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Leslie Citrome - One of the best experts on this subject based on the ideXlab platform.

  • 41 a modified delphi consensus approach to clinical guidelines for tardive dyskinesia
    Cns Spectrums, 2019
    Co-Authors: Stanley N Caroff, Leslie Citrome, Jonathan M Meyer, Leslie Lundt, Kimberly Riggs, Martha Sajatovic, Terence A Ketter
    Abstract:

    Objective Vesicular monoamine transporter 2 (VMAT2) inhibitors are the first class of drugs approved to treat tardive dyskinesia (TD). With the recent approval of these medications, a modified Delphi process was implemented to address the need for updated clinical guidelines for TD screening, diagnosis, and treatment. Methods A Steering Committee of 11 TD experts met in a Nominal Group meeting format to discuss/prioritize questions to be addressed about TD and identify individuals to be invited to serve as Delphi survey panelists. Two survey rounds were conducted anonymously; responses were collected, collated, and analyzed. Respondent agreement was defined a priori by the Steering Committee as unanimous (100%), consensus (75–99%), or majority (50–74%). For questions using a 5-point Likert scale, agreement was based on percentage of respondents choosing ≥4 (“agree completely” or “agree”). Round 1 survey included questions on TD screening, diagnosis, and treatment. Round 2 questions were refined per panelist feedback and excluded Round 1 questions with 75% agreement). Results Online surveys were sent to 60 individuals; 29 agreed to participate as panelists (23 psychiatrists; 6 neurologists). Respondents unanimously agreed (100%) that all patients currently taking Dopamine Receptor Blocking agents (DRBAs) should be screened for TD, and that the Abnormal Involuntary Movement Scale (AIMS) is the standard structured assessment for monitoring severity of TD. There was consensus (76%) that a semi-structured assessment could be used for more frequent routine TD screening. Respondents unanimously agreed that treatment with first generation antipsychotics, older age, and longer cumulative exposure to antipsychotics were risk factors for TD. For TD diagnosis, consensus (89%) was reached that a patient with an AIMS score >2 (mild) affecting 1 body area should be considered as having possible TD; consensus (93%) was also reached that TD was most often evident in orofacial musculature, although other body areas may be affected and should not be neglected. Consensus was not reached on minimum cumulative duration of DRBA exposure for TD diagnosis, but a majority (70%) agreed that minimum cumulative exposure of 1month may be sufficient. For TD treatment, unanimity or consensus was reached on 4 strategies to consider: discussion of treatment options with patients/caregivers (100%), modification of antipsychotic regimen (100%), treatment with VMAT2 inhibitor (100%), and modification of anticholinergic regimen (86%). Conclusions Using a Nominal Group and modified Delphi process, consensus was reached within 1−2 rounds on several key aspects of TD screening, diagnosis, and treatment. This process may offer an expedient method to identify gaps in agreement and facilitate updated management guidelines. Funding Acknowledgements: Sponsored by Neurocrine Biosciences,Inc.

  • antipsychotic related movement disorders drug induced parkinsonism vs tardive dyskinesia key differences in pathophysiology and clinical management
    Neurology and Therapy, 2018
    Co-Authors: Kristen M Ward, Leslie Citrome
    Abstract:

    Drug-induced parkinsonism (DIP) and tardive dyskinesia (TD) are stigmatizing movement disorders associated with exposure to Dopamine Receptor Blocking agents such as antipsychotics, but they differ in their pathophysiology and clinical management. Treatment for one may worsen the other, and there are important diagnostic clues that assist in making an accurate assessment and instituting a rational treatment plan. A literature review was executed to identify articles relating to the presentation, pathophysiology, epidemiology, and management of DIP and TD. DIP and TD prevalence estimates range from approximately 20 to 35% among antipsychotic users, but may be higher in select populations. DIP often presents as bradykinesia and rigidity, as well as rhythmic tremor, and the majority of cases appear within hours to weeks of initiation of therapy with an antipsychotic, or if dosage of the antipsychotic is increased. TD onset is delayed, typically appearing after at least 3 months or longer of treatment, and patients will commonly present with involuntary, abnormal facial movements such as lip smacking, puckering, chewing, or tongue protrusion. DIP often resolves with discontinuation of the causative agent, but TD may be permanent. Broadly, proposed mechanisms underlying these adverse events include decreased Dopamine concentrations in the nigrostriatal pathway of the striatum and Dopamine hypersensitivity, for DIP and TD, respectively. Pharmacologic treatment approaches for DIP have commonly included anticholinergic agents such as benztropine; however, anticholinergic medications can make TD worse. Switching the antipsychotic medication to one with lower propensity for DIP is an option for some patients. Amantadine, a non-anticholinergic agent used for the treatment of DIP, may be preferred in patients with comorbid DIP and TD. In TD, treatment options include the new reversible vesicular monoamine 2 transporter inhibitors, valbenazine and deutetrabenazine. It is important for clinicians to be able to recognize DIP and TD in patients using antipsychotics so that they can minimize the impact of these adverse events on their patients’ quality of life. Accurate diagnosis will drive the selection of the correct treatment. Plain language summary available for this article.

  • tardive dyskinesia placing vesicular monoamine transporter type 2 vmat2 inhibitors into clinical perspective
    Expert Review of Neurotherapeutics, 2018
    Co-Authors: Leslie Citrome
    Abstract:

    Introduction: Tardive dyskinesia (TD) is an iatrogenic movement disorder caused by exposure to Dopamine Receptor Blocking agents. Two vesicular monoamine transporter type 2 (VMAT2) inhibitors for t...

  • epidemiology prevention and assessment of tardive dyskinesia and advances in treatment
    The Journal of Clinical Psychiatry, 2017
    Co-Authors: John M Kane, Christoph U Correll, Leslie Citrome
    Abstract:

    ​​ Tardive dyskinesia (TD) is a disorder characterized by involuntary movements, typically of the orofacial muscles and also of the extremities and other muscle groups. The condition is associated with exposure to Dopamine Receptor Blocking agents, including antipsychotics. Because the indications and off-label uses for these agents have expanded over the last 2 decades, a larger number of patients are receiving antipsychotic medications than in the past. While evidence suggests that patients being treated with second-generation antipsychotics have less risk for developing TD than those treated with first-generation antipsychotics, the decreased risk is not as great as was originally expected. In addition, patients with chronic psychiatric conditions often require long-term use of antipsychotics, putting them at risk for TD. This article addresses the prevalence, risk factors, and prevention of TD; assessment strategies including diagnostic criteria and rating scales; and evidence for TD treatments, including 2 newly approved medications: deutetrabenazine and valbenazine. ​​​.

Joseph Jankovic - One of the best experts on this subject based on the ideXlab platform.

  • treatment of tardive dyskinesia
    Neurologic Clinics, 2020
    Co-Authors: Hassaan Bashir, Joseph Jankovic
    Abstract:

    Tardive dyskinesia (TD) is an iatrogenic condition that encompasses a wide phenomenological spectrum of movement disorders caused by exposure to Dopamine Receptor Blocking agents (DRBAs). TD may cause troublesome or disabling symptoms that impair quality of life. Due to frequent, often inappropriate, use of DRBAs, TD prevalence rates among patients exposed to DRBAs continue to be high. The judicious use of DRBAs is key to the prevention of TD, reduction of disease burden, and achieving lasting remission. Dopamine-depleting vesicular monoamine transporter type 2 inhibitors are considered the treatment of choice of TD.

  • the nosology of tardive syndromes
    Journal of the Neurological Sciences, 2018
    Co-Authors: Karen Frei, Joseph Jankovic, Daniel Truong, Stanley Fahn, Robert A Hauser
    Abstract:

    Since the original description of side effects of neuroleptics, different terminologies and definitions for tardive dyskinesia (TD) and tardive syndrome (TS) have been used by different authors, and often these two terms have been used interchangeably. This paper proposes a nosology designed to define and clarify various terms and phenomenologies within the TS spectrum. We propose to use the term tardive dyskinesia to refer to the original description of repetitive and complex oral-buccal-lingual (OBL) movements, as well as to the analogous repetitive movements that can appear in the limbs, trunk, or pelvis. The repetitive, relatively rhythmic nature of the movements is the common denominator of this phenomenologic category. The term tardive syndrome refers to the spectrum of all persistent hyperkinetic, hypokinetic and sensory phenomenologies resulting from chronic Dopamine Receptor Blocking agents (DRBA) exposure. Thus, TS is an umbrella term. When dystonia is the main feature of TS it is considered to be tardive dystonia (TDyst). Retrocollis appears to be the predominant form of cervical dystonia in this condition. Cranial dystonias, particularly oromandibular dystonia, are also common forms of TDyst. Tardive akathisia refers to the inability to remain still with an urge to move, giving the appearance of restlessness. It is a sensory phenomenon and a common and disabling form of TS. Unlike acute akathisia, tardive akathisia tends to occur late and persists after the drug is withdrawn. In tardive tourettism, the patient exhibits the features of Tourette syndrome with complex motor and phonic tics associated with premonitory urge and relief of tension after performing the tic behavior. Tardive tremor differs from the resting tremor seen in drug-induced parkinsonism in that it is mainly a postural and kinetic greater than resting tremor. Tardive pain has been reported in association with chronic use of DRBA's. The pain involved the mouth, tongue and the genital region. The patients tended to obsess over the pain and usually had some other form of motor tardive syndrome, either tardive dyskinesia, tardive akathisia or tardive dystonia. The term tardive parkinsonism has been proposed for those drug induced parkinsonism patients who have persistent symptoms following discontinuation of the DRBA. However, there is a strong possibility that the DRBA may have simply unmasked subclinical parkinsonism or that there is coincident Parkinson disease developing during the period the patient is taking the DRBA.

  • Treatment of Tardive Dyskinesia: A General Overview with Focus on the Vesicular Monoamine Transporter 2 Inhibitors
    Drugs, 2018
    Co-Authors: Nicki Niemann, Joseph Jankovic
    Abstract:

    Tardive dyskinesia (TD) encompasses the spectrum of iatrogenic hyperkinetic movement disorders following exposure to Dopamine Receptor-Blocking agents (DRBAs). Despite the advent of atypical or second- and third-generation antipsychotics with a presumably lower risk of complications, TD remains a persistent and challenging problem. Prevention is the first step in mitigating the risk of TD, but early recognition, gradual withdrawal of offending medications, and appropriate treatment are also critical. As TD is often a persistent and troublesome disorder, specific antidyskinetic therapies are often needed for symptomatic relief. The vesicular monoamine transporter 2 (VMAT2) inhibitors, which include tetrabenazine, deutetrabenazine, and valbenazine, are considered the treatment of choice for most patients with TD. Deutetrabenazine—a deuterated version of tetrabenazine—and valbenazine, the purified parent product of one of the main tetrabenazine metabolites, are novel VMAT2 inhibitors and the only drugs to receive approval from the US FDA for the treatment of TD. VMAT2 inhibitors deplete presynaptic Dopamine and reduce involuntary movements in many hyperkinetic movement disorders, particularly TD, Huntington disease, and Tourette syndrome. The active metabolites of the VMAT2 inhibitors have high affinity for VMAT2 and minimal off-target binding. Compared with tetrabenazine, deutetrabenazine and valbenazine have pharmacokinetic advantages that translate into less frequent dosing and better tolerability. However, no head-to-head studies have compared the various VMAT2 inhibitors. One of the major advantages of VMAT2 inhibitors over DRBAs, which are still being used by some clinicians in the treatment of some hyperkinetic disorders, including TD, is that they are not associated with the development of TD. We also briefly discuss other treatment options for TD, including amantadine, clonazepam, Gingko biloba , zolpidem, botulinum toxin, and deep brain stimulation. Treatment of TD and other drug-induced movement disorders must be individualized and based on the severity, phenomenology, potential side effects, and other factors discussed in this review.

  • movement disorders from the use of metoclopramide and other antiemetics in the treatment of migraine
    Headache, 2016
    Co-Authors: Subhashie Wijemanne, Joseph Jankovic, Randolph W Evans
    Abstract:

    Nausea and vomiting are a frequent accompaniment of migraine and anti-nausea medications are frequently used in its management. The majority of anti-nausea medications that are used in migraine are Dopamine Receptor Blocking agents and therefore have the potential to cause drug-induced movement disorders. This article explores the risk of such drug-induced movement disorders in migraineurs who were treated with these medications.

  • Reviews An Update on Tardive Dyskinesia: From Phenomenology to Treatment
    2015
    Co-Authors: Olga Waln, Joseph Jankovic
    Abstract:

    Tardive dyskinesia (TD), characterized by oro-buccal-lingual stereotypy, can manifest in the form of akathisia, dystonia, tics, tremor, chorea, or as a combination of different types of abnormal movements. In addition to movement disorders (including involuntary vocalizations), patients with TD may have a variety of sensory symptoms, such as urge to move (as in akathisia), paresthesias, and pain. TD is a form of tardive syndrome—a group of iatrogenic hyperkinetic and hypokinetic movement disorders caused by Dopamine Receptor-Blocking agents. The pathophysiology of TD remains poorly understood, and treatment of this condition is often challenging. In this update, we provide the most current information on the history, nomenclature, etiology, pathophysiology, epidemiology, phenomenology, differential diagnosis, and treatment of TD

Joohi Jimenezshahed - One of the best experts on this subject based on the ideXlab platform.

  • deutetrabenazine for treatment of involuntary movements in patients with tardive dyskinesia
    Expert Review of Neurotherapeutics, 2021
    Co-Authors: Benjamin J Dorfman, Joohi Jimenezshahed
    Abstract:

    Introduction: Tardive dyskinesia (TD) is a hyperkinetic movement disorder that arises as a complication of exposure to Dopamine Receptor Blocking agents. Vesicular monoamine transporter type 2 (VMA...

  • a randomised double blind placebo controlled study of topiramate in the treatment of tourette syndrome
    Journal of Neurology Neurosurgery and Psychiatry, 2010
    Co-Authors: Joseph Jankovic, Joohi Jimenezshahed, Lawrence W Brown
    Abstract:

    Objective: To investigate the effects of topiramate on Tourette syndrome (TS). Background: Dopamine-Receptor-Blocking drugs have been traditionally used to control tics in patients with TS, but these neuroleptics are associated with potentially limiting side effects. Methods: This is a randomised, double-blind, placebo-controlled, parallel group study. To be included in the study, subjects required a DSM-IV diagnosis of TS, were 7–65 years of age, had moderate to severe symptoms (Yale Global Tic Severity Scale (YGTSS) ⩾19), were markedly impaired as determined by the Clinical Global Impression (CGI) scale severity score of ⩾4 and were taking no more than one drug each for tics or TS comorbidities. Results: There were 29 patients (26 males), mean age 16.5 (SD 9.89) years, randomised, and 20 (69%) completed the double-blind phase of the study. The primary endpoint was Total Tic Score, which improved by 14.29 (10.47) points from baseline to visit 5 (day 70) with topiramate (mean dose 118 mg) compared with a 5.00 (9.88) point change in the placebo group (p = 0.0259). There were statistically significant improvements also in the other components of the YGTSS as well as improvements in various secondary measures, including the CGI and premonitory urge CGI. No differences were observed in the frequency of adverse events between the two treatment groups. Conclusion: This double-blind, placebo-controlled trial provides evidence that topiramate may have utility in the treatment of moderately severe TS.

Benjamin J Dorfman - One of the best experts on this subject based on the ideXlab platform.

Kailash P Hatia - One of the best experts on this subject based on the ideXlab platform.

  • recurrent acute dystonic reaction and oculogyric crisis despite withdrawal of Dopamine Receptor Blocking drugs
    Movement Disorders, 2009
    Co-Authors: Susanne A Schneide, Vrajesh Udani, Charulata Sankhla, Kailash P Hatia
    Abstract:

    Adverse events of Dopamine-Blocking agents include acute dystonic reactions and oculogyric crises (OGCs). OGCs may be recurrent on maintenance of or re-exposure to the drug. Thus, complete withdrawal is recommended. Recurrent episodes of acute dystonia despite withdrawal and the lack of further exposure to antiDopaminergic agents are usually not seen. Here, we report three cases with recurrent OGCs despite complete withdrawal of neuroleptics. Triggering or priming factors were a single dose of haloperidol in two cases and a single dose of metoclopramide in one case. Episodes reoccurred spontaneously, but responded to anticholinergics. The pathomechanisms of acute dystonic reactions and OGCs remain unclear. Parallels to levodopa-induced dyskinesias in Parkinson's disease, as well as to dopa-responsive dystonia, paroxysmal dyskinesias, and channelopathies are discussed here. Whether there is a genetic susceptibility or some other reason for only some patients developing this phenomenon remains unclear.