9.1 Cerebral Palsy Classification & GMFCS

Overview of Cerebral Palsy Definition & Etiology

Cerebral Palsy (CP) represents a group of permanent, non-progressive disorders of movement and posture development causing activity limitation. The motor disturbances are attributed to non-progressive brain lesions occurring in the developing fetal or infant brain. Although the primary brain lesion is static, secondary musculoskeletal manifestations (muscle contractures, bony deformities, and joint subluxations) evolve dynamically with growth.

In premature infants (gestational age <32 weeks), the predominant neuropathological mechanism is periventricular leukomalacia (PVL)—ischemic necrosis of white matter surrounding the lateral ventricles, affecting descending pyramidal fibers supplying the lower extremities. In term infants, mechanisms include hypoxic-ischemic encephalopathy (HIE), middle cerebral artery stroke, and intrauterine infections.

Motor Classification and Topographic Distribution

Cerebral palsy is classified by abnormal tone pattern (spastic, dyskinetic, ataxic, mixed) and anatomical distribution (diplegia, hemiplegia, quadriplegia).

Spastic Cerebral Palsy

Spastic CP accounts for ~80% of cases, presenting with velocity-dependent hypertonia, hyperreflexia, and clonus.

• Spastic Diplegia: Lower extremities are affected significantly more than upper extremities. Classically associated with prematurity and PVL. Demonstrates a scissoring gait (hip adductor spasticity) and crouch gait (hamstring/hip flexor tightness paired with weak plantarflexors). Cognition is frequently preserved.
• Spastic Hemiplegia: Unilateral motor impairment (arm > leg). Caused by focal cortical/subcortical stroke. Early handedness (preference before 12 months) is a primary red flag. Independent ambulation (GMFCS I-II) is typical.
• Spastic Quadriplegia: All four limbs and trunk are severely involved. Caused by diffuse cerebral insult (severe HIE). High incidence of intellectual disability, epilepsy, dysphagia, and severe hip dislocation.

Dyskinetic and Ataxic Cerebral Palsy

• Dyskinetic CP: Accounts for 10-15% of cases, caused by basal ganglia lesions secondary to kernicterus or severe asphyxia. Manifests as dystonia (sustained twisting postures) or choreoathetosis (involuntary writhing movements). Cognition is often preserved.
• Ataxic CP: Caused by cerebellar injury, manifesting with hypotonia, wide-based gait, intention tremor, and dysmetria.

Gross Motor Function Classification System (GMFCS)

The Gross Motor Function Classification System (GMFCS) categorizes gross motor function in children with CP across 5 ordinal levels, focusing on self-initiated movement and assistive technology needs in daily life:

• GMFCS Level I: Walks indoors and outdoors and climbs stairs without using a handrail. Gross motor skills (running, jumping) are limited in speed and balance.
• GMFCS Level II: Walks indoors/outdoors and climbs stairs holding a railing. Experiences limitations on uneven terrain or inclines; cannot run or jump effectively.
• GMFCS Level III: Walks using a hand-held mobility device (forearm crutches, rolling walker) indoors. Uses wheeled mobility for long distances outdoors.
• GMFCS Level IV: Relies on wheeled mobility in most settings. May achieve self-mobility with a powered wheelchair or walk short distances at home with a body-support walker.
• GMFCS Level V: Transported in a manual wheelchair in all settings. Severe head and trunk control limitations; requires complete physical assistance for positioning and transfers.

Focal Spasticity Management & Serial Casting

Focal spasticity management integrates physical therapy, orthoses, serial casting, and chemodenervation. Botulinum toxin A injections target dynamic muscle overactivity (e.g., gastrocnemius, hamstrings, adductors), peaking at 2-4 weeks with effects lasting 3-4 months. When dynamic spasticity is complicated by early fixed soft-tissue tightness (such as Achilles tendon tightness), serial casting is performed by applying weekly below-knee casts for 3-6 weeks, progressively stretching the soft tissues into dorsiflexion.

Hip Surveillance Protocol by GMFCS Level

Progressive hip displacement affects up to 90% of children at GMFCS V due to muscle imbalance (hypertonic adductors/iliopsoas vs weak gluteals) and delayed weight-bearing. Surveillance uses AP pelvis radiographs to measure Migration Percentage (MP). Normal MP is <20%; an MP >30% indicates hip displacement requiring orthopedic referral.

Radiographic Screening Schedule:

• GMFCS I: Baseline AP pelvis radiograph at 12-24 months; annual clinical monitoring.
• GMFCS II: Baseline radiograph at 12 months; repeat every 2 years until age 8.
• GMFCS III-IV: Baseline radiograph at 12 months; repeat every 6-12 months until age 8-10, then annually until skeletal maturity.
• GMFCS V: Baseline radiograph at 6-12 months; repeat every 6 months until age 8-10, then annually until skeletal maturity.

When MP >30%, interventions include soft tissue releases (adductor/psoas tenotomy) or Varus Derotation Osteotomy (VDRO). Preventive bracing does not halt hip displacement.

Selective Dorsal Rhizotomy (SDR)

Selective Dorsal Rhizotomy (SDR) transects abnormal sensory nerve rootlets at L2-S1 to interrupt hyperactive stretch reflexes and reduce spasticity.

Candidate Selection Criteria

• Ideal Candidate: Pure spastic diplegia due to PVL; age 3 to 8 years; GMFCS Level II or III; good underlying trunk strength and selective motor control; no fixed contractures or deformities.
• Exclusion Criteria: Presence of dystonia, athetosis, or ataxia; severe trunk weakness; fixed structural contractures; lack of family support for intensive therapy.

Post-operatively, patients require 6-12 months of intensive physical therapy (4-5 days/week) to strengthen unmasked underlying muscle weakness and retrain gait.