Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0013421 (dystonia)
 8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ventricular fluid concentrations of homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA), the respective metabolites of dopamine and serotonin, were measured in 57 patients undergoing thalamotomy for relief of movement disorders. The diseases included were Parkinson disease, dystonia, cerebral palsy, multiple sclerosis, and posttraumatic or posthypoxic encephalopathy. Untreated parkinsonian patients had the lowest mean HVA level (119 ng per milliliter). Patients with multiple sclerosis or with posttraumatic or posthypoxic encephalopathy with both intellectual impairment and bilateral motor involvement had lower mean HVA levels (197 and 177 ng per milliliter, respectively) than cerebral palsy patients with bilateral motor disease (233 ng per milliliter), dystonia patients (246 ng per milliliter), or multiple sclerosis patients with normal intellect (376 ng per milliliter). The data suggest that diffuse cerebral disease may lead to diminished dopaminergic activity. Ventricular fluid 5-HIAA levels were similar in all groups of patients. Chronic cerebellar stimulation markedly increased ventricular fluid HVA and 5-HIAA levels, indicating that cerebellar stimulation affected cerebral dopaminergic and serotonergic systems.
 ...
PMID:Ventricular fluid homovanillic acid and 5-hydroxyindoleacetic acid concentrations in patients with movement disorders. 56 83

Similar movement disorders developed in two 8-year-old retarded children while they were receiving phenytoin. Seizures subsequent to a diphtheria-pertussis-tetanus immunization had developed in each child at 1 to 2 months of age. A static encephalopathy ensued, characterized by mental retardation, ataxia, spasticity, and a mixed seizure disorder. Intermittent dystonia and choreoathetosis developed insidiously while serum phenytoin concentrations were in the therapeutic range. Sustained dystonia and choreoatheosis developed 2 hours after an oral provocation with phenytoin. The baseline abnormalities on the electroencephalogram remained unchanged during the choreoathetosis. Recognizable metabolic abnormalities known to be associated with similar movement disorders were excluded. It was concluded from these studies that the movement disorder is secondary to phenytoin and can occur at therapeutic serum concentrations. Phenytoin is a central anticholinergic agent and a central stimulant of serotonin, and may induce movement disorders as a result of altering these neurotransmitters in the brain. The variable expression of these movement disorders may relate to the nature of the preexisting striatal insult.
 ...
PMID:Phenytoin-induced dystonia and choreoathetosis in two retarded epileptic children. 94 1

Cavinton was used for 10 years in 967 patients with different cerebrovascular diseases. The highest effect was seen in patients with early forms and primarily chronic forms: vegetovascular (neurocirculatory) dystonia, initial manifestations of brain blood supply insufficiency, circulatory encephalopathy in the first and second stages. Improvement of the subjective status and a decrease of the intensity of vestibulocerebellar disorders were recorded by the end of the treatment in 75-85% of such patients. In ischemic brain stroke, regress of general cerebral and focal symptoms was more rapid and significant in the adequate reaction type of cerebral hemodynamics to cavinton administration (a rise of pulse blood content of the brain and a reduction of the vascular tone according to the REG data) and was less noticeable in the hypertonic and, in particular, in the hypotonic type. Cavinton should not be used in severe general cerebral hypertensive crises, as well as in elderly or senile patients with acute cardio-cerebral or cerebro-cardiac syndrome, postinfarction cardiosclerosis, marked disorders of heart rhythm.
 ...
PMID:[10-year experience with using Cavinton in cerebrovascular disorders]. 131 51

We report six previously healthy children who several days after a prodromal illness had an acute encephalopathy that ran a biphasic course. It appears to constitute a recognizable syndrome with a good prognosis that can be differentiated from other encephalopathies of obscure origin as previously defined by Lyon et al. The active phase was dominated by coma or confusion and by abnormal movements, including disordered gesticulation and attacks of orofacial dyskinesia or limb dystonia associated with permanent rigidity and culminating in opisthotonic posturing. Repeated seizures were observed in only two patients. Permanent slow waves were recorded on the electroencephalogram in all patients, even during bursts of abnormal movements. Cerebrospinal fluid and results of serologic studies were normal throughout the course of the disease, and attempts at viral isolation and antiviral antibody detection yielded negative results. Brain imaging either showed no abnormalities or suggested a moderate degree of brain edema. The recovery phase, which extended for several weeks, was characterized by a rapid return of motor function and persistent behavioral and cognitive disturbances. Nonverbal reasoning recovered long before verbal expression returned to normal. Four patients eventually recovered fully, whereas two had mild sequelae.
 ...
PMID:Coma associated with intense bursts of abnormal movements and long-lasting cognitive disturbances: an acute encephalopathy of obscure origin. 144 43

Two patients with acute encephalopathy with bilateral striatal necrosis are presented and the literature on the subject is reviewed. The disease is characterized by abrupt onset following a systemic infectious illness, with disturbance of consciousness, absence of speech, dystonic movements of the limbs, general stiffness, opisthotonus, tremor, facial grimacing, and stereotyped reaction to painful stimuli. After a variable period of time, there is gradual improvement of the neurological status with clearing of consciousness and recovery of motor functions. Mild CSF pleocytosis is the only abnormal laboratory test encountered. Cranial imaging shows from the beginning of the illness, bilateral involvement of the striatum that may persist indefinitely. The pathogenesis of this disorder remains unknown although an infectious or para-infectious mechanism seems to be the most likely possibility.
 ...
PMID:Acute encephalopathy with bilateral striatal necrosis. A distinctive clinicopathological condition. 149 50

According to the authors' observations, the symptoms of nervous system derangement associated with legionnaires' disease rather often enter the disease structure and can virtually be characterized as a manifestation of infectious and toxic encephalopathy and polyneuropathy (encephalopolyneuropathy). In the majority of cases, the neurological disorders develop acutely or subacutely after or simultaneously with respiratory lesions. The clinical picture of encephalopathy is marked by permanent headache, mental abnormalities, memory disturbances, insomnia, pronounced astheno-vegetative and vascular manifestations. In patients with legionellosis, polyneuropathy is manifested by paresthesias, less frequently by pains in the distal parts of the limbs and myasthenia without visible atrophies. Vegetative disorders such as vegetative polyneuropathy of the hands and legs, visceral polyneuropathies are typical symptoms of the disease whatever its gravity. Vegetovascular dystonia together with long-term AP instability is an obligate sign of the disease. Electrophysiological examinations (EEG, REG, EMG) support the clinical findings and may serve the basis for an objective evaluation of the gravity of the neurological disorders. The degree of pulmonary lesions and the intensity of vegetative disorders eventually determine the torpidity and characteristics of the disease course.
 ...
PMID:[Nervous system involvement in legionellosis (legionnaires' disease)]. 164 36

The reported cases of betolepsy, namely convulsive fits and syncopal attacks induced by cough were observed in patients suffering from different pulmonary diseases, vegetovascular dystonia, and venous encephalopathy. The extracerebral mechanism occurring by the Valsalva type related to the lowering of cardiac output and blood supply to the brain was assumed to be implicated in the origin of betolepsy. In the described group of the patients with multiple occlusive lesions of the cerebral arteries, the pathogenesis of betolepsy is obviously connected with a decrease of the arteriovenous gradient of cerebral circulation to the level close to the critical one. In this case, enhancement of the cerebral blood flow attained by different approaches including reconstructive operations on cerebral vessels rather than administration of anticonvulsants is an effective means of counteracting betolepsy.
 ...
PMID:[Betolepsy in patients with multiple lesions of major cerebral blood vessels]. 166 74

A large kindred, in which either Leber's hereditary optic atrophy, or a hereditary spastic dystonia, or a combination of both manifested over many generations was restudied after the first report on it in 1964. NMR scans revealed bilateral, and, in two patients with hemidystonia, unilateral necrosis with shrinkage of the putamen, in one case associated with total disappearance of the head of the caudate nucleus. Except for age-appropriate cortical atrophy in one instance, no other changes were observed in the brain, brainstem, and cerebellum. The putaminal necrosis appears as typical "striatal slits" on the NMR scans. It is argued that this rare disease, since the princeps description in 1964 only reported in England (1986) and the U.S.A (1986), is most likely a singular type of mitochondrial encephalopathy: it is associated with Leber's optic atrophy, and the NMR changes observed have been signalled in other mitochondrial encephalomyelopathies, such as Leigh's disease and MELAS.
 ...
PMID:Hereditary spastic dystonia: a new mitochondrial encephalopathy? Putaminal necrosis as a diagnostic sign. 188 May 38

A 13-year-old boy was the victim of attempted strangulation. His condition had returned to normal by the sixth day after the assault; however, from the seventh day, choreoathetosis, dystonia, and marked pseudobulbar paralysis developed in the boy. The computed tomographic scans and T2-weighted magnetic resonance images that were obtained at this time revealed low-density and high-signal intensities in the region of the bilateral putamen and caudate nucleus. These symptoms and the changes in his computed tomographic scans and magnetic resonance images subsided gradually during a 2-month period. Sequential analysis of the cerebrospinal fluid for gamma-aminobutyric acid and dopamine concentrations during his illness revealed reciprocal changes with normal recovery. Because of the delayed onset of neurological changes and the cerebrospinal fluid showing reversible symptoms, the delayed encephalopathy after strangulation had been related to the biochemical alterations that followed anoxia in the vulnerable basal ganglia.
 ...
PMID:Delayed postanoxic encephalopathy after strangulation. Serial neuroradiological and neurochemical studies. 189 66

A 13-year-old boy was the victim of a strangulation attempt. His behavior was normal by the 6th day after the assault. However, from the 7th day, he developed choreoathetosis, dystonia and marked pseudobulbar palsy. CT and T2-weighted MRI at this time revealed a low density and high signal intensity in the region of the bilateral putamen and caudate respectively for the first time. Thereafter, these symptoms and changes in CTs and MRIs subsided gradually over two months. Sequential analysis of CSF for GABA and dopamine during illness revealed reciprocal changes each other with normal recovery. Because of delayed onset of neurological changes, and findings of CSF with reversible symptoms the delayed encephalopathy after strangulation is probably related to biochemical alteration secondary to anoxia in vulnerable basal ganglia.
 ...
PMID:[Delayed postanoxic encephalopathy after strangulation--the serial neuroradiological and neurochemical studies]. 210 26


1 2 3 4 5 6 7 8 9 10 Next >>