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Neurology India 2021Lamotrigine (LMT) is a phenyltriazine derivative that was originally described as an antiepileptic drug. (Review)
Review
BACKGROUND
Lamotrigine (LMT) is a phenyltriazine derivative that was originally described as an antiepileptic drug.
OBJECTIVE
This literature review aims to evaluate the clinical epidemiological profile, pathological mechanisms, and management of lamotrigine-associated movement disorders.
METHODS
Relevant reports in six databases were identified and assessed by two reviewers without language restriction. Reports that the individuals only developed tremor or ataxia after LMT use were not included.
RESULTS
In total 48 reports of 108 cases from 19 countries were assessed. The movement disorders associated with LMT found were 29 tics, 21 dyskinesias, 14 myoclonus, 13 parkinsonism, 10 dystonia, and 1 stuttering. The not clearly defined cases included 10 akathisia, 4 myoclonus, 4 cerebellar syndromes, 1 hypertonia, 1 dyskinesia, and an unknown number of dystonia cases. The mean reported age was 33.34 years (range: 1.574 years). The male was the predominant sex and the most common LMT indication was epilepsy. The mean LMT-dose at the movement disorder onset was 228 mg. The time from LMT start to the onset of movement disorder was within 6 months in 81%. The time from LMT withdrawal to complete recovery was within 1 month in 83%. The most common management was LMT withdrawal.
CONCLUSIONS
In the literature, the majority of the cases did not give a clear picture of the individual, and the times of movement disorder onset and recovery are not described. We believe that before withdrawal LMT, a dose adjustment based on the benefits and adverse events with careful evaluation case-by-case can be done.
Topics: Anticonvulsants; Ataxia; Epilepsy; Humans; Infant; Lamotrigine; Male; Movement Disorders
PubMed: 34979637
DOI: 10.4103/0028-3886.333440 -
Ugeskrift For Laeger Jul 2021This is a case report of a patient, who was diagnosed with epilepsy (atypical infantile convulsions) at the age of one year and unspecific myopathy at the age of three...
This is a case report of a patient, who was diagnosed with epilepsy (atypical infantile convulsions) at the age of one year and unspecific myopathy at the age of three years. At the age of 25 years, the patient was referred to a neuromuscular clinic due to myopathy, but the diagnose was changed to atypical infantile convulsions with seizures in adulthood and paroxysmal choreoathetosis due to a pathogenic variant c.970G>A, p. (Gly324Arg) in the PRRT2 gene.
Topics: Adult; Dyskinesias; Epilepsy, Benign Neonatal; Humans; Infant; Membrane Proteins; Mutation; Nerve Tissue Proteins; Pedigree
PubMed: 34356019
DOI: No ID Found -
The Journal of Clinical Psychiatry Dec 2019Because the symptoms of tardive dyskinesia (TD) have an insidious onset and fluctuating nature, and the risk of TD associated with second-generation antipsychotic (SGA)... (Review)
Review
Because the symptoms of tardive dyskinesia (TD) have an insidious onset and fluctuating nature, and the risk of TD associated with second-generation antipsychotic (SGA) treatment has been underestimated, it has been challenging for clinicians to make an early and accurate TD diagnosis. More patients are at risk of developing this potentially permanent, disabling condition than ever before because of the widespread use of SGAs; therefore, prevention of TD, if possible, is of utmost importance. Clinicians must use reliable screening tools and diagnostic criteria to assess patients for TD, rule out other abnormal movement conditions, and make an accurate TD diagnosis.
Topics: Antipsychotic Agents; Early Diagnosis; Humans; Risk Factors; Tardive Dyskinesia
PubMed: 31846242
DOI: 10.4088/JCP.NU18041BR1C -
Tremor and Other Hyperkinetic Movements... 2020Telemedicine is the use of electronic communication technology to facilitate healthcare between distant providers and patients. In addition to synchronous video... (Review)
Review
Telemedicine is the use of electronic communication technology to facilitate healthcare between distant providers and patients. In addition to synchronous video conferencing, asynchronous video transfer has been used to support care for neurology patients. There is a growing literature on using telemedicine in movement disorders, with the most common focus on Parkinson's disease. There is accumulating evidence for videoconferencing to diagnose and treat patients with hyperkinetic movement disorders and to support providers in remote underserviced areas. Cognitive testing has been shown to be feasible remotely. Genetic counseling and other counseling-based therapeutic interventions have also successfully performed in hyperkinetic movement disorders. We use a problem-based approach to review the current evidence for the use of telemedicine in various hyperkinetic movement disorders. This Viewpoint attempts to identify possible telemedicine solutions as well as discussing unmet needs and future directions.
Topics: Dystonic Disorders; Genetic Counseling; Humans; Huntington Disease; Hyperkinesis; Medically Underserved Area; Movement Disorders; Myoclonus; Neuropsychological Tests; Parkinson Disease; Remote Consultation; Telemedicine; Tic Disorders; Tremor; Videoconferencing
PubMed: 32195039
DOI: 10.7916/tohm.v0.698 -
Arquivos de Neuro-psiquiatria May 2022Parkinson's disease (PD) is a complex neurodegenerative condition. Treatment strategies through all stages of disease progression could affect quality of life and... (Review)
Review
BACKGROUND
Parkinson's disease (PD) is a complex neurodegenerative condition. Treatment strategies through all stages of disease progression could affect quality of life and influence the development of future complications, making it crucial for the clinician to be on top of the literature.
OBJECTIVE
This paper reviews the current treatment of PD, from early to advanced stages.
METHODS
A literature review was conducted focusing on the treatment of PD, in the different stages of progression.
RESULTS
Every individual with a new diagnosis of PD should be encouraged to start exercising regularly. In the early stage, treatment should focus on using the lowest dose of levodopa or combination therapy that provides maximum functional capacity, and does not increase the risk of complications, such as peak dose dyskinesias and impulse control disorders. At the moderate and advanced stages, motor fluctuations and complications of treatment dominate the picture, making quality of life one important issue. Rehabilitation programs can improve motor symptoms and should be offered to all patients at any stage of disease progression.
CONCLUSION
Many factors need to be considered when deciding on the best treatment strategy for PD, such as disease progression, presence of risk factors for motor and behavioral complications, potential side effects from dopaminergic therapy and phenotypical variabilities. Treatment should focus on functional capacity and quality of life throughout the whole disease course.
Topics: Antiparkinson Agents; Disease Progression; Dyskinesias; Humans; Levodopa; Parkinson Disease; Quality of Life
PubMed: 35976316
DOI: 10.1590/0004-282X-ANP-2022-S126 -
Neurobiology of Disease May 2022This review provides an overview of the synaptic dysfunctions of neuronal circuits and underlying neurochemical alterations observed in the hyperkinetic movement... (Review)
Review
This review provides an overview of the synaptic dysfunctions of neuronal circuits and underlying neurochemical alterations observed in the hyperkinetic movement disorders, dystonia and dyskinesia. These disorders exhibit similar changes in expression of synaptic plasticity and neuromodulation. This includes alterations in physical attributes of synapses, synaptic protein expression, and neurotransmitter systems, such as glutamate and gamma-aminobutyric acid (GABA), and neuromodulators, such as dopamine, acetylcholine, serotonin, adenosine, and endocannabinoids. A full understanding of the mechanisms and consequences of disruptions in synaptic function and plasticity will lend insight into the development of these disorders and new ways to combat maladaptive changes.
Topics: Antiparkinson Agents; Corpus Striatum; Dyskinesias; Dystonia; Dystonic Disorders; Humans; Levodopa
PubMed: 35139431
DOI: 10.1016/j.nbd.2022.105650 -
Cell Reports. Medicine Oct 2023Dyskinesia is involuntary movement caused by long-term medication with dopamine-related agents: the dopamine agonist 3,4-dihydroxy-L-phenylalanine (L-DOPA) to treat...
Dyskinesia is involuntary movement caused by long-term medication with dopamine-related agents: the dopamine agonist 3,4-dihydroxy-L-phenylalanine (L-DOPA) to treat Parkinson's disease (L-DOPA-induced dyskinesia [LID]) or dopamine antagonists to treat schizophrenia (tardive dyskinesia [TD]). However, it remains unknown why distinct types of medications for distinct neuropsychiatric disorders induce similar involuntary movements. Here, we search for a shared structural footprint using magnetic resonance imaging-based macroscopic screening and super-resolution microscopy-based microscopic identification. We identify the enlarged axon terminals of striatal medium spiny neurons in LID and TD model mice. Striatal overexpression of the vesicular gamma-aminobutyric acid transporter (VGAT) is necessary and sufficient for modeling these structural changes; VGAT levels gate the functional and behavioral alterations in dyskinesia models. Our findings indicate that lowered type 2 dopamine receptor signaling with repetitive dopamine fluctuations is a common cause of VGAT overexpression and late-onset dyskinesia formation and that reducing dopamine fluctuation rescues dyskinesia pathology via VGAT downregulation.
Topics: Mice; Animals; Dopamine Agonists; Levodopa; Dopamine; Antiparkinson Agents; Parkinsonian Disorders; Dyskinesia, Drug-Induced; Oxidopamine; gamma-Aminobutyric Acid
PubMed: 37774703
DOI: 10.1016/j.xcrm.2023.101208 -
Neurology India 2023
Topics: Humans; Chorea; Dyskinesias; Hyperglycemic Hyperosmolar Nonketotic Coma
PubMed: 37635540
DOI: 10.4103/0028-3886.383864 -
The Journal of Clinical Psychiatry Dec 2019Tardive dyskinesia (TD), a condition of potentially irreversible abnormal involuntary movements that is associated with dopamine receptor blocking agents (DRBAs),... (Review)
Review
Tardive dyskinesia (TD), a condition of potentially irreversible abnormal involuntary movements that is associated with dopamine receptor blocking agents (DRBAs), produces significant impairment of functioning and quality of life for patients. Contrary to expectations, TD has not vanished despite the introduction of SGAs. Instead, changing prescription practices and increased off-label prescription of DRBAs have placed more patients than ever at risk of this potentially dangerous and disabling condition. This activity provides an overview of treatment strategies for TD as part of an individualized management plan, including DRBA medication adjustment and antidyskinetic treatment.
Topics: Antipsychotic Agents; Dopamine Antagonists; Humans; Tardive Dyskinesia
PubMed: 31880872
DOI: 10.4088/JCP.NU18041BR4C -
Movement Disorders : Official Journal... May 2021Autophagy is intensively studied in cancer, metabolic and neurodegenerative diseases, but little is known about its role in pathological conditions linked to altered...
BACKGROUND
Autophagy is intensively studied in cancer, metabolic and neurodegenerative diseases, but little is known about its role in pathological conditions linked to altered neurotransmission. We examined the involvement of autophagy in levodopa (l-dopa)-induced dyskinesia, a frequent motor complication developed in response to standard dopamine replacement therapy in parkinsonian patients.
METHODS
We used mouse and non-human primate models of Parkinson's disease to examine changes in autophagy associated with chronic l-dopa administration and to establish a causative link between impaired autophagy and dyskinesia.
RESULTS
We found that l-dopa-induced dyskinesia is associated with accumulation of the autophagy-specific substrate p62, a marker of autophagy deficiency. Increased p62 was observed in a subset of projection neurons located in the striatum and depended on l-dopa-mediated activation of dopamine D1 receptors, and mammalian target of rapamycin. Inhibition of mammalian target of rapamycin complex 1 with rapamycin counteracted the impairment of autophagy produced by l-dopa, and reduced dyskinesia. The anti-dyskinetic effect of rapamycin was lost when autophagy was constitutively suppressed in D1 receptor-expressing striatal neurons, through inactivation of the autophagy-related gene protein 7.
CONCLUSIONS
These findings indicate that augmented responsiveness at D1 receptors leads to dysregulated autophagy, and results in the emergence of l-dopa-induced dyskinesia. They further suggest the enhancement of autophagy as a therapeutic strategy against dyskinesia. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
Topics: Animals; Antiparkinson Agents; Autophagy; Corpus Striatum; Disease Models, Animal; Dyskinesia, Drug-Induced; Humans; Levodopa; Mice; Oxidopamine; Parkinsonian Disorders
PubMed: 33460487
DOI: 10.1002/mds.28480