Cerebral palsy

Hypoxic-ischemic injury and PVL

One of the leading causes of CP is brain hypoxia and ischemia in the neonatal period. The nature of the damage directly depends on the degree of maturation of the nervous system: in full-term infants, the gray matter is predominantly affected, whereas in premature infants (under 36 weeks of gestation), the white matter is affected.

The most common type of injury in premature infants is periventricular leukomalacia (PVL). It is recognized as the main cause of long-term neurological, cognitive, and behavioral disorders.

Screening using ultrasound (neurosonography) is critical for predicting the risk of CP. Ultrasound is performed at the bedside and allows for the detection of cyst formation or resolution in PVL. If the scan shows major structural anomalies, the probability of developing cerebral palsy ranges from 50 to 80% (depending on the diagnostician's experience). With a normal ultrasound picture, the risk of severe disability does not exceed 3–4%. Magnetic resonance imaging is ordered only in the presence of pronounced neurological symptoms, as routine performance lacks sufficient justification.

Hemolytic disease of the newborn (HDN)

Another significant factor in the development of CP is severe HDN. The prognosis in this disease strictly correlates with the degree of hemolysis. In severe forms, there is a high risk of severe psychomotor retardation and subsequent cerebral palsy.

To prevent such outcomes, prevention of Rhesus sensitization in women is applied (administration of anti-Rhesus immunoglobulin). If sensitization has already occurred, intrauterine exchange transfusion (at 25–27 weeks) and early delivery starting from the 29th week of gestation are used to protect the fetus and prevent severe HDN.

Orthopedic consequences: pathological flatfoot

CP belongs to the group of neuromuscular diseases that act as an etiological factor for the development of severe foot deformations. One of the frequent manifestations is pathological flatfoot.

The pathogenesis is based on the disruption of normal relationships in the tarsal joints. Anatomically, this manifests as an increase in talocalcaneal divergence, plantarflexion of the talus, and dorsolateral displacement of the navicular bone. Clinically, the patient exhibits increased hindfoot valgus, as well as forefoot supination and abduction.

These changes disrupt the propulsive function of the foot and cause biomechanical shifts throughout the lower extremity. In severe stages, the main load is transferred to the sustentaculum tali, maximal pronation of the calcaneus occurs, and a severe rocker-bottom foot deformation develops.

Acquired clubfoot in cerebral palsy

Cerebral palsy is also a classic neurological cause for the development of acquired clubfoot.

The main mechanism of this pathology in CP is pronounced muscle imbalance. The physiological equilibrium between the flexor and extensor muscles of the foot is disrupted.

Due to neuromuscular disorders and subsequent structural changes, a persistent equinovaneovarus deformation forms, requiring complex and prolonged orthopedic correction.

Class and exam questions

What else to study on this topic

• Mechanisms of development and stages of periventricular leukomalacia (PVL)
• Brain ultrasound screening protocols in premature newborns
• Biomechanics and stages of foot deformation in pathological flatfoot
• Specific prevention and management tactics for pregnancy in Rh-sensitization
• Aneurysmal malformations of the vein of Galen as a cause of stroke in pediatrics

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