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)

Over a 7-year period (February 1974 through February 1981), 318 patients underwent the implantation of cerebellar stimulation systems for the reduction of spasticity (98%) or epilepsy (2%). A total of 518 procedures were carried out to implant and maintain the equipment during this period. Fourteen patients developed infections in the tissue around their implanted systems, which represented 4.4% of the patients or 2.7% of the procedures performed. Staphylococcus aureus was the infectious agent in 7 cases (50%), the clinical features of which occurred usually within 1 month. Staphylococcus epidermidis infected 5 patients with features presenting late (more than 2 years) after the initial implantation. The management involved antibiotic therapy for 2 weeks in all 14 patients. In 12 patients, the entire system was removed, with 100% eradication of the infection. In the other 2 patients, the radio receiver and lead wires up to but not including the cerebellar electrode pads were removed. One of these 2 patients has been free of infection for 4 years. The other had S. aureus cultured from removed electrode pads after 6 weeks. Of the 14 cases, morbidity was severe in only 1 patient. Seven patients underwent reimplantation 6 weeks after the infection.
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PMID:Management of infected cerebellar stimulation systems. 697 69

An unselected series of 116 dyskinetic cerebral palsy cases born 1959-70 was delineated and subgrouped according to neurological criteria into 35 hyperkinetic (30%) and 81 dystonic (70%) cases. Of the hyperkinetics, 80% had a mild motor disability, while 90% of the dystonics had moderate or severe disability. Subordinated spastic signs were found in 9% of the hyperkinetic and in 44% of the dystonic cases. IQ was greater than 90 in 69% of the hyperkinetics and 25% of the dystonics and less than 50 in 11% and 41%, respectively. Two or more additional neurological abnormalities (spasticity, mental retardation, epilepsy, anarthria, dysarthria, hearing deficit) were detected in 46% hyperkinetic and 81% dystonic cases. A heavy multihandicap complex was present predominantly in the dystonic subgroup. The 5-19 year mortality rate was 6% and was confined to the most severely handicapped dystonic cases. The twin rate was 5%. A total of 9% had birth weights less than or equal to 1500 g, and 31% had less than or equal to 2500 g. The weight- and age-specific incidences increased rapidly with decreasing birth weights and gestational ages. The crude incidence of hyperkinetic cerebral palsy was 0.07 and dystonic cerebral palsy 0.17 per thousand live births.
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PMID:Dyskinetic cerebral palsy. I. Clinical categories, associated neurological abnormalities and incidences. 713 69

There is a growing body of evidence that the central nervous system (CNS), even in the adult animal, is capable of adaptation and reorganization not only as a result of partial damage to the CNS but also in response to stimulation. Environmental stimulation produces changes including expansion of visual cortex, increases in dendritic branching, glia and cholinesterase. Environmental stimulation also produces behavioural changes. Experimental electrical stimulation produces changes in synapse size, synaptic vesicle change, dendritic branching and changes in synaptic transmission. In man, repetitive electrical stimulation via epidural electrodes increases plasma levels of norepinephrine, epinephrine, and dopamine, and CSF levels of norepinephrine. Repetitive electrical stimulation in man dates back to 1967 and has been used for the control of pain, to improve spasticity, bladder control, motor deficit and the autonomic hyperreflexia of spinal cord injury. In addition, improvement has been reported in epilepsy, cerebral palsy, torticollis and peripheral vascular diseases. The best controlled studies are in multiple sclerosis and peripheral vascular disease, and these results will be presented in more detail.
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PMID:Rehabilitation following brain damage: some neurophysiological mechanisms. The effects of repetitive stimulation in recovery from damage to the central nervous system. 718 88

Many therapeutic effects of benzodiazepines are mediated by neuronal high-affinity binding sites, i.e. benzodiazepine receptors (BR), located on GABAA receptors. Recently, endogenous BR ligands have partially been identified which, as agonists, either increase or, as inverse agonists, decrease GABAergic inhibition in the brain. BR antagonists, previously described as intrinsically inactive, induce effects in animals and humans under particular circumstances emphasizing a functional relevance of endogenous BR ligands. Several brain disorders, e.g. anxiety, insomnia, epilepsy, spasticity, alcoholism, coma, dementia, may be associated with a disequilibrium of opposing endogenous BR ligands changing the excitability of neurons implicated in aforementioned diseases. It is proposed that, depending on the relative role endogenous BR ligands play in the pathophysiology of these disorders, BR antagonists might demonstrate a variable efficacy in improving their symptomatology. In fact, such therapy would restore the homeostatic balance among various endogenous BR ligands being disturbed during an illness.
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PMID:Involvement of endogenous benzodiazepine receptor ligands in brain disorders: therapeutic potential for benzodiazepine antagonists? 747 87

We describe a male patient with late onset globoid cell leukodystrophy (GLD) (Krabbe's disease) still alive at 24 years of age, with a well preserved intellectual and communicative capacity, in contrast to visual failure and severe central pyramidal and extrapyramidal motor disability with spasticity, dystonia, ataxia and peripheral neuropathy. Visual dysfunction began at 4 years of age, limping and balance problems at 8 years and epilepsy at 14 years of age. Neuroimaging at 15 years of age revealed white matter lesions, and nerve conduction velocity examinations showed a slowly developing polyneuropathy. Galactosylceramidase activity was reduced in leukocytes to 0.07 mu kat/kg protein compared with 0.02 (SD 0.01) mu kat/kg protein in infantile GLD.
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PMID:Late onset globoid cell leukodystrophy (Krabbe's disease)--Swedish case with 15 years of follow-up. 775 15

A 55-year-old mildly hypertensive woman died after having developed a subcortical dementia during the past 9 years, with focal neurological signs. She presented at the age of 46 years with short episodes of dizziness and diplopia, suggesting that transient ischemic attacks involved the posterior fossa structures. Over the next 8 years, she developed difficulty in walking, urinary incontinence and seizures. On examination in 1989, she was severely demented. There was tetraparesis, bilateral arm and leg spasticity with hyperreflexia and bilateral Babinski signs. She showed epilepsia partialis continua involving the eyes, left hemiface and limbs. CT showed hypodensity of the white matter and lacunes in the basal ganglia and centrum semiovale, moderate hydrocephalus with cerebellar and cortical atrophy. Clinical and radiological features were similar to those of Binswanger's disease. Similar cases had occurred in the family affecting the patient's grandfather, father and two brothers, suggesting an autosomal dominant hereditary disease. Postmortem examination disclosed a Binswanger type of leukoencephalopathy caused by a peculiar microangiopathy characterized by a slightly basophilic small arterial granular degeneration of the medial sheath associated with the presence of ballooned smooth muscle cells with clear cytoplasm. Electron microscopic study revealed degenerative changes in the parietal vessels with notable increase of basal-membrane-type material and electron-dense granular deposits. These lesions could correspond to a specific familial pathology of the small arteries of the brain. They are identical to those reported in some patients with autosomal dominant inheritance. For other patients with similar clinical features and the same familial pattern, reported as "hereditary multi-infarct dementia'' and "chronic familial vascular encephalopathy'', there are no sufficient objective pathological facts to consider that they have the same disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Small arterial granular degeneration in familial Binswanger's syndrome. 814 Aug 99

Fourteen patients (10 boys, 4 girls) aged from 4 months to 14 years old were diagnosed with mitochondrial disease based on the clinical manifestations together with abnormal muscle mitochondrial morphologies. Their clinical diagnoses included Leigh syndrome, three; Menkes' syndrome, three; Kearns-Sayre syndrome, two; myoclonic epilepsy with ragged fibres, one; and infant-onset progressive myoclonic epilepsy, one; fatal infantile mitochondrial myopathy, one; fatty acid oxidation defect, two; and myopathy with cardiopathy, one. Organs involved other than muscles included central nervous system, ten; heart, six; eye, two; liver, two; and kidney, two. Clinical manifestations varied to include hypotonia, seizures, myoclonus, mental retardation, nystagmus, ataxia, ptosis, ophthalmoplegia, retinal degeneration, muscle atrophy, spasticity etc. Nine had an abnormal rise in lactate after glucose loading. Ragged-red fibres were found in four patients. Abnormal mitochondrial morphology included abnormal accumulation, abnormal cristae pattern of tubular, concentric, or parallel form, some contained osmiophilic inclusion bodies. One patient of Leigh syndrome had had brain necropsy which showed intramyelin splitting of myelinated axons.
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PMID:Clinical manifestation of mitochondrial diseases in children. 821 54

Baclofen is a central nervous system agent that is commonly used for the treatment of muscle spasticity in spinal cord injury patients. Acute withdrawal of this medication can induce the development of neurological symptoms, including seizure disorder, psychosis, hallucinations and visual disturbances. We report 3 cases of acute central nervous system symptoms that developed in spinal cord injury patients. Each patient had been chronically maintained on a baclofen regimen to control muscle spasticity. Symptoms developed shortly after baclofen therapy was interrupted following genitourinary surgery. It is important that urologists become familiar with the symptomatology of baclofen withdrawal, the methods of its prevention and the appropriate therapy should the syndrome develop.
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PMID:Neurological manifestations of baclofen withdrawal. 823 May 32

We abstracted the results of all English language reports of the outcomes of bacterial meningitis published after 1955. We used hierarchical Bayesian meta-analysis to determine the overall and organism-specific frequencies of death and persistent neurologic sequelae in children 2 months to 19 years of age. A total of 4920 children with acute bacterial meningitis were included in 45 reports that met the inclusion criteria. Children described in the 19 reports of prospectively enrolled cohorts from developed countries had lower mortality (4.8% vs. 8.1%) and were more likely to have no sequelae (82.5% vs. 73.9%). In these 19 studies 1602 children were evaluated for at least 1 sequela after hospital discharge. The mean probabilities of these sequelae were: deafness, 10.5%; bilateral severe or profound deafness, 5.1%; mental retardation, 4.2%; spasticity and/or paresis, 3.5%; seizure disorder, 4.2%; and no detectable sequelae, 83.6%. Mean probabilities of outcomes varied significantly by etiologic bacteria, e.g. mortality: Haemophilus influenzae, 3.8%; Neisseria meningitis, 7.5%; Streptococcus pneumoniae, 15.3%.
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PMID:Outcomes of bacterial meningitis in children: a meta-analysis. 832

Cortical laminar necrosis is a histopathological entity, related to conditions of cerebral energy depletion. Clinical correlates are supposed to be spastic motor deficits, decreased intellectual capacity and epilepsy. A study was performed in 45 children with cortical laminar abnormalities in signal intensity on MRI. The purpose of the study was to evaluate causes and clinical consequences of these cortical abnormalities on MRI in order to find indirect evidence for the hypothesis that they may represent cortical laminar necrosis. In view of the frequently present concomitant white matter damage, two contrast groups were formed: one group of 40 children with periventricular white matter abnormalities, part of them with subcortical extensions of the white matter damage; and another group of 53 children without abnormalities on MRI. Data concerning history, present clinical condition and final diagnosis were collected. The presence of cortical laminar abnormalities on MRI was found to be strongly associated with a history of cerebral energy depletion, especially hypoxia-ischemia, either in the perinatal period or later in life. Whereas white matter abnormalities tended to be more frequent in premature children, cortical laminar abnormalities tended to occur more frequently in term neonates and older children. The presence of cortical laminar abnormalities on MRI was correlated with an increased risk of spasticity in children without concomitant white matter abnormalities. In children with white matter lesions, cortical laminar abnormalities did not contribute to the risk of spasticity, which was already highly increased by the presence of white matter damage. No association was found between cortical abnormalities on MRI and epilepsy or psychomotor retardation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cortical laminar abnormalities--occurrence and clinical significance. 835 19


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