Lithium monotherapy-induced tardive dyskinesia

Fountoulakis, Konstantinos Ν.; Tegos, Thomas; Kimiskidis, Vasilios Κ.

doi:10.1016/j.jad.2018.10.094

Cited by 12 publications

(3 citation statements)

References 14 publications

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“…The conventional mood stabilizer lithium is associated with parkinsonism and, in a few case reports, tardive dyskinesia. 3 , 4 More commonly, lithium is associated with postural and action tremors (estimates of frequency range from 4% to 65%). It is important to note that lithium-induced tremors are not characteristic of the tremor featured in parkinsonism, which is a resting tremor.…”

Section: Discussionmentioning

confidence: 99%

Extrapyramidal side effects with nonantipsychotic medications

Koch,

Launio,

Williams

2024

Mental Health Clinician

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Section: Discussionmentioning

confidence: 99%

Extrapyramidal side effects with nonantipsychotic medications

Koch,

Launio,

Williams

2024

Mental Health Clinician

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“…[22] TD may also occur due to dose reduction or abrupt discontinuation of antipsychotics. [30] Other drugs such as antidepressants (e.g., duloxetine), [26] mood stabilizers (lithium), [31] and calcium channel blockers (e.g., flunarizine) have been reported to trigger TD (e.g., flunarizine). Table 2).…”

Section: Pathophysiologymentioning

confidence: 99%

Drug-Induced Tardive Dyskinesia

Marianto¹,

Kosim

Wedastra

2021

Int J Res Rev

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Drug-induced movement disorders could be classified into acute, subacute, and chronic based on the time of occurrence. Tardive dyskinesia (TD) is one of the most frequent long-term drug-induced movement disorders. Delay in treatment often caused TD to be irreversible. In this review, we will discuss TD in-depth to enhance clinician knowledge regarding the diagnosis, prevention, and comprehensive management of patients with TD. Keywords: tardive dyskinesia, movement, disorder, antipsychotic.

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“…In addition to TDZD8, other direct inhibitors of potential interest include various drugs such as tideglusib, lithium, valproic acid, and CHIR 99021. Lithium rarely triggers TD by itself, and its role as a potentiating factor in patients under polypharmacy developing TD is unclear . Chronic lithium use has been reported to protect and attenuate TD in a population of patients with schizophrenia, whereas short‐term effects were disappointing .…”

Section: Gsk‐3β As a Key Signaling Molecule In Tdmentioning

confidence: 99%

Time for a New Slate in Tardive Dyskinesia Research

Blanchet

Lévesque

2020

Movement Disorders

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Despite high hopes and expectations that modern antipsychotic drug therapy would finally come to grips with tardive dyskinesia (TD) and pave the way for its burial, this potentially irreversible complication remained a fearsome and challenging issue, particularly in older age groups. Long-term prevalence rates >20% are still reported even in patients never exposed to firstgeneration drugs. 1-3 The gospel of TD has taught generations that striatal dopamine D 2 receptors become supersensitive during antipsychotic drug treatment. In the interval, the body of research supporting this hypothesis in human TD has remained deceptively thin, only to promote the development of novel antipsychotic drugs lacking robust affinity and selectivity for D 2 receptors supposed to avoid TD. Evidently, this has not panned out yet. Unfortunately, drug management of moderate-to-severe TD remains limited, attributable, in large part, to knowledge gaps in pathophysiology. Alleviation of TD scores afforded by vesicular monoamine transporter type 2 (VMAT2) blockade with tetrabenazine, deutetrabenazine, and valbenazine 4 proved their clinical relevance and supported two basic points in TD: (1) relative integrity of VMAT2 function and (2) implication of dopamine signaling. The proportion of responders' rate (≥50% reduction in baseline TD scores on the Abnormal Involuntary Movements Scale) <50% with these drugs 5 is a good indicator of the challenge awaiting clinicians managing TD. In this brief article, we present recent molecular findings indirectly suggesting the presence of enhanced striatal dopamine signaling in TD beyond D 2 receptors and wish to call out researchers and clinicians in considering new dopaminergic and nondopaminergic targets to improve management through modulation of glycogen synthase kinase (GSK)-3 activity.The mechanisms underlying delayed induction and maintenance of TD, as well as susceptibility of elderly subjects, remain elusive. The research community has relied essentially on experimental rodent models in order to achieve progress in the field. The short-acting dosing methods used for drug exposure in rodents have been questioned, given that they yield excessive peak and rapid trough levels in accordance with the short half-life of haloperidol in rodents (2-3 hours) relative to humans (>24 hours). 6 Furthermore, the relevance of the brief 3-week drug exposure proposed to assess the resulting vacuous chewing movements (VCM) response has also been raised, susceptible to reflect acute extrapyramidal reactions rather than genuine TD, leading some groups to advocate an extension of the haloperidol exposure to 6 months with more continuous forms of drug delivery with the drinking water or long-acting intramuscular depot preparations, before conducting further experiments. 7,8 Differences in phenomenology between early versus late VCM responses are also difficult to appreciate, but the acute impact of a shortacting haloperidol injection on VCM scores and distinct striatal dynorphin mRNA expression have argued for late ...

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Lithium monotherapy-induced tardive dyskinesia

Cited by 12 publications

References 14 publications

Extrapyramidal side effects with nonantipsychotic medications

Extrapyramidal side effects with nonantipsychotic medications

Drug-Induced Tardive Dyskinesia

Time for a New Slate in Tardive Dyskinesia Research

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