Disease relevance of Cerebral Palsy

• Hypertonia, which results from motor pathway defects in the central nervous system (CNS), is observed in numerous neurological conditions, including cerebral palsy, stroke, spinal cord injury, stiff-person syndrome, spastic paraplegia, dystonia and Parkinson disease [1].
• We report on a 16-year-old girl with spastic quadriplegic cerebral palsy associated with premature birth and typical periventricular leukomalacia, who had a dramatic improvement in motor function after treatment with carbidopa/levodopa [2].
• A history of epilepsy or febrile seizures in the mother, febrile seizures, neonatal convulsions, cerebral palsy, head trauma, and viral encephalitis were significantly more common in patients than in control subjects (p less than 0.05) [3].
• We suspect that activated protein C resistance may be an important cause of in utero cerebrovascular disease and hemiplegic cerebral palsy [4].
• Neurological abnormality in the first year of life before any seizure, and the presence of minor motor seizures, were associated with an increased rate of mental retardation and cerebral palsy at age 7, but early age at onset appeared to have little prognostic value regarding intellectual function, cerebral palsy, and epilepsy [5].

Psychiatry related information on Cerebral Palsy

• OBJECTIVE: To examine the relationship between prenatal magnesium sulfate exposure and the risk for cerebral palsy (CP) or mental retardation (MR) among very low-birth-weight (VLBW; <1500 g) children [6].
• MAIN OUTCOME MEASURE: Diagnosis of MR by age 7 years considered as being mild or severe and as occurring without other developmental disabilities (isolated MR) or as occurring with other developmental disabilities, including cerebral palsy, epilepsy, or a pervasive developmental disorder [7].
• People with FAS have high rates of comorbid conditions: attention deficit hyperactivity disorder (40%), mental retardation (15-20%), learning disorders (25%), speech and language disorders (30%), sensory impairment (30%), cerebral palsy (4%), epilepsy (8-10%) [8].
• Treatment with oral B12 quickly corrected her anaemia and there was a gradual improvement in speech, gait, tremor, disorientation and mood but mild spastic diplegia remained [9].
• MMPI characteristics associated with cerebral palsy and dystonia musculorum deformans [10].

High impact information on Cerebral Palsy

• More on prenatal magnesium sulfate and risk of cerebral palsy [11].
• Intrathecal baclofen for spasticity in cerebral palsy [12].
• These findings suggest that caspase inhibitors may be able to provide benefit over a prolonged therapeutic window after hypoxic-ischemic events in the developing brain, a major contributor to static encephalopathy and cerebral palsy [13].
• VIP and neurotrophic analogs, acting through a cAMP-independent mechanism and inducing ADNF release, could represent new avenues in the understanding and prevention of human cerebral palsy [14].
• INTERPRETATION: Our study suggests that children born after IVF have an increased risk of developing neurological problems, especially cerebral palsy [15].

Chemical compound and disease context of Cerebral Palsy

• The prevalence at school age of cerebral palsy and severe education subnormality in children of low birthweight (less than or equal to 4 lb=1814 g) born to residents in the region served by the South East Thames Regional Health Authority in the early 1970s was compared with that in children of the same birthweight born in 1950-53 [16].
• Methylphenidate for cerebral palsy with choreoathetosis [17].
• Motor benefit from levodopa in spastic quadriplegic cerebral palsy [2].
• Perinatal white matter lesions associated with cerebral palsy appears to involve glutamate excitotoxicity and excess free radical production [18].
• Concerns about their long-term neurodevelopmental consequences arose in the late 1990s when follow-up of randomised controlled trials indicated an increased risk of cerebral palsy after postnatal dexamethasone exposure [19].

Biological context of Cerebral Palsy

• The extent of this impact was much greater among children with multiple disabilities or with either cerebral palsy, epilepsy or seizures, delays in growth and development, or emotional or behavioral problems [20].
• Of 960 live births in this weight group, 669 (70%) survived to 1 year adjusted age; 646 (96.6%) were assessed at follow-up, and 80 (12.4%) of these were disabled: cerebral palsy, 8.7%; vision loss, 2.9%; hearing loss, 1.3%; epilepsy, 0.6%; mental retardation, 4.8%; more than one disability per child, 3.6%; and projected dependent disability, 1.4% [21].
• No phenotype associated with established lipopolysaccharide model for cerebral palsy [22].
• Gastric emptying in children with cerebral palsy and gastroesophageal reflux [23].
• Fetal stroke, or that which occurs between 14 weeks of gestation and the onset of labor resulting in delivery, has been associated with postnatal epilepsy, mental retardation, and cerebral palsy [24].

Anatomical context of Cerebral Palsy

• To investigate some of the pathophysiological mechanisms in cerebral palsy, surface electromyograms (EMG) were recorded from pairs of flexor/extensor muscles during both voluntary and passive flexion/extension of upper and lower limbs of 20 patients [25].
• We conclude that IFN can adversely affect the immature central nervous system and produce spastic diplegia, which is potentially reversible [26].
• METHODS: Brain injury patterns were analyzed in 43 children whose exposure to meconium in the AF was their only identified risk for quadriplegic cerebral palsy [27].
• The corpus callosum is a major white matter tract that undergoes protracted myelination, underpins higher order cognitive processing and developmental damage to which is associated with, for example, cerebral palsy, mental retardation and attention deficit hyperactivity disorder [28].
• Shed deciduous teeth from patients with tuberous sclerosis, cerebral palsy, Down syndrome, phenylketonuria and healthy persons were examined with a surface microscope [29].

Gene context of Cerebral Palsy

• Intracerebral injection of the glutamatergic analogue ibotenate to newborn mice induces cortical plate and white matter lesions mimicking the brain damage associated with cerebral palsy, and pretreatment with proinflammatory cytokines such as interleukin-1-beta or with interleukin-9 significantly exacerbates these lesions [30].
• These findings suggest that EPO may provide benefit after hypoxic-ischemic events in the developing brain, a major contributor to static encephalopathy and cerebral palsy [31].
• Possible correlation between high levels of IL-18 in the cord blood of pre-term infants and neonatal development of periventricular leukomalacia and cerebral palsy [32].
• Serum prealbumin and albumin concentrations do not reflect nutritional state in children with cerebral palsy [33].
• Preliminary results demonstrate an increase in IL-1, IL-6, and TNF-alpha in those children who are deceased at 1 year or who have a diagnosis of cerebral palsy versus those with normal neuromotor outcome [34].

Analytical, diagnostic and therapeutic context of Cerebral Palsy

• Triggering factors, seizure patterns, and ictal electroencephalograms were the same as in startle epilepsy occurring in children with cerebral palsy but differed in that there was no clinical or radiological evidence of a focal brain lesion in the vicinity of the motor supplementary cortex [35].
• The authors examined the relation between intrapartum magnesium sulfate exposure and risk of cerebral palsy in a case-control study of low birth weight children designed to control for confounding by the clinical indications for magnesium in pregnancy [36].
• METHODS: We conducted a retrospective review of the data on all patients with cerebral palsy who had a sagittal plane spinal deformity but no coronal plane deformity, had undergone posterior spinal fusion with unit rod instrumentation at our institution, and had been followed for at least two years [37].
• We examined the contributions to vecuronium resistance made by cerebral palsy and anticonvulsants in a study of children with cerebral palsy and a control group [38].
• Statistically significant increased ORs were seen for hospitalization for cerebral palsy (1.7), epilepsy (1.5), congenital malformation (1.8) or tumour (1.6), but also for asthma (1.4) or any infection (1.4) [39].

References