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PubMed2000

Use of selective thalamotomy for various kinds of movement disorder, based on basic studies.

Methods of selective thalamotomy with microrecording for several kinds of movement disorder are described. Precise thalamotomy (Vim, VO or Vim+VO) depends on the understanding of the functional organization of the human thalamus on the one hand, and the patient's specific feature of movement disorders on the other. To realize selective thalamotomy, microrecording and a computerized planning system are essential. Thus, a properly selected thalamotomy for movement disorders is quite useful.

Antiparkinson Agents↗

PubMed1996

Dyskinetic movement disorder among adults with mental retardation: phenomenology and co-occurrence with stereotypy.

We screened for the occurrence of dyskinetic and stereotypic movement disorders using item-independent screening protocols to determine whether these forms of movement disorder can be distinguished among adults with mental retardation. Stereotypies and dyskinesias were reliably distinguished in terms of topography. Tardive dyskinesia occurred in 18.2% of a cohort of individuals receiving chronic neuroleptic treatment. Stereotypic movement disorder was associated with increased dyskinesia scores and increased prevalence of tardive dyskinesia. Increased dyskinesia scores were also found for subjects exhibiting stereotypy who had been free of neuroleptic treatment for 3 years. Results indicate that dyskinesia and stereotypy are discriminable movement disorders and provide preliminary support for the hypothesis that they may be related by common mechanisms.

Adolescent↗

PubMed2006

Referrals for movement disorder surgery: under-representation of females and reasons for refusal.

OBJECTIVE: Referral of movement disorder patients for deep brain stimulation surgery was examined to determine whether referred patients were representative of gender proportions in our population, and reasons why patients do not proceed to surgery. METHODS: Demographic information on referrals to the surgical program was retrospectively reviewed from our database and from a detailed chart review. RESULTS: Although almost equal numbers of movement disorder patients are male and female, of the 91 patients referred for surgery, only 31% were female. Sixty-one percent of referred patients did not undergo surgery. Of these, the majority were denied for medical reasons, including cognitive decline (21%), psychiatric concerns (5%) and neurological reasons (42%). CONCLUSIONS: Almost one-third of patients referred for movement disorder surgery were denied for medical reasons. This underscores the importance of evaluation of all potential patients by a multidisiplinary team to fully assess suitablity for stereotactic surgery. Interestingly, women were under-represented in those referred. In order that all appropriate patients have the opportunity to consider surgery, education of both physicians and patients, and different strategies to approach females regarding surgery may allow more patients to benefit from this treatment.

Deep Brain Stimulation↗

PubMed1997

Long-term effects of tetrabenazine in hyperkinetic movement disorders.

Over the past 15 years we have treated 526 patients with severe hyperkinetic movement disorders with tetrabenazine (TBZ), a monoamine-depleting and a dopamine-receptor-blocking drug. We report here the results in 400 patients with adequate follow-up. The response was rated on a scale of 1 to 5 (1 = marked improvement, 4 = no response, 5 = worsening) and was assessed initially and at the last clinic visit. The average duration of TBZ treatment was 28.9 months (+/- 31.1; range, 0.25 to 180 months). The global response rating of 1 (marked improvement) was recorded in 89.2% of 93 patients with tardive stereotypy, 83.3% of 12 with myoclonus, 82.8% of 29 with Huntington's disease, 80.5% of 82 with tardive dystonia, 79.3% of 29 with other movement disorders, 62.9% of 108 with idiopathic dystonia, and in 57.4% of 47 with Tourette's syndrome. The most common side effects included drowsiness (36.5%), parkinsonism (28.5%), depression (15.0%), insomnia (11.0%), nervousness or anxiety (10.3%), and akathisia (9.5%). The side effects were controlled with reduction in the dosage. TBZ is an effective and safe drug for the treatment of a variety of hyperkinetic movement disorders. In contrast to typical neuroleptics, TBZ has not been demonstrated to cause tardive dyskinesia.

Adult↗

PubMed2003

[Movement disorders and botulinum toxin in neurology].

Botulinum toxin has been a useful treatment in many movement disorders and more recently in other non-neurological motor dysfunctions for more than 15 years. Here, we review the various indications in neurology, mainly in the field of movement disorders. From 1973 to 2002, we searched the Medline database on this topic. We selected the most useful and relevant papers, with a special interest in dystonia. We summarized the results in the main indications (spasmodic torticollis, bleparospasm, hemifacial spasm) and in other manifestations such as writer's cramp, oromandibular dystonia, tremor, tics and myoclonus. We discuss the data of literature and compare them with the experience of the French movement disorders groups.

Anti-Dyskinesia Agents↗

PubMed1997

Hyperkinetic movement disorders during and after acute stroke: the Lausanne Stroke Registry.

BACKGROUND AND OBJECTIVE: To study consecutive patients with acute or delayed hyperkinetic movement disorders in the Lausanne Stroke Registry. METHODS: We have identified 29 patients with acute or delayed movement disorders among 2500 patients who had their first-ever acute stroke in the Lausanne Stroke Registry. SETTING: Department of Neurology, Lausanne University Hospital. RESULTS: Our patients presented with hemichorea-hemiballism (11 patients), hemidystonia (5 patients), stereotypias (2 patients), jerky dystonic unsteady hand (3 patients), asterixis (2 patients), initial limb-shaking (2 patients), bilateral tremor (1 patients), bilateral jaw myoclonus (1 patient), hemiakathisia (1 patient) and dysarthria-dyskinetic hand (1 patient). On neuroimaging a lesion was found in 25 of the 29 cases in the territory of the middle cerebral artery (7 deep, 2 superficial and 2 complete), the posterior cerebral artery (11 patients), both middle and posterior cerebral arteries (2 patients) or the anterior cerebral artery (1 patient). The jerky dystonic unsteady hand syndrome was associated with a specific lesion, an infarct in the territory of the posterior choroidal artery. Presumed small-vessel disease was the commonest cause of stroke (15 patients). Only 3 patients had persistent movements (> 6 months). CONCLUSION: Hyperkinetic movement disorders are uncommon in acute stroke (1%), the commonest types being hemichorea-hemiballism and hemidystonia. These movement disorders are associated with stroke involving the basal ganglia and adjacent white matter in the territory of the middle or the posterior cerebral artery. The jerky dystonic unsteady hand syndrome is specifically associated with a small infarct in the territory of the posterior choroidal artery. The abnormal movements usually regress spontaneously.

Adult↗

PubMed1994

Neuropharmacological evaluation of movement disorders that are adverse reactions to specific foods.

Three cases are reported of patients who had episodic movement disorders triggered by foods or components of the diet. In the first patient, the movement consisted of shaking the head from side to side that was triggered by milk and a number of other foods. In the second patient, the movement consisted of a repeated shrugging of the shoulders that was triggered by egg and coffee. In the third, the movement consisted of rhythmic contractions of the arms and legs that were triggered by aspartame. The first patient agreed to participate in a study in which she drank 250 ml of skim milk, an amount sufficient to trigger head shaking, after pretreatment with drugs known to alter neurotransmission across beta-adrenergic, dopaminergic, GABAergic or purinergic synapses. At the doses used, propranolol and diazepam had no effect on the milk evoked movement disorder. Levodopa (plus carbidopa) blocked the reaction to milk. Haloperidol, salbutamol and theophylline by themselves triggered a reaction similar to that evoked by milk. These observations suggest that, in susceptible individuals, foods can trigger movement disorders through an action on dopamine and other neurotransmitter pathways in the brain. A videotape of the reactions of the first two patients is available.

Adult↗

PubMed1989

Movement disorder of premature infants with severe bronchopulmonary dysplasia: a new syndrome.

A previously unrecognized, striking movement disorder has been observed in 10 premature infants with severe bronchopulmonary dysplasia. Chronic hypoxemia, hypercarbia, bronchospasm, and inadequate nutrition were present in all. The movement disorder developed from approximately the third postnatal month. The dominant movements involve the limbs, neck, trunk, and oral-buccal-lingual structures. The limb movements were most prominent distally and consisted of rapid, random, jerky movements (similar to chorea) and "restless" movements (similar to akathisia). Similar movements of the neck and face were observed; tongue movements had a "darting" quality. The oral-buccal-lingual movements were similar to the dyskinesia of older patients. Movements were exacerbated during episodes of respiratory failure and attenuated during sleep. All infants exhibited feeding disorders, largely due to tongue movements. In 3 infants treated with clonazepam, there was striking improvement in motor function, including feeding. The natural history was partial or complete resolution or a static course. Thus, of the 7 surviving infants, the movements were absent (without therapy) at 15, 18, and 30 months of age. In the remaining 4 infants (3 of whom receive clonazepam), the movements, though attenuated, persisted at 6, 12, 15 and 21 months of age, respectively. Neuropathologically, 1 infant showed neuronal loss with astrocytosis in caudate, putamen, globus pallidus, and thalamus. These data defined a previously unrecognized extrapyramidal movement disorder of infants with severe bronchopulmonary dysplasia; pathogenesis may be related to chronic hypoxemia.

Bronchopulmonary Dysplasia↗

PubMed2000

Intracortical inhibition of the motor cortex in movement disorders.

We have studied the function of inhibitory interneurons within the motor cortex in several movement disorders using a paired-pulse magnetic stimulation technique. Their function was disturbed in patients with dystonia or focal lesions of the basal ganglia. On the other hand, the inhibition was normal in patients with chorea or essential tremor. The inhibitory circuit in the motor cortex must be functionally involved in some movement disorders probably because of changes of the inputs from basal ganglia to motor cortices, but not involved in the others. This difference in the functional involvement of inhibitory interneurons of the motor cortex may reflect different pathogenesis of these movement disorders.

Adult↗

PubMed1988

Association of psychosis and movement disorders in the elderly.

There are a number of different relationships among aging, psychosis and movement disorders, most of which have been proposed to involve the neurotransmitter dopamine. Dopamine content and dopamine receptors have been shown to decrease with age, which may relate to the time of onset of different motor and psychotic disorders, as well as to the appearance of these disorders. For example, some so-called senile movement disorders, such as senile tremor and senile chorea, may relate to alterations in dopaminergic transmission with age, as might the general findings of increased slowing of movements and mildly increased rigidity with age, although it is not clear how common some of these changes are in the medically healthy elderly. Decrease in dopamine with age may also be associated with the findings that choreiform and psychotic disorders (which have been proposed to be related to excess dopaminergic activity) tend to predominate at younger ages, whereas parkinsonism is more common at later ages. Certain findings support this notion, such as the appearance of both dyskinesia and psychosis in patients treated with L-dopa, the finding that psychosis may be less common in patients with later-onset Huntington's disease, and the fact that neuroleptic-induced parkinsonism is often more severe in the elderly. However, the situation is more complicated than this, because there are a number of phenomena that do not fit the pattern, including the observation of an increased incidence of tardive dyskinesia in the elderly. Age-related changes in other transmitters are undoubtedly important in both movements disorders and psychosis, and even dopamine has been proposed to have both trophic and toxic properties over the aging process. In general, care is warranted in the use of any psychotropic medications in the elderly, because there can be widespread and often unpredictable effects of these drugs on both motor and mental function.

Aged↗

PubMed1979

The trial use of clozapine for abnormal involuntary movement disorders.

Twelve patients with abnormal involuntary movement disorders were treated with clozapine in a double-blind, placebo-controlled trial. The cohort consisted of individuals with Gilles de la Tourette's syndrome, Huntington's disease, and atypical persistent dyskinesia that was drug induced. Two subjects were dropped from the protocol due to complications. Two patients with Huntington's disease showed a marked decrease in movements; other individuals obtained no significant therapeutic benefits. Seven of the 10 patients completing the trial experienced moderate or marked side effects.

Adolescent↗

PubMed1995

Selective putaminal excitotoxic lesions in non-human primates model the movement disorder of Huntington disease.

While dyskinetic movements have been reported in primates with unilateral excitotoxic lesions following stimulation by dopaminergic agonists, the presence and intensity of the dyskinetic syndromes have varied extensively with size and location of lesion. With the intent of producing a more reliable behavioral model of Huntington disease, anatomically-defined lesions of limited size were produced by magnetic resonance imaging-guided stereotaxic injection of quinolinic acid in specific regions within the caudate and putamen of rhesus monkeys. The location and extent of the lesions were verified by magnetic resonance imaging as well as quantitative positron emission tomography imaging with the dopamine D1 specific receptor ligand SCH 39166 as a marker for striatal output neurons. The quality, frequency and duration of dyskinetic movements were assessed and quantified before and after administration of 0.5 mg/kg apomorphine in multiple test sessions over several months. Selective unilateral lesions in the posterior putamen, but not in the anterior putamen or the head of the caudate, produced marked dystonia and dyskinesia after apomorphine administration. While combined unilateral lesions of the caudate and posterior putamen produced dyskinesia similar to selective posterior putaminal lesions, combined unilateral lesions of the anterior and posterior putamen did not elicit dyskenesia. On the basis of these results, one monkey received a bilateral selective lesion in the posterior putamen. This animal remained healthy and exhibited marked spontaneous Huntington-like chorea spontaneously in the first 48 h after lesioning and persistent apomorphine-induced dyskinesia thereafter. We conclude that bilateral selective excitotoxic lesions of the posterior putamen provide an improved model of the movement disorder of Huntington disease.

Animals↗

PubMed2003

The role of positron emission tomography imaging in movement disorders.

PET imaging provides the means to study neurochemical, hemodynamic, or metabolic processes that underlie movement disorders in vivo. Because the extent of presynaptic nigrostriatal dopaminergic denervation can be quantified in PD even at an early or preclinical stage of the disease, PET imaging may allow the selection of at-risk subjects for neuroprotective intervention trials. These techniques may also provide markers to follow progression of disease or evaluate the effects of neurorestorative interventions in patients who have more advanced disease. PET is expected to play an increasing role in the selection of patients who have PD for deep brain stimulation. Dopaminergic studies may have a limited clinical role in the diagnosis of patients who have symptoms that suggestive of PD yet do not respond to typical dopaminergic drugs, such as patients who have vascular parkinsonism or ET with mild resting tremor who may have normal dopaminergic innervation. The differential diagnosis between PD and multiple system atrophy, progressive supranuclear palsy, or corticobasal degeneration is not yet clearly established by PET, but combined pre- and postsynaptic dopaminergic imaging may be able to distinguish early idiopathic PD from atypical parkinsonian disorders, in general. Huntington's chorea is characterized by more prominent striatal dopamine receptor loss, whereas nigrostriatal denervation is present to a lesser degree. Patients who have TS may have enhanced synaptic dopamine release in the putamen. Functional imaging studies have generally failed to demonstrate nigrostriatal denervation in essential tremor or idiopathic dystonia. Studies have shown striatal dopamine receptor loss in selected subtypes of dystonic patients. In conclusion, it is expected that PET will help us to better understand the pathophysiology of movement disorders, increase the diagnostic accuracy, allow preclinical diagnosis, monitor disease progression, and evaluate the efficacy of therapeutic agents. Pharmacologic radioligand displacement studies and the development of new nondopaminergic ligands may further aid in the unraveling of cerebral mechanisms that underlie movement disorders.

Brain↗

PubMed2003

Neuroepithelial cysts presenting with movement disorders: two cases.

BACKGROUND: The authors present two cases of movement disorders caused by neuroepithelial cysts and highlight their management. Neuroepithelial cysts are ependymal or epithelial lined fluid collections of unknown etiology within the central nervous system parenchyma with no obvious ventricular or subarachnoid connection. Most cysts are asymptomatic, however, some present with seizures, mass effect, or rarely with movement disorders. CASE REPORTS: The first patient, a 27-year-old female, presented with progressive weakness, dystonic posturing, tremor, ballismus and choreoathetotic movements of her right upper extremity. Her symptoms improved after stereotactic drainage of a neuroepithelial cyst in her basal ganglia but recurred within a year. The second case, a 56-year-old female, presented with diplopia, nystagmus, gait imbalance and hemiparesis. Her symptoms improved after stereotactic drainage of a midbrain neuroepithelial cyst. The cyst reaccumulated over the next few years and she became symptomatic with left arm tremor and facial weakness. Aspiration was again performed with symptomatic improvement for nine months. Her tremor recurred and a cyst access device was placed stereotactically. She improved and has remained stable for over a year. CONCLUSION: Simple stereotactic drainage of neuroepithelial cysts has a high recurrence rate. The authors recommend considering placement of a drainage device to facilitate aspiration of the cyst fluid during follow-up, if needed.

Adult↗

PubMed1998

Pathophysiology of akinetic movement disorders: a paradigm for studies in fibromyalgia?

Patients with fibromyalgia sometimes have sign of a movement disorder in addition to sensory disturbances sometimes similar as those found in akinetic syndromes. Akinesia is due to disturbances in the functions of the cortico-thalamo-nigro-striatal system and associated areas. The reason of this dysfunction in Parkinson's disease is a decreased nigral dopaminergic efferent innervation due to a neuronal degeneration in the pars compacta of the substantia nigra. Changes in other neurotransmitters, like GABA or serotonin, and in receptors and second messengers also occur, with additional modulation due to therapy. The aetiology of nigral malfunction is in only rarely known. Drugs and mutations of some genes are examples which give much insight in the pathogenesis of movement disorders in general. In other akinetic disorders, like multisystem atrophy, corticobasal ganglionic degeneration, and progressive supranuclear palsy, more complex patterns of degeneration have been found. This pathological anatomical disturbances have typical clinical effects which can be studied physiologically and with imaging in vivo. Since basal ganglia play also a role in pain, a comparative study of their involvement in movement disorders and nociception seems to be fruitful, especially in devising new therapeutic strategies.

Animals↗

PubMed1987

Application of SCS for movement disorders and spasticity.

20 patients with movement disorders and spasticity were treated with SCS to decrease tonus and improve impaired motor function. 12 patients with multiple sclerosis had gait disorders and slight up to considerable increase in tonus. We observed quantitative changes in diminution of spasticity, voluntary motor function, bladder function, lessening of ataxia and pain relief. During a follow-up of up to 4 years no deterioration in the patients' condition could be observed. 11 patients reported a more fluent gait in 6 cases accompanied by a decrease in tonus. Increase in tonus and deterioration of gait pattern were observed after break down of the stimulation. Although the indications for electrostimulation still remains uncertain in some cases with definite diagnosis without any progressive character of the disease and without severe neurological disturbances improvement can be obtained.

Adult↗

PubMed2002

Stereotypic movement disorder after acquired brain injury.

Stereotypic movement disorder (SMD) consists of repetitive, non-functional motor behaviour that interferes with daily living or causes injury to the person. It is most often described in patients with mental retardation. However, recent evidence indicates that this condition is common among otherwise normal individuals. This case study describes a patient with new-onset SMD occurring after subdural haematoma and brain injury. SMD has rarely been reported after acquired brain injury, and none have documented successful treatment. The current psychiatric literature regarding neurochemistry, neuroanatomy, and treatment of SMD are reviewed with particular application to one patient. Treatment options include serotonin re-uptake inhibitors, opioid antagonists and dopamine antagonists. SMD has been under-appreciated in intellectually normal individuals, and may also be unrecognized after brain injury. Further investigation is needed in this area, which may benefit other individuals with SMD as well.

Adult↗

PubMed2002

Applications of transcranial magnetic stimulation in movement disorders.

The author reviews the applications of transcranial magnetic stimulation (TMS) in a series of movement disorders--namely, Parkinson's disease, corticobasal degeneration, multiple system atrophy, progressive supranuclear palsy, essential tremor, dystonia, Huntington's chorea, myoclonus, the ataxias, Tourette's syndrome, restless legs syndrome, Wilson's disease, Rett syndrome, and stiff-person syndrome. Single- and paired-pulse TMS studies have been done mainly for pathophysiologic purposes. Repetitive TMS has been used largely for therapy. Many TMS abnormalities are seen in the different diseases. They concur to show that motor cortical areas and their projections are the main target of the basal ganglia dysfunction typical of movement disorders. Interpretation has not always been clear, and sometimes there were discrepancies and contradictions. Largely, this may be the result of the extreme heterogeneity of the methods used and of the patients studied. It is premature to give repetitive TMS a role in treatment. Overall, however, TMS gives rise to a new, outstanding enthusiasm in the neurophysiology of movement disorders. There is reason to predict that TMS, with its continuous technical refinement, will prove even more helpful in the near future. Then, research achievements are reasonably expected to spill over into clinical practice.

Electric Stimulation↗