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181. Effects of surgical adductor releases for hip subluxation in cerebral palsy: an AACPDM evidence report

eligible for inclusion. The studies included children (mean age 3 to 15 years, where reported) with cerebral palsy, spastic quadriplegia, spastic paraplegia, spastic diplegia, spastic triplegia, paraplegia, hemiplegia, athetosis, athertosis/spastic, dystonic quadriplegia and mixed quadriplegia. Outcomes assessed in the review There were no specific inclusion criteria relating to the outcomes. The included studies used a range of outcome measures relating to the range of movement of the hip, number

2003 DARE.

182. Guanidinoacetate methyltransferase deficiency

and manifest as chorea, athetosis and ataxia. Etiology GAMT deficiency is due to mutations in the GAMT gene (19p13.3). Different mutations (missense, nonsense, splice site, insertions, deletions) have been identified, located on various exons of the GAMT gene. The most frequently identified mutation, c.327G>A (p.K109K, splice site exon 2), is present in at least one allele in over 50% of families. c.59G>C is most frequently encountered in Portuguese patients. To date no genotype phenotype correlation has

2004 Orphanet

183. Energy Costs of Spasticity in Spinal Cord Injury: A Pilot Investigation

amount (65-75% TDEE) and is the most sensitive to changes in spasticity. Dampening spasticity has been reported to increase weight gain and necessitate reduced caloric intake in a child with spastic quadriplegia. Similarly, athetosis in patients with cerebral palsy increased resting metabolic rate (RMR) as compared to control subjects with no athetotic movements. Although several studies have reported energy requirements for persons with neurodevelopmental disabilities, and even SCI, however, none

2007 Clinical Trials

184. Supported Speed Treadmill Training Exercise Program (SSTTEP) for Marginally Ambulatory Children With Cerebral Palsy

in Baclofen dosing, or casting procedures to the lower extremities; Passive range of motion of lower extremity joints: < 30º contracture of hip in extension as measured by the Thomas Test; passive dorsiflexion range of motion to -15º with the knee extended, and knee extension range (90º/90º test) to 70º and <-20º knee extension. At least 2 years post- dorsal rhizotomy. Exclusion Criteria: Children with "mixed" types of CP (i.e. athetosis) or other movement disorders (e.g. ataxia); Children receiving

2007 Clinical Trials

185. Outcomes of Orthopaedic Surgery Using Gait Laboratory Versus Observational Gait Analysis in Children With Cerebral Palsy

with their physical function. Patients are candidates for orthopaedic surgery including soft tissue and/or bony procedures involving at least 2 levels, in one or both lower extremities (e.g. knee & ankle). Patients must be able to undergo instrumented gait analysis in a motion laboratory. Exclusion Criteria: Presence of dystonia, athetosis, or mixed tone abnormalities. History of orthopaedic lower extremity procedures within the previous 2 years. Patients who have had previous gait laboratory analysis that has

2007 Clinical Trials

186. The Effect of Botox on Children With Cerebral Palsy

, and at least 0 degrees of ankle dorsiflexion with the knee extended while the foot is in varus Children who are planning to undergo botulinum toxin injections of the gastrocnemius and/or soleus muscles without serial casting as clinically dictated for the treatment of muscle spasticity Exclusion Criteria: Children who have a diagnosis of "mixed" types of CP (i.e. athetosis) or other movement disorders (i.e. ataxia) Children who have had a selective dorsal rhizotomy, are presently are receiving intrathecal

2007 Clinical Trials

187. Diagnosis, Treatment, and Prevention of Cerebral Palsy in Near-Term/Term Infants Full Text available with Trip Pro

limitation, that are attributed to non-progressive disturbances that occurred in the developing fetal or infant brain." In a majority of cases, the predominant motor abnormality is spasticity; other forms of cerebral palsy include dyskinetic (dystonia or choreo-athetosis) and ataxic cerebral palsy. In preterm infants, about one-half of the cases have neuroimaging abnormalities, such as echolucency in the periventricular white matter or ventricular enlargement on cranial ultrasound. Among children born

2008 Clinical Obstetrics and Gynecology

188. The effects of therapeutic taping on gross motor function in children with cerebral palsy. Full Text available with Trip Pro

cerebral palsy. Subjective observation, however, suggested that one child with athetosis benefited from therapeutic taping over the paraspinal region.

2006 Pediatric physical therapy : the official publication of the Section on Pediatrics of the American Physical Therapy Association Controlled trial quality: uncertain

189. Effectiveness of the Innsbruck Sensorimotor Activator and Regulator in improving saliva control in children with cerebral palsy. (Abstract)

7 years 10 months, range 4 to 13 years) were selected. Measures of drooling and feeding skills were taken at baseline, at the completion of a 6-month control phase, and at two more 6-monthly time points after the ISMAR was fitted. Children varied greatly in both the length of time taken to tolerate wearing the ISMAR and duration for which the appliance was worn. Only six children (four females, two males) completed the full study. Their motor disabilities were athetosis (n=3), spastic

2004 Developmental Medicine and Child Neurology

190. Clinical (video) findings and cerebrospinal fluid neurotransmitters in 2 children with severe chronic bilirubin encephalopathy, including a former preterm infant without marked hyperbilirubinemia VIDEO. (Abstract)

structures has been described at autopsy after only moderate hyperbilirubinemia, but classic chronic bilirubin encephalopathy without marked hyperbilirubinemia has been reported only rarely. We report a case of a 7-year-old, former 29-weeks' gestation, gravely ill premature infant with a peak bilirubin level of 13.3 mg/dL in the neonatal period. We compare this case with a 12-year-old, former term infant with a peak bilirubin level of 49.4 mg/dL on day 10 of life. Both children have dystonia, athetosis

2005 Pediatrics

191. The neurotoxicity and safety of treatment with cefepime in patients with renal failure. Full Text available with Trip Pro

conscience, confusion, agitation, global aphasia, myoclonus, chorea-athetosis, convulsions and coma. The latency, the period between the start of treatment and neurological deterioration, was 4,75 +/- 2,55 days (range: 1-10 days). All patients died 17 +/- 14,7 days (range: 1-42 days) after becoming symptomatic. Three of them died shortly after neurological deterioration. Five patients developed a neurological "tableau" with global aphasia. Three patients showed clinical improvement after

2008 Transplantation

192. Recessive Twinkle mutations in early onset encephalopathy with mtDNA depletion. Full Text available with Trip Pro

involvement. The clinical manifestations included hypotonia, athetosis, sensory neuropathy, ataxia, hearing deficit, ophthalmoplegia, intractable epilepsy and elevation of serum transaminases. The liver showed mtDNA depletion, whereas the muscle mtDNA was only slightly affected. Alpers-Huttenlocher syndrome has previously been associated with mutations of polymerase gamma, a replicative polymerase of mtDNA. We show here that recessive mutations of the close functional partner of the polymerase

2007 Brain

193. Mitochondrial Complex III Deficiency Associated with a Homozygous Mutation in UQCRQ. Full Text available with Trip Pro

Mitochondrial Complex III Deficiency Associated with a Homozygous Mutation in UQCRQ. A consanguineous Israeli Bedouin kindred presented with an autosomal-recessive nonlethal phenotype of severe psychomotor retardation and extrapyramidal signs, dystonia, athetosis and ataxia, mild axial hypotonia, and marked global dementia with defects in verbal and expressive communication skills. Metabolic workup was normal except for mildly elevated blood lactate levels. Brain magnetic resonance imaging (MRI

2008 American Journal of Human Genetics

194. Rating scale for psychogenic movement disorders: scale development and clinimetric testing. Full Text available with Trip Pro

, tics, athetosis, ballism, cerebellar incoordination), 2 functions (gait, speech), and 14 body regions. To study interrater agreement, three movement disorder neurologists independently rated 88 videotapes of PMD patients. Data analysis was performed using a kappa coefficient of agreement, Kendall's coefficient of concordance, Spearman correlations, and intraclass correlation coefficients. Validity and scale responsiveness were tested as well. All phenomena and speech and gait dysfunction occurred

2005 Movement Disorders

195. Neurological manifestations in Wilson's disease: Report of 119 cases. (Abstract)

%), rigidity (66%), tremor (60%), and dysphagia (50%). Less frequent manifestations were chorea (16%) and athetosis (14%). Rare neurological presentations were seizures (4.2%), and pyramidal signs (3%).Copyright 2006 Movement Disorder Society.

2006 Movement Disorders

196. Kernicterus

aged over 1 year, the classical features develop, which include abnormalities in the extrapyramidal, visual and auditory systems. Minor intellectual deficits may be present. Extrapyramidal signs These may occur and the most common and most severe is athetosis, although chorea can also occur. Upper extremities are more severely affected than the lower ones and bulbar nerves may also be involved. Chronic bilirubin encephalopathy causes damage to the basal ganglia. Visual problems These most commonly (...) appear to be very sensitive to bilirubin, even at relatively low levels. This may present as delayed language and so any baby at risk must have hearing assessed. The presenting feature of kernicterus may be childhood deafness. Cognitive defects These do not feature prominently in kernicterus but athetosis or chorea along with hearing defects may give the false impression of learning disability. Dental enamel Shows some hypoplasia and some may show green staining of teeth. More subtle alterations

2008 Mentor

197. Neurological Examination of the Upper Limbs

. Note whether it is focal or diffuse. Look for involuntary movements such as tremor, tics, myoclonic jerks, chorea or athetosis. Look for muscle fasciculation (sign of lower motor neurone disease process). These are subcutaneous twitches over a muscle belly at rest. Tapping the belly may stimulate fasciculation. [ ] Examination of the sensory system Examination of each of the sensory modalities: Light touch Use the light touch of a finger, a piece of cotton wool or a piece of tissue paper

2008 Mentor

198. Neurological Examination of the Lower Limbs

. Neuropathic ulcers and neuropathic joints develop because of a lack of pain perception. Pain is a protective mechanism. When inspecting the motor system, the following points should be assessed: Note the resting posture. Establish whether there is unusual rotation or posture of a joint. Note whether the patient is symmetrical. Look for muscle wasting or hypertrophy: note whether it is focal or diffuse. Look for involuntary movements such as tremor, tics, myoclonic jerks, chorea or athetosis. Look

2008 Mentor

199. Chorea

be considered to be related but some experts call these 'unvoluntary' because there is an element of voluntary control. Cerebrovascular diseases are a common cause of secondary movement disorders. Post-stroke movement disorders include Parkinsonism and a wide range of hyperkinetic movement disorders, including chorea, ballism, athetosis, dystonia, tremor, myoclonus, stereotypies and akathisia. Classification Athetosis Sinuous, slow, involuntary writhing movements affecting the fingers, hands, toes and feet (...) . Chorea may occur with athetosis and is then called choreoathetosis. Dystonias A dystonia is a sustained muscle contraction, frequently causing repetitive twisting movements or abnormal postures. [ , ] It is a dynamic condition that often changes in severity depending on the posture assumed and on voluntary activity of the area of the body involved. The diagnosis is clinical and there are no specific tests available; therefore, expert opinion should be sought. Dystonias may be primary or secondary

2008 Mentor

200. Pelizaeus-Merzbacher Disease

of learning difficulty than is present. These patients may survive to the sixth decade of life or longer. SPG2-like disease - there is spastic paraplegia from childhood, mild , ataxia and athetosis (continual slow movements, especially of the extremities). They usually live to the sixth decade or beyond. Neurological signs progress gradually with periods of relative stability. If they learn to walk they tend to lose it during adolescence (occasionally adulthood). Other general observations may be made

2008 Mentor

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