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PubMed2003

Do disorders of movement cause movement disorders and dementia?

Neurons require long-distance microtubule-based transport systems to ferry vital cellular cargoes and signals between cell bodies and axonal or dendritic terminals. Considerable progress has been made on developing a molecular understanding of these processes and how they are integrated into normal neuronal functions. Recent work also suggests that these transport systems may fail early in the pathogenesis of a number of neurodegenerative diseases.

Animals↗
PubMed1997

Guidelines for the therapeutic use of botulinum toxin in movement disorders. Italian Study Group for Movement Disorders, Italian Society of Neurology.

Since its introduction in the early '80s the use of botulinum toxin has improved the quality of life of the patients affected by movement disorders. Toxin's neuromuscular blocking action allows a symptomatic treatment of those clinical conditions characterised by excessive muscular activity. Although the dosages used are safe and the side-effects are reversible, a correct use of botulinum toxin depends on the knowledge of its clinical pharmacology and of the anatomy of the body segments to be injected. In addition, the treatment of more complex conditions, i.e. laringeal dystonia, imposes an inter-disciplinary approach and specialised injection techniques. In this review, the Italian Study Group on Movement Disorders presents the consensus guidelines for the therapeutic use of botulinum toxin in movement disorders. The main toxin types, their use and administration modalities, and the training guidelines will be presented.

Botulinum Toxins↗
PubMed2005

Autism and Asperger's disorder: are they movement disorders involving the cerebellum and/or basal ganglia?

Autism and Asperger's disorder (AD) are childhood developmental disorders of unknown aetiology. Autism and AD share several behavioural features, and it is not clear whether they are distinct disorders or variants of the same disorder. Recent studies indicate that disordered movement may be another feature of autism and AD, and that this may reflect dysfunction within the frontostriatal and/or cerebellar motor circuits. While disordered movement in autism and AD has been examined in a variety of ways, it is relatively under-researched compared to the cognitive, affective, and behavioural disturbances seen in these disorders. This review examines the role of the frontostriatal and cerebellar motor systems in the behavioural features of autism and AD, with gait as a proxy, and discusses difficulties with their diagnosis and their possible pathogenesis.

Animals↗
PubMed1998

Ablative therapy for movement disorders. Complications in the treatment of movement disorders.

Presently, there is a renaissance in the surgical treatment of movement disorders. Prompted by the growing recognition of the limitations of drug therapy, this resurgence has been further promoted by progress in neuronal transplantation, advances in neuroimaging and stereotactic surgical techniques, and innovative therapies, such as deep brain stimulation for abnormal movements. Mortality associated with thalamotomy and pallidotomy is rare, but morbidity is not inconsiderable, particularly in the elderly and those with preexisting brain damage. Judicious patient selection and physiologic confirmation of stereotactic targets are cornerstones to complication avoidance.

Antiparkinson Agents↗
PubMed2003

Psychogenic Movement Disorders.

Psychogenic movement disorders are one of the most challenging conditions encountered by clinicians. Patients with these disorders represent the overlap of psychiatry and neurology and need care from these specialties. Issues within the patient's family, questions about secondary gain, and prejudices among other clinicians often complicate evaluation and treatment. Diagnosis is further complicated by lack of laboratory and other tests to reliably diagnose movement disorders; most movement disorders are diagnosed based on history and clinical phenomena. Treatment is best conducted within the context of a multidisciplinary team experienced in working with these patients and with one another. Identification and treatment of underlying psychopathology, such as major depression or anxiety disorders, is also of great importance.

Journal Article↗
PubMed2001

6: Movement disorders II: the hyperkinetic disorders.

Involuntary movements or hyperkinesias are classified into syndromes of chorea, ballism, tremor, dystonia, myoclonus and tics. The hyperkinesias are caused by disturbances in the circuitry connecting the cerebral cortex, thalamus, basal ganglia and cerebellum. Drugs are a common cause of movement disorders. The aim of management is to characterise the movement disorder, identify and treat the cause or institute symptomatic treatment. The genetic basis of many movement disorders is increasingly recognised. Where there are potential implications for family members, accurate diagnosis and counselling are particularly important.

Humans↗
PubMed2005

Diagnosis and management of acute movement disorders.

Most movement disorders, reflecting degenerative disorders, develop in a slowly progressive fashion. Some movement disorders, however, manifest with an acute onset. We wish to give an overview of the management and therapy of those acute-onset movement disorders.Drug-induced movement disorders are mainly caused by dopamine-receptor blockers (DRB) as used as antipsychotics (neuroleptics) and antiemetics. Acute dystonic reactions usually occur within the first four days of treatment. Typically, cranial pharyngeal and cervical muscles are affected. Anticholinergics produce a prompt relief. Akathisia is characterized by an often exceedingly bothersome feeling of restlessness and the inability to remain still. It is a common side effect of DRB and occurs within few days after their initiation. It subsides when DRB are ceased. Neuroleptic Malignant Syndrome is a rare, but life-threatening adverse reaction to DRB which may occur at any time during DRB application. It is characterised by hyperthermia, rigidity, reduced consciousness and autonomic failure. Therapeutically immediate DRB withdrawal is crucial. Additional dantrolene or bromocriptine application together with symptomatic treatment may be necessary. Paroxysmal dyskinesias are childhood onset disorders characterised by dystonic postures, chorea, athetosis and ballism occurring at irregular intervals. In Paroxysmal Kinesigenic Dyskinesia they are triggered by rapid movements, startle reactions or hyperventilation. They last up to 5 minutes, occur up to 100 times per day and are highly sensitive to anticonvulsants. In Paroxysmal Non-Kinesiogenic Dyskinesia they cannot be triggered, occur less frequently and last longer. Other paroxysmal dyskinesias include hypnogenic paroxysmal dyskinesias, paroxysmal exertional dyskinesia, infantile paroxysmal dystonias, Sandifer's syndrome and symptomatic paroxysmal dyskinesias. In Hereditary Episodic Ataxia Type 1 attacks of ataxia last for up to two minutes, may be accompanied by dysarthria and dystonia and usually respond to phenytoin. In Type 2 they can last for several hours, may be accompanied by vertigo, headache and malaise and usually respond to acetazolamide. Symptomatic episodic ataxias can occur in a number of metabolic disorders, but also in multiple sclerosis and Behcet's disease.

Adolescent↗
PubMed2005

Movement disorders: classifications.

Movement disorders (ataxia, dystonic disorders, gait disorders, Huntington disease, myoclonus, parkinsonism, spasticity, tardive dyskinesia, tics and tremor) are clinically, pathologically and genetically heterogeneous and are characterized by impairment of the planning, control or execution of movement. Current classifications of these disorders have inherent shortcomings due to the complex nature of movement disorders and the lack of diagnostic tests for the majority. Undiscriminating terminology, as well as the clinical, pathological and genetic heterogeneity, further complicate the development of comprehensive categorizations. Modern classification schemes tend to focus on clinical, pathological or genetic/molecular criteria, but more recent attempts have been made to integrate across these levels. From a historical perspective, two 'golden ages' have shaped the current and evolving classification schemes: (1) the definition of clinical pathological entities in the early twentieth century and (2) the application of molecular neurogenetics in the past 10-15 years. However, the classification of movement disorders on clinical grounds (according to age at onset, distribution of symptoms, disease course, provoking factors and therapeutic response) remains one of the most useful modes of categorization. Postmortem criteria have been employed to distinguish between degenerative and nondegenerative disorders, and specific hallmarks may be required to establish or confirm a diagnosis. Genetic features used for classification purposes include mode of inheritance and molecular genetic data, such as linkage to a known gene locus or identification of a specific genetic defect. A final classification scheme is based on alterations in molecular mechanisms (e.g. trinucleotide expansions) or protein function (e.g. channelopathies). Despite recent advances, it may not be possible to develop the 'ultimate' classification of movement disorders, and different patterns of lumping and splitting may be useful for the clinician, the pathologist or the geneticist/molecular biologist. Furthermore, certain individual cases with unique features may not fit into any particular category. Continued research by both clinicians and basic scientists is necessary in order to refine and redefine classification schemes of movement disorders.

Dystonia↗
PubMed2006

Long-term prognosis of patients with psychogenic movement disorders.

Psychogenic movement disorders (PMD) are hyper- or hypokinetic movement disorders associated with underlying psychological or psychiatric disorders. Structured telephone interview was administered to 228 patients with PMD seen in our clinic between 1990 and 2003. The mean age of the subjects was 42.3+/-14.3 years (range 14-70 years), mean duration of symptoms was 4.7+/-8.1 years (range 2-14 years), and mean duration of follow-up was 3.4+/-2.8 years (6 months-12 years). Improvement of symptoms was noted in 56.6% patients; while 22.1% were worse, and 21.3% remained the same at the time of follow-up. In this longitudinal study of patients with PMD we found that indices of strong physical health, positive social life perceptions, patient's perception of effective treatment by the physician, elimination of stressors, and treatment with a specific medication contributed to a favorable outcome.

Adolescent↗
PubMed1977

Therapeutics of disordered movement.

Human motor behavior is organized around two major neurotransmitter systems in the basal ganglia--dopaminergic and cholinergic. Hypokinetic disease may result from hypofunction of the dopaminergic system or cholinergic hyperfunction. The reverse seems true for many hyperkinetic movement disorders. Drugs which facilitate dopaminergic neurotransmission or which block cholinergic transmission relieve many hypokinetic disorders; the opposite approach is useful in treating many hyperkinetic disorders.

Carbidopa↗
PubMed2000

An unusual case of rhythmic movement disorder.

Rhythmic movement disorder is one of the sleep-wake transition disorders listed in the International Classification of Sleep Disorders. According to this classification, the condition commonly occurs in infants and toddlers, and persistence beyond 4 years of age is unusual. Recently, we encountered a case in which rhythmic movement disorder persisted up until the age of 12 years with spikes registering on the sleep electroencephalogram. Epileptic seizure was ruled out because of the characteristic rolling movement, absence of any other epileptic symptoms (e.g. vocalization and tonic-clonic seizure) and cessation as a result of removal of the blanket.

Child↗
PubMed2003

Pathophysiology of pediatric movement disorders.

Pediatric movement disorders constitute a relatively small cluster of symptoms that can be associated with many different underlying diseases. To provide effective treatment, it is essential to understand the relationship between etiology and clinical expression. This article reviews the recent literature on several common pediatric movement disorders, including spasticity, dystonia, chorea, myoclonus, bradykinesia, and tics, and it discusses current models of physiology that may help link the cellular pathology of specific diseases to the expression of clinical symptoms.

Ataxia↗
PubMed2005

Movement disorder emergencies.

Movement disorders may present acutely, and failure to recognize and exclude important differential diagnoses can result in significant morbidity or mortality. Unfortunately, much of the literature pertaining to this topic is scattered and not easily accessible. This review aims to address this deficit. Movement disorder emergencies are discussed according to their most likely mode of presentation. Diagnostic considerations and early management principles are reviewed, along with appropriate pathophysiology where relevant.

Acute Disease↗
PubMed2003

An unusual family with multiple movement disorders.

Multiple movement disorders presenting in the same family are rare. We present an unusual family where generalized dystonia, Huntington's disease, progressive supranuclear palsy and secondary paroxysmal dyskinesia co-exist. The index case presented with young-onset dystonia and tested negative for the DYT1 gene deletion. Her father was similarly affected. The father's brother (paternal uncle of the index) also had abnormal movements-a mixture of chorea and dystonia-and tested positive for the HD expansion. His son had secondary paroxysmal dyskinesia, and tested negative for the HD expansion. The index case and her father were also negative for the HD expansion. A paternal aunt of two of the cases had a clinical diagnosis of progressive supranuclear palsy. Dystonia is known to be a genetically heterogeneous condition. The co-existence of inherited generalized dystonia with other movement disorders may provide clues to its genetic localization.

Adolescent↗
PubMed1998

Botulinum toxin for neurological disorders in a movement disorders clinic in Singapore.

AIM OF STUDY: This study was done to examine the usefulness of botulinum toxin A injections in treating various neurological disorders such as hemifacial spasm, blepharospasm, focal dystonia and task-specific dystonia. METHODS: This was a prospective, open-labelled trial of patients seen in a Movement Disorders Clinic with dyskinesias potentially treatable with botulinum toxin. All patients were assessed before and after injections using clinical rating scales, and those with focal and task-specific dystonias were also recorded on videotape. RESULTS: There were 102 patients with hemifacial spasm, 3 with blepharospasm, 13 with neck dystonia, 6 with writer's cramp, I with musician's cramp, and I with jaw dystonia. All patients with hemifacial spasm and blepharospasm obtained good results, while 77% of those with cervical dystonia received substantial benefit. Only half of those with writer's cramp improved. Hemifacial spasm seems more prevalent in Singapore compared with Western populations. CONCLUSION: Injections of botulinum toxin are useful in treating the various neurological disorders studied. This is an advancement in the treatment of these dyskinesias which respond poorly to oral medications.

Adult↗
PubMed2001

Tardive dyskinesia--diagnostic issues, subsyndromes, and concurrent movement disorders: a study of state hospital inpatients referred to a movement disorder consultation service.

Of 49 state hospital patients referred for movement disorder consultation for tardive dyskinesia (TD), 11 (23.9%) of 46 meeting inclusion criteria had movement disorders other than TD. These other disorders led to a false diagnosis of TD in 6 subjects (12.2%). Between-day dyskinesia variability affected TD ascertainment in only 3.2 percent of subjects. Prevalences of other neurological conditions in the 30 patients identified with definite TD were parkinsonism (90%), dystonia (25%), akathisia (16%), cerebellar signs (40%), dysmetria (23%), cerebellar tremor (17%), tardive dystonia (3.3%), and tardive akathisia (3.3%). Concurrence rates of parkinsonism with TD varied significantly according to which clinical signs were used to define parkinsonism. Using a rating score threshold of at least mild, rigidity occurred in 79.3 percent, bradykinesia in 55.2 percent, and resting tremor in 41.4 percent of subjects with TD; more significant rigidity occurred in 41.4 percent, bradykinesia in 31.0 percent, and resting tremor in 20.7 percent. Concurrence rates of neurological conditions with TD subsyndromes were distributed rather evenly according to condition prevalences, except for an association of cervicotruncal TD with bradykinesia (perhaps because of ventromedial striatal presynaptic and postsynaptic D2 blockade, respectively). These findings, as well as the occurrence of equal gender ratio and relative under-representation of bipolar and alcohol disorders in subjects with definite TD, are discussed.

Aged↗
PubMed2005

Controlled sleep restriction for rhythmic movement disorder.

Rhythmic movement disorder is a parasomnia that is difficult to treat. In our study, 3 weeks of controlled sleep restriction with hypnotic administration in the first week resulted in almost complete resolution of the movements in 6 children. This therapeutic success suggests that rhythmic movement disorder results from a voluntary self-soothing behavior.

Child↗