These patients are especially at risk of developing osteoporosis because of decreased weight bearing, so following their calcium intake and vitamin D levels is important.Gastrointestinal and nutritional complications include the following:Failure to thrive due to feeding and swallowing difficulties secondary to poor oromotor control; patients may require a gastrostomy tube (G-tube) or a jejunostomy tube (J-tube) to augment nutrition.Gastroesophageal reflux and associated aspiration pneumoniaDental problems also include enamel dysgenesis, malocclusion, and Increased risk of aspiration pneumonia because of oromotor dysfunctionHearing loss (particularly in patients who had acute bilirubin encephalopathy [kernicterus]; also seen in patients who were born prematurely or who were exposed to ototoxic drugs)Epilepsy occurs in 15-60% of children with cerebral palsy and is more common in patients with spastic quadriplegia or mental retardation.

Jan 25 2013. In most cases, the exact cause is unknown but is most likely multifactorial.Interpretation of the literature is limited by the lack of strict definitions in studies attempting to define a pathogenesis of cerebral palsy and the relatively small size of certain studies. Pediatrics.

Cerebral palsy epidemiology: where are we now and where are we going?. Such scores may reflect circumstances unrelated to birth asphyxia, such as infections and other preexisting prenatal conditions.The following postnatal factors may contribute to cerebral palsy:Intracranial hemorrhage (eg, due to prematurity, vascular malformations, or trauma)Periventricular leukomalacia (in premature infants)Persistent fetal circulation or persistent pulmonary hypertension of the newbornPossible causes of cerebral palsy by type are discussed below.Of all cases of cerebral palsy, 70-90% are congenital and 10-30% are acquired (eg, vascular, inflammatory, traumatic). The phrase is sometimes used pejoratively for writing that focuses on the aesthetic qualities of language rather than its practical application.

2002

Pascual-Pascual SI, Pascual-Castroviejo I.

There are no definitive laboratory studies for diagnosing the condition, only studies, including the following, to rule out other symptom causes:Thyroid function studies: Abnormal thyroid function may cause abnormalities in muscle tone or deep tendon reflexes or movement disordersLactate and pyruvate levels: Abnormalities may indicate an abnormality of energy metabolism (ie, mitochondrial cytopathy)Ammonia levels: Elevated ammonia levels may indicate liver dysfunction or urea cycle defectOrganic and amino acids: Serum quantitative amino acid and urine quantitative organic acid values may reveal inherited metabolic disordersChromosomal analysis: Chromosomal analysis, including karyotype analysis and specific DNA testing, may be indicated to rule out a genetic syndrome, if dysmorphic features or abnormalities of various organ systems are presentCerebrospinal protein: Levels may support asphyxia in the neonatal period; protein levels can be elevated, as can the lactate-to-pyruvate ratioCranial imaging studies to help evaluate brain damage and identify persons who are at risk for cerebral palsy include the following:Cranial ultrasonography: Can be performed in the early neonatal period to delineate clear-cut structural abnormalities and show evidence of hemorrhage or hypoxic-ischemic injuryComputed tomography scanning of the brain: Is particularly helpful for imaging of blood, calcification, and bone, and may be performed quickly in a sleeping infant, but emits radiation. Spasticity in patients with spastic quadriplegia can be more resistant even with services and orthopedic and rehabilitative intervention.Patients with severe forms of cerebral palsy may have a significantly reduced life span, although this continues to improve with improved health care and gastrostomy tubes.Cerebral palsy complications may affect multiple systems. The overall rate of mental retardation in affected persons is thought to be 30–50%. Hoving MA, van Raak EP, Spincemaille GH, Palmans LJ, Becher JG, Vles JS. Du RY, McGrath CP, Yiu CK, King NM. Hemming K, Hutton JL, Colver A, Platt MJ. Evidence of diffuse polymicrogyria and thinning of the corpus callosum is noted in this image.