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Results for “MOVEMENT DISORDERS”

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At least 19 recordsLinked to original sources
PubMed2003

State of the art review: molecular diagnosis of inherited movement disorders. Movement Disorders Society task force on molecular diagnosis.

This review is designed to provide practical help for the clinical neurologist to make appropriate use of the possibilities of molecular diagnosis of inherited movement disorders. Huntington's disease, Parkinson's disease and parkinsonian syndromes, ataxias, Wilson disease, essential tremor, dystonias, and other genetic diseases associated with a variety of movement disorders are considered separately.

Chromosome Mapping↗
PubMed1999

Pediatric movement disorders.

Movement disorders in children encompass disorders of motor control--both hyperkinetic (excessive movement) and hypokinetic (decreased movement). This article focuses on the hyperkinetic movement disorders, particularly tremor, Wilson's disease, dystonia, tics and Tourette syndrome, chorea, myoclonus, neuroleptic-induced movement disorders, and psychogenic movement disorders. Phenomenology of the disorders as well as clinical presentation, basic pathophysiology, genetics, and treatment are discussed.

Antipsychotic Agents↗
PubMed1992

Trauma and movement disorders.

Movement disorders have been linked to trauma; however, these cases are uncommon and best substantiated if the movement disorder occurs in close temporal association with the trauma, occurs in context of other clinical signs of neurologic damage, and if evidence of CNS lesions on neuroimaging scans is evident. The pathophysiology of movement disorders relates to basal ganglia dysfunction, and traumatic lesions of peripheral nervous system structures or cortical regions could theoretically alter basal ganglia function indirectly and influence movement disorders. Parkinson's disease, the prototype of movement disorders, does not appear to be caused by trauma.

Brain↗
PubMed1999

What is new in movement disorders?

Movement disorders is a term applied for a heterogeneous group of diseases and syndromes sharing deficits of voluntary motor function or movement patterns. In clinical practice, the term movement disorders is usually employed to designate those syndromes and diseases that are linked to a pathology or dysfunction of cortico-basal ganglia circuits. The last years have witnessed a rapid expansion in our understanding of the etiological and pathophysiological factors underlying movement disorders such as Parkinson's disease or dystonia. The discovery of new gene mutations is bound to give rise to new insights into the molecular pathogenesis of movement disorders related to neurodegenerative processes. It is already becoming apparent that pathological protein aggregation may be a common link in the neuronal degeneration underlying such diverse entities as spinocerebellar ataxia, idiopathic torsion dystonia and Parkinson's disease. So far, these new findings have not been translated into new forms of symptomatic or preventive therapies. Nevertheless, symptomatic treatment of movement disorders, as evident in the field of Parkinson's disease, is one of the most rewarding and innovative areas of neurological therapy.

Antiparkinson Agents↗
PubMed2003

Oral pharmacotherapy of childhood movement disorders.

Movement disorders, a common problem in children with neurologic impairment, are receiving increasing clinical attention. The differences in movement disorders between adults and children are striking; presentation is frequently insidious and may be characterized by mild hypotonia. The clinical manifestations of extrapyramidal disorders are profoundly influenced by the age of onset. The conditions reviewed in this article are expressed clinically by the occurrence of abnormalities of movement and posture, often in association with disturbances of muscle tone. This article reviews empiric drug use and recommendations for childhood movement disorders.

Administration, Oral↗
PubMed2003

Movement disorders.

Movement disorders are commonly encountered in clinical practice. The diagnosis of movement disorders relies on a focused history and neurologic examination. Diagnostic steps include (1) identification of the phenomenology of the movements (eg, tremor); (2) characterization of appropriate clinical syndromes; and (3) differential diagnosis of specific disease entities. Accurate diagnosis is essential because symptomatic treatment exists for most movement disorders.

Adult↗
PubMed2002

The feasibility of statistical parametric mapping for the analysis of positron emission tomography studies using 11C-2-beta-carbomethoxy-3-beta-(4-fluorophenyl)-tropane in patients with movement disorders.

Movement disorders, including Parkinson's disease and parkinsonian syndromes, e.g. progressive supranuclear palsy, multiple system atrophy, and Lewy body dementia, may be difficult to differentiate among each other at an early stage, since they may share similar clinical features and response to dopaminergic drugs. As new tracers for imaging the dopamine transporters become available, the use of positron emission tomography (PET) for the differential diagnosis of movement disorders is gaining clinical relevance. Visual interpretation is generally used for PET image analysis. However, the use of some form of less subjective analysis is desirable in order to detect subtle changes that may be difficult to identify by visual interpretation and to achieve an operator independent analysis. To this end this study was aimed at assessing the feasibility of using statistical parametric mapping (SPM) for the clinical evaluation of single PET scans performed with 2-beta-carbomethoxy-3-beta-(4-fluorophenyl)-tropane ( C-beta-CIT-FE). Eleven healthy volunteers and five patients with movement disorders (Parkinson's disease, essential tremor, PSP and Lewy body dementia) were included in this study. Each subject underwent a PET study after i.v. injection of C-beta-CIT-FE. The PET images of C-beta-CIT-FE distribution acquired between 60 and 90 min were spatially fitted into the Talairach and Tournoux space. A template of normal C-beta-CIT-FE distribution was derived from studies in the 11 normal control subjects. Different patterns of reduction of the uptake of the tracer were detected in the basal ganglia of the five patients, in relation to each pathological condition. The patterns of distribution were all consistent with the severity and type of disease. The results of this study demonstrate the feasibility of differentiating among different states of dopaminergic impairment, due to Parkinson's disease and parkinsonian syndromes, by using PET scans with C-beta-CIT-FE and by using the SPM procedure for analysis of the data.

Adult↗
PubMed1990

Treatment of hyperkinetic movement disorders.

Movement disorders are subdivided based on a variety of criteria. One useful and popular approach to movement disorders, based on clinical phenomenology, categorizes these disorders into two groups, those displaying a poverty of movement (akinesia) and those displaying excessive movement (hyperkinesia). This article discusses diagnosis and treatment of the latter. By necessity, certain hyperkinesias such as hyperexplexia, akathisia, and restless leg syndrome are omitted or only briefly discussed. The major hyperkinesias, dystonia, tremor, tics, chorea (including tardive dyskinesia and ballism), and myoclonus are reviewed and a guide to practical management emphasizing symptomatic treatment is presented.

Benzodiazepines↗
PubMed1999

Movement disorders.

Movement disorders cause difficulty with ambulation. Hypokinetic disorders produce a slow gait with short strides and impairment of balance. The hyperkinetic disorders are also marked by an impairment of balance, caused by rapid or uncontrollable movements of the limbs or trunk, that interferes with the normal rhythm of walking. The gaits of different movement disorders help the clinician to classify them. Appropriate diagnosis and treatment of the disorder may significantly improve ambulation and quality of life.

Gait↗
PubMed2004

Deep brain stimulation for movement disorders.

Movement disorders remain the primary indication for the use of intracranial neurostimulation techniques. This review will discuss the history of this technology as well as the mechanisms of action, current clinical indications, and future prospects for the treatment of movement disorders.

Brain↗
PubMed2003

Genetics of pediatric movement disorders.

Movement disorders in children often have a genetic basis. An explosion of genetic information in the past decade has led to the discovery of genetic defects in many forms of ataxia, parkinsonism, dystonia, tremor, and spastic paraparesis. This review focuses on genetically defined, early-onset diseases characterized primarily or exclusively by movement disorders. Particular emphasis is placed on disorders for which clinical or research testing is available.

Child↗
PubMed2002

[Clinical neurophysiology of movement disorders].

Movement disorders are physiologically studied based on three principles; 1. relation between movements and brain activities, 2. excitability and inhibitory mechanisms of motor cortices, and 3. sensorimotor integration. Regardless of voluntary or involuntary movements, the study on how the movement in question is related to brain activities provides an important information as to its pathophysiology. This can be studied by jerk-locked averaging of electroencephalogram or magnetoencephalogram in case of involuntary movements and movement-related cortical potentials for voluntary movements, change of cortical rhythmic activities in relation to movement (event-related desynchronization or synchronization), cortico-muscular coupling(coherence), and neuroimaging techniques such as PET, SPECT and fMRI. Excitability and inhibitory mechanisms of motor cortices can be studied by applying transcranial magnetic stimulation. Positive and negative myoclonus of cortical origin is related to abnormal hyperexcitability of the positive and negative components, respectively, of the primary motor cortex (M1). Focal dystonia is associated with impairment of inhibitory mechanisms in M1. The simplest form of abnormal sensorimotor integration is cortical reflex myoclonus. In the choice reaction time task, contingent negative variation is reduced in a task-specific way in focal dystonia. Effect of movement on somatosensory processing (gating) is abnormal immediately before the movement onset in focal dystonia, again in a task-specific way. Daily activities like gait can be studied by SPECT which does not require fixation of the subject's head during the task performance.

Brain↗
PubMed1998

Models of basal ganglia function and pathophysiology of movement disorders.

Movement disorders are categorized as hypokinetic (Parkinson's disease) or hyperkinetic (Huntington's disease, hemiballism, or dystonia). Neuroscience research over the last several years, using data obtained in animal models for these disorders and data from patients undergoing stereotactic surgery, has greatly advanced the knowledge of the pathophysiologic basis of these diseases. This article offers a summary and critique of current models of the pathophysiology underlying hypokinetic and hyperkinetic diseases and a discussion of the implications of these models for neurosurgical procedures as treatment for these disorders.

Basal Ganglia↗
PubMed2000

Neuro-ophthalmology of movement disorders.

Movement disorders are a diverse group of neurologic disorders that share in common the frequent development of clinical abnormalities in ocular motility or visual perception. This article reviews the recent literature pertaining to the neuro-ophthalmologic advances in the basal ganglia disorders (Parkinson disease, progressive supranuclear palsy, corticobasal degeneration, multiple system atrophy, and Huntington disease), the spinocerebellar ataxias and episodic ataxias, amyotrophic lateral sclerosis, benign essential blepharospasm, hemifacial spasm, and Tourette syndrome.

Humans↗
PubMed2001

Neurosurgery for movement disorders.

Movement disorders have been treated neurosurgically since the 1930s. Current diagnoses for neurosurgical interventions are Parkinson's disease, essential tremor, multiple sclerosis, and some dystonic disorders such as idiopathic torsions dystonia. By using stereotactic image-guided techniques, targets can be chosen to treat different symptoms: the ventrointermediate nucleus of thalamus for tremor; the internal globus pallidus for dyskinesia, dystonia, rigidity, akinesia, and tremor; and the subthalamic nucleus for all cardinal symptoms in advanced Parkinson's disease, including drug-induced hyperkinesia (secondary to reduced drugs). The surgical approaches can be divided into three main groups: destructive (e.g., lesional surgery), reversible and adjustable (e.g., permanent electro-inhibition/stimulation), and reconstructive (e.g., fetal nerve cell transplantation). Reconstructive procedures, which are not discussed here, are still in the early developmental phase. All the methods have advantages and disadvantages; therefore, it is important that the right target and technique be chosen for each patient.

Brain↗
PubMed1991

Movement disorders--limb movement and the basal ganglia.

The primary concern of this article is to review experimental methods that may lead to a better understanding of the functional role of the basal ganglia in the control of movement. Two models of basal ganglia impairment are considered: Parkinson's disease and Huntington's disease. The review focuses primarily on akinesia and bradykinesia because they are key abnormalities of basal ganglia dysfunction. In general, through electromyography and kinematic analysis of movement, it may be possible to characterize specific movement disorders. Specifically, if damage sustained by the central nervous system is traced to a certain structure, it may provide insight on the extent of involvement and functional role of that structure in the control of movement. Much of the data reviewed suggests that the basal ganglia may play a specific role in the initiation and regulation of force control.

Basal Ganglia↗
PubMed2006

Drug Insight: from disturbed motility to disordered movement--a review of the clinical benefits and medicolegal risks of metoclopramide.

Metoclopramide, the only drug approved by the FDA for treatment of diabetic gastroparesis, but used off-label for a variety of other gastrointestinal indications, has many potentially troublesome adverse neurologic effects, particularly movement disorders. In this article, we comprehensively review the indications and side effects of metoclopramide, and describe some common pitfalls and strategies to minimize the medicolegal risks to the prescribing physician. Metoclopramide accounts for nearly a third of all drug-induced movement disorders, a common reason for a malpractice suit. The entire spectrum of drug-induced movement disorders, ranging from subtle to life-threatening, can ensue from its use; akathisia and dystonia are generally seen early in the course of metoclopramide-induced movement disorders, whereas tardive dyskinesia and parkinsonism seem to be more prevalent in chronic users. Female sex, age and diabetes are the major risk factors for metoclopramide-induced movement disorders. It is therefore incumbent on gastroenterologists and other prescribing physicians to become familiar with the adverse neurologic effects associated with the use of metoclopramide, and to take appropriate preventive and defensive measures.

Dopamine Antagonists↗