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Tremor and Other Hyperkinetic Movements... 2022Multiple sclerosis (MS), a subset of chronic primary inflammatory demyelinating disorders of the central nervous system, is closely associated with various movement... (Review)
Review
BACKGROUND
Multiple sclerosis (MS), a subset of chronic primary inflammatory demyelinating disorders of the central nervous system, is closely associated with various movement disorders. These disorders may be due to MS pathophysiology or be coincidental. This review describes the full spectrum of movement disorders in MS with their possible mechanistic pathways and therapeutic modalities.
METHODS
The authors conducted a narrative literature review by searching for 'multiple sclerosis' and the specific movement disorder on PubMed until October 2021. Relevant articles were screened, selected, and included in the review according to groups of movement disorders.
RESULTS
The most prevalent movement disorders described in MS include restless leg syndrome, tremor, ataxia, parkinsonism, paroxysmal dyskinesias, chorea and ballism, facial myokymia, including hemifacial spasm and spastic paretic hemifacial contracture, tics, and tourettism. The anatomical basis of some of these disorders is poorly understood; however, the link between them and MS is supported by clinical and neuroimaging evidence. Treatment options are disorder-specific and often multidisciplinary, including pharmacological, surgical, and physical therapies.
DISCUSSION
Movements disorders in MS involve multiple pathophysiological processes and anatomical pathways. Since these disorders can be the presenting symptoms, they may aid in early diagnosis and managing the patient, including monitoring disease progression. Treatment of these disorders is a challenge. Further work needs to be done to understand the prevalence and the pathophysiological mechanisms responsible for movement disorders in MS.
Topics: Chorea; Dyskinesias; Humans; Movement Disorders; Multiple Sclerosis; Tremor
PubMed: 35601204
DOI: 10.5334/tohm.671 -
Journal of Parkinson's Disease 2020In people with young onset Parkinson's disease (YOPD), onset of symptoms is between 21 and 40 years of age. The distinction between YOPD and late-onset Parkinson's... (Review)
Review
In people with young onset Parkinson's disease (YOPD), onset of symptoms is between 21 and 40 years of age. The distinction between YOPD and late-onset Parkinson's disease is supported by genetic differences (a genetic etiology is more common in people with YOPD) and clinical differences (e.g., dystonia and levodopa-induced dyskinesias are more common inYOPD). Moreover, people with YOPD tend to have different family and societal engagements compared to those with late-onset PD. These unique features have implications for clinical management, and call for a tailored multidisplinary approach involving shared-decision making.
Topics: Adult; Age of Onset; Disease Management; Dystonia; Female; Humans; Male; Parkinson Disease; Pregnancy; Pregnancy Complications; Social Interaction; Work Schedule Tolerance; Young Adult
PubMed: 32651336
DOI: 10.3233/JPD-202135 -
Brazilian Journal of Physical Therapy 2021Scapular focused exercise interventions are frequently used to treat individuals with shoulder pain. However, evidence for changes in scapular motion after intervention...
BACKGROUND
Scapular focused exercise interventions are frequently used to treat individuals with shoulder pain. However, evidence for changes in scapular motion after intervention is limited.
OBJECTIVE
To compare the effects of scapular movement training versus standardized exercises for individuals with shoulder pain.
METHODS
This will be a single-blinded randomized controlled trial. Sixty-four individuals with shoulder pain for at least 3 months, scapular dyskinesis, and a positive scapular assistance test will be randomly allocated to one of two groups: Scapular Movement Training (group 1) and Standardized Exercises (group 2). Group 1 will receive education about scapular position and movement, and be trained to modify the scapular movement pattern. Group 2 will perform stretching and strengthening exercises. Both groups will be treated twice a week for eight weeks. Three-dimensional scapular kinematics and muscle activity of the serratus anterior and upper, middle, and lower trapezius during elevation and lowering of the arm will be assessed at baseline and after 8 weeks of treatment. Pain intensity, function, fear avoidance beliefs, and kinesiophobia will be assessed at baseline and after 4 and 8 weeks of treatment, and 4 weeks after the end of treatment.
CONCLUSIONS
The results of this study may contribute to a better understanding of the efficacy of scapular focused treatments for individuals with shoulder pain.
CLINICAL TRIAL REGISTRATION
NCT03528499.
Topics: Humans; Biomechanical Phenomena; Dyskinesias; Exercise; Exercise Therapy; Movement; Scapula; Shoulder Pain; Superficial Back Muscles; Randomized Controlled Trials as Topic
PubMed: 32855073
DOI: 10.1016/j.bjpt.2020.08.001 -
Neurotherapeutics : the Journal of the... Oct 2020Levodopa is the most effective medication for the treatment of the motor symptoms of Parkinson's disease. However, over time, the clinical response to levodopa becomes... (Review)
Review
Levodopa is the most effective medication for the treatment of the motor symptoms of Parkinson's disease. However, over time, the clinical response to levodopa becomes complicated by a reduction in the duration and reliability of motor improvement (motor fluctuations) and the emergence of involuntary movements (levodopa-induced dyskinesia). Strategies that have been attempted in an effort to delay the development of these motor complications include levodopa sparing and continuous dopaminergic therapy. Once motor complications occur, a wide array of medical treatments is available to maximize motor function through the day while limiting dyskinesia. Here, we review the clinical features, epidemiology, and risk factors for the development of motor complications, as well as strategies for their prevention and medical management.
Topics: Antiparkinson Agents; Carbidopa; Catechol O-Methyltransferase Inhibitors; Delayed-Action Preparations; Disease Management; Dyskinesias; Humans; Levodopa; Parkinson Disease
PubMed: 32761324
DOI: 10.1007/s13311-020-00889-4 -
CNS Spectrums Apr 2022Accurate diagnosis and appropriate treatment of tardive dyskinesia (TD) are imperative, as its symptoms can be highly disruptive to both patients and their caregivers.... (Review)
Review
Accurate diagnosis and appropriate treatment of tardive dyskinesia (TD) are imperative, as its symptoms can be highly disruptive to both patients and their caregivers. Misdiagnosis can lead to incorrect interventions with suboptimal or even deleterious results. To aid in the identification and differentiation of TD in the psychiatric practice setting, we review its clinical features and movement phenomenology, as well as those of other antipsychotic-induced movement disorders, with accompanying links to illustrative videos. Exposure to dopamine receptor blocking agents (DRBAs) such as antipsychotics or antiemetics is associated with a spectrum of movement disorders including TD. The differential diagnosis of TD is based on history of DRBA exposure, recent discontinuation or dose reduction of a DRBA, and movement phenomenology. Common diagnostic challenges are the abnormal behaviors and dyskinesias associated with advanced age or chronic mental illness, and other movement disorders associated with DRBA therapy, such as akathisia, parkinsonian tremor, and tremor related to use of mood stabilizing agents (eg, lithium, divalproex). Duration of exposure may help rule out acute drug-induced syndromes such as acute dystonia or acute/subacute akathisia. Another important consideration is the potential for TD to present together with other drug-induced movement disorders (eg, parkinsonism, parkinsonian tremor, and postural tremor from mood stabilizers) in the same patient, which can complicate both diagnosis and management. After documentation of the phenomenology, severity, and distribution of TD movements, treatment options should be reviewed with the patient and caregivers.
Topics: Antipsychotic Agents; Humans; Movement Disorders; Psychomotor Agitation; Tardive Dyskinesia; Tremor
PubMed: 33213556
DOI: 10.1017/S109285292000200X -
Translational Neurodegeneration Feb 2021Paroxysmal dyskinesias are a group of neurological diseases characterized by intermittent episodes of involuntary movements with different causes. Paroxysmal kinesigenic... (Review)
Review
Paroxysmal dyskinesias are a group of neurological diseases characterized by intermittent episodes of involuntary movements with different causes. Paroxysmal kinesigenic dyskinesia (PKD) is the most common type of paroxysmal dyskinesia and can be divided into primary and secondary types based on the etiology. Clinically, PKD is characterized by recurrent and transient attacks of involuntary movements precipitated by a sudden voluntary action. The major cause of primary PKD is genetic abnormalities, and the inheritance pattern of PKD is mainly autosomal-dominant with incomplete penetrance. The proline-rich transmembrane protein 2 (PRRT2) was the first identified causative gene of PKD, accounting for the majority of PKD cases worldwide. An increasing number of studies has revealed the clinical and genetic characteristics, as well as the underlying mechanisms of PKD. By seeking the views of domestic experts, we propose an expert consensus regarding the diagnosis and treatment of PKD to help establish standardized clinical evaluation and therapies for PKD. In this consensus, we review the clinical manifestations, etiology, clinical diagnostic criteria and therapeutic recommendations for PKD, and results of genetic analyses in PKD patients performed in domestic hospitals.
Topics: China; Chorea; Consensus; Dystonia; Humans; Membrane Proteins; Nerve Tissue Proteins
PubMed: 33588936
DOI: 10.1186/s40035-021-00231-8 -
Tremor and Other Hyperkinetic Movements... 2023Episodic ataxia (EA), characterized by recurrent attacks of cerebellar dysfunction, is the manifestation of a group of rare autosomal dominant inherited disorders. EA1... (Review)
Review
BACKGROUND
Episodic ataxia (EA), characterized by recurrent attacks of cerebellar dysfunction, is the manifestation of a group of rare autosomal dominant inherited disorders. EA1 and EA2 are most frequently encountered, caused by mutations in and . EA3-8 are reported in rare families. Advances in genetic testing have broadened the and phenotypes, and detected EA as an unusual presentation of several other genetic disorders. Additionally, there are various secondary causes of EA and mimicking disorders. Together, these can pose diagnostic challenges for neurologists.
METHODS
A systematic literature review was performed in October 2022 for 'episodic ataxia' and 'paroxysmal ataxia', restricted to publications in the last 10 years to focus on recent clinical advances. Clinical, genetic, and treatment characteristics were summarized.
RESULTS
EA1 and EA2 phenotypes have further broadened. In particular, EA2 may be accompanied by other paroxysmal disorders of childhood with chronic neuropsychiatric features. New treatments for EA2 include dalfampridine and fampridine, in addition to 4-aminopyridine and acetazolamide. There are recent proposals for EA9-10. EA may also be caused by gene mutations associated with chronic ataxias (), epilepsy syndromes (), GLUT-1, mitochondrial disorders (), metabolic disorders (Maple syrup urine disease, Hartnup disease, type I citrullinemia, thiamine and biotin metabolism defects), and others. Secondary causes of EA are more commonly encountered than primary EA (vascular, inflammatory, toxic-metabolic). EA can be misdiagnosed as migraine, peripheral vestibular disorders, anxiety, and functional symptoms. Primary and secondary EA are frequently treatable which should prompt a search for the cause.
DISCUSSION
EA may be overlooked or misdiagnosed for a variety of reasons, including phenotype-genotype variability and clinical overlap between primary and secondary causes. EA is highly treatable, so it is important to consider in the differential diagnosis of paroxysmal disorders. Classical EA1 and EA2 phenotypes prompt single gene test and treatment pathways. For atypical phenotypes, next generation genetic testing can aid diagnosis and guide treatment. Updated classification systems for EA are discussed which may assist diagnosis and management.
Topics: Humans; Ataxia; Cerebellar Ataxia; Acetazolamide; Mutation
PubMed: 37008993
DOI: 10.5334/tohm.747 -
Scientific Reports Nov 2020Upper crossed syndrome (UCS) refers to the altered muscle activations and movement patterns in scapulae along with some abnormal alignment in the upper quarter, which... (Clinical Trial)
Clinical Trial Randomized Controlled Trial
Upper crossed syndrome (UCS) refers to the altered muscle activations and movement patterns in scapulae along with some abnormal alignment in the upper quarter, which may contribute to the dysfunction of the cervicothoracic and glenohumeral joints. The present study aimed to investigate the effectiveness of a comprehensive corrective exercise program (CCEP) and subsequent detraining on alignment, muscle activation, and movement pattern in men with the UCS. This randomized controlled trial included 24 men. The intervention group conducted CCEP (8 weeks), followed by four weeks of detraining and the control group maintained normal daily activities. Electromyography of selected muscles, scapular dyskinesis test, head, shoulder, and thoracic spine angle were measured at baseline, post-test, and follow-up. There were significant differences for Group x time interaction and also for within-group from pre-test to post-test and follow-up in all outcomes. Also, significant differences were observed in three outcomes at post-test and follow-up between the CCEP and control group in favor of the CCEP. In Conclusion, the present study demonstrates that the CCEP for individuals with UCS is feasible and effective, improving muscle activation imbalance, movement patterns, and alignment. Importantly, these improvements were maintained after four weeks of detraining, suggesting lasting neuromuscular re-training adaptations.
Topics: Adult; Dyskinesias; Electromyography; Exercise; Exercise Therapy; Humans; Male; Movement; Muscles; Scapula; Shoulder; Shoulder Joint; Spine
PubMed: 33244045
DOI: 10.1038/s41598-020-77571-4 -
Journal of Veterinary Internal Medicine May 2021Movement disorders are a heterogeneous group of clinical syndromes in humans and animals characterized by involuntary movements without changes in consciousness. Canine...
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.
Topics: Animals; Chorea; Dog Diseases; Dogs; Dyskinesias; Mutation; Phenotype
PubMed: 33769611
DOI: 10.1111/jvim.16108 -
Journal of Postgraduate Medicine 2016Asterixis is a type of negative myoclonus characterized by irregular lapses of posture of various body parts. It is an uncommon but important sign in clinical neurology.... (Review)
Review
Asterixis is a type of negative myoclonus characterized by irregular lapses of posture of various body parts. It is an uncommon but important sign in clinical neurology. Initially described as a "liver flap," its utility encompasses a galaxy of neurological and nonneurological situations. Asterixis has a rich history. Despite being described over 70 years ago, its exact pathogenesis remains unknown. Its significance as a tool for the evaluation and prognosis of encephalopathies has been suggested. This review presents its history, clinical implications and its significance.
Topics: Brain; Dyskinesias; Humans; Movement Disorders; Myoclonus
PubMed: 27089111
DOI: 10.4103/0022-3859.180572