Neurology Advisor: In addition to those developments, what are some ways in which TD treatment could be improved? 

Dr Gonzalez-Alegre: Physician and patient education, mostly geared toward prevention. We should never forget this is an iatrogenic condition. I have personally observed that the educational efforts in the field of psychiatry in the last few decades led to a more judicial use of offending agents. In contrast, in my subjective opinion, there is perhaps a higher proportion of cases caused by agents used to treat gastrointestinal symptoms. An important area of research is pharmacogenomics.


Continue Reading

Dr Pierre: Given the limited effect size of treatments such as valbenazine, it would be great if future treatments are developed that eliminate TD more completely. It would also be a significant advancement if novel medications were developed that had a lower risk for TD in the first place. This occurred 2 decades ago, as SGAs replaced first-generation antipsychotics, but it would be great if there were antipsychotic medications associated with minimal TD risk.

TD had become something of a “forgotten disorder” during the last 2 decades as SGAs replaced first-generation antipsychotics and with no other established treatments for TD. With the approval of valbenazine and deutetrabenazine, there has been a resurgence of awareness. Although that no doubt has occurred in part as a result of pharmaceutical marketing, increased awareness and early recognition of TD is a good thing and could help improve patient outcomes.

Neurology Advisor: What should be the focus of future research in this area?

Dr Gonzalez-Alegre: Hopefully, a better understanding of the underlying biological bases of TD could lead to improved design of dopamine-receptor blocking drugs that do not cause this debilitating syndrome. The newer generation of antipsychotics were a step in the right direction, but there is still much room for improvement. Furthermore, we should not forget that most patients treated with these drugs do not develop TD. Although we know some risk factors for TD, such as older age and female sex, there is likely a genetic predisposition in those who develop it. If we are able to identify in advance who is most likely to develop TD or not, we could better tailor treatments as we move toward precision medicine; this is a research area that should be heavily pursued.

Neurology Advisor: Are there any additional points on the topic that our readers should know about?

Related Articles

Dr Gonzalez-Alegre: After many decades without a uniform approach to the treatment of TD and lack of scientific evidence supporting the use of available therapies, the availability of new FDA-approved drugs should hopefully result in an overall improvement in the management of this condition. In the long run, however, the goal should be to make TD a disease of the past. Improvement in drug design and advances in pharmacogenomics should help us reach that goal.

Dr Pierre: We still have a very poor understanding of how antipsychotics and other medications cause TD. As with other medical conditions, the hope is that better understanding will pave the way to more effective treatments.

References

  1. Teva announces FDA approval of AUSTEDO® (deutetrabenazine) tablets for the treatment of tardive dyskinesia in adults [news release]. Jerusalem, Israel: Teva Pharmaceuticals newsroom; August 30, 2017.
  2. Caroff SN, Campbell EC, Carroll B. Pharmacological treatment of tardive dyskinesia: recent developments. Expert Rev Neurother. 2017;17(9):871-881.
  3. Carbon M, Hsieh CH, Kane JM, Correll CU. Tardive dyskinesia prevalence in the period of second-generation antipsychotic use: a meta-analysis. J Clin Psychiatry. 2017;78(3):e264-e278.
  4. Jankovic J, Clarence-Smith K. Tetrabenazine for the treatment of chorea and other hyperkinetic movement disorders. Exp Rev Neurother. 2011;11(11):1509-1523.
  5. Hauser R, Factor S, Marder S, et al. KINECT 3: a Phase 3 randomised, double-blind, placebo-controlled trial of valbenazine for tardive dyskinesia. Am J Psychiatry. 2017;174(5):476-484.