Cases reported "Hyperkinesis"

Filter by keywords:



Filtering documents. Please wait...

1/11. Hyperkinetic movement disorders caused by corpus striatum infarcts: brain MRI/CT findings in three cases.

    Three patients with hemichorea/hemiballismus/hemidystonia caused by discrete contralateral infarction of the corpus striatum are presented. The infarcts were all small on CT or MRI brain scan and were lacunar in type. Small discrete infarction of basal ganglionic structures allows such adventitious movements to be manifested. Involvement of contiguous areas, seen with larger infarcts, can suppress such movements. The infrequency of such hyperkinetic movement disorders, and the subtle infarct appearance on brain scan, can lead to a delay in the diagnosis.
- - - - - - - - - -
ranking = 1
keywords = dystonia
(Clic here for more details about this article)

2/11. Hyperkinetic movement disorder in an 11-year-old child treated with bilateral pallidal stimulators.

    Pallidal stimulation is widely used in the treatment of movement disorder in adults but is less well reported in the treatment of dystonia in children. Despite inconsistent results in the past, its use in dystonia in Parkinson's disease is again attracting interest with promising results. Bilateral as well as unilateral pallidotomies have been performed and are felt to be required in some cases of dystonia. Use of depth electrodes to provide long-term electrical stimulation to pallidum and other basal ganglia structures has recently become more widespread. This technique is felt to have a lower morbidity, especially in bilateral procedures. Here we present the case of an 11-year-old boy with severe hyperkinetic movement disorder who showed sustained improvement after bilateral pallidal stimulation implantation.
- - - - - - - - - -
ranking = 3
keywords = dystonia
(Clic here for more details about this article)

3/11. Involuntary vocalisations and a complex hyperkinetic movement disorder following left side thalamic haemorrhage.

    A variety of involuntary speech phenomena as for example palilalia have been described as consequences of neurological disorders. Palilalia is the involuntary repetition of syllabels, words and phrases in ongoing speech. We describe a 73 year old woman who suffered from a hypertensive thalamic haemorrhage. MRI revealed that the lesion was predominantly located within the pulvinar, extending to the lateroposterior thalamic nuclei and to the pretectal area with possible involvement of the medial geniculate body. Few months after the event she developed involuntary vocalisations with whole words and meaningless syllables being rapidly reiterated. In contrast to typical palilalia these vocalisations were not meaningfully related to the ongoing speech of the patient. In addition, the patient developed a complex hyperkinetic movement disorder with right-sided painful hemidystonia and bilateral clonic jerks and a right-sided postural tremor.
- - - - - - - - - -
ranking = 1
keywords = dystonia
(Clic here for more details about this article)

4/11. A nonsense mutation of the sodium channel gene SCN2A in a patient with intractable epilepsy and mental decline.

    Mutations, exclusively missense, of voltage-gated sodium channel alpha subunit type 1 (SCN1A) and type 2 (SCN2A) genes were reported in patients with idiopathic epilepsy: generalized epilepsy with febrile seizures plus. Nonsense and frameshift mutations of SCN1A, by contrast, were identified in intractable epilepsy: severe myoclonic epilepsy in infancy (SMEI). Here we describe a first nonsense mutation of SCN2A in a patient with intractable epilepsy and severe mental decline. The phenotype is similar to SMEI but distinct because of partial epilepsy, delayed onset (1 year 7 months), and absence of temperature sensitivity. A mutational analysis revealed that the patient had a heterozygous de novo nonsense mutation R102X of SCN2A. Patch-clamp analysis of Na(v)1.2 wild-type channels and the R102X mutant protein coexpressed in human embryonic kidney 293 cells showed that the truncated mutant protein shifted the voltage dependence of inactivation of wild-type channels in the hyperpolarizing direction. Analysis of the subcellular localization of R102X truncated protein suggested that its dominant negative effect could arise from direct or indirect cytoskeletal interactions of the mutant protein. haploinsufficiency of Na(v)1.2 protein is one plausible explanation for the pathology of this patient; however, our biophysical findings suggest that the R102X truncated protein exerts a dominant negative effect leading to the patient's intractable epilepsy.
- - - - - - - - - -
ranking = 0.017400621402597
keywords = idiopathic
(Clic here for more details about this article)

5/11. Botulinum toxin to suppress hyperkinesias after hypoglossal-facial nerve anastomosis.

    Facial hyperkinesias are a common side effect of hypoglossal-facial nerve anastomoses. We report a patient whose facial hyperkinesias were suppressed by botulinum toxin injections a treatment recently introduced in the therapy of craniocervical dystonias. EMG studies are used to document the effect of botulinum toxin on the facial hyperkinesias as well as on voluntary muscle activation.
- - - - - - - - - -
ranking = 1
keywords = dystonia
(Clic here for more details about this article)

6/11. Idiopathic dystonia and cervical spondylotic myelopathy.

    Cervical myelopathy developed in two patients with idiopathic torsion dystonia. There were marked spondylotic changes in both patients, probably attributable to the incessant dystonic movements of the neck. Previous cervical spine surgery may have exacerbated the myelopathy in one of the patients. Cervical myelopathy complicating idiopathic dystonia must be distinguished from other causes of neurological deterioration, since it may be improved by appropriate neurosurgical treatment.
- - - - - - - - - -
ranking = 6.0348012428052
keywords = dystonia, idiopathic
(Clic here for more details about this article)

7/11. Clinical and experimental studies of phenytoin-induced hyperkinesias.

    phenytoin administration occasionally leads to the induction of hyperkinetic movement disorders. The pathophysiologic basis of this phenomena is unknown, but thought to be a toxic effect of phenytoin. Study of two cases of this disorder and a review of the literature suggest that antecedant pathologic changes in the basal ganglia are prerequisites for the development of phenytoin-induced hyperkinesias. In an animal model of tardive dyskinesia, phenytoin was found to enhance neuroleptic-induced behavioral supersensitivity but have no effect in control animals. We conclude that phenytoin induced hyperkinesias reflect a specific effect of phenytoin on an abnormal neural substrate and suggest the presence of an otherwise silent pathological alteration of the corpus striatum. The diagnostic value of an episode of phenytoin-induced hyperkinesia is discussed.
- - - - - - - - - -
ranking = 16.365319844809
keywords = dyskinesia
(Clic here for more details about this article)

8/11. Hyperkinetic dysarthria as an early indicator of impending tardive dyskinesia.

    Tardive dyskinesia is a potentially irreversible disturbance of the central nervous system that is associated with the chronic ingestion of neuroleptic medications. Abnormal movements within the oral musculature are characteristic of tardive dyskinesia and are manifested in motor speech production as hyperkinetic dysarthria. Early detection of hyperkinetic dysarthria in patients who have chronically ingested neuroleptic agents may play a critical role in preventing an irreversible condition of tardive dyskinesia.
- - - - - - - - - -
ranking = 114.55723891366
keywords = dyskinesia
(Clic here for more details about this article)

9/11. methylphenidate, neuroleptics and dyskinesia-dystonia.

    Methlyphenidate is one of two stimulant drugs used in the management of the Hyperkinetic Reaction in children. It has been known to have side effects such as dyskinesia, but this case details the emergence of dystonia and dyskinesia when the simultaneous use of methylphenidate and a phenothiazine was followed by withdrawal of the phenothiazine. It is postulated that the use of phenothiazine resulted in a post-synaptic supersensitivity which precipitated dystonia and dyskinesia when phenothiazine was withdrawn and methylphenidate reinstituted. It is also suggested that the phenothiazine dopamine-blocking action may necessitate the use of larger quantities of stimulant in order to produce the desired effect.
- - - - - - - - - -
ranking = 120.55723891366
keywords = dyskinesia, dystonia
(Clic here for more details about this article)

10/11. The "jerky dystonic unsteady hand": a delayed motor syndrome in posterior thalamic infarctions.

    We report the cases of three patients with a thalamic infarct in the territory of the posterior choroidal artery involving the posterior thalamic nuclei. These patients developed delayed complex hyperkinetic motor syndromes, associating ataxia, tremor, dystonia, myoclonus and chorea, which we call "the jerky dystonic unsteady hand". One patient had a severe myoclonic and ataxic-dystonic choreoathetosis; another showed a so-called rubral tremor (myoclonic ataxia with resting, action, and wing-beating tremor) with dystonia; and the third one had a dystonic and ataxic hand with intermittent mild action myoclonus. All of them had sensory dysfunction; two had also presented with a painful Dejerine-Roussy syndrome. All had CT or MRI-proven infarcts in the territory of the posterior cerebral artery involving the posterior choroidal territory with an abnormal signal in the posterior area of the thalamus (pulvinar nucleus) but sparing the other thalamic, subthalamic and midbrain structures. These delayed myoclonic complex hyperkinetic syndromes have not been reported before, and we did not observe them in other topographic forms of thalamic infarcts. They may thus represent a new entity of movement disorders due to lesions in the posterior thalamic nuclei, with specificity for posterior choroidal artery infarcts.
- - - - - - - - - -
ranking = 2
keywords = dystonia
(Clic here for more details about this article)
| Next ->


Leave a message about 'Hyperkinesis'


We do not evaluate or guarantee the accuracy of any content in this site. Click here for the full disclaimer.