Cerebral Palsy: An Overview

Cerebral palsy (CP) is a non-progressive neuromotor disorder of cerebral origin. It encompasses various clinical conditions of differing etiology and severity, ranging from mild impairment to profound disability. Most cases involve multiple neurological deficits and varying degrees of cognitive impairment. CP does not include progressive, degenerative, or metabolic disorders of the nervous system1.

Epidemiology

Determining the exact prevalence of CP is challenging, as milder cases may go undiagnosed. However, an estimated 1-2 per 100 live births are affected by CP2.

Enteropathogenesis

CP can arise from prenatal, perinatal, or postnatal factors. Potential causes include cerebral malformations, perinatal hypoxia, birth trauma, chorioamnionitis, prothrombotic factors, acid-base imbalances, indirect hyperbilirubinemia, metabolic disturbances, and intrauterine or acquired infections. Most affected infants have multiple risk factors. Prematurity is a significant risk factor for spastic diplegia, whereas term infants are more likely to develop quadriparesis or hemiparesis. The exact pathophysiology remains unclear, though primary neurological abnormalities may be identified in the future1,3. Recent data challenge the significance of birth asphyxia, suggesting that it may be a consequence rather than the cause of brain injury2. Various pathological lesions, including cerebral atrophy, porencephaly, periventricular leukomalacia, and basal ganglia, thalamic, or cerebellar lesions, may be present3.

Types of Cerebral Palsy:

CP are classified based on topographic distribution, neurological findings, and etiology1,3:

1. Spastic Cerebral Palsy: The most common type (65%), further categorized into spastic quadriparesis, diplegia, or hemiparesis. Key features include persistent neonatal reflexes, feeding difficulties, and an abnormal posture, such as scissoring due to adductor spasm. Spastic quadriparesis is common in term infants, whereas spastic diplegia is more frequent in preterm infants with periventricular leukomalacia. Spastic hemiplegia typically becomes evident between 4-6 months of age, presenting with early hand preference and abnormal fisting2.

2. Hypotonic (Atonic) Cerebral Palsy: Despite pyramidal involvement, these patients exhibit hypotonia, normal or brisk tendon reflexes, and a positive Babinski response. They often have severe intellectual disabilities3.

3. Extrapyramidal CP: Present in 30% of cases, it includes athetosis, choreiform movements, dystonia, tremors, and rigidity. Mental retardation and hearing deficits may also be present. High-frequency audiometry is recommended, especially in cases related to bilirubin encephalopathy1,2.

4. Cerebellar Involvement: Less than 5% of cases exhibit hypotonia, hyporeflexia, ataxia, and intention tremors by the age of two. Nystagmus is uncommon, and cognitive abilities may be preserved3.

5. Mixed Type: Some patients exhibit features of multiple types due to widespread neurological involvement2.

Severity of Lesion: CP severity varies:

1. Mild cases (20%): Patients can walk independently.

2. Moderate cases (50%): Require assistance but can be managed on an outpatient basis.

3. Severe cases (30%): Involve multiple disabilities and may require institutional care1.

Clinical Evaluation

1. Visual Deficits: Nearly 50% of CP patients exhibit strabismus, gaze paralysis, cataracts, coloboma, retrolental fibroplasia, and refractive errors2.
2. Hearing Impairment: Often seen in kernicterus and rubella-related CP3.
3. Speech Disorders: Aphasia, dysarthria, and dyslalia are prevalent in dyskinetic CP1.
4. Sensory Deficits: One-third of cases exhibit astereognosis and spatial disorientation2.
5. Seizures: Common in spastic CP, often resistant to antiepileptic therapy. EEG abnormalities are frequently observed3.
6. Cognitive Impairment: About 25% of children have borderline intelligence (IQ 80-100), while approximately 50% have severe intellectual disabilities1,2.
7. Other Complications: Thermoregulation issues, dental anomalies, and increased infection susceptibility are noted3.

Diagnosis:

CP should be suspected in children with low birth weight, perinatal insults, increased muscle tone, feeding difficulties, and developmental delays. Diagnosis is based on perinatal history, neurological assessment, and evaluation of associated deficits. Laboratory investigations, including metabolic screening, may be necessary. Neuroimaging (CT/MRI) can help assess cerebral damage2,3.

Differential Diagnosis:

Conditions mimicking CP include:

• Neurodegenerative Disorders: Progressive symptoms, familial occurrence, and metabolic abnormalities1.

• Hydrocephalus & Subdural Effusion: Macrocephaly and bulging fontanelles2.

• Brain Tumours: Progressive neurological deficits with increased intracranial pressure3.

• Muscle Disorders: Myopathies and muscular dystrophies present with hypotonia and diminished reflexes1.

• Ataxia-Telangiectasia: Early ataxia with later-onset ocular telangiectasia2.

Prevention

Reducing maternal infections, ensuring optimal perinatal care, and early detection can lower CP prevalence. Early intervention can minimize residual disabilities and improve quality of life3.

Management

A holistic, multidisciplinary approach involving families is crucial:

• Physiotherapy & Occupational Therapy: Improve posture, reduce spasticity, and enhance motor function1.

• Medications: Baclofen, tizanidine, diazepam, and dantrolene sodium can manage spasticity. Botulinum toxin or phenol nerve blocks may address contractures2.

• Surgical Interventions: Orthopaedic procedures for contractures and spasticity in selected cases3.

• Speech & Special Education: Address vision, speech, and learning disabilities1.

• Social & Emotional Support: Counseling for families, vocational training, and institutionalization for severely affected cases2,3.

Conclusion

CP is a complex disorder requiring early identification and comprehensive management to enhance the quality of life for affected individuals. A multidisciplinary approach with medical, rehabilitative, and social support can optimize outcomes1,3.

References

1. Ghai OP, Paul VK, Bagga A. Essential Pediatrics. 10th ed. New Delhi: CBS Publishers; 2023. p. 398-402.

2. Kliegman RM, St Geme JW, Blum NJ, Shah SS, Tasker RC, Wilson KM. Nelson Textbook of Pediatrics. 21st ed. Philadelphia: Elsevier; 2020. p. 2051-2055.

3. Hockenberry MJ, Wilson D, Rodgers CC. Wong’s Essentials of Pediatric Nursing. 10th ed. St. Louis: Elsevier; 2017. p. 1121-1124.

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