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PubMed1988

Spontaneous and harmaline-stimulated Purkinje cell activity in rats with a genetic movement disorder.

The genetically dystonic rat (dt) displays a complex movement disorder in the absence of morphological defects in the nervous system. This mutant is also insensitive to the tremorogenic effects of harmaline. Because harmaline is known to act on the cells of the inferior olive to induce activity at the tremor frequency in the olivocerebellobulbar pathway, this pathway has been investigated as a possible site of a defect in the dt rat. Biochemical studies suggested the presence of abnormalities at the level of the Purkinje cell or its afferent input. Thus, the present study investigated the harmaline response of Purkinje cells in dt rats and unaffected littermate controls with extracellular single-unit recording techniques. The spontaneous, simple spike and complex spike firing rates of dt rats were significantly lower than those of normal littermate controls. In normal rats, 2 responses to systemic harmaline injection were seen. Simple spikes were either completely suppressed for periods of 30-180 min, or were intermittently suppressed, pausing repeatedly for periods of 1-18 sec. Cells that showed complete suppression of simple spike activity also showed increased frequency and rhythmicity of complex spikes. In dt rats, intermittent simple spike responses were seen in a proportion (41%) similar to that in normal rats (53%). However, the proportion of cells showing high-frequency, rhythmic, complex spikes and complete suppression of simple spikes was low in the dt rats in comparison with littermate controls (18 versus 47%). In addition, 41% of the cells from dt rats displayed no change, or an anomalous change, in firing patterns in response to harmaline. Since the rhythmic activation of olivary neurons that results in the rhythmic, complex spike discharge of Purkinje cells is assumed to be responsible for the appearance of harmaline tremor, the failure of the dt rat to display tremor is most likely due to a failure at the olivocerebellar level, rather than at a site efferent to the cerebellum.

Action Potentials↗
PubMed2006

A systematic review of the methodology of telemedicine evaluation in patients with postural and movement disorders.

We reviewed the methodology used in telemedicine research concerning patients with postural and movement disorders. Literature searches were performed using various computerized databases through to October 2005. Twenty-two studies met the criteria for review. Two broad models of telemedicine delivery were represented in the literature: (1) telemedicine between health-care professionals at each telemedicine site (n=16) and (2) telemedicine between health-care professionals and a patient at a remote site (n=6). Disparate research methodologies were used to investigate these two models. Most studies were limited to investigating the technical feasibility and acceptability of a telemedicine service rather than focusing on the overall effect of introducing the telemedicine service into routine health care. Nonetheless, it is possible to conclude that telemedicine is acceptable for both patients and professionals when used in rehabilitation. Since the two models of telemedicine evaluation tend to explore different outcomes (diagnostic accuracy versus health status), it is recommended that separate methodologies should be used. In contrast to evaluations of telemedicine model 2, randomized controlled trials appear to be less valuable for telemedicine model 1.

Delivery of Health Care↗
PubMed1983

Eye movement disorders in multiple sclerosis and optic neuritis.

Horizontal saccadic and smooth pursuit eye movements were studied in 84 patients with multiple sclerosis (MS) and 21 patients with optic neuritis (ON). The MS patients were clinically classified as 'definite', 'probable', or 'possible'; subclinical eye movement disorder was found in 80 per cent of the definite, 74 per cent of the probable and 60 per cent of the possible category. Five of the ON patients (25 per cent) showed a subclinical eye movement deficit; these 5 were young patients with a recent history of ON. In a group of 27 MS patients with symptoms of spinal cord involvement only, 14 showed subclinical oculomotor disorder indicating the involvement of cerebral structures in the demyelination process. A study of the correlation between specific eye movement parameters and results of visual evoked response (VER) tests revealed that saccadic latency or smooth pursuit abnormalities are not correlated with prolonged VER latencies (P-100 peak latency). This indicates that lesions beyond the primary visual pathway contribute substantially to both parameters of oculomotor dysfunction. A significant correlation was found between prolonged saccadic latency and smooth pursuit deficit. An explanation for this finding based on functional aspects of the saccadic and smooth pursuit systems and their mutual interaction is presented. The occurrence of internuclear ophthalmoplegia (INO) is significantly related to an increase of saccadic latency. This finding indicates that demyelination in the patients manifesting INO may not be restricted exclusively to one or both medial longitudinal fasciculi, but may extend to other brainstem structures which are functionally involved in the programming of saccades. The findings confirm the value of standardized objective examination of eye movements in the detection and clarification of subclinical lesions in the central nervous system of patients with an early diagnosis of MS or ON.

Adolescent↗
PubMed2002

Movement disorders associated with atypical antipsychotic drugs.

Data from clinical trials reviewed in this article fulfill predictions based on preclinical findings that atypical antipsychotic drugs are associated with a reduced potential for inducing extrapyramidal symptoms (EPS) and other movement disorders. Atypical drugs have been shown to reduce all subtypes of acute EPS, the frequency of EPS-related patient dropouts, and the need for concomitant antiparkinsonian drug use. Clozapine remains superior to other atypicals in treating psychosis without worsening motor symptoms in patients with Parkinson's disease. Atypicals may be selectively advantageous in treating schizophrenic patients with a predisposition to catatonia. Although the risk of developing lethal neuroleptic malignant syndrome may be diminished with atypical drugs, clinicians must remain alert to the signs of this disorder. Atypicals have reduced liability for inducing tardive dyskinesia (TD) and show antidyskinetic properties in patients with preexisting TD. Passive resolution of TD may be facilitated in some patients by the use of these agents. Thus, the risk of movement disorders has become only one of several considerations in choosing among antipsychotic drugs.

Akathisia, Drug-Induced↗
PubMed1993

[Movement disorders induced by neuroleptic therapy].

Neuroleptics are drugs frequently used in clinical psychiatric and neurologic daily practice. They share the ability to block postsynaptic dopamine D2 receptors in the Central Nervous System. Their potency is directly proportional to that block. Movement disorders are the most frequent and important adverse effects induced by these antipsychotic drugs. This work will highlight some of the essential aspects of distinct neuroleptic-induced movement disorders.

Antipsychotic Agents↗
PubMed2004

The restless legs syndrome and periodic limb movement disorder: a review of management.

The restless legs syndrome (RLS) and periodic limb movement disorder (PLMD) are distinguishable but overlapping disorders. Both feature nocturnal involuntary limb movements (periodic limb movements) that can cause sleep disruption, but each has distinct clinical features that are relevant to the diagnosis and management of the patient. The diagnosis of RLS is made by meeting established clinical criteria, not from discovery of periodic limb movements of sleep (PLMS) on a sleep study. PLMD, however, does require the presence of PLMS on polysomnography as well as an associated sleep complaint. Moreover, PLMS are themselves nonspecific, occurring both with RLS and with other sleep disorders as well as in normal individuals. The diagnosis of PLMD, then, requires not merely finding a significant number of PLMS but also excluding other potential causes for the associated sleep complaint. Treatment of RLS is based on consideration of the pattern and severity of the disorder, with dopaminergic drugs generally favored for initial treatment. Anticonvulsants, opioids, and sedative/hypnotics also have a role. A treatment algorithm is provided to assist with the management of RLS. Treatment of PLMD relies on many of the same medications, but is generally more straightforward and places a greater reliance on levodopa compounds and sedative-hypnotics.

Diagnosis, Differential↗
PubMed1994

Movement disorders following lesions of the thalamus or subthalamic region.

Reports of 62 cases with a movement disorder associated with a focal lesion in the thalamus and/or subthalamic region were analyzed. Thirty-three cases had a lesion confined to the thalamus. Sixteen cases had a thalamic lesion extending into the subthalamic region and/or midbrain. Thirteen cases had a lesion in the subthalamic region or a subthalamic lesion extending into the midbrain. Nineteen cases with dystonia, 18 with asterixis, 17 with ballism-chorea, three with paroxysmal dystonia, and five with clonic or myorhythmic movements have been described. No case with isolated tremor has been described. In 53 cases with unilateral thalamic or subthalamic lesions, all but one with bilateral blepharospasm (associated with right posterior thalamic, pontomesencephalic, and bilateral cerebellar lesions) had dyskinesias in the limbs contralateral to the lesion. The other nine cases had bilateral paramedian thalamic lesions; seven developed bilateral dyskinesias, and the remaining two had unilateral dyskinesias. Regarding the 19 patients with dystonia, the two with bilateral blepharospasm had thalamic and upper brainstem lesions, and one with hemidystonia and torticollis had a subthalamic lesion. The other 16 patients all had a unilateral thalamic lesion with contralateral dystonia (10 hemidystonia, five focal dystonia affecting a hand and/or and one segmental dystonia involving face, arm, and hand). The exact location of the thalamic lesion was mentioned in 10 cases; the posterior or posterolateral thalamus was involved in six and the paramedian thalamus in four. These areas are more posterior or medial to the ventrolateral and ventroanterior thalamic nuclei, which receive pallido-thalamic and nigro-thalamic afferents. Two cases developed dystonia immediately after thalamotomy, and one case developed it 4 days after head trauma. The others initially had a hemiplegia and developed dystonia 1-9 months after the acute insult. Fifteen of the 17 patients with chorea had a unilateral lesion in the subthalamic nucleus or subthalamic region (eight due to infarcts, one to hemorrhage, five to mass lesions, and one to multiple sclerosis). All had contralateral hemichorea or hemiballism. One other case had bilateral chorea of the hands and tongue due to paramedian thalamic infarction. Another case with generalized chorea and thalamic atrophy was complicated by stereotaxic surgery. Thirteen of the 18 cases with asterixis had lesions confined to the thalamus. Eight were associated with thalamotomy, and five others had a stroke (four infarction and one hemorrhage) affecting the contralateral thalamus.(ABSTRACT TRUNCATED AT 400 WORDS)

Dominance, Cerebral↗
PubMedDate not supplied

Movement disorders and new azapirone anxiolytic drugs.

Dopamine is a neurotransmitter affecting motor function, and the dopamine system is the focus of abnormality in dyskinetic diseases. An important side effect of many psychotropic drugs possessing dopamine activity is the production of movement disorders; this potential problem needs to be examined carefully with any new central nervous system drug, such as the azapirone anxiolytic drugs. The pharmacology of the azapirones, represented by the prototype, buspirone, involves several different neuroreceptor systems. Current evidence indicates that buspirone's anxiolytic activity is mediated through serotonergic mechanisms. It also displays some binding affinity for dopamine receptors, which necessitates comparisons between buspirone and neuroleptic agents in preclinical tests, clinical studies, and case reports. Although similarities occurred in some biochemical studies, neuroleptics, and not buspirone, caused an increase in dopamine receptors with chronic use. Neuroleptics typically produce this change after long-term use, which is thought to be a key factor leading to tardive dyskinesia. In standard animal behavior studies, buspirone's profile failed to match neuroleptic agents. Most notably, neuroleptics produce catalepsy; however, buspirone failed to induce catalepsy and instead reversed this effect. Isolated case reports have described buspirone as causing movement disorders, but these patients were previously exposed to neuroleptic agents. Furthermore, buspirone has been used successfully to treat anxiety in parkinsonism without exacerbating existing movement problems. In psychotropic drug use, careful patient monitoring, complete drug histories, and a full appreciation for a drug's pharmacology are necessary to decipher any likelihood of a drug relation with an adverse effect.

Aged↗
PubMed1994

Movement disorder following excitotoxin lesions in primates.

We previously reported on the histologic and neurochemical features of quinolinic acid lesions in primates which produce many of the characteristic features of Huntington's disease (HD). We now report on the effects of apomorphine in generating a movement disorder in four of these animals. Animals were tested with saline or apomorphine both before and after the lesions. All animals showed few spontaneous abnormal movements after lesioning, but showed marked dyskinetic movements following apomorphine administration. These results show that excitotoxin lesions in primates can produce an apomorphine-inducible movement disorder which closely resembles that of HD.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2006

Dopa-responsive hypersomnia and mixed movement disorder due to sepiapterin reductase deficiency.

Sepiapterin reductase deficiency (SRD) is a rare, treatable disorder of monoamine metabolism with cognitive delay and l-dopa responsive movement disorder. We describe a patient with SRD and distinctive phenotypic feature of marked hypersomnolence. Our patient showed improvement with therapies directed at both serotonergic and dopaminergic deficiencies. This case illustrates symptoms that characterize the SRD phenotype and demonstrates the importance of systematic treatment trials addressing the various biochemical abnormalities present.

Adult↗
PubMed2005

[Movement disorders of functional origin (psychogenic) in children].

PATIENTS AND METHODS: Sixteen cases of functional (psychogenic) pediatric movement disorders (PMD) have been analyzed. They represents 2.4% of a PMD personal series (age of onset less than 18). RESULTS: Apart from a case, age of onset was older than 10 years. 81% (13/16 cases) were females. Tremor (68%) was the predominant abnormal movement followed by mioclonus. These facts are according with the scarce studies reported of functional PMD. We emphasize the diagnostic difficulties of this kind of conditions. CONCLUSIONS: Diagnostic clues are age of onset older than 10 years, female gender, clinical inconsistency of the movement, increasing or decreasing of the movements with attention to the movements or distraction, normality of the exams including neurophysiological studies. However in some cases a follow-up is necessary to confirm the diagnosis.

Humans↗
PubMed2005

Non-movement disorder heralds symptoms of Machado-Joseph disease years before ataxia.

We describe three patients with the Machado-Joseph disease (MJD) genetic abnormality who had non-movement disorder neurological symptoms or signs that preceded the gait ataxia by several years. This implies that some clinical manifestations other than ataxia may be considered part of the herald symptoms of MJD, especially in the setting of a positive family history.

Adult↗