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 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Numerous factors need to be taken into account when managing a patient with Parkinson's disease (PD) after deep brain stimulation (DBS). Questions such as when to begin programming, how to conduct a programming screen, how to assess the effects of programming, and how to titrate stimulation and medication for each of the targeted sites need to be addressed. Follow-up care should be determined, including patient adjustments of stimulation, timing of follow-up visits and telephone contact with the patient, and stimulation and medication conditions during the follow-up assessments. A management plan for problems that can arise after DBS such as weight gain, dyskinesia, axial symptoms, speech dysfunction, muscle contractions, paresthesia, eyelid, ocular and visual disturbances, and behavioral and cognitive problems should be developed. Long-term complications such as infection or erosion, loss of effect, intermittent stimulation, tolerance, and pain or discomfort can develop and need to be managed. Other factors that need consideration are social and job-related factors, development of dementia, general medical issues, and lifestyle changes. This report from the Consensus on Deep Brain Stimulation for Parkinson's Disease, a project commissioned by the Congress of Neurological Surgeons and the Movement Disorder Society, outlines answers to a series of questions developed to address all aspects of DBS postoperative management and decision-making with a systematic overview of the literature (until mid-2004) and by the expert opinion of the authors. The report has been endorsed by the Scientific Issues Committee of the Movement Disorder Society and the American Society of Stereotactic and Functional Neurosurgery.
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PMID:Deep brain stimulation: postoperative issues. 1681 Jul 19

As people grow old, their need for medications increases dramatically because of the higher incidence of chronic pain, diabetes mellitus, cardiovascular and neurological diseases in the elderly population. Furthermore, the elderly require special consideration with respect to drug delivery, drug interactions and adherence. In particular, patients with chronic neurological diseases often require multiple administration of drugs during the day to maintain constant plasma medication levels, which in turn increases the likelihood of poor adherence. Consequently, several attempts have been made to develop pharmacological preparations that can achieve a constant rate of drug delivery. For example, transdermal lisuride and apomorphine have been shown to reduce motor fluctuations and duration of 'off' periods in advanced Parkinson's disease, while rotigotine allows significant down-titration of levodopa without severe adverse effects. Thus, parkinsonian patients with long-term levodopa syndrome or motor disorders during sleep could benefit from use of transdermal lisuride and apomorphine. Moreover, transdermal dopaminergic drugs, particularly rotigotine, seem the ideal treatment for patients experiencing restless legs syndrome or periodic limb movement disorder during sleep, disorders that are quite common in elderly people or in association with neurodegenerative diseases. Unlike dopaminergic drugs, transdermal treatments for the management of cognitive and behavioural dysfunction in patients with Parkinson's disease and Alzheimer's disease have inconsistent effects and no clearly established role. Nevertheless, because of their favourable pharmacological profile and bioavailability, the cholinesterase inhibitors tacrine and rivastigmine are expected to show at least the same benefits as oral formulations of these drugs, but with fewer severe adverse effects. Transdermal delivery systems play an important role in the management of neuropathic pain. The transdermal lidocaine (lignocaine) patch is recommended as first-line therapy for the treatment of postherpetic neuralgia. Furthermore, in patients with severe persistent pain, transdermal delivery systems using the opioids fentanyl and buprenorphine are able to achieve satisfactory analgesia with good tolerability, comparable to the benefits seen with oral formulations. Transdermal administration is the ideal therapeutic approach for chronic neurological disorders in elderly people because it provides sustained therapeutic plasma levels of drugs, is simple to use, and may reduce systemic adverse effects. Several transdermal delivery systems are currently under investigation for the treatment of Parkinson's disease, Alzheimer's disease and neuropathic pain. Although most transdermal delivery systems treatments cannot be considered as first-line therapy at present, some of them provide clear advantages compared with other routes of administration and may become the preferred treatment in selected patients. In general, however, most transdermal treatments still require long-term evaluation in large patient groups in order to optimise dosages and evaluate the actual incidence of local and systemic adverse effects.
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PMID:Transdermal treatment options for neurological disorders: impact on the elderly. 1682 90

Tardive dyskinesia (TD) is an umbrella term typically used to describe a movement disorder associated with the use of neuroleptic (anti-psychotic) medication. It is characterized by abnormal, repetitive and involuntary movements. The movements may be around the mouth and face (orofacial dyskinesia) and less frequently, in the trunk and limbs (trunk and limb dyskinesia). TD occurs in over 20% of those using neuroleptic medication continually for longer than three months. A case report is presented of a patient affected by TD who suffered mechanical musculoskeletal pain secondary to its effects, and was managed by chiropractic care.
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PMID:Chiropractic management of musculoskeletal pain secondary to tardive dyskinesia. 1754 98

Although still considered a paradigmatic movement disorder, Parkinson's disease (PD) is associated with a broad spectrum of non-motor symptoms. These include disorders of mood and affect with apathy, anhedonia and depression, cognitive dysfunction and hallucinosis, as well as complex behavioural disorders. Sensory dysfunction with hyposmia or pain is almost universal, as are disturbances of sleep-wake cycle regulation. Autonomic dysfunction including orthostatic hypotension, urogenital dysfunction and constipation is also present to some degree in a majority of patients. Whilst overall non-motor symptoms become increasingly prevalent with advancing disease, many of them can also antedate the first occurrence of motor signs - most notably depression, hyposmia or rapid eye movement sleep behaviour disorder (RBD). Although exact clinicopathological correlations for most of these non-motor features are still poorly understood, the occurrence of constipation, RBD or hyposmia prior to the onset of clinically overt motor dysfunction would appear consistent with the ascending hypothesis of PD pathology proposed by Braak and colleagues. Screening these early non-motor features might, therefore, be one approach towards early 'preclinical' diagnosis of PD. This review article provides an overview of the clinical spectrum of non-motor symptoms in PD together with a brief review of treatment options.
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PMID:Non-motor symptoms in Parkinson's disease. 1835 32

Awake bruxism is defined as the awareness of jaw clenching. Its prevalence is reported to be 20% among the adult population. Awake bruxism is mainly associated with nervous tic and reactions to stress. The physiology and pathology of awake bruxism is unknown, although stress and anxiety are considered to be risk factors. During sleep, awareness of tooth grinding (as noted by sleep partner or family members) is reported by 8% of the population. Sleep bruxism is a behaviour that was recently classified as a 'sleep-related movement disorder'. There is limited evidence to support the role of occlusal factors in the aetiology of sleep bruxism. Recent publications suggest that sleep bruxism is secondary to sleep-related micro-arousals (defined by a rise in autonomic cardiac and respiratory activity that tends to be repeated 8-14 times per hour of sleep). The putative roles of hereditary (genetic) factors and of upper airway resistance in the genesis of rhythmic masticatory muscle activity and of sleep bruxism are under investigation. Moreover, rhythmic masticatory muscle activity in sleep bruxism peaks in the minutes before rapid eye movement sleep, which suggests that some mechanism related to sleep stage transitions exerts an influence on the motor neurons that facilitate the onset of sleep bruxism. Finally, it remains to be clarified when bruxism, as a behaviour found in an otherwise healthy population, becomes a disorder, i.e. associated with consequences (e.g. tooth damage, pain and social/marital conflict) requires intervention by a clinician.
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PMID:Bruxism physiology and pathology: an overview for clinicians. 2373 57

It has been recognized that head trauma can induce movement disorders including tremor, dystonia, parkinsonism and tics. Likewise, lesions involving the peripheral nervous system have been held responsible for such extrapyramidal manifestations, However, involuntary movements secondary to electric injury have seldom been described. Here we report a patient who developed limb dystonia 6 years after receiving an electric discharge in the ipsilateral limb. Although imaging and laboratory studies failed to ascribe the lesion either to the central or peripheral nervous system, initial symptoms such as local bruises, edema and pain would favor peripheral damage. Botulinum toxin injections markedly improved dystonia. Analysis of cases of dystonia following electric injury reported to date suggest that: (a) dystonia may be expected to develop immediately or even years after the electric insult; (b) dystonia usually develops in or adjacent to the area initially injured; (c) dystonia remains limited to a distinct body segment; (d) severity of dystonia as well as the interval between injury and the onset of the movement disorder fails to correlate with trauma severity; (e) no evidence supports the hypothesis that previous history of movement disorders or neuroleptic exposure are predisposing factors; and (f) botulinum toxic provides symptomatic relief.
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PMID:Delayed onset limb dystonia following electric injury. 1859 Oct 86

The aim of the present study was to review the history, clinical course, treatment, and outcome of movement disorders in children and young people with complex regional pain syndrome (CRPS). Case notes were reviewed retrospectively of children and young people who presented with movement disorders in CRPS to our tertiary paediatric pain service over a period of 13 years. Ten children with CRPS presented with movement disorders (eight females, two males). The age at first presentation with symptoms of CRPS ranged from 8 to 15 years (mean 11 y 2 mo, median 13 y). The most common movement disorder was dystonia (n=8), followed by tremors (n=3) and myoclonus (n=3); two patients had all three movement disorders. The movement disorder affected mainly the lower limb (n=9) with a predilection for the foot (n=7) and was frequently initiated by minor trauma (n=7). Follow-up ranged from 6 months to 14 years. The outcome was variable, with good prognosis in nearly half of the cases: four children experienced complete resolution of symptoms. Two children showed a slight improvement. Four children showed no improvement. Movement disorders in CRPS are under-recognized in children. The management has to be multidisciplinary with an expertise in paediatric pain.
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PMID:Movement disorders associated with complex regional pain syndrome in children. 1901 46

Cervical dystonia (CD) or spasmodic torticollis is the most frequent form of focal dystonia. Cervical dystonia is characterized by sustained neck spasms, abnormal head posture, head tremor, and pain. A 53-year-old male patient with the diagnosis of CD developed an episode of delusional depression and was treated with electroconvulsive therapy (ECT). An unexpected and dramatic improvement of CD was seen during the first 2 days after each ECT session. That therapeutic effect was not sustained and vanished soon afterward. The effectiveness of ECT for CD, although too brief to be recommended as a useful treatment, may shed light on the pathophysiology of this problematic movement disorder.
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PMID:Short-lived response of cervical dystonia to electroconvulsive therapy. 1914 11

Machado-Joseph disease or spinocerebellar ataxia 3 (MJD/SCA3) is a clinically heterogeneous, neurodegenerative disorder characterized by varying degrees of ataxia, ophthalmoplegia, peripheral neuropathy, pyramidal dysfunction and movement disorder. MJD/SCA3 is caused by a CAG repeat expansion mutation in the protein coding region of the ATXN3 gene located at chromosome 14q32.1. Current hypotheses regarding pathogenesis favor the view that mutated ataxin-3, with its polyglutamine expansion, is prone to adopt an abnormal conformation, engage in altered protein-protein interactions and aggregate. Expanded CAG repeat length correlates with the range and severity of the clinical manifestations and inversely correlates with age of disease onset. Though MJD/SCA3 is classically described as affecting the cerebellum, brainstem and basal ganglia, recent neuropathology and neuroimaging series demonstrate involvement of other areas such as the thalamus and cerebral cortex. Clinically, much emphasis has been placed in the description and recognition of the non-motor symptoms observed in these patients, such as pain, cramps, fatigue and depression. Currently, no disease modifying treatment exists for MJD/SCA3. Standard of care includes genetic counseling, exercise/physical therapy programs, and speech and swallow evaluation. Symptomatic treatment for clinical findings such as depression, sleep disorders, parkinsonism, dystonia, cramps, and pain is important to improve the quality of life for those with MJD/SCA3.
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PMID:Caring for Machado-Joseph disease: current understanding and how to help patients. 1981 45

Oromandibular dystonia (OMD) is a focal neurological movement disorder characterized by involuntary sustained and often painful muscle contraction, usually producing repetitive movements or abnormal positions of the mouth, jaw and/or tongue. We report on a 30-year-old woman affected with OMD with a 12-year follow-up. Focal dystonia involved an involuntary activity of the lateral pterygoid muscles causing forceful jaw displacement in the maximal protrusive position. These episodes initially occurred during jaw function and increased up to an open-lock with bilateral pre-auricular pain. Dystonic spasms were absent during sleep and were reduced temporarily by sensory tricks. Treatment with botulinum toxin type A (BTX) was performed during three different sessions over a 1-year period. Electromyographic-guided BTX injections into the lateral pterygoid muscles were given with cannula electrodes. Botox reduced the involuntary activity of the muscles. Recurrence and exacerbation of dystonic symptoms occurred during the two pregnancies and completely disappeared immediately after both deliveries with prolonged symptom-free periods. During the last 8 years, the patient had a slight relapse of symptoms during flu attacks, periods of stress and during menses. The temporal pattern of these symptoms indicates a possible relationship between OMD and hormonal factors.
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PMID:Oromandibular dystonia and hormonal factors: twelve years follow-up of a case report. 1984 Mar 57


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