SEARCH · PubMed Health

Results for “Movement Disorders”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24Linked to original sources

PubMedDate not supplied

[Nocturnal paroxysmal dystonia, movement disorder and epilepsy].

INTRODUCTION: Nocturnal paroxysmal dystonia (NPD) is a disorder which appears during sleep. It is characterized by generally brief paroxysmal motor events which are complex when clinically expressed and are often repetitive. The origin of this disorder has been a matter for discussion for some time. Initially it was considered a specific movement disorder, but recently it has been suggested that it is epileptic in nature. CASE REPORT: In this study we present the case of a patient who is hospitalized in the Unit for epileptic surgery, suffering from epilepsy which does not respond to medical treatment and requires surgery. The patient is treated with conventional methodology, prolonged and continuous presurgical videoelectroencephalographic monitoring. EEG registers were used via electrodes placed in the scalp and skull, electrodes placed in the skull on adequate indication. Two types of perfectly defined electroclinical events occurred: some not epileptic and others clearly epileptic. On one occasion a convulsive tonic clonic epileptic crisis was recorded typical of frontal focal origin preceded by non epileptic motor phenomena. CONCLUSION: The presence of paroxysmal motor episodes during sleep, atypical as a form of epilepsy, the absence of unquestionable specific data in the EEG, and in the light of our discoveries, force us to consider the possibility that NPD is in fact a form of epilepsy caused in a reflex manner by a specific type of movement disorder during sleep, and whose origin should be more widely discussed.

Adult↗

PubMed1984

Neurochemical anatomy of movement disorders.

Recent advances in our understanding of the neurochemical anatomy of the pyramidal and extrapyramidal motor systems have led to more logical and effective pharmacotherapies for movement disorders. Our knowledge of the neurochemistry of Parkinson's and Huntington's diseases is the most complete. In the future, the same approaches used in these diseases need to be used on the somewhat less common disorders such as progressive supranuclear palsy, dystonia, Tourette's syndrome, and cerebellar ataxias. Postmortem neurochemical analyses of these diseases should be exciting and will improve our overall understanding of the neurochemistry of movement disorders. The second area that is moving rapidly is investigations of the role of neuropeptides and the excitatory neurotransmitter glutamate. These agents are in high concentrations in motor pathways and projection areas. Further elucidation of their functional roles in the pathogenesis and pathophysiology of basal ganglia diseases should provide new approaches and therapies for motor disorders.

Basal Ganglia↗

PubMed2004

New nomenclature for drug-induced movement disorders including tardive dyskinesia.

Psychotropic agents are increasingly being prescribed by different specialty clinicians for a variety of psychiatric illnesses, making it necessary to improve understanding of the etiology, diagnosis, and management of drug-induced movement disorders (D-IMD) across medical specialties. Early descriptions of movement disorders were based on identifiable disease states such as parkinsonism, dystonia deformans, and Huntington's chorea, which introduced complicated and often overlapping nomenclature. This has hindered communication about, description of, and diagnosis of these drug-induced disorders. Research criteria for tardive dyskinesia, a specific, purposeless, involuntary, hyperkinetic, potentially persistent D-IMD, have varied, with relatively few data-driven conclusions available to support clinical decision-making. The differences in research criteria among published reports on rates of tardive dyskinesia with atypical antipsychotics make it difficult to find meaningful comparisons and conclusions between atypicals. A novel system for classifying D-IMD according to whether they are reversible or persistent, hypokinetic or hyperkinetic, and dystonic or nondystonic is proposed. This new classification system will provide clinicians and researchers across specialties a more precise language, which will hopefully improve the diagnosis of and research criteria for D-IMD.

Adult↗

PubMed1995

Treatment of various movement disorders with botulinum A toxin injection: an experience of 900 patients.

A prospective open study of botulinum toxin A treatment for patients with various movement disorders at Siriraj Hospital, Mahidol University was analysed to evaluate its efficacy. The grand total of 900 patients comprised of a) 592 patients (65.78 per cent) with hemifacial spasm; b) 92 patients (10.22 per cent) with occupational cramp; c) 79 patients (8.78 per cent) with blepharospasm and Meige syndrome; d) 72 patients (8.00 per cent) with spasmodic torticollis; e) 19 patients (2.11 per cent) with hemidystonia and generalised dystonia; f) 11 patients (1.22 per cent) with spasmodic dysphonia; g) 10 patients (1.11 per cent) with spastic hemiparesis; and h) 25 patients (2.78 per cent) with miscellaneous group (i.e. tics, Gilles de la Tourette, facial myokimia, benign fasciculation, etc.). The results of treatment for hemifacial spasm were classified as excellent in 486 patients (82.09 per cent), moderate improvement in 60 patients (10.14 per cent), mild improvement in 39 patients (6.59 per cent) and no improvement or worse in 7 patients (1.18 per cent). There were complications of mild transient facial weakness in 50 patients (8.45 per cent) and mild ptosis in 12 patients (2.02 per cent). The effect of botulinum toxin treatment lasted 3-6 months. In occupational cramp and spasmodic torticollis the good response rate was around two-thirds of all patients, whereas, blephalospasm, spasmodic dysphonia, spastic hemiparesis and tics responsed in 79-88 per cent of the patients. Botulinum toxin A injection is thus a simple, safe, and effective out-patient treatment for patients with various kinds of movement disorders but it is a costly therapy.

Botulinum Toxins↗

PubMed2004

[Movement disorders in childhood: therapeutic update].

Abnormal movements are not uncommon in childhood. Due to the severity of the abnormal movements or to the functional disability, a medical treatment is often required; the wide range of available pharmacological molecules and the absence of therapeutic consensus highlight the limited efficacy of the medical treatment on dystonic or athetoid movements, or severe tic disorders. The recent identification of the enzymatic defect implicated in metabolic diseases led to the development of specific treatment for newly recognized disorders, with more or less interesting results (creatine ou biotine supplementation). Recent progress in functional neurosurgery opened new fields in the treatment of movement disorders. Intrathecal baclofen was proved effective in the treatment of secondary dystonia, especially in patients with cerebral palsy. Deep brain stimulation is now an established therapy for patients with a generalized dystonic syndrome. Given the successful results of pallidal stimulation in dystonia, the indication of this procedure has been discussed in other types of abnormal movements.

Anti-Dyskinesia Agents↗

PubMed2004

Parkinsonism and other movement disorders in outpatients in chronic use of cinnarizine and flunarizine.

The purpose of this study is to determine the prevalence and the patterns of movement disorders (MD) in outpatients submitted to the chronic use of cinnarizine (cz) or flunarizine (fz), and to establish the main risk factors for MD development. Over a period of 3 months, data were collected from outpatients who were chronic users of cz or fz in a municipal health institute. A total of 26 outpatients were included and all of them were submitted to a protocol that included DSM-4 diagnosis criteria for drug-induced movement disorders, parkinsonism (PK) and depression. Parkinsonism was diagnosed in 34% of the patients, PK plus akathisia, PK plus akathisia and bucco-linguo-masticatory syndrome (BLMS), isolated BLMS and dystonia were found in 4% patients each. Patients with BLMS had the highest median age and the longest average period in which they used the drugs. The affected group, when compared to the non-affected one, presented with higher rates of depression. This study demonstrates the existence of a direct relationship between the time of use of cz and fz, the age and the prevalence of PK and other MD. It also suggests that these drugs increase the incidence of depression.

Adult↗

PubMed1980

An unusual movement disorder associated with neuroleptic treatment: tardive dyskinesia?

This case report describes a chronically psychotic man presenting signs of a movement disorder exacerbated by neuroleptic treatment and repeatedly diagnosed as tardive dyskinesia. However, this movement disorder differed from classical tardive dyskinesia both in the nature of specific symptoms and in their relationship to neuroleptic treatment. Closer examination revealed evidence of neurolgical disorder preceding the earliest neuroleptic treatment. Although the nature of this disorder remains unclear, serious doubt exists whether it properly deserved a diagnosis of tardive dyskinesia, which opened the way for medicolegal dispute. The numerous ramifications of tardive dyskinesia speak for restrictive use of this diagnosis and for clear diagnostic criteria.

Adult↗

PubMedDate not supplied

Rationales, values, and DSM-IV: the case of "medication-induced movement disorders".

The DSM-IV has improved psychiatric diagnostic classification through initiating, among other things, the open disclosure of rationales for nosologic changes. It will be argued that a consideration of values is necessary in justifying nosologic changes, considerations missing from the DSM-IV rationales. In illustration of this, I examine the reasons for including the medication-induced movement disorders (MIMDs) on axis I by using a literature review, then compare the published rationales for including the MIMDs with the DSM-IV Task Force's own guidelines for including categories. Discrepancies are found between the Task Force's guidelines for including categories and the published rationales for including MIMDs. Strict adherence to the Task Force guidelines more strongly supports placing MIMDs in axis III. Discussion emphasizes the importance of value commitments in nosology development.

Akathisia, Drug-Induced↗

PubMed1999

Secondary periodic limb movement disorder and restless legs syndrome.

Periodic limb movement disorder (PLMD) and restless legs syndrome (RLS) are well-known entities from a clinical and polysomnographic point of view. PLMD and RLS are seen mostly as primary or hereditary diseases, but may occur in conjunction to other diseases such as uremia, polyneuropathy, Parkinson's disease, and deficiencies of iron and magnesium. This review will discuss the prevalence, etiology and pathophysiology of secondary PLMD and RLS.

Journal Article↗

PubMed2001

Recent advances in the understanding of tau protein and movement disorders.

Tau plays an important role in movement disorders. The accumulation of pathological tau is a major substrate of frontotemporal dementia and parkinsonism linked to chromosome 17, progressive supranuclear palsy, and corticobasal degeneration. Over the past year, several new mutations on the tau gene have been found. These mutations have been classified into three groups: (i) mutations in constitutively spliced exons; (ii) mutations in the alternatively spliced exon 10; and (iii) mutations of the exon 10 5' splice site. Some patients presenting with frontotemporal dementia and parkinsonism linked to chromosome 17 transiently respond to levodopa therapy. The significance of Pick bodies was recognized by a recent study on kindred with the Glu342Val tau mutation. In sporadic cases of progressive supranuclear palsy, the presence of the H1 haplotype was found to be a risk factor. Corticobasal degeneration shares a common genetic background with progressive supranuclear palsy. This opens the question of whether corticobasal degeneration represents a separate disorder or a spectrum of disease with progressive supranuclear palsy. However, distinguishing features are observed, and include oculomotor abnormalities, which may help to differentiate these two disorders on clinical grounds. Despite recent advances in the understanding of the tauopathies, there are still no curative therapies available. It is hoped that studies in transgenic tau animal models will lead to the development of successful treatments.

Atrophy↗

PubMed2000

Bupropion SR reduces periodic limb movements associated with arousals from sleep in depressed patients with periodic limb movement disorder.

BACKGROUND: Antidepressant-induced periodic limb movement disorder (PLMD) may limit the tolerability of some antidepressant medications and interfere with treatment response. Given the role of dopamine in PLMD and the effects of bupropion sustained-release (SR) on central dopaminergic function, we hypothesized that bupropion SR would not be associated with antidepressant-induced PLMD. METHOD: In an expanded case-series design, we compared the effects of bupropion SR, after about 10 weeks of treatment, on measures of PLMD, depression, and sleep in 5 depressed (Research Diagnostic Criteria) patients who also met criteria for having pretreatment PLMD. Depression was measured using the Beck Depression Inventory and the Hamilton Rating Scale for Depression. Patients were considered to have PLMD if polysomnographic recordings showed > 5 periodic limb movements/hour of sleep that were associated with arousals from sleep. RESULTS: Bupropion SR treatment was associated with a reduction in measures of PLMD and an improvement in depression. CONCLUSION: These results show that bupropion SR is not associated with antidepressant-induced PLMD. Rather, bupropion SR treatment reduces objective measures of PLMD in depressed patients with the disorder.

Adult↗

PubMedDate not supplied

Ethnicity and movement disorders.

This article is a review of studies involving ethnicity and spontaneous as well as iatrogenic movement disorder. We have focused on Parkinson's disease and tardive dyskinesia. Some early studies reported that African Americans had lower rates of Parkinson's disease than Caucasians, whereas more recent surveys have not found such a difference. Several studies suggested that African Americans have a higher risk of developing tardive dyskinesia than Caucasians, even when differences in neuroleptic drug use are accounted for. Asians seem to have a lower or equal risk of developing tardive dyskinesis as compared with Caucasians. We discuss the possible contribution of ethnicity to the etiology of movement disorders and the implications thereof.

Adolescent↗

PubMed2006

Movement disorders in Latin America.

The authors review some particularities of movement disorders (MDs) in the ethnically diverse population of Latin America. Although idiopathic diseases are evenly prevalent, access to treatment encounters difficulties that are worth discussing. Infectious-parasitic diseases observed throughout the continent occasionally present as MDs, and will be individually reviewed. Inherited MDs with regional foci of increased prevalence, particularly spinocerebellar ataxias, will also be considered. Whereas there is no treatment for genetic disorders, most of the other conditions are preventable or amenable to adequate treatment. Hope for better health standards for the Latin American population lies in profound social and political changes that are still to come.

Humans↗

PubMed1986

[Psychogenic movement disorders in the mental handicapped. Differential diagnosis and therapy. Case report].

The problems involved in treating psychogenic movement disorders in mentally retarded persons are pointed out. A psychoanalytic approach is doomed to failure because of the mental handicap. The authors report positive therapeutic results with a 17-year-old girl who had a severe hysterical movement disorder including sudden falls and a grotesque gait. Successful behavior therapy with this patient supports the hypothesis that conditioning was the chief factor in the maintenance of the symptoms and indicates that even severe mental retardation does not necessarily imply that there will be resistance to extinction. The individuals of greatest significance to the patient should, in the author's view, play an important part in the treatment program.

Adolescent↗

PubMed2005

Apraxia in movement disorders.

The definition of apraxia specifies that the disturbance of performed skilled movements cannot be explained by the more elemental motor disorders typical of patients with movement disorders. Generally this does not present a significant diagnostic problem when dealing with 'higher-level' praxic disturbances (e.g. ideational apraxia), but it can be a major confound in establishing the presence of limb-kinetic apraxia. Most motor disturbances characteristic of extrapyramidal disorders, particularly bradykinesia and dystonia, will compromise the ability to establish the presence of loss of dexterity and deftness that constitutes this subtype. The term 'apraxia' has also been applied to other motor disturbances, such as 'gait apraxia' and 'apraxia of eyelid opening', that perhaps are misnomers, demonstrating the lack of a coherent nomenclature in this field. Apraxia is a hallmark of corticobasal degeneration (CBD) and historically this has received the most attention among the movement disorders. Corticobasal degeneration is characterized by various forms of apraxia affecting limb function, particularly ideomotor apraxia and limb-kinetic apraxia, although buccofacial and oculomotor apraxia can be present as well. The syndrome of parkinsonism and prominent apraxia, designated the 'corticobasal syndrome' (CBS), may be caused by a variety of other central nervous system pathologies including progressive supranuclear palsy (PSP), Alzheimer's disease, dementia with Lewy bodies and frontotemporal dementias. Distinct from the CBS, PSP and Parkinson's disease can demonstrate varying degrees of apraxia on selected tests, especially in those patients with more severe cognitive dysfunction. Diseases that cause the combination of apraxia and a primary movement disorder most often involve a variety of cerebral cortical sites as well as basal ganglia structures. Clinical-pathological correlates and functional imaging studies are compromised by both this diffuse involvement and the confusion experienced in the clinical evaluation of apraxia in the face of the additional elemental movement disorders. Finally, although apraxia results in clear disability in patients with the CBS, it is not clear how milder ideomotor apraxia found on specific testing contributes to patients' overall day-to-day motor disability.

Alzheimer Disease↗

PubMed1988

Serotonin in involuntary movement disorders.

Several recent studies have emphasized that serotonergic pathways in the CNS are intimately involved in the modulation of motor behavior, and in the pathophysiology of human involuntary movement disorders. These observations are supported by recent reports demonstrating large serotonergic innervation of the striatum and substantia nigra, and a close interaction between the activity of serotonergic neurons with the dopamine system in the striatum and nigra. In the following communication we summarize evidence demonstrating defective serotonergic functions in a number of human movement disorders and discuss their management with serotonergic drugs.

Basal Ganglia↗

PubMed2001

Complex movement disorders following bilateral paramedian thalamic and bilateral cerebellar infarcts.

Complex movement disorders (CMD; including tremor, dystonias, choreoatheosis, and myoclonus) following infarcts in the posterior and posterolateral thalamic nuclei have been reported. This case of a 59-year-old man who developed CMD following bilateral paramedian and bilateral cerebellar infarcts illustrates the lack of anatomic specificity and the diverse pathophysiology which may underlie CMD.

Athetosis↗

PubMed1989

PET and movement disorders.

In this paper the use of PET for determining the patterns of disruption of both regional cerebral metabolism, and the pre- and post-synaptic dopaminergic systems, associated with movement disorders is reviewed. That the various akinetic-rigid syndromes result in distinctive PET findings is shown, making functional imaging valuable in their differential diagnosis. PET may also be useful for detecting the presence of sub-clinical disease in Huntington's disease and other inherited movement disorders.

Blood Glucose↗