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)

In approximately 10,000 admissions in a 12 months period, at University Teaching Hospital, Lusaka 85 cases of meningitis were recorded. The signs and symptoms in these patients do not greatly differ from other similar studies in Africa. The commonest organism isolated was pneumococcus. There was high mortality rate which was to a large extent due to parents not bringing their children to hospital early enough for medical treatment to be instituted. This is borne out by the fact that 50% of the children with meningitis died within the first 24 hours. The C.S.F. protein and peripheral white blood count may be of prognostic value. Spasticity, cranial nerve palsises hydrocephalus and subdural effusion were the commonest complications.
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PMID:Bacterial meningitis in infancy and childhood in Lusaka (One year prospective sturdy). 0 34

Two siblings of consanguinous parents were noted to have a neurologic syndrome marked by developmental delay, regression of psychomotor performance, marked spasticity and progressive central nervous system degeneration. Markedly delayed nerve conduction times and a sural nerve biopsy which demonstrated changes typical of metachromatic leukodystrophy (MLD) were evident. Impairment of sulfated glycolipid metabolism was documented by analysis of glycospingolipid in urinary sediment. In spite of these findings, activities of arylsulfatase A and cerebroside sulfatidase in white blood cells and cultured skin fibroblasts were near normal. However, when intact growing fibroblasts were loaded with 35SO4-sulfatide a clear defect in sulfatide cleavage, comparable to that seen in MLD patients, was observed. Thus, these patients represent a new form of sulfatide storage disease -- MLD characterized by intact enzyme activity in cell homogenates but defective sulfolipid metabolism in vivo and in intact fibroblasts.
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PMID:Metachromatic leukodystrophy without arylsulfatase A deficiency. 4 Dec 11

Rud's syndrome is a neuroichthyosis with hypogonadism, associated with mental deficiency and epilepsy. Short stature is a frequent component of the syndrome. The primary genetic defect and the pattern of inheritance have not yet been determined. A typical patient is presented, with mental deficiency, short stature, pypoacusia, muscular atrophy, tylosis, pseudoacanthosis nigricans and endocrine disturbances. The neuroichthyosis with hypogonadism must be considered Rud's syndrome. A classification of neuroichthyosis is proposed. In a first group is neuroichthyosis with hypogonadism, in the second group is neuroichthyosis with spasticity and in the third group, neuroichthyosis without hypogonadism or spasticity.
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PMID:Neuroichthyosis with hypogonadism (Rud's syndrome). 5 Feb 99

At the light of authors' present experience, radicletomy appears as an excellent antalgic operative procedure in the case of roots with high functional risk (brachial plexus and lumbar plexus). In the absence of any motor deficiency or ataxia, it appears that radicletomy is of help in the cure of severe hypertonies of the extremities (sequelae of cerebral stem contusions). Conversely, in the spastic sequelae of hemi- or paraparesias, lumbar-sacral posterior selective radicotomy is a sure procedure that procures results nearly super-imposable to radicletomy with an appreciable gain in time. At last, for what concerns the motor involvements of the upper extremity ending in spasticity, selective radicletomy recovers its rights and has to be preferred to S.P.R. The indications may be summarized as follows: -- At the level of the lower extremities: in the case of paraparetic sequelae or of sequelae due to spastic paraplegia, a S.P.R. has to be performed; for what concerns antalgic surgery, in the absence of motor deficiency, the best indication is radicletomy. -- At the level of the upper extremities: in the case of dystonic sequeale of the cerebral stem, spastic pain bound with hemiplegia or with carcinoma etc. (herpes zoster..), radicletomy constitutes the ideal surgical procedure.
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PMID:[Results of selective posterior radiculetomy at the lumbar and cervical level]. 5 51

Drug-induced diseases constitute up to 5% of hospital admissions,a figure which almost certainly understates the total morbidity due to drugs1. Sever drug-induced myopathies are uncommon, but milder forms may be more prevalent than is generally appreciated, since skeletal muscle constitutes some 45% of total body-weight and has a major metabolic role in addition to its mechanical function2. Knowledge of possible effects of drugs on the neuromuscular system is of increasing importance both because the range of therapeutic agents continues to expand and because the resulting syndromes, through usually reversible at the outset, may progress and lead to grave consequences if the drug responsible is not stopped. Drug-induced neuropathies3 will not be considered here, but it will be appreciated that muscle weakness may also be feature of such disorders and that some drugs may cause both a neuropathy and a myopathy. The features of the main drug-induced syndromes are summarised in the table. To these one could justifiably add the unwanted effects of srugs given for the treatment of central-nervous-system or neuromuscular disorders per se-e.g., the cholinergic block which may be produced by anticholinesterases alone or with corticosteroids in the myasthenic,4 and the profound weakness which may supervene after relief of spasticity with dantrolene sodium5.
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PMID:Drug-induced myopathies in man. 7 27

Two patients are reported with a chronic progressive illness characterized by dementia, ataxia and spasticity. There were no myoclonic jerks and both had normal electroencephalograms (EEG). Pathological findings in three brain biopsies were those of viral meningoencephalitis with perivenous demyelination. Serological data in both patients indicated the presence of measles virus infection. Intracytoplasmic structures resembling measles virus nucleocapsids were found in the brain biopsy of one patient. Immunofluorescent staining showed antibody in the temporal lobe biopsy of both patients. It is suggested that these patients are examples of a chronic form of measles meningoencephalitis hitherto undescribed.
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PMID:An unusual form of measles meningoencephalitis. A report of two cases. 9 70

The clinical features in 2 second cousins with neuronopathic Gaucher disease include slowly progressive ataxia, spasticity, myoclonus, and seizures with relative preservation of intellectual function. Organomegaly was noted only in Patient 1. Both patients had diffuse slowing with paroxysmal features in electroencephalograms and a deficiency of beta-glucosidase activity in leukocytes and skin fibroblast cultures. The parents of Patient 1 and the related father of Patient 2 had levels of beta-glucosidase activity consistent with the carrier state for Gaucher disease. The value of beta-glucosidase activity in the mother of Patient 2 suggests a different mutation, the result being a defective enzyme component not detectable by measuring total activity.
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PMID:Clinical variation in 2 related children with neuronopathic Gaucher disease. 9 23

Two patients had the variable clinical features of unilateral cryptophthalmia. A 5-month-old boy had isolated unilateral cryptophthalmia: a small boney orbit, deformed optic canal, and a small amorphous mass with no normal intraocular tissue representing the globe. No extraocular muscles or optic nerve were identified by B-scan ultrasound or by computed axial tomography x-ray techniques. The second patient, a 13-year-old girl, had unilateral cryptophthalmia, and numerous systemic abnormalities including a head circumference less than the third percentile, severe mental retardation, hypoplasia of the left side of the head, and a left facial cleft deformity. She also had contractures of hips, knees and ankles, and bilateral spasticity and jerky movements. The left boney orbit was contracted and deformed and contained a small amorphous tissue with no ocular detail, as revealed by B-scan and computed tomography scan.
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PMID:Unilateral cryptophthalmia. 10 6

A young epileptic presented with spasticity as well as ataxia, diplopia and nystagmus; his serum phenytoin level was very high. All the abnormal signs disappeared after withdrawal of phenytoin. Spasticity, hyperreflexia, and clonus are features of phenytoin intoxication, present in this case, which are not commonly seen, and which have rarely been mentioned previously in the literature.
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PMID:Spasticity due to phenytoin toxicity. 10 44

In rats the application of 10 mg/kg 6-amino-nicotinamide (6-AN) leads to an accumulation of 6-phosphogluconate, by inhibition of 6-phosphogluconate dehydrogenase in the pentose phosphate pathway, in the cells of the spinal cord. The accumulation reaches its maximum after 18-24 h. It seems that there exists a relationship between the accumulation of 6-phosphogluconate and the lesion of the neuroglia, which is found in electron microscopic studies. Symptoms of a spastic paresis only develop later when the spinal interneurones are destroyed as a consequence of the lesion of the neuroglia. The accumulation of 6-phosphogluconate almost exceeds the 400 fold of the norm. No considerable differences are found between the effects of a dose of 35 mg 6-AN/kg and one of 10 mg 6-AN/kg. Free gluconate is identified enzymically in the cells of the spinal cords of the rats treated with 6-AN. The compound is very probably formed by dephosphorylation and diffuses into the blood. 6-Phosphogluconate is an inhibitor of the phosphoglucose isomerase. Its accumulation shifts the equilibrium towards glucose 6-phosphate. The lactate concentration decreases as compared with the untreated controls. Muscular action potentials are recorded extracellularly with a concentric needle electrode from the musculus gastrocnemius of rats treated with 6-AN. First activations of the electromyograms are found 48 h after the application of 10 mg 6-AN/kg. The electrical activities increase during the time in which a progressive destruction of the interneurones occurs. The electromyogram displays a permanent state of excitation with high amplitudes and an increased frequency. The continuity and intensity of the increased activity recorded by the electromyograph is the most important pathological finding. p-Chlorophenyl-GABA and, still more so, chlorpromazine cause temporary reduction of the excitation processes and an electromyogram nearly at rest. Under the same conditions, haloperidol is only slightly effective. The symptoms developed by the chemical destruction of the interneurones of the spinal cord, with rigidity and spasticity of the hind limbs, are suitable for testing antispastic drugs.
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PMID:Spastic paresis after 6-aminonicotinamide: metabolic disorders in the spinal cord and electromyographically recorded changes in the hind limbs of rats. 13 91


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