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Summary Table

Domain	Details
Risk Factors	Prematurity (strongest single risk factor), low birth weight (<2500 g), perinatal asphyxia/hypoxic-ischemic encephalopathy (HIE), intrauterine infections (TORCH), multiple gestation, chorioamnionitis, periventricular leukomalacia (PVL), intraventricular hemorrhage (IVH), neonatal seizures, kernicterus, maternal substance abuse
Etiology	Non-progressive injury to the developing brain occurring prenatally (most common, ~70-80%), perinatally, or postnatally (up to age 2-3 years). NOT a degenerative process.
Patient Presentation	Delayed motor milestones (not sitting by 9 months, not walking by 18 months), abnormal muscle tone noticed by parents or pediatrician, hand preference before 12 months of age, feeding difficulties in infancy
Classic Physical Exam	Spasticity (velocity-dependent increase in tone), hyperreflexia, scissoring gait, toe-walking, persistent primitive reflexes beyond expected age, clenched fists, asymmetric crawling. In dyskinetic forms: involuntary writhing (athetoid) or jerky (choreiform) movements.
Key Diagnostic Results	Brain MRI showing periventricular leukomalacia (in preterm) or basal ganglia injury (in term asphyxia). No single lab test confirms the diagnosis. Diagnosis is fundamentally clinical.
Management	Multidisciplinary rehabilitation (physical therapy, occupational therapy, speech therapy), oral baclofen or diazepam for generalized spasticity, botulinum toxin A injections for focal spasticity, intrathecal baclofen pump for severe refractory spasticity, orthopedic surgery for fixed contractures, anticonvulsants if comorbid epilepsy
Keywords	"Non-progressive motor disorder," "delayed milestones," "scissoring gait," "periventricular leukomalacia," "persistent primitive reflexes," "upper motor neuron signs in a child," "hand preference before age 1"

1. Pathophysiology

Cerebral palsy (CP) is defined as a non-progressive disorder of movement and posture caused by a static lesion or injury to the immature, developing brain. The word "non-progressive" is one of the most tested concepts: the brain lesion itself does not worsen over time, but the clinical manifestations can evolve as the child grows and the nervous system matures. This distinction is critical because if a vignette describes a child whose neurological function is actively deteriorating, you must consider a neurodegenerative condition instead of CP.

The timing of injury determines the pattern of brain damage and, consequently, the clinical subtype. In preterm infants, the most vulnerable brain region is the periventricular white matter, which carries the descending corticospinal fibers for the lower extremities. Damage here, called periventricular leukomalacia (PVL), preferentially affects the leg motor fibers, producing the classic pattern of spastic diplegia (legs more affected than arms). This is why prematurity is so tightly linked to the diplegic pattern, and why PVL on MRI in the setting of a former premature infant with bilateral lower extremity spasticity is a textbook combination.

In term infants, the most metabolically active regions of the brain are the basal ganglia, thalamus, and the parasagittal cortex. Hypoxic-ischemic injury at term therefore tends to damage these deeper gray matter structures, leading to either spastic quadriplegia (if the cortex and deep structures are widely involved) or dyskinetic (athetoid/choreoathetoid) CP (if the basal ganglia bear the brunt of injury). Kernicterus from severe unconjugated hyperbilirubinemia is another classic cause of basal ganglia injury and dyskinetic CP; this association remains high-yield even though exchange transfusions have made it rare.

The upper motor neuron (UMN) pathway is almost always involved in the spastic forms, which account for roughly 70-80% of all CP. Damage to the corticospinal tract produces the familiar UMN constellation: spasticity, hyperreflexia, clonus, a positive Babinski sign, and scissoring gait. Understanding that CP is an UMN disease helps you quickly differentiate it from lower motor neuron conditions (such as spinal muscular atrophy) that present with hypotonia and absent reflexes.

A key pathophysiological point for the exam: the motor deficit is the defining feature of CP, but most children with CP also have associated comorbidities including intellectual disability (about 50%), epilepsy (25-45%), visual impairment, hearing loss, speech and language disorders, and behavioral problems. The vignette may focus on one of these comorbidities, but the underlying diagnosis is still CP.

2. Classification and Clinical Manifestation

By Motor Type

Type	Frequency	Brain Lesion	Clinical Features
Spastic	~70-80%	Cortex or pyramidal (corticospinal) tracts	Increased muscle tone (velocity-dependent), hyperreflexia, clonus, positive Babinski. Tone increases with rapid passive movement.
Dyskinetic (Athetoid/Choreoathetoid)	~10-15%	Basal ganglia, thalamus	Involuntary, writhing movements (athetosis) or rapid, jerky movements (chorea). Tone fluctuates. Worsened by stress, improved during sleep.
Ataxic	~5%	Cerebellum	Wide-based gait, intention tremor, dysmetria, difficulty with rapid alternating movements. Hypotonia rather than spasticity.
Mixed	Variable	Multiple areas	Combination of spasticity and dyskinesia most common. Features of more than one motor type.

By Topography

Subtype	Limbs Affected	Typical Etiology	Key Clinical Features
Spastic Diplegia	Both legs >> arms	Prematurity, PVL	Scissoring gait, toe-walking, relatively preserved upper limb function and cognition. "Typical CP of prematurity."
Spastic Hemiplegia	One side (arm often > leg)	Prenatal stroke, focal cortical injury, middle cerebral artery infarct	Unilateral fisting, early hand preference before 12 months, circumduction gait, affected arm held in flexion.
Spastic Quadriplegia	All four limbs, trunk, and often bulbar muscles	Severe global HIE in term infants, severe bilateral brain injury	Most severe form. Often associated with intellectual disability, epilepsy, swallowing dysfunction, and pseudobulbar signs. Limited functional mobility.

By Functional Severity (Gross Motor Function Classification System, GMFCS)

Level	Functional Ability
I	Walks without limitations
II	Walks with limitations (difficulty on uneven surfaces, stairs)
III	Walks using a hand-held mobility device (walker, crutches)
IV	Self-mobility with limitations; may use powered wheelchair
V	Transported in a manual wheelchair; severely limited voluntary movement

The GMFCS is testable because it guides prognosis and treatment planning. A child classified as GMFCS Level I has a very different rehabilitation plan and surgical candidacy compared to GMFCS Level V.

3. Diagnostic Workup

Test	Role	Key Findings
Clinical assessment of milestones and tone	Best initial step	Delayed motor milestones, abnormal tone, persistent primitive reflexes
Brain MRI	Best initial imaging / Most informative test	PVL (preterm), basal ganglia injury (term HIE), focal infarct (hemiplegia), cortical/subcortical atrophy
Cranial ultrasound	Screening in neonates (especially preterm)	IVH, PVL in the neonatal period
EEG	Adjunctive, if seizures suspected	Epileptiform discharges (25-45% of CP patients have epilepsy)
Metabolic and genetic testing	To exclude mimics	Normal results expected in CP; abnormal results redirect to metabolic/genetic diagnoses
TORCH screening	If prenatal infection suspected	Positive serology redirects to congenital infection as etiology

The diagnosis of cerebral palsy is clinical. There is no single laboratory test, imaging study, or biomarker that "confirms" CP. The diagnosis rests on recognizing a child with a non-progressive motor disorder that originated from injury to the developing brain, combined with the characteristic physical exam findings.

The best initial step in evaluating a child with suspected CP is a thorough developmental and neurological examination. You are looking for delayed motor milestones (the child who is not sitting unsupported by 9 months, not walking by 15-18 months), abnormal muscle tone (most commonly increased tone with spasticity, but hypotonia can be the initial presentation in young infants before spasticity develops), persistent primitive reflexes (such as the Moro reflex persisting beyond 6 months or the asymmetric tonic neck reflex persisting beyond 6-7 months), and early hand dominance before 12 months (a red flag for hemiplegia, since children normally do not establish handedness until 18-24 months).

Brain MRI is the most informative neuroimaging study and should be obtained in virtually all children with suspected CP. MRI is abnormal in approximately 80-90% of cases and helps establish the etiology and timing of the brain injury. In former preterm infants, the hallmark finding is periventricular leukomalacia, visible as white matter volume loss and signal abnormality around the lateral ventricles. In term infants with a history of perinatal asphyxia, you will see basal ganglia and thalamic signal abnormality. In children with spastic hemiplegia, MRI may reveal a focal infarct in the territory of the middle cerebral artery. A normal MRI does not exclude the diagnosis but should prompt careful reconsideration and further workup for mimics.

Metabolic and genetic testing is not routinely performed when the clinical picture is straightforward and the MRI shows a pattern consistent with CP. However, if the MRI is normal, if the history lacks clear risk factors, or if there are atypical features (such as progressive neurological decline, family history of similar disease, or episodic worsening), you must investigate for metabolic disorders (e.g., glutaric aciduria type I, which mimics dyskinetic CP), genetic conditions (e.g., hereditary spastic paraplegia, dopa-responsive dystonia), and structural brain malformations. This is a frequently tested concept: the exam wants you to know when CP is not CP.

4. Management and Treatment

Intervention	Indication	Details
Physical therapy (PT)	All patients	Stretching, strengthening, gait training. Cornerstone of management at every GMFCS level.
Occupational therapy (OT)	Fine motor and self-care deficits	Hand function, feeding skills, adaptive equipment
Speech-language therapy	Speech/language delays, swallowing dysfunction	Augmentative communication devices if needed
Oral baclofen	Generalized spasticity	Starting dose 5 mg three times daily, titrate up to 60-80 mg/day in divided doses. Sedation is the main side effect.
Diazepam	Generalized spasticity (second line)	0.12-0.8 mg/kg/day divided; sedation and dependence limit long-term use
Botulinum toxin A (BoNT-A)	Focal/regional spasticity	Injected into targeted muscles (e.g., gastrocnemius for equinus). Effect lasts 3-6 months. Repeat as needed.
Intrathecal baclofen (ITB) pump	Severe generalized spasticity refractory to oral agents	Surgically implanted pump delivers baclofen directly to the spinal cord. Requires careful monitoring for pump malfunction and withdrawal.
Selective dorsal rhizotomy (SDR)	Spastic diplegia, GMFCS II-III, good underlying strength	Irreversible surgical cutting of selected dorsal (sensory) rootlets to reduce spasticity. Best outcomes in carefully selected patients.
Orthopedic surgery	Fixed contractures, hip subluxation/dislocation, scoliosis	Tendon lengthening, hip reconstruction, spinal fusion as indicated. Often deferred until skeletal maturity when possible.
Anticonvulsants	Comorbid epilepsy (25-45%)	Chosen based on seizure type; no agent is uniquely preferred for CP-associated epilepsy
Nutritional support	Failure to thrive, feeding difficulties	Gastrostomy tube placement if oral feeding is unsafe or inadequate

Rehabilitation therapy is the foundation of CP management at every level of severity. Physical therapy aims to maintain range of motion, prevent contractures, strengthen functional muscles, and optimize gait. Occupational therapy targets fine motor skills, feeding, dressing, and adaptive equipment use. Speech-language therapy addresses both communication (many children benefit from augmentative and alternative communication devices) and swallowing safety. These therapies should begin as early as possible and continue throughout childhood.

For spasticity management, the approach is stepwise. The first-line pharmacological option for generalized spasticity is oral baclofen, a GABA-B receptor agonist that reduces spasticity at the spinal cord level. It is started at a low dose (5 mg two to three times daily) and titrated gradually. Sedation, weakness, and lowered seizure threshold are notable side effects. Diazepam (a GABA-A agonist) is an alternative, but its use is limited by sedation, tolerance, and risk of dependence.

For focal spasticity (e.g., isolated equinus due to calf spasticity, or wrist flexor spasticity), the treatment of choice is botulinum toxin A injection into the affected muscles. The toxin blocks acetylcholine release at the neuromuscular junction, producing a temporary, localized reduction in tone lasting 3-6 months. This allows a window for intensive therapy and functional gains. Repeat injections are often needed but must be spaced appropriately to avoid antibody formation.

For severe, generalized, refractory spasticity, the next step is an intrathecal baclofen pump. This delivers baclofen directly into the cerebrospinal fluid, allowing therapeutic concentrations at the spinal cord with much lower systemic doses and fewer systemic side effects. The exam tests awareness of a critical complication: acute baclofen withdrawal from pump malfunction or catheter issues, which can cause rebound spasticity, hyperthermia, rhabdomyolysis, seizures, and death. This is a medical emergency treated with high-dose oral or enteral baclofen and supportive care.

Selective dorsal rhizotomy (SDR) is a neurosurgical procedure reserved for carefully selected children, typically those with spastic diplegia, GMFCS levels II-III, good underlying strength, and no significant dystonia. By selectively cutting sensory nerve rootlets that contribute to the spasticity reflex arc, SDR can permanently reduce spasticity. It is not reversible, and patient selection is critical.

Orthopedic interventions are common and include soft tissue surgery (adductor releases, hamstring lengthening, Achilles tendon lengthening) for dynamic contractures, and bony procedures (femoral and pelvic osteotomies for hip displacement, spinal fusion for scoliosis) for structural deformities. Hip surveillance with serial radiographs is standard of care in children with CP, as the incidence of hip displacement increases with GMFCS level (approaching 90% in GMFCS V).

5. Differential Diagnosis and Distractors

Differential	Why It Looks Similar	Key Discriminator
Spinal muscular atrophy (SMA)	Presents in infancy with motor delay and hypotonia	SMA is a lower motor neuron disease: hypotonia with areflexia and fasciculations, no spasticity or hyperreflexia. Tongue fasciculations are a hallmark.
Hereditary spastic paraplegia (HSP)	Progressive lower limb spasticity, can look like spastic diplegia	Progressive course, often with a positive family history. MRI may be normal or show thin corpus callosum. CP is non-progressive.
Glutaric aciduria type I	Can mimic dyskinetic CP after acute metabolic crisis with basal ganglia injury	Macrocephaly, acute encephalopathic crisis triggered by illness, elevated urine glutaric acid, characteristic widened Sylvian fissures on MRI
Dopa-responsive dystonia (Segawa disease)	Dystonia presenting in childhood, diurnal fluctuation	Symptoms worsen throughout the day and improve with sleep, dramatic response to low-dose levodopa. CP dystonia does not show this pattern.
Rett syndrome	Developmental regression, hand stereotypies, acquired microcephaly	Loss of previously acquired hand skills (hand-wringing stereotypies), primarily affects girls, MECP2 mutation. CP does not involve regression of skills.
Leukodystrophies (e.g., metachromatic, Krabbe)	White matter disease on MRI, progressive spasticity	Progressive neurological decline with worsening cognition and motor function. CP is static. MRI shows diffuse, progressive demyelination rather than the stable PVL of CP.
Muscular dystrophy (Duchenne)	Motor delay, abnormal gait in a young boy	Proximal weakness, Gowers sign (climbing up legs to stand), pseudohypertrophy of calves, markedly elevated creatine kinase. No spasticity or hyperreflexia.
Benign developmental delay	Delayed milestones	Exam and tone are normal; child catches up over time. No spasticity, no persistent primitive reflexes, no abnormal posturing.

6. Traps and High-Yield Pearls

The single most common way students get questions about CP wrong is confusing CP with a progressive or degenerative neurological condition. The vignette for CP will never describe worsening brain pathology or loss of previously acquired cognitive milestones. If the stem mentions that the child was "developing normally and then started to lose skills," you are being steered toward a neurodegenerative disease, not CP. The clinical manifestations of CP may change as the child grows (for example, an infant may initially present with hypotonia before spasticity becomes apparent), but this evolution of signs is not the same as disease progression.

A second classic trap involves early hand preference. Normal children do not establish hand dominance until approximately 18-24 months of age. If a vignette describes a 6 or 8-month-old infant who "always reaches with the right hand" or "never uses the left hand," this is not a normal developmental variant. This is a red flag for spastic hemiplegia affecting the contralateral side, and the question is testing whether you recognize this subtle early sign.

Third, remember that a normal MRI does not rule out CP. About 10-15% of children with CP have normal neuroimaging. In such cases, the exam expects you to pursue additional workup for treatable mimics, particularly metabolic and genetic disorders. The core competency being tested is your ability to recognize when the clinical picture does not fully fit CP and to appropriately expand your differential.

Fourth, be aware of the intrathecal baclofen withdrawal scenario. If a vignette presents a child with CP who has an implanted baclofen pump and develops acute onset of worsening spasticity, high fever, and altered mental status, the answer is acute baclofen withdrawal, and it is a medical emergency requiring immediate intervention.

Finally, the exam frequently tests the association between prematurity, periventricular leukomalacia, and spastic diplegia as a linked triad. When you see a former premature infant presenting with bilateral lower extremity spasticity, scissoring gait, and relatively spared upper limbs and cognition, you should recognize spastic diplegia and anticipate PVL on MRI. This pattern is one of the most predictable and testable vignettes in pediatric neurology.

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