetic or metabolic etiology

• MRI with T1, T2, FLAIR, DWI, and susceptibility-weighted sequences
• DTI (Diffusion Tensor Imaging) and tractography for white matter tract visualization (specialist centers)
• Performed under sedation/general anesthesia in young or uncooperative children
• Optimal timing: 2-8 years of age (myelination complete, lesions most visible)
• In the neonatal period, early MRI (day 3-5 of life) and term-equivalent age MRI (36-40 weeks corrected) are most informative in preterm infants

"Imaging generally correlates with the findings on clinical examination - involvement of the pyramidal tract in spastic CP and of the basal ganglia or cerebellum in dyskinetic or ataxic subtypes. It is estimated that up to 70% of patients with dyskinetic CP have imaging evidence of involvement of the thalamus and basal ganglia." - Bradley and Daroff's Neurology in Clinical Practice

• Refers to injury to deep cerebral white matter in two patterns:
  • Focal periventricular necrosis: Coagulative necrosis → cyst formation or focal glial scars, most common at trigone of lateral ventricles and foramen of Monro
  • Diffuse white matter injury: Affects premyelinating oligodendrocytes → global loss of oligodendrocytes → white matter volume loss and ventriculomegaly
• Pathogenesis: hypoxia-ischemia → free radical exposure + cytokine toxicity + excitatory neurotransmitter (glutamate) excess
• Classic sequela: spastic diplegia (descending motor fibers for lower limbs traverse periventricular area)
• MRI more sensitive than cranial ultrasound for diffuse PVL

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B. Cranial Ultrasound (Head Ultrasound - HUS)

• Used in the neonatal and early infant period (before anterior fontanelle closes, ~18 months)
• Portable, no sedation required, safe, repeatable
• Indications: All preterm infants <32 weeks; term infants with HIE, suspected IVH, or clinical risk factors
• Findings:
  • Intraventricular hemorrhage (IVH) - Papile grading I-IV:
    • Grade I: Subependymal (germinal matrix) hemorrhage
    • Grade II: IVH without ventricular dilatation
    • Grade III: IVH with ventricular dilatation
    • Grade IV: Intraparenchymal hemorrhage (periventricular hemorrhagic infarction)
  • Periventricular echogenicity - suggesting PVL (though less sensitive than MRI for diffuse injury)
  • Periventricular cysts - cystic PVL (highly predictive of CP)
  • Hydrocephalus - post-hemorrhagic
• Limitation: Fails to identify subtle diffuse white matter injury; MRI is superior for confirmation
• Serial HUS recommended: at birth (for IVH), 7-14 days, 36-40 weeks corrected age

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C. CT Scan (Computed Tomography)

• Less preferred than MRI due to radiation exposure and lower soft tissue contrast
• Use in emergencies: Acute postnatal injury, suspected non-accidental trauma, urgent assessment where MRI is unavailable
• May identify:
  • Calcifications (congenital infections: TORCH)
  • Subdural hemorrhage
  • Gross structural abnormalities
• Not recommended as routine first-line investigation in stable children

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D. Advanced MRI Techniques (Specialist Indications)

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II. ELECTROENCEPHALOGRAM (EEG)

• Routine EEG (awake and sleep): First-line; minimum 30-60 minutes including sleep
• Prolonged/Ambulatory EEG (24-72 hours): When seizures are frequent but not captured on routine EEG
• Video-EEG Telemetry: Gold standard for seizure characterization and pre-surgical epilepsy evaluation; correlates clinical behavior with EEG changes
• Neonatal EEG / aEEG (amplitude-integrated EEG): Continuous monitoring in NICU for birth asphyxia; identifies subclinical seizures; predicts neurodevelopmental outcome

• Focal epileptiform discharges (sharp waves, spikes): Hemiplegic CP, focal cortical injury
• Multifocal epileptiform activity: Quadriplegic, extensive cortical damage
• Hypsarrhythmia: Infantile spasms (West syndrome) - associated with severe structural CP
• Diffuse slowing: Severe cortical dysfunction
• Background abnormalities (burst suppression): Severe HIE in neonatal period; poor prognostic indicator

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III. METABOLIC INVESTIGATIONS

• MRI is normal or nonspecific
• Clinical course appears progressive (challenging a pure CP diagnosis)
• Symptoms worsen with fasting, febrile illness, or intercurrent stress
• Atypical features are present (family history, consanguinity, regression of milestones)
• Initial genetic testing is negative but suspicion persists

Routine Metabolic Screen

CSF Analysis (Cerebrospinal Fluid)

"Inborn errors of metabolism can sometimes go undetected under the guise of a CP diagnosis, some potentially treatable. The absence of visible structural CNS injury (especially if the history lacks risk factors) should raise concern for an underlying genetic condition." - Bradley and Daroff's Neurology in Clinical Practice

Key Metabolic CP Mimics to Identify (as they are treatable)

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IV. GENETIC INVESTIGATIONS

• 10% of CP cases have pathogenic chromosomal copy number variants (Oskoui et al., 2015)
• 14% of CP cases have identifiable single gene disorders on whole exome sequencing (McMichael et al., 2015)

• Normal or atypical MRI
• No plausible acquired perinatal/postnatal etiology
• Progressive features or regression of milestones
• Dysmorphic features, microcephaly, or multiple congenital anomalies
• Family history of similar condition; consanguinity
• Bilateral cortical malformations (lissencephaly, polymicrogyria, heterotopia)
• Ataxic CP without clear structural cerebellar lesion
• Clinical actionability expected (e.g., precision therapy available)

Genetic Tests Available

• L-serine or memantine in GRIN1/GRIN2A (NMDA receptor variants)
• 4-aminopyridine or acetazolamide in CACNA1A
• Caffeine in ADCY5
• JAK inhibitors in interferonopathies
• Deep brain stimulation for dyskinetic crises: GNAO1, UBA5, KMT2B

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V. NEONATAL INVESTIGATIONS (Perinatal Period)

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VI. HEARING ASSESSMENT

• Hearing loss present in approximately 10% of children with CP
• Increased risk of both conductive (recurrent otitis media) and sensorineural hearing loss
• Sensorineural hearing loss particularly associated with kernicterus (bilirubin damage to cochlear nuclei and auditory pathways) and neonatal meningitis

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VII. VISION AND OPHTHALMOLOGICAL ASSESSMENT

• Vision problems in 30-50% of children with CP
• Strabismus (squint): Most common; occurs in ~40%
• Cortical Visual Impairment (CVI): Due to injury to visual cortex or optic radiations; most common cause of visual impairment in children with CP
• Refractive errors (myopia, hypermetropia, astigmatism): Common
• Homonymous hemianopia: In hemiplegia (damage to optic radiations)
• Nystagmus: Associated with cerebellar CP
• Optic atrophy: In severe global brain injury

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VIII. COGNITIVE AND DEVELOPMENTAL ASSESSMENT

• Intellectual disability in up to 45% of children with CP (range highly variable by subtype)
• Formal assessment before school entry to guide educational placement and support

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IX. SPEECH AND LANGUAGE ASSESSMENT

• Communication disability is common, from dysarthria to complete anarthria
• Feeding/swallowing problems are major causes of morbidity

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X. MUSCULOSKELETAL AND ORTHOPEDIC INVESTIGATIONS

Hip Surveillance X-ray

• Most important routine orthopedic investigation in CP
• Mandatory surveillance program because hip dislocation is a major preventable complication
• Reimer's Migration Percentage (MP): Proportion of femoral head lateral to Perkin's line; normal <25%

• MP 25-40%: Close surveillance + physiotherapy
• MP >40%: Surgical referral indicated
• Spastic quadriplegia (GMFCS IV-V) has ~60-70% risk of hip displacement if untreated

Spinal X-ray

• Screening for scoliosis; lateral/AP views
• Particularly important in GMFCS III-V
• Cobb angle measurement to quantify curvature
• Serial X-rays to monitor progression
• GMFCS IV-V patients have ~50% risk of scoliosis

Gait Analysis (3D Instrumented Gait Analysis - IGA)

• Kinematics (joint angles), kinetics (forces and moments), EMG (muscle activity), energy expenditure
• Gold standard for surgical decision-making in ambulatory CP
• Performed at specialist gait labs; age >4-5 years for reliable data

Bone Density (DEXA Scan)

• Osteopenia/osteoporosis common in non-ambulatory CP (GMFCS IV-V)
• Indicated in: non-ambulatory children, limited sun exposure, nutritional deficiency, long-term AED use
• DXA scan of lumbar spine and total body

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XI. NUTRITIONAL AND GROWTH MONITORING

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XII. UROLOGICAL INVESTIGATIONS

• Neurogenic bladder common in CP (up to 50% of quadriplegic CP)
• May present as urinary incontinence, retention, recurrent UTI, or upper tract damage

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XIII. RESPIRATORY INVESTIGATIONS

• Restrictive lung disease, aspiration pneumonia, and sleep-disordered breathing are common

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XIV. SUMMARY TABLE: Investigation Pathway in CP

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• Bradley and Daroff's Neurology in Clinical Practice - Chapter 111
• Creasy & Resnik's Maternal-Fetal Medicine - Periventricular Leukomalacia
• The Harriet Lane Handbook 23rd Edition - Chapter 9
• Royal Children's Hospital Clinical Practice Guidelines: Cerebral Palsy (RCH Melbourne)
• Metabolic and Genetic Disorders Mimicking Cerebral Palsy - PMC8015517
• Oskoui et al. (2015); McMichael et al. (2015) - Genetic causes of CP