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PubMed2005

Movement disorders and Creutzfeldt-Jakob disease: a review.

Movement disorders are reported in a significant number of patients within the course of Creutzfeldt-Jakob disease (CJD). Although myoclonus is more frequent, dystonia, choreoathetosis, tremor, hemiballismus, and atypical parkinsonian syndromes have also been reported. In this review, we report the principal movement disorders associated with CJD and evaluate their correlations with neuroradiological and neuropathological findings that could in fact suggest a basal ganglia dysfunction. Further studies are warranted in order to clarify these correlations.

Animals↗

PubMed2003

[Movement disorders in childhood: classification and genetic update].

Abnormal movements are not unusual in childhood. Recent genetic progresses provide a new approach of childhood movement disorders. Several loci have been identified in paroxysmal dyskinesia, or in Gilles de la Tourette syndrome. A gene has been cloned in Hallervorden-Spatz syndrome, and a gene has recently been implicated in benign hereditary chorea. Considerable advances concern the genetic of dystonic syndromes: several chromosomal localizations have been identified, and several genes have been cloned. Genetic advances allow nosographic reclassification of some entities and offer new molecular tools for a more appropriate diagnosis. The increasing wealth of genetic knowledge will provide further insight in the understanding of abnormal movement disorders in childhood.

Child↗

PubMed1995

Psychogenic movement disorders.

The diagnosis of PMDs is by no means a simple task. Organic movement disorders are more often misdiagnosed as psychogenic rather than the reverse. The degree to which psychological factors underlie movement disorders may range from being the exclusive cause to being a reaction to the movement disorder. The most common psychiatric illnesses associated with PMDs are depression, conversion reactions, and anxiety disorders. Although the diagnosis of psychogenicity may seem elusive, the definitions and diagnostic criteria of PMDs outlined in this article serve as useful guidelines for obtaining a more accurate diagnosis. The emphasis on a multidisciplinary approach with a strong alliance of neurologist and psychologist or psychiatrist is essential to assure proper diagnoses and treatment.

Adult↗

PubMed1998

Evolution of neuroablative surgery for involuntary movement disorders: an historical review.

Surgical therapy of involuntary movement disorders has evolved during the past century from gross destructive ablations of the central nervous system to refined, accurate, discrete lesioning of sites deep within the brain. The understanding of neuroanatomic and physiological systems improved tremendously through experimentation in animals and empirical observations of surgery in humans. A continuum of accumulated knowledge has been achieved through ablation or lesioning of virtually all aspects of the central and peripheral nervous system predicated on previous successes or failures. This compilation of surgical history of involuntary movement disorders has provided present neurosurgeons with the foundations on which they base their therapeutic measures and will direct future endeavors within this field.

Basal Ganglia↗

PubMed2004

Botulinum toxin B treatment in children with spastic movement disorders: a pilot study.

The treatment of adult and pediatric patients suffering from movement disorders with elevated muscle tone includes the application of focally denervating botulinum toxins. Dystonic movement disorders in adult patients have been treated successfully using botulinum toxin type B (NeuroBloc). Thus far, there has been no systematic treatment of children with botulinum toxin type B. This study reports on the treatment of 29 children with spastic or dystonic movement disorders using botulinum toxin type B in an open-label pilot study. Sixty-two treatment sessions were performed. In 33 of these sessions, the therapy goal that had been defined before intervention was attained or surpassed. Seventeen nonresponders to botulinum toxin type A were also included in the treatment, 11 of whom attained the therapy goal. Side effects were observed in 24% of all treatments, dry mouth being the most frequent (10%), in some cases having a desirable clinical effect. With this preliminary data as a basis, we recommend a maximum dose for children of 400 U botulinum toxin type B per kg body weight, which should not exceed a total of 10,000 U botulinum toxin type B.

Adolescent↗

PubMed2001

Chronic posttraumatic movement disorder alleviated by insertion of meso-diencephalic deep brain stimulating electrode.

Incapacitating and drug-resistant posttraumatic movement disorders have successfully been treated by stereotactic thalamotomy. We describe the case of a young man with a posttraumatic hemiballismoid type movement disorder of the left arm, persistent for 2 years, who was selected for treatment with a thalamic deep brain stimulator. However, placement of the stimulating electrode tip at the junction of the zona incerta and subthalamic regions caused abolition of the movement disorder, and the pulse generator was not required. Reassessment over a 44-month period using multiple clinical and functional tests has confirmed continued benefit. This case adds to the reports of alleviation of movement disorders following either stereotactic thalamic mapping or placement of stimulating electrodes without macroscopic thalamic lesioning.

Activities of Daily Living↗

PubMed1986

Electrophysiology of the corticomotoneurone pathways in patients with movement disorders.

The corticomotoneurone pathways were examined in 21 patients with movement disorders, using the technique of percutaneous electrical stimulation of the motor cortex. Conduction in these pathways was assessed by measuring the latency to onset of electromyographic activity in the muscles of the upper limb after cortical stimulation. In all patients [five with primary (idiopathic) torsion dystonia and two with secondary (symptomatic) hemidystonia, seven with Huntington's disease, four with essential tremor, and three with Parkinson's disease] central motor conduction was normal. This and other evidence suggests that the origin of the disorder of movement in these conditions lies in the delivery of abnormal motor commands to a normal corticomotoneuronal system.

Adult↗

PubMed2005

Treatment issues in psychogenic-neuropsychiatric movement disorders.

Patients with PNMDs pose a fascinating challenge to clinicians at the neurology-psychiatry interface. We have outlined a diagnostic and therapeutic approach to these complex disorders. Patients with PNMDs typically manifest abnormal movements and postures that do not fit expected patterns of movement disorder phenomenology. The first goal of neurologic consultation is to make an accurate diagnosis, with a view to either ruling out or defining the extent of any organic substrate. The next task is an effective referral to a psychiatrist capable of diagnosing relevant psychopathology and collaborating in a treatment plan. A supportive explanation of the diagnosis, one that is sensitive to the patient's intellectual capacity, conception of the illness, and self-esteem, appears to be a crucial determinant that influences the patient's capacity to be engaged effectively in treatment. The treatment for each patient with PNMD is individualized and may include psychotherapy, hypnosis, pharmacotherapy, physical therapy, and other approaches. To date, no treatment approach has been shown to be superior, and very few long-term outcome data are available. Although many factors influence response to treatment, those of particular importance are the effectiveness of communication among the neurologist, the psychiatrist, and the patient; the nature, severity, and chronicity of relevant psychopathology and environmental stressors; and the quality of external support and intrinsic resources available to the patient.

Humans↗

PubMed1997

Psychopharmacogenetic basis of medication-induced movement disorders.

In light of the emerging evidence for genetic vulnerability to adverse drug reactions, this article attempts to elucidate the natural history of medication-induced movement disorders from a psychopharmacogenetic perspective. Studies of the risk factors, neurobiology, and pharmacogenetics are reviewed concurrently. The relevant variables associated with 10 genetically mediated movement disorders are tabulated and compared with those of medication-induced movement disorders without a clear-cut genetic basis. As a result of this integrated analysis, it is evident that there is an intimate genetic and pathophysiological link between neuropsychiatric movement disorders of diverse origins. The emergence of drug-induced movement disorders seems to reflect a spectrum of basal ganglia derangement attributable to genetic predisposition; psychotropic medications only augment the genetic vulnerability to clinical phenotypes. It is proposed that a multidimensional analysis of the interacting variables is essential for understanding the natural history of these conditions, and that the scope of psychopharmacology should be broadened to include psychopharmacogenetics for improving therapeutic objectivity and prevention research.

Animals↗

PubMed1993

Tardive stereotypy and other movement disorders in tardive dyskinesias.

We reviewed the medical records and videotapes of 100 patients with tardive dyskinesia (TD) referred to our movement disorders clinic to characterize the spectrum of hyperkinetic movement disorders caused by dopamine receptor blocking drugs (DRBD). Tardive stereotypy, present in 78 patients, was the most common type of TD, followed by tardive dystonia, akathisia, tremor, chorea, and myoclonus. Sixty-four had a combination of these hyperkinesias. In a second study, a "blind" review of videotapes of patients with a variety of movement disorders found that DRBD were the cause of stereotypic movements in 89.3% of patients, and 96.1% of patients with TD had stereotypy. We conclude that stereotypy can be readily differentiated from other hyperkinetic movement disorders and that its presence in an adult is highly suggestive of prior exposure to DRBD.

Adult↗

PubMedDate not supplied

Movement disorders after status epilepticus and other brain injuries.

A retrospective medical record review was conducted of 173 consecutive children hospitalized for acquired brain injuries on a specialized pediatric rehabilitation service. The chart review identified children who developed movement disorders with acquired brain injuries: 8 with status epilepticus, 2 with trauma, and 1 with anoxia. Movement disorders were observed more frequently following status epilepticus (8 of 12) than following other causes of acquired brain injury (3 of 161; P = .0001). Four additional children had severe neurologic deficits following status epilepticus but did not develop movement disorders. The 11 patients who developed movement disorders had choreiform movements predominantly. Even though status epilepticus is a clinical phenomenon resulting from a variety of etiologies, the features of movement disorders in these children were strikingly similar. The pathophysiology of this complication is unknown.

Anticonvulsants↗

PubMed2005

Novel movement disorder of the lower lip: is it epilepsia partialis continua? Clues from a secondary case.

A 28-year-old woman developed an acute-onset novel movement disorder of the lower lip mimicking focal dystonia. Investigations showed it to be a presentation of epilepsia partialis continua occurring in association with agenesis of the corpus callosum. It responded favorably to anti-epileptic drug therapy. Recently, Kleopa and Kyriakides reported on 4 patients who developed sudden-onset movement disorder characterized by a tonic sustained, lateral and outward protrusion of half of the lower lip. They failed to find any causative factors, despite extensive investigation. Treatment with anticholinergics, clonazepam, and botulinum toxin injection failed to improve the movement disorder. I present an additional case of similar focal movement disorder occurring in the presence of agenesis of the corpus callosum. A scalp electroencephalogram revealed focal epileptic activity, and the movement disorder responded favorably to treatment with antiepileptic drugs.

Adult↗

PubMed2006

Movement disorders: neurodevelopment and neurobehavioural expression.

Braak and co-workers have recently shown that movement disorders such as Parkinson's disease develop progressively over years with early neuronal losses in brainstem regions caudal to the substantia nigra. The relevance of this finding to notions of comorbidity between movement disorders and psychiatric symptoms was recognised at the recent meeting concerning, "Implications of Comorbidity for the Etiology and Treatment of Neuropsychiatric Disorders" held in Oct. 2005 in Mazagon, Spain. The identification of stages in the early development of neurodegenerative disorders appeared to unify multiple, diverse findings. These included: novel therapeutic innovations for Parkinson's disease, Alzheimer's disease and depression in the aged; the neurochemical ontogeny of drug-induced oral dyskinesias; the types of chemical agents abused in neuropsychiatric states; postnatal iron overload effects upon the functional and interactive role of dopaminergic and noradrenergic pathways that contribute to the expression of movement disorders; and the spectrum of motor symptoms expressed in schizophrenia and attention deficit hyperactivity disorder and the eventual treatment of these disorders. A continued focus on a number of neuropsychiatric diseases as progressive disorders may lead to further advances in understanding their etiology and in developing better therapeutics.

Animals↗

PubMed2000

Clinical report of three patients with hereditary hemochromatosis and movement disorders.

Neurologic manifestations are rarely described in hereditary hemochromatosis (HH). We describe three patients with HH and movement disorders. Patient 1, a 69-year-old man, had a 13-year history of disabling cerebellar syndrome, action tremor and myoclonus, and secondary dementia. Patient 2 was a 40-year-old man with a 9-year history of cerebellar syndrome, head and arm tremor, and cervical dystonia. Patient 3, a 75-year-old woman, had a 5-year history of rapidly disabling parkinsonian syndrome unresponsive to levodopa. The diagnosis of HH was established in the three patients by iron tests, evidence of a C282Y mutation, and, in two patients, by liver biopsy. High-field T2-weighted magnetic resonance imaging showed hyperintense signals in hemispheric white matter in patient 1, cerebellar atrophy in patient 2, and cerebellar and cerebral atrophy in patient 3 and no significant hypointense signals in the three patients. Phlebotomies and symptomatic treatments did not change the course of the disease. Our cases are compared with the five previously reported observations of HH with movement disorders. This rare association is one cause of the chronic acquired non-Wilsonian hepatocerebral degeneration syndromes and represents a separate entity from aceruloplasminemia. The pathophysiologic mechanism of movement disorders in HH is unresolved. No hepatic insufficiency and portosystemic encephalopathy is evidenced in our cases, whereas the putative role of abnormal iron load remains to be ascertained. HH should be investigated more systematically in patients with movement disorders.

Adult↗

PubMed2001

[Contributions of Charcot and Marsden to the development of movement disorders in the 19th and 20th centuries].

Charcot described many neurological diseases in the 19th century, particularly in movement disorders. Charcot contributed in the clinical description of Parkinson's disease, and introduced its first pharmacological treatment. He also studied the hyperkinesias, e.g. of Tourette syndrome, differential diagnosis of tremors, dystonias, choreas and startle disease. Marsden, who died recently, was an exponent in the study of Movement Disorders, with many publications in this field in the 20th century. His most important contributions are definitions and classifications of movement disorders, such as Parkinson's disease, dystonia, myoclonus, essential tremor, the description of the syndromes "Painful Legs Moving Toes", "Gait Ignition Failure" and "Primary Writing Tremor". The contributions of Charcot in the 19th century and Marsden in the 20th century to the movement disorders allow us to conclude that both of them were the most representative icons in this field in the past two centuries.

History, 19th Century↗

PubMed2006

Movement disorders fellowship training program at Columbia University Medical Center in 2001-2002.

Data regarding the clinical experience of movement disorders subspecialty training are currently not available. In order to provide information to help design a well-rounded clinical experience, we reviewed the number and types of patients seen by all clinical movement disorders fellows over the course of 1 year at Columbia University Medical Center (CUMC). We conducted a retrospective analysis of all patients seen by four full-time clinical fellows and one part-time fellow during the 2001-2002 academic year, using billing records to tabulate all clinic visits and patient charts to certify diagnosis. One thousand six hundred sixty-two patients (1,132 new and 530 follow-ups) were seen by five fellows. Each full-time fellow evaluated and treated a mean of 263 new patients, 116 follow-up patients, and 15 in-patient consultations. The part-time clinical fellow evaluated and treated 81 new patients and 65 follow-up patients. Approximately half of the new patients had idiopathic Parkinson's disease. Full-time fellows saw equivalent numbers of patients but they evaluated few patients with uncommon movement disorders. Weekly video rounds allowed all fellows to see many more patients, aiding the recognition of movement phenomenology and enhancing understanding of diagnoses and treatment strategies. Thus, CUMC fellows evaluate a large number of patients with a wide range of diagnoses within a 1-year period. Video rounds allow greater exposure to uncommon diagnoses. Similar data from other movement disorder training programs are needed to help create guidelines for formal accreditation and to improve clinical training in this subspecialty.

Academic Medical Centers↗

PubMed1994

Mitochondrial dysfunction in movement disorders.

A major theory regarding the mechanism of neuronal degeneration in several movement disorders is that mitochondrial defects may play a role. Biochemical studies in Parkinson's disease, Huntington's disease, multiple system atrophy, and idiopathic dystonia have shown defects in enzymes of oxidative phosphorylation in postmortem brain tissue, platelets, muscle, or lymphocytes. The basal ganglia and substantia nigra are also particularly susceptible to the accumulation of age-dependent mitochondrial DNA deletions, which may contribute to the delayed onset of movement disorders. The 1-methyl-4-phenyl 1,2,3,6-tetrahydropyridine model of Parkinson's disease involves conversion to 1-methyl-4-phenylpyridinium, which then inhibits complex I of the electron transport chain. Our studies show that the complex II inhibitor 3-nitropropionic acid can closely replicate the neurochemical, histologic, and clinical features of Huntington's disease. The mechanism of neuronal death in both these models may be slow excitotoxicity. Both direct biochemical studies and animal models of movement disorders therefore suggest that mitochondrial dysfunction may play a direct role in their pathogenesis.

Animals↗

PubMed2003

Movement disorders in children: definitions, classifications, and grading systems.

Disorders that affect movement in children are relatively common. However, they have received little attention, especially when compared with epilepsy and neuromuscular disorders. In this review article, we address the major types of movement disorders that affect children, their clinical characteristics and etiologies, and, when available, the scales used to grade them. A discussion on spasticity, which traditionally is not addressed in reviews of "movement disorders," is also included.

Ataxia↗