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At least 631 records · Page 35Linked to original sources
PubMed1989

Movement disorders and depression due to flunarizine and cinnarizine.

Over the last few years, cases of movement disorders induced by flunarizine and cinnarizine have been increasingly reported. We describe a series of 101 patients, whose ages ranged from 37 to 84 years (mean 69.1), developing abnormal movements frequently associated with depression, secondary to treatment with either or both drugs. Symptoms closely resembled those induced by neuroleptic drugs and remitted on drug discontinuance in all but five cases after 5-22 months' follow-up. Whether or not such undesirable side effects are attributable to calcium antagonism and/or dopamine receptor blockade, long-term treatment with flunarizine or cinnarizine should be discouraged, particularly in the elderly.

Adult↗
PubMed1983

Supranuclear eye movement disorders in Fisher's syndrome of ophthalmoplegia, ataxia, and areflexia. Report of a case and literature review.

Eye movements in a patient with Fisher's syndrome were examined clinically and documented photographically when palsies were most severe and on repeated occasions during the recovery period. Two recordings of horizontal eye movements were made using the infrared reflection method. Particular attention was paid to signs indicating supranuclear eye movement disorders. We also reviewed cases in which signs suggesting brain-stem involvement were reported. Mild ptosis in the presence of severe ophthalmoplegia, preservation of Bell's phenomenon despite paralysis of voluntary upward gaze, conjugate palsies of vertical gaze, and horizontal dissociated nystagmus have been found relatively often. Convergence spasm was reported only once, however, and there were no prior reports of rebound nystagmus or vertical vestibulo-ocular reflex disorder.

Ataxia↗
PubMed1992

Periodic limb movement disorder is associated with normal motor conduction latencies when studied by central magnetic stimulation--successful use of a new technique.

This study prospectively tested the hypothesis that patients with periodic limb movement disorder (PLMD) have longer motor conduction latencies than normals. Six healthy adults, 13 patients with PLMD, and 8 patients with long-term multiple sclerosis (MS) had recordings of motor conduction latencies during wake and sleep. MS subjects were included only to show that we could detect prolongation of central conduction; nonMS subjects were used to test the hypothesis. Subjects had no other medical or sleep problems. A novel magnetic stimulator, the Cadwell MES-10, was discharged over the vertex and the C7 cervical spine. It triggered compound muscle action potentials that were recorded in the abductor digiti minimi in the hand. The conduction latencies were the total conduction time (TCT), measured vertex to hand, and the peripheral conduction time (PCT), measured C7 to hand. The difference was the central conduction time (CCT). Only TCT could be obtained during sleep. Supporting the use of TCT as an indirect measure of central conduction was that, in all waking subjects, TCT correlated with CCT (r = 0.91, p = 0.001) but not with PCT. Reliabilities during wake and sleep were 0.95 or higher for TCT and PCT measurements. Waking CCT was greater in MS subjects (13.77 milliseconds) than those without MS (9.21 milliseconds), p = 0.001. Sleeping TCT was much less impressive in distinguishing MS subjects [27.08 milliseconds in nonrapid eye movement (NREM) sleep; 28.64 milliseconds in rapid eye movement (REM) sleep] from nonMS subjects (24.45 milliseconds in NREM; 24.84 milliseconds for REM), p = 0.07 for NREM and p = 0.04 for REM.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1978

Ventricular fluid homovanillic acid and 5-hydroxyindoleacetic acid concentrations in patients with movement disorders.

Ventricular fluid concentrations of homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA), the respective metabolites of dopamine and serotonin, were measured in 57 patients undergoing thalamotomy for relief of movement disorders. The diseases included were Parkinson disease, dystonia, cerebral palsy, multiple sclerosis, and posttraumatic or posthypoxic encephalopathy. Untreated parkinsonian patients had the lowest mean HVA level (119 ng per milliliter). Patients with multiple sclerosis or with posttraumatic or posthypoxic encephalopathy with both intellectual impairment and bilateral motor involvement had lower mean HVA levels (197 and 177 ng per milliliter, respectively) than cerebral palsy patients with bilateral motor disease (233 ng per milliliter), dystonia patients (246 ng per milliliter), or multiple sclerosis patients with normal intellect (376 ng per milliliter). The data suggest that diffuse cerebral disease may lead to diminished dopaminergic activity. Ventricular fluid 5-HIAA levels were similar in all groups of patients. Chronic cerebellar stimulation markedly increased ventricular fluid HVA and 5-HIAA levels, indicating that cerebellar stimulation affected cerebral dopaminergic and serotonergic systems.

Adult↗
PubMedDate not supplied

[Movement disorders in David Copperfield].

Charles Dickens' novels are a source of vivid neurological descriptions. Besides Pickwickian syndrome, many other neurological descriptions can be found in Dickens' novels. David Copperfield contains several characters with movement disorders including generalized dystonia (Mr. Uriah Heep), restless legs syndrome (the waiter), cervical dystonia (Mr. Sharp) and spasmodic dysphonia (Mr. Creakle). These neurological descriptions an probably based on the observation of actual patients.

Humans↗
PubMed1990

Movement disorders in mitochondrial myopathies. A study of nine cases with two autopsy studies.

Of 85 consecutive patients with mitochondrial myopathy, 29 had clinically significant central nervous system involvement. Nine of these had movement disorders that included dystonia, chorea, parkinsonism, and myoclonus. Autopsy studies of one patient with ataxia, dementia, and parkinsonism followed by dystonia showed the features of olivopontocerebellar atrophy with additional degenerative changes in the basal ganglia. Postmortem in a further case with myoclonus, deafness, muscle weakness, retinopathy, and ataxia showed symmetrical mineralisation of the striatopallidodentatal system.

Adult↗
PubMed1988

Primary CNS lymphoma presenting as a choreic movement disorder followed by segmental dystonia.

Clinical presentation of primary CNS lymphoma with an extrapyramidal movement disorder has not been recorded. A 66-year-old woman presented with chorea involving her left arm and subsequently developed right-sided segmental dystonia with prominent hemifacial dystonic spasms, milder torticollis and dystonia of the right arm. Investigations revealed primary CNS lymphoma with extensive involvement of the right-sided basal ganglia as well as lesions confined to the head of the left caudate nucleus and the corpus callosum. Chorea of her left arm subsided with progressing disease while remission of right-sided segmental dystonia was observed following radiotherapy of the brain. This patient's findings and a review of the literature suggest a possible relation between cranio-cervical dystonia and pathology affecting the head of the caudate nucleus.

Aged↗
PubMed2006

Respiratory retraining therapy and management of laryngopharyngeal reflux in the treatment of patients with cough and paradoxical vocal fold movement disorder.

OBJECTIVES: We describe the outcome of patients with cough and paradoxical vocal fold movement disorder (PVFMD) treated with respiratory retraining therapy and management of laryngopharyngeal reflux (LPR). METHODS: Twenty patients with the complaint of cough were given a diagnosis of PVFMD and treated with proton pump inhibitors for a minimum of 6 months followed by 3 to 5 sessions of respiratory retraining therapy. Pulmonary function testing (PFT) and subjective rating of cough and reflux (reflux symptom index; RSI) were performed. Also, PFT and rating of cough were performed on a group of 10 healthy volunteers with no complaint of cough. RESULTS: The study group comprised 13 women and 7 men. The baseline cough rating and ratio of forced inspiratory volume at 0.5 second to forced inspiratory vital capacity (FIV0.5/FIVC) on PFT were significantly worse in the treatment group than in the control group. After therapy, 20 patients (100%) experienced improvement in cough, 19 patients (95%) experienced improvement on PFT, and 17 patients (85%) experienced improvement in the RSI score. The differences were statistically significant. CONCLUSIONS: Respiratory retraining therapy combined with management of LPR is an effective treatment for patients with cough and PVFMD when a single-modality treatment is not sufficient.

Adolescent↗
PubMed2003

[Botulinum toxin--interventional neuropediatrics in spastic movement disorders in childhood].

Botulinumtoxin A (BTX) is widely used for the treatment of spastic movement disorders in childhood. Safety and local efficacy of BTX are well documented by the experience of many users and verified by several clinical trials. Indications for the use of BTX in children include facilitation of care, better tolerance of ortheses as well as the quantitative and qualitative improvement of motor abilities. This article differentiates clinical indications for which the use of BTX has been proven from those in which effectiveness is only suspected or is yet unclear.

Botulinum Toxins, Type A↗
PubMed2003

The KickStrip: a novel testing device for periodic limb movement disorder.

STUDY OBJECTIVES: In light of the ongoing debate over the clinical significance of periodic limb movement disorder (PLMD) and its monitoring in overnight sleep studies, we introduce a novel, portable, low-cost device for PLMD testing. The KickStrip is a disposable device, which includes a movement sensor, a central processing unit with real-time software, and a display. In the present study, the KickStrip final score (Kscore) is validated against the traditional periodic limb movement index (PLMI) based on overnight recordings in the sleep laboratory. DEISGN: Patients underwent full polysomnographic recordings concomitantly with the use of the KickStrip for a single night. SETTING: Sleep Disorders Unit at Loewenstein Rehabilitation Hospital and Sleep Medicine Center at Rambam Medical Center, Israel. PATIENTS: Eighty-two patients referred for overnight sleep recordings due to sleep disturbance of any kind. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: The Kscores were collected and the PLMI computed for each leg separately. Pearson correlations between Kscores and PLMI ranged between r = 0.83 to r = 0.88 (p < 0.001). Sensitivity and specificity values of the Kscores for increasing PLMD thresholds showed sensitivity ranging from 50% to 100% and specificity ranging from 83% to 100%. Receiver operating characteristic curves showed area-under-the-curve values ranging from 82% to 92%. Bland-Altman plot showed high agreement between the methods. CONCLUSIONS: Comparisons between the Kscores and the traditional PLMI show increased accuracy with severity level and excellent agreement. The KickStrip is a valuable tool for PLMD testing for both clinical and research purposes.

Adolescent↗
PubMed1985

Progabide in the treatment of hyperkinetic extrapyramidal movement disorders.

The ability of the selective GABA-receptor agonist, progabide, to suppress abnormal involuntary movements was evaluated in a preliminary open pilot study. 17 patients, 10 males and 7 females, aged 10-78 years, with hyperkinetic movement disorders were included in the study. Daily doses of progabide ranged from 900 to 3600 mg (median 2400 mg) corresponding to 14-45 mg/kg (median 45 mg/kg), while the duration of treatment varied from 2 to 52 weeks. Improvement, with a reduction of involuntary movements exceeding 25%, occurred in two of four patients with Gilles de la Tourette's syndrome, and in two of three patients with postanoxic intention myoclonus, while no consistent beneficial effects were registered in ten patients with Huntington's chorea, postanoxic choreoathetosis, torsion dystonia, tardive dyskinesia, action tremor, essential myoclonus, or oro-branchio-respiratory myoclonus.

Adolescent↗
PubMed2002

Mutations of voltage-gated sodium channels in movement disorders and epilepsy.

Spontaneous and induced mutations of neuronal Na+ channels in human patients and mutant mice result in a broad range of neurological-disease. Epilepsy, a disorder of neuronal hyperexcitability, has been associated with delayed inactivation of SCN2A in mice, and with altered kinetics of SCN1A in human patients. Movement disorders including tremor, ataxia, dystonia and paralysis have been observed in mice with mutations of SCN8A. Electrophysiological recordings from neurons isolated from mice with mutations in individual channels reveal the contributions of each channel to in vivo firing patterns. In addition to monogenic disease, Na+ channel mutations are likely to contribute to polygenic disease susceptibility and to normal variation in neuronal function. Advances in molecular methods coupled with genomic sequences from the Human Genome Project will permit identification of many new patient mutations and generation of animal models to dissect their physiological and cellular consequences.

Amino Acid Sequence↗
PubMed2006

Evolution of basal ganglia surgery for movement disorders.

In 1942, it was thought that basal ganglia surgery would cause permanent unconsciousness and significant impairment of motor control. By 1947, when human stereotactic surgery was introduced, the first target was the globus pallidus in a patient with chorea. What happened during those 5 years to set the stage for stereotactic surgery? During the last half of the 19th century, it was first noted that motor disorders were often accompanied by atrophy of various parts of the basal ganglia, and when histopathology became part of necropsy, that relationship between movement disorders and the basal ganglia was strengthened. The impairment of fine motor control was noted in experiments that involved lesioning the basal ganglia, which led to the conclusion that disease of the basal ganglia might cause motor impairment. Finally, in 1939, Russel Meyers took the bold move of surgically resecting the head of the caudate nucleus at craniotomy in a patient with Parkinson's disease, demonstrating that Dandy was wrong in the view that the basal ganglia were the center of consciousness, and that symptoms and motor control might be improved by caudate lesions without motor impairment. He reported his first patient in a meeting in 1940, which was published in 1942, and was encouraged to investigate basal ganglia surgery further. Although results were encouraging, the mortality rate was prohibitive. Since the introduction of pallidoansotomy in 1947, basal ganglia surgery has become both safe and effective and has been expanded and refined.

Basal Ganglia Diseases↗
PubMed2002

Movement disorders in 28 HIV-infected patients.

From 1986 to 1999, 2460 HIV-positive inpatients were seen in our Hospital. Neurological abnormalities were detected in 1053 (42.8%) patients. In this group, 28 (2.7%) had involuntary movements, 14 (50%) with secondary parkinsonism, six (21.4%) with hemichorea/hemiballismus, four (14.2%) with myoclonus, two (7.2%) with painful legs and moving toes, one (3.6%) with hemidystonia and one (3.6%) with Holmes' tremor. The HIV itself (12 patients), toxoplasmosis of the midbrain (1) and metoclopramide-related symptoms (1) were the most probable causes for the parkinsonism. All patients with hemichorea/hemiballismus were men and in all of them toxoplasmosis of the basal ganglia, mostly on the right side, was the cause of the involuntary movements. Generalized myoclonus was seen in two patients and they were due to toxoplasmosis and HIV-encephalopathy respectively; two others presented with spinal myoclonus. The two patients with painful legs and moving toes had an axonal neuropathy. The patient with hemidystonia suffered from toxoplasmosis in the basal ganglia and the patient with Holmes' tremor had co-infection with tuberculosis and toxoplasmosis affecting the midbrain and cerebellum. We conclude that HIV-infected patients can present almost any movement disorder. They can be related to opportunistic infections, medications, mass lesions and possibly to a direct or indirect effect of the HIV itself.

AIDS-Related Opportunistic Infections↗
PubMed2004

Psychogenic movement disorders in children.

A common problem in neurology is the existence of disorders that present with neurologic symptoms but do not have an identifiable neurologic basis. These disorders are often thought to have a psychologic basis. Abnormal movements are among the most frequent symptoms in psychogenic neurologic disorders. Although these disorders have not been studied extensively in children, clinical experience in our busy pediatric movement disorders clinic and many case reports support their existence in this age group. Elements of history, physical examination, and therapeutic intervention must be combined to construct a clear diagnosis of a psychogenic movement disorder. This article reviews the diagnosis and treatment of these disorders and includes two illustrative cases. Review of the current literature reveals a need for prospective trials to provide a solid foundation for better diagnosis and treatment of these disorders.

Adolescent↗
PubMed2001

Exogenous melatonin in periodic limb movement disorder: an open clinical trial and a hypothesis.

STUDY OBJECTIVES: The etiology of Periodic Limb Movement Disorder (PLMD) as well as the precise role of melatonin in human physiology remains poorly understood. Inspired by a single case observation we performed the presented study in order to obtain first evidence for the hypothesis that exogenous melatonin would decrease PLM's and thereby improves symptoms of PLMD patients. DESIGN: N/A. SETTING: N/A. PATIENTS/PARTICIPANTS: Nine patients with first time diagnosis of PLMD without RLS were treated over a six-week period with 3 mg melatonin, taken between 10 and 11 p.m. INTERVENTIONS: N/A. RESULTS: Melatonin improved well-being in 7 of the 9 patients. Polysomnography, performed prior and at the end of melatonin treatment, demonstrated a significant reduction of investigated movement parameters, such as PLMs, PLM index, PLMs with arousals and PLM-arousal index. Actigraphy, measured over 14 nights prior and during the last 14 days of melatonin treatment, showed a significant reduction in movement rate and minutes with movements during Time in Bed. CONCLUSIONS: The temporal distribution of PLMs, as well as the coupling of PLMs with the phase position of circadian temperature curve, suggest an involvement of the circadian timing system in the pathophysiology of PLMD. Locomotor activity in animals clearly exhibits a circadian pattern and can be strongly influenced by exogenous melatonin. Results suggest a chronobiotic effect of exogenous melatonin in PLMD. More specifically, we hypothesize that the mode of action of melatonin in the presented PLMD patients might have been an increase of output-amplitude of the circadian timing system, thereby enhancing the circadian rhythmicity of locomotor activity with a reduction of sleep motor activity.

Adult↗