نظرة عامة على الشلل الدماغي

Cerebral Palsy Overview

• Cerebral palsy (CP) is a group of permanent movement and posture disorders.
• These disorders arise from non-progressive disturbances in the developing fetal or infant brain.
• CP onset can be during pregnancy, childhood, or after birth, up to about age 5.
• CP is a common cause of chronic childhood disability.
• CP symptoms can change over time, sometimes improving, and sometimes worsening.

Causes of Cerebral Palsy

• Prenatal: Vascular events (like a middle cerebral artery infarct), maternal infections (like rubella, cytomegalovirus, and toxoplasmosis), and rarer conditions (like metabolic disorders, maternal toxin ingestion, and genetic syndromes).
• Perinatal: Problems during labor and delivery (like obstructed labor, antepartum hemorrhage, cord prolapse), neonatal stroke (often targeting the middle cerebral artery), severe hypoglycemia, untreated jaundice, and severe neonatal infection.
• Postnatal: Metabolic encephalopathy (including storage disorders, intermedullary metabolism disorders, metabolic disorders, and miscellaneous disorders), and toxicity (like alcohol).
• Infections: Meningitis, septicemia, and malaria (in developing countries).
• Injuries: Cerebrovascular accidents, post-surgery for congenital malformations, near-drowning experiences, trauma from motor vehicle accidents, and child abuse (like shaken baby syndrome).

Risk Factors

• During Pregnancy: Preeclampsia (in term, but not preterm, infants), multiple pregnancies (associated with preterm delivery and poor intrauterine growth), birth defects, and intrapartum complications.
• During Labor: Prolapsed cord, massive intrapartum hemorrhage, prolonged or traumatic delivery due to cephalopelvic disproportion or abnormal presentation, large baby (shoulder dystocia), and maternal shock from various causes.
• Additional factors (associated with causal factors): Prolonged second-stage labor, emergency Cesarean section, premature separation of the placenta, abnormal fetal position, meconium-stained fluid, and tight nuchal cord.
• Preterm Infants: Patent ductus arteriosus, hypotension, blood transfusion, prolonged ventilation, pneumothorax, sepsis, hyponatremia, total parenteral nutrition, seizures, and parenchymal damage with appreciable ventricular dilatation.

Classification of Cerebral Palsy

• Physiological Classification: Spastic CP, Ataxic CP, Athetoid CP, Mixed type CP, and Hypotonic CP.

• Anatomical Classification: Monoplegia (one limb affected), Hemiplegia (upper and lower limbs on one side affected), Diplegia (all limbs affected, but lower limbs more than upper limbs), and Quadriplegia (all four limbs affected).

Specific Types of Cerebral Palsy

• Spastic CP: Most common type (about 80% of cases). Characterized by hypertonia and mobility impairment due to lesions in the motor cortex. Often includes clonus(involuntary muscle spasms) of the affected limbs. Can cause early-onset arthritis and tendinitis, hip dislocations, and frequent epilepsy.
• Ataxic CP: Results from damage to the cerebellum, occurring in less than 10% of cases. Symptoms include hypotonia, tremors, and difficulty with motor skills (especially writing, typing, using scissors, or balance, especially while walking).
• Athetoid CP: Also known as dyskinetic CP, it's characterized by mixed muscle tone (both hypertonia and hypotonia) and involuntary movements. This affects the ability to hold a steady position while sitting, standing, or walking. Can create challenges with fine motor skills.
• Mixed CP: Combines features of two or more types. Diagnosed MR in 60% of cases, and learning disabilities are common.
• Hypotonic CP: Characterized by low muscle tone (hypotonia), which can be permanent but often transient. Often transient, and doesn't always represent a particular CP type. Can later develop spasticity (beginning distally moving progressively proximally with the trunk and extremities).

Signs and Symptoms

• General: Delayed milestones, lack or loss of head control, frequent epilepsy, drooling, deformities in limbs due to muscle tightness.
• Additional signs: Presence of primitive reflexes, spastic features, flaccidity, involuntary movements, lack or loss of movement in limbs, lack of social response, hip dislocations, inability to sit without support, mental retardation, learning disabilities, spinal deformities, urinary and fecal incontinence, dysarthria, and speech impairments. Difficulty with feeding.

Diagnosis

• Clinical: Delayed development, primitive reflexes, abnormal tone, involuntary movements.
• CT/MRI: Brain cell degeneration (atrophy).

Treatment

• Rehabilitation Team: Neurologist, orthopedician, physiotherapist, occupational therapist, speech therapist, special educators, and parents.
• Medical Management: Anti-convulsive drugs (like dantrolene, sodium, baclofen), botulinum toxin injections, and proper dietary supplements.
• Orthopedic interventions: Corrective surgeries for deformities and muscle length correction.
• Physiotherapy: Passive/active movements, Active assisted/active exercises, passive stretching, proper positioning, proper orthotics, gait training, and supportive devices. Therapy may utilize Rood’s approach (managing muscle tone), NDT approach (using primitive reflexes to stimulate development), Brunnstrom's approach (developing voluntary control), and sensory integration (addressing learning disabilities).

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