PubMed Health⌕ Search

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 343 records · Page 19Linked to original sources
PubMedDate not supplied

[Effect of intracerebral administration of somatostatin and neurotensin on posture and movement disorders].

Experiments were performed on male Wistar rats to study posture-movement disorders after intracerebroventricular, intraamygdalar, intrahippocampal and intranigral (pars reticulata) injections of somatostatin and neurotensin. Development of movement disturbances characterized by changes in the posture-movement syndrome was observed after somatostatin and neurotensin administration. Manifestation of movement disorders, their duration and the posture-movement syndrome structure depended on the structure to which neuropeptides were injected as well as on the neuropeptides themselves. Prolonged changes characterized by appearance of the so called "Sphinx" posture in animals developed after somatostatin intranigral administration. The obtained data permit concluding that somatostatin and neurotensin may have pathogenic significance in cataleptic syndrome development.

Animals↗
PubMed2003

Stereotactic neurosurgery for movement disorders.

Stereotactic neurosurgery for the treatment of movement disorders focuses primarily on the treatment of Parkinson's disease (PD), essential tremor (ET), and dystonia. The surgical targets in use are the subthalamic nucleus (STN) and the globus pallidus internus (GPi) for PD, GPi for dystonia, and ventralis intermedius (Vim) nucleus of the thalamus for ET. Following target selection, procedures include the generation of lesions or the placement of deep brain stimulating electrodes in the selected target. Additionally, transplantation has been used in the treatment of PD. The indications, outcomes, and risks of the various procedures are reviewed.

Dystonia↗
PubMed2004

Rehabilitation of movement disorders.

UNLABELLED: This self-directed learning module highlights several movement disorders. These include dystonia, chorea, tremors, and myoclonus. A description of the clinical presentation and associated disease processes is presented. Although the discussion on treatment focuses on pharmacologic intervention, surgical options are presented when appropriate. Other movement disorders (ie, parkinsonism) are discussed elsewhere in the Study Guide. OVERALL ARTICLE OBJECTIVES: (a) To define the various symptoms and etiologies of dystonia; (b) to define chorea and its treatment; (c) to define tremors, including associated neurologic disorders, plus pharmacologic and potential surgical interventions; and (d) to describe the symptoms, classification, and treatment of primary and secondary myoclonus.

Dyskinesias↗
PubMed1994

Prevalence of movement disorders in elderly community residents.

We studied movement disorders (MD) in community residents of Saskatchewan aged > or = 65 years. A representative sample of 70 individuals had detailed neurological evaluation. Those who had definite and possible MD at first examination had a second neurological assessment by a senior neurologist. The most prevalent MD was essential tremor (ET) (14%) followed by Parkinson's disease (PD) (3%). The marked difference in prevalence ratios for PD and ET are attributed to: (a) higher incidence of ET in the general population; (b) a greater possibility that most, if not all, ET cases would reside in the community whereas a sizable proportion of elderly PD cases may be institutionalized, and (c) shortened survival in PD but a normal life expectancy in ET.

Aged↗
PubMed2004

Anti-basal ganglia antibodies: a possible diagnostic utility in idiopathic movement disorders?

BACKGROUND: The spectrum of post-streptococcal brain disorders includes chorea, tics, and dystonia. The proposed mediators of disease are anti-basal ganglia (neuronal) antibodies (ABGA). AIM: To evaluate ABGA as a potential diagnostic marker in a cohort of UK post-streptococcal movement disorders. METHODS: Forty UK children presenting with movement disorders associated with streptococcal infection were recruited. ABGA was measured using ELISA and Western immunoblotting. To determine ABGA specificity and sensitivity, children with neurological diseases (n = 100), children with uncomplicated streptococcal infection (n = 40), and children with autoimmune disease (n = 50) were enrolled as controls. RESULTS: The mean ELISA result was increased in the post-streptococcal movement disorder group compared to all controls and derived a sensitivity of 82.4% and specificity of 79%. The Western immunoblotting method to detect ABGA derived a sensitivity and specificity of 92.5% and 94.7% respectively. There was common binding to basal ganglia antigens of 40, 45, and 60 kDa. Immunofluorescence localised the antibody binding to basal ganglia neurones. CONCLUSION: ABGA appears to be a potentially useful diagnostic marker in post-streptococcal neurological disorders. Western immunoblotting appears to be the preferred method due to good sensitivity and specificity and the ability to test several samples at once.

Adolescent↗
PubMed1990

The effect of nocturnal physiological sleep on various movement disorders.

Thirty-one subjects affected by different movement disorders underwent polygraphic and videotape monitoring during nocturnal sleep, to assess movement patterns during the night. It was possible to distinguish two categories of disorders according to their pattern of movements. In the largest group (Meige's syndrome, blepharospasm, amyotrophic choreoacanthocytosis, Tourette syndrome, tonic foot, hemiballism) abnormal movements were still present during sleep, but decreased in frequency and amplitude in all stages. The second group presented three syndromes (nocturnal paroxysmal dystonia, nocturnal myoclonus, restless legs syndrome), in which light non-rapid-eye-movement sleep induced a strong activation of abnormal movements, whereas rapid-eye-movement sleep suppressed them.

Adult↗
PubMed2001

Autonomic dysfunction in movement disorders.

Dysfunction of the autonomic nervous system is an under-recognised but important aspect of the aetiological and clinical manifestation of primary degenerative dysautonomias such as multiple system atrophy (MSA) and Parkinson's disease (PD). Although the clinical presentation of dysautonomia in these two disorders may overlap, yet pathological and in vivo imaging studies suggest considerable differences. Functional imaging studies suggest that selective cardiac sympathetic denervation may occur early in PD but not in other parkinsonian syndromes. The clinical implication of this apparently disease specific peripheral dysautonomia is unknown and would be the subject of much interest in future years. Dysautonomia in degenerative disorders also affect respiration, genitourinary function and sleep. Sleep related disorders such as rapid eye movement behaviour disorder and urinary voiding dysfunction appear to precede the development of PD related symptoms while patients with sporadic ataxia have been shown to progress to develop MSA. Dysautonomia has also been recognised in other movement disorders, examples being the combination of dystonia and complex regional pain syndrome with elevated HLA-DR13 and late onset Huntington's disease presenting with dominant parkinsonism and minimal chorea. These studies have helped progress in various diagnostic and management parameters in relation to autonomic dysfunction and movement disorders.

Autonomic Nervous System Diseases↗
PubMed1977

Neurophysiology of movement disorders.

The relation of the cortex, cerebellum, and basal ganglia and their participation in movement disorders is presented. Studies have shown that lesions to the cortex will produce contralateral paralysis while damage to the basal ganglia or cerebellum will result in movement abnormalities. These data provide support for the view that subcortical but not cortical structures initiate the control movement activity. It would appear that the basal ganglia and cerebellum receive signals from the auditory, visual, and somatosensory cortex integrate this information, and relay signals back to the motor cortex, which in turn sends out efferent fibers to the motor neurons of the spinal cord. The electronic and neurophysiological basis of the somatosensory evoked responses (SER) test following peripheral nerve stimulation and sensory recording in human cortex is given. Control values of SER peak to peak latency waveforms from 66 normal volunteers show the practicality of this test. Preliminary results using SER in patients are discussed from clinical case reports. The subjects had mild to marked movement disorders secondary to Parkinson's disease, vascular occlusion, multiple sclerosis, and spino-cerebellar degeneration. The potential of the SER as a clinical and experimental tool in evaluating movement abnormalities and other neuropathological conditions is presented.

Adult↗
PubMed2004

Respiratory retraining of refractory cough and laryngopharyngeal reflux in patients with paradoxical vocal fold movement disorder.

OBJECTIVES/HYPOTHESIS: The objective was to describe a case series of patients with refractory cough and paradoxical vocal fold movement disorder treated with respiratory retraining therapy. STUDY DESIGN: Retrospective review of a case series in a tertiary medical care center. METHODS: Five patients with laryngopharyngeal reflux were identified with refractory cough and paradoxical fold movement disorder on transnasal fiberoptic laryngoscopy by a greater than 50% reduction in airway during inspiration. The were four women and one man (age range, 42-67 y). All patients had normal forced vital capacity and forced expiratory flow but decreased ratio of forced inspiratory volume at 0.5 seconds (FIV(0.5)) to forced inspiratory vital capacity (FIVC) before starting therapy. All patients were treated with more than 6 months of twice-daily proton pump inhibitor therapy with improvement in reflux symptoms but persistent and severe daytime cough. They were subsequently treated with respiratory retraining therapy. Patients were asked to rate subjectively the severity of cough at the onset and conclusion of therapy. All patients underwent pulmonary function testing before and after therapy. Long-term follow-up ranged from 5 to 17 months. RESULTS: Patients received two to seven sessions of respiratory retraining therapy. The mean severity score changed from 9.2 before therapy to 1.3 after therapy. All patients subjectively described an improvement in the severity of their cough. Transnasal flexible laryngoscopy demonstrated improvement in paradoxical vocal fold movement, and pulmonary function testing showed improvement in the FIV(0.5)/FIVC ratio. CONCLUSION: Patients with laryngopharyngeal reflux and refractory cough in the absence of pulmonary disease should be evaluated for paradoxical vocal fold movement disorder. Respiratory retraining therapy may represent an effective therapy for cough in the absence of relief from standard management of laryngopharyngeal reflux.

Adult↗
PubMed2001

Clinical characteristics and topography of lesions in movement disorders due to thalamic lesions.

OBJECTIVE: To determine which thalamic subnuclei are involved in symptomatic unilateral movement disorders due to localized thalamic infarction, and the clinical characteristics of these abnormal movements. METHODS: The authors studied 22 patients with thalamic infarcts for their clinical presentation and the topography of the lesions, using three-dimensional T1-weighted MRI sequencing and stereotaxic analysis of the lesions. RESULTS: Patients were divided into four groups: 1) absence of abnormal involuntary movements (AIM) (nine patients); 2) isolated dystonic posture (two patients); 3) myoclonic dystonia (five patients); and 4) tremor or myoclonus (six patients). In patients with AIM, thalamic lesions were contralateral to the abnormal movements, involving the thalamogeniculate territory, centered on the ventral intermediate (Vim) and ventral caudal (Vc) nuclei. No significant difference in the volumes or center of mass of the lesions was found between patients with tremor and myoclonus and patients with dystonia, although the central nucleus and the internal part of the Vim nucleus were more consistently damaged in dystonic patients. CONCLUSION: Movement disorders related to thalamic lesions included: 1) myoclonic dystonia with predominating myoclonus and "thalamic" hand associating dystonic posture and slow, pseudo-athetoid movements, both related to lesions in the Vim and Vc nuclei of the thalamus; and 2) postural and action tremor, also related to lesions in the Vim, similar to tremor associated with midbrain lesions, as a result of abnormal functioning of the cerebello-thalamic pathways.

Aged↗
PubMed1997

Drug-induced movement disorders.

Parkinsonism, tremor, chorea-ballismus, dystonia, tardive dyskinesia, myoclonus, tics and akathisia can be induced by many drugs. The drugs that are most frequently implicated in movement disorders are antipsychotics, calcium antagonists, orthopramides and substituted benzamides (e.g. metoclopramide, sulpiride, clebopride, domperidone), CNS stimulants, antidepressants, anticonvulsants, antiparkinsonian drugs and lithium. It is possible for a single drug to induce 2 or more types of movement disorders in the same patient. Movement disorders are not always reversible after drug withdrawal.

Akathisia, Drug-Induced↗
PubMed2004

Antibasal ganglia antibodies and their relevance to movement disorders.

PURPOSE OF REVIEW: Recently, autoaggressive immunological responses were included among the causative agents of basal ganglia dysfunction. Autoaggressive immune-mediated illnesses secondary to group A beta-haemolytic streptococcal infections present with motor and psychiatric symptoms, due to basal ganglia involvement. These disorders have been associated with serum antineuronal antibodies, relatively specific to human basal ganglia tissue. This review summarizes the most recent studies concerning antibasal ganglia antibodies, focusing on the associated phenotypes and the hypotheses concerning their pathogenicity. RECENT FINDINGS: The spectrum of post-streptococcal neuropsychiatric disorders associated with antibasal ganglia antibodies seems broader than previously recognized. Other than chorea, tics and obsessive-compulsive disorder, which constituted the bulk of previously described disorders associated with antibasal ganglia antibodies, post-streptococcal neuropsychiatric disturbances include a wider range of motor and behavioural abnormalities, in keeping with the multifunctional role of the basal ganglia. An encephalitis lethargica-like illness following streptococcal infection was reported, and unusual adult-onset movement disorders associated with antibasal ganglia antibodies were documented. Moreover, investigators provided preliminary evidence for a pathogenic role of autoantibodies in Sydenham's chorea, the prototypic post-streptococcal neuropsychiatric disorder. SUMMARY: Antibasal ganglia antibodies are relatively specific in identifying post-streptococcal neuropsychiatric disorders, which constitute a wider spectrum of movement disorders than previously recognized. Although their sensitivity in diagnosing Sydenham's chorea seems excellent, it is not yet possible to extrapolate this sensitivity to all the recently identified post-streptococcal neuropsychiatric disorders. The antigens targeted by these autoantibodies and their pathogenic importance are currently under investigation. Preliminary evidence suggests that antibasal ganglia antibodies may be pathogenic.

Autoantibodies↗
PubMed1999

[Movement disorders: dystonias which are apparently psychosomatic. Torsion dystonias].

In neuropediatric clinical practice, disorders of movement include a wide diversity of conditions, amongst which the dystonias are uncommon in our practice, although they have to be considered amongst the possible diagnoses in some cases. The great variety of clinical symptoms and age of onset together with the nonspecific, erratic clinical course make diagnosis difficult. Some clinical pictures of genuine torsion disorders may be confused with hysterical conversion disorders, somatizations or Munchausen's syndrome. Diagnosis requires clinical knowledge of both conditions--torsion dystonia as opposed to hysteria or a conversion reaction--and considerable ability and experience. Genetics and molecular studies have helped to clarify some difficult diagnostic problems and facilitated both diagnosis and treatment. In a diagnostic video session we show the case of a seven year old boy who initially presented with a dystonic disorder. There was some doubt as to the aetiology and different types of treatment were given by different specialists. The true diagnosis was reached after molecular genetic studies.

Antiparkinson Agents↗
PubMed1996

Genetics of movement disorders.

Trinucleotide repeat expansions or unstable mutations are the cause of a growing number of hereditary movement disorders, especially inherited ataxias. Diagnostic practice as well as disease classifications have altered accordingly. Genes responsible for "Parkinsonian plus' syndromes and episodic movement disorders have also been recently mapped.

Chromosome Aberrations↗
PubMed2004

Practice parameters for the dopaminergic treatment of restless legs syndrome and periodic limb movement disorder.

Dopaminergic agents, particularly dopamine agonists, have been used with increasing frequency in the treatment of restless legs syndrome and periodic limb movement disorder. These evidence-based practice parameters are complementary to the Practice Parameters for the Treatment of Restless Legs Syndrome and Periodic Limb Movement Disorder, published in 1999. These practice parameters were developed by the Standards of Practice Committee and reviewed and approved by the Board of Directors of the American Academy of Sleep Medicine. Recommendations are based on the accompanying comprehensive review of the medical literature regarding the dopaminergic treatment of restless legs syndrome (RLS) and periodic limb movement disorder (PLMD), which was developed by a task force commissioned by the American Academy of Sleep Medicine. The following recommendations serve as a guide to the appropriate use of dopaminergic agents in the treatment of RLS and PLMD. Levodopa with decarboxylase inhibitor, and the dopaminergic agonists pergolide, pramipexole, and ropinirole are effective in the treatment of RLS and PLMD. Other dopamine agonists (talipexole, cabergoline, piribidel, and alpha-dihydroergocryptine) and the dopaminergic agents amantadine and selegiline may be effective in the treatment of RLS and PLMD, but the level of effectiveness of these medications is not currently established. Lastly, no specific recommendations can be made regarding dopaminergic treatment of children or pregnant women with RLS or PLMD.

Dopamine Agonists↗
PubMed1993

Reliability and applicability of movement disorder rating scales in the elderly.

Geriatric research clinicians were readily trained to use three scales initially developed for rating neuroleptic-induced movement disorders in mixed-age patients: the Abnormal Involuntary Movements Scale (AIMS), Simpson Extra Pyramidal Side Effect Scale (SEPSE), and Barnes Akathisia Scale (BAS). Interrater reliability, calculated by intraclass correlation coefficients, ranged from 0.79 to 0.93. Of elderly psychiatric inpatients tested, 97% were able to complete the examination, despite significant psychiatric, cognitive, and physical disabilities. AIMS, SEPSE, and BAS are reliable instruments for assessment of movement disorders in the elderly, representing an important first step in standardized evaluation of dyskinesia, parkinsonism, and akathisia in elderly psychiatric populations.

Aged↗
PubMed1997

Mood Disorders Secondary to Demyelinating and Movement Disorders.

Mood disorders are recognized in several neurologic diseases. This chapter reviews three specific disorders, Parkinson's disease, Huntington's disease, and multiple sclerosis. The demographics of mood disorders and unique clinical characteristics are discussed for each disease. The possible causes for neurobiologically based affective symptoms are explored.

Journal Article↗