Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Orthopedic surgery (OS) plays an important role in the management of cerebral palsy (CP). The objectives of OS are to optimize functions and prevent deformity. Newer developments in OS for CP include emphasis on hip surveillance, minimally invasive procedures, use of external fixators instead of plates and screws, better understanding of lever arm dysfunctions (that can only be corrected by bony OS), orthopedic selective spasticity-control surgery, and single-event multilevel lever arm restoration and anti spasticity surgery, which have led to significant improvements in gross motor function and ambulation, especially in spastic quadriplegia, athetosis, and dystonia. The results of OS can be dramatic and life altering for the person with CP and their caregivers if it is performed meticulously by a specialized surgical team, at the appropriate age, for the correct indications, employing sound biomechanical principles and is followed by physician-led, protocol based, intensive, multidisciplinary, institutional rehabilitation, and long term followup. However, OS can be a double-edged sword, and if performed less than optimally, and without the supporting multidisciplinary medical and rehabilitation team, expertise and infrastructure, it often leads to significant functional worsening of the person with CP, including irretrievable loss of previous ambulatory capacity. OS must be integrated into the long term management of the person with CP and should be anticipated and planned at the optimal time and not viewed as a "last resort" intervention or failure of rehabilitation. This instructional course lecture reviews the relevant contemporary principles and techniques of OS in CP.
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PMID:Orthopedic surgery in cerebral palsy: Instructional course lecture. 2856 75

Involuntary movements and parkinsonism have been interesting and important topics in neurology since the last century. The development of anatomical and physiological studies of the neural circuitry of motor systems has encouraged the study of movement disorders by means of pathophysiology and brain imaging.Multichannel electromyography from affected muscles has generated objective and analytical data on chorea, ballism, athetosis, and dystonia. Studies using floor reaction forces revealed the pathophysiology of freezing of gait in parkinsonism. Akinesia and bradykinesia are attributable to dysfunctions in the basal ganglia, frontal lobe, and parieto-occipital visual association cortex.Reciprocal innervation is an essential mechanism of smooth voluntary movement. Spinal reflexes on reciprocal innervation has been investigated in awake humans, and the pathophysiology of spasticity and Parkinson's disease were revealed as a result. Clinical applications for the treatment and evaluation of status have been developed.For future studies, detailed neural mechanisms underlying the development of motor disorders in basal ganglia diseases and recovery by interventions including surgery and neurorehabilitation are important.
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PMID:Functions and dysfunctions of the basal ganglia in humans. 3007 28

Ratios of physical activity and sports participation in people with cerebral palsy (CP) are still low compared with people without a disability. For an adequate and useful practice, physical activity professionals should understand how different types of CP profiles constrain the performance of motor skills that are required during sports practice. This study aims to develop an observation-based assessment tool to evaluate activity limitations in individuals with a moderate level of CP when performing skills requiring jumping, sprinting, change of direction, coordination, and balance. Nineteen observers with different backgrounds from five world regions were recruited for this study, with accredited experience classifying/observing para-athletes with CP. All observers watched videos of 20 international para-athletes with different CP profiles (bilateral spasticity, athetosis/ataxia, unilateral spasticity; all Gross Motor Function Classification System level I) performing 16 motor tasks, and their observations were recorded throughout an ad-hoc data collection instrument. A total of 6080 units of qualitative information were recorded for data analysis. An observation-based tool with qualitative descriptors is derived from data analyses, describing how coordination and balance affected mainly in those with dyskinesia/ataxia, range of movement in those with diplegia, and asymmetries in those with hemiplegia. This tool would help sports practitioners and physical educators to better understand how different CP profiles constrain the performance of motor skills.
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PMID:An Observational Tool to Assess Activity Limitation in Ambulatory People with Cerebral Palsy When Performing Motor Skills. 3218 25

Despite its first description more than 75 years ago, effective treatment for "Allan-Herndon-Dudley-Syndrome (AHDS)", an X-linked thyroid hormone transporter defect, is unavailable. Mutations in the SLC16A2 gene have been discovered to be causative for AHDS in 2004, but a comprehensive understanding of the function of the encoded protein, monocarboxylate transporter 8 (MCT8), is incomplete. Patients with AHDS suffer from neurodevelopmental delay, as well as extrapyramidal (dystonia, chorea, athetosis), pyramidal (spasticity), and cerebellar symptoms (ataxia). This suggests an affection of the pyramidal tracts, basal ganglia, and cerebellum, most likely already during fetal brain development. The function of other brain areas relevant for mood, behavior, and vigilance seems to be intact. An optimal treatment strategy should thus aim to deliver T3 to these relevant structures at the correct time points during development. A potential therapeutic strategy meeting these needs might be the delivery of T3 via a "Trojan horse mechanism" by which T3 is delivered into target cells by a thyroid hormone transporter independent T3 internalization.
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PMID:Allan-Herndon-Dudley-Syndrome: Considerations about the Brain Phenotype with Implications for Treatment Strategies. 3224 26


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