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PubMed1993

[Clinical diagnosis of movement disorders--evoked potentials].

As a clinical diagnostic approach, the evoked potential has been used to differentiate movement disorders, especially myoclonic movements, Giant somatosensory evoked potentials (SEPs) and long-loop reflex to electrical stimulation of the peripheral nerve are commonly employed in the evaluation of patients with myoclonus. Recently, abnormality in a specific component of SEP frontal N30 has been reported in focal dystonia. Jerk locked back averaging has been applied to cortical reflex myoclonus, minipolymyoclonus, cortical tremor, simple tics, chorea-acanthocytosis, Huntington's chorea, etc. Silent period locked averaging is also used for asterixis. With these new electrophysiological techniques, evaluation of functional mechanisms in movement disorders may be expected, with fruitful results.

Diagnosis, Differential↗

PubMed2005

Fragile X-associated tremor/ataxia syndrome and movements disorders.

PURPOSE OF REVIEW: Fragile X-associated tremor/ataxia syndrome (FXTAS) is a multiple-system neurologic disorder caused by expansion of 55-200 CGG repeats in the FMR1 (fragile site mental retardation 1) gene. The presence of both hyperkinetic and hypokinetic movement disorders such as ataxia, tremor, and parkinsonism are clinical features of FXTAS. The purpose of this review is to summarize the description of movement disorders associated with FXTAS and to discuss recent observations regarding the relationship between abnormal expansion in the FMR1 gene and development of neurodegenerative disorders. RECENT FINDINGS: The clinical expression of FXTAS occasionally resembles the phenotypes of other idiopathic neurodegenerative disorders. However, the unique pathological feature - appearance of the intranuclear inclusions in the neurons and astrocytes, is discriminatory from those in other neurodegenerative disorders. Several studies found no association between the FMR1 gene premutation and development of other neurodegenerative disorders with similar movement disorders to FXTAS. However, a premutation expansion in the FMR1 gene may be a frequent genetic cause of late-onset sporadic ataxia with magnetic-resonance-image abnormality. SUMMARY: FXTAS exhibits various movement-disorder phenotypes. However, the FMR1 gene premutation is unlikely to be a common genetic cause of neurodegenerative disorders with tremor or ataxia. Patients with sporadic late-onset ataxia associated with magnetic-resonance-image abnormality should be considered for testing for a CGG-repeat expansion in the FMR1 gene.

Ataxia↗

PubMed2006

Movement disorders induced by gastrointestinal drugs: two paediatric cases.

A number of frequently prescribed gastrointestinal drugs can cause movement disorders in children, as well as in adults. In our centre for paediatric neurology, we saw a 3-year-old girl with abnormal movements mostly of the legs with an inner restlessness (akathisia) while using cisapride. Another patient, a 17-year-old male, developed a hemiballism (a fierce movement of one arm and shoulder with a hurling appearance) while using ranitidine for gastric distress. In both children, the movement disorder disappeared after discontinuing the drug. The pathophysiological mechanisms of these drug-induced movement disorders might be related to the central function of histamine in the developing brain. These cases illustrate the importance of being alert for possible drug-induced events early in the process of diagnosing abnormal movement disorders.

Adolescent↗

PubMed1993

Movement disorders.

This article focuses on the current knowledge about movement disorders associated with alcohol and drug abuse. Chronic alcohol use can produce a wide spectrum of movement disorders including tremor, withdrawal parkinsonism and dyskinesias, cerebellar ataxia, and asterixis. MPTP, a neurotoxin first reported to cause parkinsonism in a group of drug abusers, has provided important insights into the pathogenesis of Parkinson's disease. There is a growing body of literature providing evidence that dyskinesias such as tics and dystonia may be precipitated or exacerbated by cocaine. Amphetamines have been implicated in the production of stereotypies and exacerbation of tics.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed1993

Hereditary motor-sensory neuropathy and movement disorders.

To explore the relationship between hereditary motor and sensory neuropathy (HMSN) and movement disorders, we examined 7 patients with HMSN referred to our Movement Disorders Clinic and surveyed members of the Charcot-Marie-Tooth association. The following movement disorders were observed in the index patients: postural tremor in 6, rest tremor in 3, and Parkinsonism and dystonia in 2. Tremor, present in 40% of the 201 patients who responded to the survey, was first noted at a mean age of 36 years, and mostly involved the hands. Family history of tremor was more frequent in the tremor group (P < 0.005), which also had a significantly worse writing score than the nontremor group (P < 0.001). The overlap in clinical features between HMSN-associated tremor and essential tremor (ET), the high frequency of family history of tremor, and the lack of a relationship between the severity of tremor and of peripheral neuropathy suggest that the tremor in HMSN is pathogenically related to ET.

Aged↗

PubMed1999

Epilepsy and paroxysmal movement disorders in families: evidence for shared mechanisms.

The epilepsies have been regarded as clinically distinct from the paroxysmal movement disorders. Recently, a variety of ion channel defects have been identified as the biological basis of certain familial epilepsies and paroxysmal movement disorders. We studied two families with the co-occurrence of epilepsy, movement disorders and migraine. Information was obtained on 147 individuals in the two families. In family WF, there was a co-occurrence of epilepsy (benign infantile convulsions, idiopathic generalized epilepsy), episodic ataxia (with cerebellar atrophy and without myokymia) and common migraine. In family CL, epilepsy (febrile seizures, febrile seizures plus), kinesigenic paroxysmal dyskinesia and migraine (including hemiplegic migraine) were observed in various combinations over 3 generations. The observations in these two families, together with review of the literature, suggest that the co-occurrence of epilepsy (particularly benign infantile convulsions), paroxysmal movement disorders and migraine is not due to chance. Thus, these distinct clinical phenomena could have a shared biological basis and ion channel defects are an attractive possibility.

Adolescent↗

PubMed1997

Movement disorders in adult hydrocephalus.

In a prospective series of symptomatic adult hydrocephalus characterized by gait disturbance, cognitive impairment, and/or urinary incontinence, 88 of 118 patients (75%) had additional akinetic, tremulous, hypertonic, or hyperkinetic movement disorders. Their prevalence was highest in patients with idiopathic normal pressure hydrocephalus (NPH) of the elderly (56/65 patients, 86%), and they were less frequent in patients with secondary NPH (10/15, 66%), with nonhydrodynamic atrophic/other hydrocephalus (20/33, 61%), and with obstructive hydrocephalus/aqueductal stenosis (2/5, 40%). Akinetic symptoms were found in 73 of 118 patients (62%), and the most frequent movement disorder was upper extremity bradykinesia (55%). Akinetic, tremulous, hypertonic, and hyperkinetic movement disorders were exclusively secondary to causes not related to hydrocephalus in 24 of 118 patients (20%). The proportion of patients with movement disorders not attributable to only such causes was highest in the idiopathic NPH group (44/65, 68%). Thirteen of 118 patients (11%) presented with a parkinsonian syndrome. There was evidence for coexistent Parkinson's disease in four of these patients. Parkinsonism was found to be secondary to NPH in five patients and was found improved after shunting. Akinetic symptoms in patients with NPH generally responded favorably to CSF diversion, which was evident in 80% of a subset of this group. Various other movement disorders did not show definite improvement. The high prevalence of bradykinesia and other akinetic symptoms in NPH and the beneficial effect of shunting on such symptoms suggest that NPH may cause a more generalized disorder of motor function.

Adolescent↗

PubMed1996

Delayed-onset progressive movement disorders after static brain lesions.

We studied 53 patients (64% females) with static brain lesions who developed progressive movement disorders. Of these, 50 (94%) had dystonia, 17 (32%) tremor, eight (15%) parkinsonism, seven (13%) myoclonus, and three (6%) chorea. The precipitating insults included perinatal hypoxia/ischemia in 22 (42%), stroke in 12 (23%), head injury in eight (15%), encephalitis in eight (15%), and carbon monoxide poisoning, kernicterus, and radiation necrosis in one patient (2%) each. Among the 30 patients with initial insult occurring at age 2 years or younger (Infant group), distribution of dystonia at follow-up was focal in three (10%), segmental in eight (27%), unilateral in 10 (33%), and generalized in nine (30%). The mean latency between the original injury and onset of movement disorder was 25.5 +/- 16.7 years. Among the nine patients who developed dystonia after an insult occurring between ages 6 and 17 (Childhood group), the distribution of dystonia at follow-up was segmental in two (33%) and unilateral in seven (78%); the mean latency of dystonia onset was 4.9 +/- 7.8 years. Of the 14 patients in the Adult group (injury at age 25 or older), 11 developed dystonia, two developed parkinsonism, and one had carbon monoxide encephalopathy and parkinsonism. The distribution of dystonia in the 11 patients at follow-up was segmental in three (27%) and unilateral in eight (73%). The mean latency of movement disorder onset in the 14 patients of the Adult group was 2.5 +/- 4.9 years. No individuals in the Childhood or Adult groups became left-hand dominant; by comparison, nine of the 30 individuals in the Infant group became left-handed. In conclusion, brain injury at a young age is associated with a longer latency to onset of subsequent movement disorder, a greater tendency to development of generalized dystonia, and a greater probability of altered handedness. These tendencies may result from differences in age-related neuroplasticity.

Adult↗

PubMed2002

Long-term efficacy of botulinum toxin A in treatment of various movement disorders over a 10-year period.

Although botulinum toxin A (BTX) has been licensed in Canada for treatment of various movement disorders since 1990, few clinical studies regarding its long-term efficacy and side effects have been reported. We conducted a retrospective analysis of 235 patients who received BTX from our movement disorders clinic over a 10-year period (January 1990 to December 1999). A total of 2,616 treatment cycles (multiple injections) were administered to 235 patients with cervical dystonia (CD), hemifacial spasm (HS), blepharospasm (BP), and other movement disorders. Substantial benefit at 5 years was seen in most patients (90% in BP, 88% in HS, 63% in CD, 100% in jaw closing and lower limb dystonia, and 56% in writer's cramp). Benefit was maintained for up to 10 years in CD, HS, and BP data, with a 75.8% benefit reported. Twenty-eight percent of patients discontinued treatment during the follow-up period due to a variety of reasons. Of these, 9.1% of patients developed primary resistance, and 7.5% of patients secondary resistance. Adverse effects, mostly minor, developed in 27% of patients at any one time, occurring over 4.5% of treatment cycles. These were most frequently reported in blepharospasm (22 of 36 patients in 40 cycles), followed by hemifacial spasm (21 of 70 patients in 46 cycles), and cervical dystonia (17 of 106 in 28 cycles). Only 1.3% of patients discontinued therapy due intolerable adverse effects. The results show that BTX is a safe and effective treatment of various types of movement disorders, and most side effects are well tolerated. Discontinuation for any reason was also low after 5 years. Efficacy was maintained after long periods of treatment with high degree of patient satisfaction.

Adult↗

PubMed1998

Osmotic demyelination syndrome with two-phase movement disorders: case report.

Osmotic demyelination syndrome (ODS) is characterized by regions of demyelination throughout the brain, which are most prominent in the pons. This demyelinating disease is associated with electrolyte disturbances and typically occurs in patients who are alcoholic or malnourished. Movement disorders are not frequently recognized in patients with ODS. This report describes a 22-year-old woman with ODS after correction of profound hyponatremia. The main neurologic symptom was two-phase movement disorder. First, she had acute onset dystonia, then the movement disorder transformed to generalized rigidity and tremors in the delayed second phase. Magnetic resonance imaging in the first phase revealed demyelinating lesions in the central pons, bilateral thalami and basal ganglia. In the second phase, the previous myelinolysis had been partially resolved. The clinical course of the two-phase movement disorder did not correlate with the resolving feature of neuroradiologic findings. During the second-phase movement disorder, the patient had a good response to propranolol and trihexyphenidyl.

Adult↗

PubMed1999

[Value of functional imaging in Parkinson's disease and related movement disorders].

Modalities for imaging morphology do not contribute significantly to the differential diagnosis of movement disorders. In contrast, functional imaging as PET or SPECT can differentiate among Parkinson's disease (PD), vascular or toxic Parkinsonism and movement disorders within multi system degeneration. Especially the decreased DOPA uptake--detected by 18F-DOPA or 123I-beta CIT--within the striate with accentuation in the posterior putamen is typical for PD, where initially D2-receptor activity--imaged by 11C-raclopride or 123I-iodobenzamide--is increased. In contrast to this typical pattern dopaminergic terminals as well as D2-receptors are diffusely reduced in multi system degeneration, where often energy metabolism is additionally disturbed. In Parkinson syndrome of vascular origin focal disturbances of pre- and postsynaptic dopaminergic sites and energy metabolism are found, movement disorders after intoxication are accompanied by selective loss of dopaminergic neurons (MPTP) or by widespread neuronal damage in the basal ganglia as well as in the cortex (Cyanide, solvents). Functional studies additionally permit the follow-up of disease progression, by which also the efficacy of therapeutic strategies can be assessed.

Diagnosis, Differential↗

PubMed2001

Restless legs syndrome (RLS) and periodic limb movement disorder (PLMD): acute placebo-controlled sleep laboratory studies with clonazepam.

Restless legs syndrome (RLS) - a common sensorimotor disorder - and periodic limb movement disorder (PLMD) are currently treated with substances of four classes: dopaminergic agents, which are considered the drugs of choice, benzodiazepines, opioids and anticonvulsants. As their effects on sleep variables differ considerably, the aim of the present placebo-controlled sleep laboratory study was to measure the acute effects of 1 mg clonazepam on objective and subjective sleep and awakening quality in ten RLS and 16 PLMD patients, utilizing polysomnography (PSG) and psychometry. Descriptive data analysis demonstrated at the confirmatory level concerning three target variables that - as compared with placebo - clonazepam significantly improved objective sleep efficiency and subjective sleep quality in both patient groups, but failed to reduce the index PLM/h of sleep. At the descriptive level, in PLMD clonazepam improved PLM during time in bed, REM and wakefulness and showed more significant changes in various sleep and awakening measures than in RLS patients, though there were no significant inter-group differences. In conclusion, in both PLMD and RLS clonazepam exhibited acute therapeutic efficacy regarding insomnia, which is quite different from the mode of action of dopamine agonists.

Adult↗

PubMed1996

Thalamic stimulation-evoked sensations in chronic pain patients and in nonpain (movement disorder) patients.

1. Little is known about the effect of central and peripheral nervous system injury on the processing of somatosensory information at the thalamic level in humans. The role of the human thalamic ventrocaudal nucleus (Vc) in nociception is not well understood because reports of nociceptive neuronal responses and stimulation-evoked pain are rare. In this study, we have characterized effects of microstimulation in the tactile region of Vc. Specifically, we investigated the incidence of painful sensations evoked by thalamic microstimulation in patients with and without chronic pain. 2. Data were obtained during stereotactic thalamic procedures for relief of pain or motor disorders. Patients were divided into three groups, those with 1) central poststroke pain (PSP, n = 13); 2) nonstroke pain (NSP, n = 23); and 3) movement disorders (controls, n = 24). Most (15 of 23) of the NSP patients had peripheral nerve damage. Tungsten microelectrodes were used to record neuronal responses in the thalamus and to deliver stimuli. Localization of tactile Vc was determined according to stereotactic coordinates and neuronal responses to innocuous somatic stimuli. At selected sites, microstimulation (1-s trains, 300 Hz, 0.1-0.2 ms pulses, < 100 microA) was performed and the patient was requested to describe the quality of the sensation and its peripheral location (projected field, PF). 3. Microstimulation in tactile Vc commonly evoked paresthesia-type sensations. Threshold stimulation never evoked pain in the NSP patients and evoked pain at only 2% of Vc sites in the movement disorder patients. In these latter 2 groups of patients, stimulation at > 98% of Vc sites evoked paresthesia. By contrast, in the PSP patients, 28% of Vc sites stimulated evoked painful sensations at threshold. Suprathreshold stimuli evoked painful sensations at 46% of Vc sites in the PSP patients but at only 8% of Vc sites in NSP patients and 12% of Vc sites in the movement disorder patients. 4. The thresholds to evoke paresthesia in the NSP and movement disorder patients were significantly lower than the thresholds in the PSP patients. However, stimulation thresholds to elicit pain were similar in all patient groups. 5. All patients were capable of differentiating stimulation-evoked paresthesia from pain. Stimulation-evoked painful sensations in the PSP patients were often described as burning and sometimes as "sharp," "shocking," or "unpleasant." By contrast, the quality of pain evoked in the other patient groups was typically described as unpleasant or shocking. Pain could be evoked at sites throughout tactile Vc, although most sites were located in the ventral 2/3 of the nucleus. 6. In the movement disorder patients, the location of the projected sensation usually corresponded to the location of the receptive fields of the tactile neurons recorded at the same site. By contrast, in both groups of pain patients there was a high incidence of mismatches between the projected and receptive fields. 7. These results suggest that the effective thalamic output from Vc to the cortex is affected by somatosensory deafferentation in pain patients. In addition, in the PSP patients there are also changes in the thalamocortical processing of noxious information. The increased incidence of thalamic-evoked pain in PSP patients may be due to 1) loss of low-threshold mechanoreceptive thalamic neurons such that nociceptive neuronal output is now prominent, 2) reduced tonic inhibition of thalamic or cortical nociceptive neurons, and/or 3) unmasking or strengthening of nociceptive pathways.

Cerebrovascular Disorders↗

PubMed2002

Control of post-stroke movement disorders using chronic motor cortex stimulation.

The effects of motor cortex (MC) stimulation on post-stroke movement disorders were analyzed in 50 patients. These individuals either underwent MC stimulation primarily for the purpose of controlling their post-stroke involuntary movements (n = 8) or underwent MC stimulation for the purpose of controlling their post-stroke central pain (n = 42). In the latter patients, the effects of MC stimulation on co-existent involuntary or voluntary movement disorders were analyzed retrospectively. Good control of involuntary movements was observed in 2 of 3 patients with hemichoreo-athetosis, 2 of 2 patients with distal resting or action tremor, and 1 of 3 patients with proximal postural tremor. Subjective improvements in motor performance were reported by 8 patients who had mild motor weakness, and the effects appeared to be attributable to attenuation of rigidity. We consider that these findings justify further clinical studies on MC stimulation for the control of post-stroke movement disorders.

Electric Stimulation Therapy↗

PubMed1994

Movement disorders in patients treated with long-acting injectable antipsychotic drugs.

The frequencies of antipsychotic drug-induced movement disorders documented by physicians and identified by researchers using standardized clinical rating scales were compared, as were the frequencies associated with use of fluphenazine decanoate and haloperidol decanoate. All outpatients at a Veterans Affairs medical center who were being maintained with intramuscular injections of fluphenazine decanoate or haloperidol decanoate and were in otherwise good health were studied. The patients were assessed by a pharmacist using the Abnormal Involuntary Movement Scale to evaluate the presence and severity of tardive dyskinesia (TD) and the Simpson-Angus EPS Rating Scale to evaluate the presence and severity of extrapyramidal symptoms (EPS). The patients' medical records for the previous two years were reviewed to determine whether a movement disorder had been documented, whether the patient's informed consent for antipsychotic drug use had been obtained, and to collect other data about the patient and his or her drug therapy. A total of 50 patients were evaluated. A neurologic examination by a physician had been documented in the chart within six months before clinical testing for 36 patients; abnormal movements had been found in 8 patients. Twenty-one subjects met the study criteria for probable TD or EPS or both. Of these patients, only six had been identified within the previous six months as having a movement disorder. Two patients with medical-record documentation of a movement disorder were not so identified by their test scores. Informed consent had been obtained from only 10 patients. Patients receiving haloperidol decanoate had a higher frequency of EPS but were also receiving higher drug dosages than patients given fluphenazine decanoate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2002

Absence of movement disorders after surgical resection of glioma invading the right striatum.

OBJECT: Despite the high frequency of striatal lesions, the rate of movement disorders reported in the literature is lower than expected (< 10%). To maximize the extent of resection in low-grade gliomas invading the right striatum, the authors performed a striatal resection in a series of 14 patients, observed the lack of movement disorders following these procedures, and discuss herein the mechanisms likely to explain these findings. METHODS: Fourteen patients harboring a low-grade glioma that was infiltrating the right nondominant striatum, and in whom the results of neurological examination were normal, underwent surgery in which intraoperative electrical mapping was used, allowing the identification of pyramidal pathways. The striatum was resected in all procedures, and corticospinal tracts were systematically detected and preserved. Ten patients presented with a transient postoperative motor deficit, and nine with a loss of interest and affect. These symptoms all resolved within 3 months, except for one case of persistent hemiparesis. No postoperative movement disorder was noted, even transitorily. All resections were categorized as either total or subtotal on control magnetic resonance images. CONCLUSIONS: These findings show that the nondominant striatum can be removed in cases of glioma invasion without inducing even transitory movement disorders. This phenomenon could be explained by the combined resection of the two classes of striatal neurons, an associated pallidal and thalamocortical resection, or a compensatory recruitment of parallel networks. Thus, these results may allow the surgeon to maximize the extent of removal of low-grade gliomas involving basal ganglia. Striatal resection may induce transient hemiparesis and "athymhormic syndrome," however, necessitating that the patient be clearly informed before surgery.

Adult↗

PubMed1969

Effect of tetrabenazine on extrapyramidal movement disorders.

Thirty patients with various extrapyramidal movement disorders were treated for prolonged periods with 75 to 225 mg. daily of tetrabenazine. In patients with choreiform and hemiballistic motor activity the involuntary movements were diminished or abolished. In patients with cerebellar or Parkinsonian tremor the tremor was aggravated in moderately severe cases, but was uninfluenced in severe cases. In all cases the dyskinesia returned when- the drug was stopped.Side-effects were inconsiderable and disappeared on reducing the dose slightly. Hence the drug may be an important alternative to neurosurgical treatment of hyperkinesias and especially suitable for severely disabled patients.

Chorea↗

PubMed1992

Genetic considerations in movement disorders.

Certain genetic aspects of the movement disorders, including parkinsonism, dystonia, ataxia, chorea, tics, and others, are reviewed. Clinical features, diagnostic techniques, and laboratory tests of newly recognized inherited syndromes are discussed. Progress in linkage analysis in several disorders is also presented.

Brain↗