Movement disorders are a heterogeneous group of clinical syndromes in humans and animals characterized by involuntary movements without changes in consciousness. Canine movement disorders broadly include tremors, peripheral nerve hyperexcitability disorders, paroxysmal dyskinesia, and dystonia. Of these, canine paroxysmal dyskinesias remain one of the more difficult to identify and characterize in dogs. Canine paroxysmal dyskinesias include an array of movement disorders in which there is a recurrent episode of abnormal, involuntary, movement. In this consensus statement, we recommend standard terminology for describing the various movement disorders with an emphasis on paroxysmal dyskinesia, as well as a preliminary classification and clinical approach to reporting cases. In the clinical approach to movement disorders, we recommend categorizing movements into hyperkinetic vs hypokinetic, paroxysmal vs persistent, exercise-induced vs not related to exercise, using a detailed description of movements using the recommended terminology presented here, differentiating movement disorders vs other differential diagnoses, and then finally, determining whether the paroxysmal dyskinesia is due to either inherited or acquired etiologies. This consensus statement represents a starting point for consistent reporting of clinical descriptions and terminology associated with canine movement disorders, with additional focus on paroxysmal dyskinesia. With consistent reporting and identification of additional genetic mutations responsible for these disorders, our understanding of the phenotype, genotype, and pathophysiology will continue to develop and inform further modification of these recommendations.

Navigate PD was an educational program established to supplement existing guidelines and provide recommendations on the management of Parkinson\'s disease (PD) refractory to oral/transdermal therapies. It involved 103 experts from 13 countries overseen by an International Steering Committee (ISC) of 13 movement disorder specialists. The ISC identified 71 clinical questions important for device-aided management of PD. Fifty-six experts responded to a web-based survey, rating 15 questions as \'critically important;\' these were refined to 10 questions by the ISC to be addressed through available evidence and expert opinion. Draft guidance was presented at international/national meetings and revised based on feedback. Key take-home points are: • Patients requiring levodopa >5 times daily who have severe, troublesome \'off\' periods (>1-2 h/day) despite optimal oral/transdermal levodopa or non-levodopa-based therapies should be referred for specialist assessment even if disease duration is <4 years. • Cognitive decline related to non-motor fluctuations is an indication for device-aided therapies. If cognitive impairment is mild, use deep brain stimulation (DBS) with caution. For patients who have cognitive impairment or dementia, intrajejunal levodopa infusion is considered as both therapeutic and palliative in some countries. Falls are linked to cognitive decline and are likely to become more frequent with device-aided therapies. • Insufficient control of motor complications (or drug-resistant tremor in the case of DBS) are indications for device-aided therapies. Levodopa-carbidopa intestinal gel infusions or subcutaneous apomorphine pump may be considered for patients aged >70 years who have mild or moderate cognitive impairment, severe depression or other contraindications to DBS.

The second international consensus conference on the scapula was held in Lexington Kentucky. The purpose of the conference was to update, present and discuss the accumulated knowledge regarding scapular involvement in various shoulder injuries and highlight the clinical implications for the evaluation and treatment of shoulder injuries. The areas covered included the scapula and shoulder injury, the scapula and sports participation, clinical evaluation and interventions and known outcomes. Major conclusions were (1) scapular dyskinesis is present in a high percentage of most shoulder injuries; (2) the exact role of the dyskinesis in creating or exacerbating shoulder dysfunction is not clearly defined; (3) shoulder impingement symptoms are particularly affected by scapular dyskinesis; (4) scapular dyskinesis is most aptly viewed as a potential impairment to shoulder function; (5) treatment strategies for shoulder injury can be more effectively implemented by evaluation of the dyskinesis; (6) a reliable observational clinical evaluation method for dyskinesis is available and (7) rehabilitation programmes to restore scapular position and motion can be effective within a more comprehensive shoulder rehabilitation programme.

Following the diagnosis of Parkinson\'s disease, treatment may be initiated with MAO-B-inhibitor, even prior to the development of any functional deficit. For patients with a functional deficit who are younger (usually under 75 years of age) and otherwise in good condition, treatment should be started with a dopamine agonist or MAO-B-inhibitor. In other patients, initial treatment with levodopa is recommended. In the case of difficult on-off-symptoms and dyskinesias in spite of optimal treatment, surgical procedures and duodenal levodopa infusion should be considered. Rehabilitation should be targeted at specific problems associated with functional skills.

Plasticity includes the ability of the nervous system to optimize neuronal activity at a cellular and system level according to the needs imposed by the environment. Neuroplasticity phenomena within sensorimotor cortex are crucial to enhance function to increase skillfulness. Such plasticity may be termed \"adaptive\" to indicate its ecologically beneficial role. In professional musicians, enhanced adaptive plasticity is associated with one of the highest level of motor skill a human being can achieve and the amount of these changes is even dependent on the age at which instrumental playing was started. In addition, adaptive neuroplastic changes occur when nervous system try to repair itself thus compensating dysfunctions. However, when these adaptive phenomena are pushed to an extreme, they can produce a maladaptive sensorimotor reorganization that interferes with motor performance rather than improving it. The model we discuss here is focal hand dystonia I which an intrinsic abnormality of neural plasticity, in some predisposed individuals, may lead to abnormal sensorimotor integration and to the appearance of a characteristic movement disorder. Deficient homeostatic control might be an important mechanism triggering this maladaptive reorganization, and future behavioral studies are needed to confirm this hypothesis. In the second part of this consensus paper, we will critically discuss as a second model, the hypothesis that levodopa-induced dyskinesia correlate with an aberrant form of plasticity in the human primary motor cortex, possibly because of abnormal oscillations within the basal ganglia loop. Disorders of cortical plasticity have not in the past been considered as possible causes of human clinical states. The recognition that this can occur, together with a speculative mechanism, generates an important and provocative hypothesis for future research at the clinical-scientific interface.

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