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At least 793 records · Page 44Linked to original sources
PubMed1989

[Writer's cramp--focal dystonia or psychogenic movement disorder? A critical literature study].

For more than 100 years there has been a discussion as to whether writer's cramp is caused by a disease of the central nervous system, or if it is to be considered as a disturbance of psychogenic origin. Whereas before 1982 there seemed to be a lot of evidence for the psychogenic theory many authors now tend to stress the opinion of Sheehy and Marsden who had explained that "writer's cramp" should be seen as a "focal dystonia". This article discusses the statements of Sheehy and Marsden in comparison with other scientific findings regarding the occupational cramps--above all "writer's cramp". It is concluded that there are different therapeutic approaches derived from the respective theory and which are considered to lessen the movement disorder. Scientific literature suggests that psychotherapy or some therapeutic approaches of behaviour therapy are more effectful in mastering this "mysterious" disorder than any pharmacological substance tested upto now.

Dystonia↗
PubMed2006

Oscillations in the basal ganglia under normal conditions and in movement disorders.

A substantial body of work within the last decade has demonstrated that there is a variety of oscillatory phenomena that occur in the basal ganglia and in associated regions of the thalamus and cortex. Most of the earlier studies focused on recordings in rodents and primates. More recently, significant advances have been made in this field of research through the analysis of basal ganglia field potentials recorded from implanted deep brain stimulation electrodes in the basal ganglia of human patients with Parkinson's disease and other disorders. It now appears that oscillatory activity may play a significant role in the pathogenesis of these diseases. The most significant finding is that in Parkinson's disease synchronized oscillatory activity in the 10- to 35-Hz band (often termed "beta-band") is prevalent in the basal ganglia-thalamocortical circuits, and that such activity can be reduced by dopaminergic treatments. The entrainment of large portions of these circuits may disrupt information processing in them and may lead to parkinsonian akinesia (and perhaps tremor). Although less firmly established than the role of oscillations in movement disorders, oscillatory activities at higher frequencies may also be a component of normal basal ganglia physiology.

Animals↗
PubMed2003

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.

Aged↗
PubMedDate not supplied

An immunoassay for anti-neuronal antibodies associated with involuntary repetitive movement disorders.

Tourette's syndrome (TS) is a complex neurobehavioral disorder emerging in childhood and is characterized by motor and vocal tics of at least one year in duration. In a portion of patients with TS, environmental (non-genetic) factors may either have an etiologic role or act to modulate the phenotype. One possible environmental factor may be antibodies to central nervous system cells, as sera from several children diagnosed with either TS or Sydenham's chorea contained anti-neuronal antibodies. Using enriched membrane preparations isolated from HTB-10 neuroblastoma cells, a sensitive and specific assay was developed for the determination of human anti-neuronal antibodies associated with involuntary repetitive movement disorders. This assay exhibited between-run and within-run precision of 11.3 percent and 5.9 percent, respectively. The sensitivity, specificity, positive predictive value, and negative predictive value of this assay for the diagnosis of TS and TS or chorea are 79.1 percent, 61.2 percent, 61.6 percent, 78.8 percent, and 71.1 percent, 60.9 percent, 68.6 percent, and 63.6 percent, respectively. In addition, there was a significant difference (p < 0.0001) between the mean optical density in the patients with TS and children determined to be clinically "normal".

Autoantibodies↗
PubMed2005

Calcium-sensitive potassium channelopathy in human epilepsy and paroxysmal movement disorder.

The large conductance calcium-sensitive potassium (BK) channel is widely expressed in many organs and tissues, but its in vivo physiological functions have not been fully defined. Here we report a genetic locus associated with a human syndrome of coexistent generalized epilepsy and paroxysmal dyskinesia on chromosome 10q22 and show that a mutation of the alpha subunit of the BK channel causes this syndrome. The mutant BK channel had a markedly greater macroscopic current. Single-channel recordings showed an increase in open-channel probability due to a three- to fivefold increase in Ca(2+) sensitivity. We propose that enhancement of BK channels in vivo leads to increased excitability by inducing rapid repolarization of action potentials, resulting in generalized epilepsy and paroxysmal dyskinesia by allowing neurons to fire at a faster rate. These results identify a gene that is mutated in generalized epilepsy and paroxysmal dyskinesia and have implications for the pathogenesis of human epilepsy, the neurophysiology of paroxysmal movement disorders and the role of BK channels in neurological disease.

Adolescent↗
PubMed1992

Abnormal cerebellar output in rats with an inherited movement disorder.

Biochemical and metabolic mapping techniques have consistently identified the deep cerebellar nuclei (DCN) of the genetically dystonic rat as a site of abnormality. Extracellular single-unit recording techniques were used to assess the functional significance of these findings in affected rats and normal littermates between 16 and 25 days of age. Cells in the medial nucleus of the mutant rats had significantly increased spontaneous firing rates in comparison with cells from normal rats. In both the medial and the interpositus nuclei, cells from the mutants fired more rhythmically than those from the normal rats. When harmaline was administered systemically to activate the olivo-cerebellar system, in normal rats, increased firing rate and bursting patterns of activity were seen. There was no reliable change in the average firing rate or rhythmicity of cells in the medial nucleus of the dystonic rats, although previous studies have shown that harmaline activates neurons in the inferior olive in the mutants. It is likely that naturally stimulated olivary activity also fails to modulate cerebellar output in this model of inherited movement disorder. Anatomical studies did not reveal any consistent changes in the number of Purkinje cells, the volume of the DCN, or the soma size of DCN neurons. Since the electrophysiological findings cannot be ascribed to a loss of the Purkinje cells that normally provide an inhibitory input to the cerebellar nuclei, the results of this study indicate the presence of a functional defect in the control of cerebellar output in the dystonic rat that accounts for the failure of these animals to display harmaline tremor and which may be critical to the motor syndrome.

Animals↗
PubMed2002

Is EQ-5D a valid measure of HRQoL in patients with movement disorders? A comparison with SF-36 and FIM questionnaires.

We assessed the descriptive part of the EQ-5D system in rehabilitation patients with validity severe moving disorders and compared it with the FIM and the SF-36 Health Survey in a sample of 60 patients. We analyzed the EQ-5D convergent validity and the correlations between EQ-5D scores and a clinical variables. The internal validity of the EQ-5D instrument proved good. Moreover, the EQ-5D discriminated symptom severity as scored by the FIM and the SF-36 correspondent subscales. We analyzed the sensitivity of the EQ-5D only with respect to the ability of patients to move with or without a wheelchair. Most patients considered "moving a wheelchair" as a good way of "getting about." This investigation can be considered a pilot study on the performance of the EQ-5D in a group of pathologies involving various degrees of movement disorders. The findings show possible problems of misinterpretation in the levels of the mobility dimension.

Journal Article↗
PubMed1989

Hand muscle reflexes following electrical stimulation in choreatic movement disorders.

Thenar reflexes following electrical stimulation of the median nerve (containing proprioceptive and cutaneous afferents) and the radial superficial nerve (cutaneous afferents only) were investigated in 23 patients with manifest Huntington's disease (HD) at an early stage, in 17 clinically healthy descendants of HD-patients and in 18 patients with choreatic hyperkinesia due to various aetiologies other than HD. In 61% of the patients with early HD the long-latency reflexes (LLR) were uni- or bilaterally absent in response to both median nerve and radial superficial nerve stimulation. The remaining patients had a diminished mean amplitude and mean duration of their LLR. In contrast, offspring and patients with symptomatic chorea had preserved LLR which did not differ in amplitude or duration from normal controls. Additionally, the mean amplitude and mean duration of the Hoffmaan-reflex (HR) was found to be increased in patients with HD and their offspring but not in patients with other aetiologies. It is concluded (1) that the loss of LLR is not related to the choreatic hyperkinesia itself but to the degeneration of a hitherto poorly defined neuronal circuit in HD; (2) that among a variety of diseases presenting with chorea, the loss of LLR seems to be specific for HD; (3) that the testing of hand muscle reflexes in choreatic movement disorders is helpful for the differential diagnosis of early HD but not for the detection of gene carriers among offspring of patients with HD.

Afferent Pathways↗
PubMed1994

A rhythmic movement disorder in REM sleep: a case report.

The case of a 34-year-old woman in good health with a complaint of diurnal fatigue and chronic repetitive rocking body movements during sleep is reported. Repeated polygraphic and video recordings during sleep allowed for a detailed analysis of rhythmic patterns of head and body rolling movements preferentially occurring during rapid eye movement sleep. The contribution of severe psychopathology or neurologic disorder was carefully examined and ruled out with personality testing, structured psychiatric interview, neurological examination with electroencephalogram, cerebral computerized tomography, magnetic resonance imaging and position emission tomography scans.

Adult↗
PubMed1972

Treatment of involuntary movement disorders with tetrabenazine.

Seventeen patients with choreiform, athetoid, or ballistic involuntary movements, or with spasmodic torticollis, were treated with tetrabenazine in doses of 25 to 200 mg daily for periods varying from two weeks to more than six months. Randomized ciné film of the patients' involuntary movements, taken before, during, and after treatment was assessed individually by seven `blind' observers. Eight patients were judged improved; two had Huntington's chorea, two athetosis, two dystonia musculorum deformans, one hemiballismus, and one spasmodic torticollis. Four of the eight improved patients have continued taking the drug for longer than six months. In a second study seven patients with Huntington's chorea were treated for two weeks each with tetrabenazine (50 mg t.d.s.) and with amantadine (100 mg t.d.s.) and the results assessed by the same method. The choreiform movements of six of these patients were strikingly improved with tetrabenazine therapy, but amantadine had no effect. Tetrabenazine is an effective agent for the suppression of choreiform and ballistic involuntary movements. It is only slightly effective in the treatment of athetosis and spasmodic torticollis. Drowsiness, insomnia, and depression were the most conspicuous unwanted effects, and these may limit the clinical usefulness of the drug.

Adolescent↗