Dr Craig Chepke, psychiatre en pratique privée et professeur adjoint adjoint de psychiatrie, faculté de médecine de l'Université de Caroline du Nord, membre du conseil d'administration de CURESZ

La dyskinésie tardive (TD) est un syndrome neurologique d'apparition retardée qui peut survenir comme effet secondaire de l'utilisation prolongée de médicaments antipsychotiques. Les personnes qui développent la TD peuvent avoir des mouvements involontaires répétitifs qui sont généralement lents et contorsionnants, ou de nature dansante. Les mouvements se produisent le plus souvent dans les muscles du visage, de la bouche et de la langue, mais peuvent également apparaître dans les bras, les jambes ou le torse. Les estimations de la fréquence de la TD diffèrent mais vont de 7% à 30% chez les personnes qui prennent des antipsychotiques pendant une période prolongée.1 La durée d'exposition nécessaire pour développer la TD est variable, mais elle peut survenir des mois voire des années après le début du traitement avec un antipsychotique. Une fois que la TD se manifeste, elle peut devenir irréversible. Par conséquent, la détection précoce et le traitement de la dyskinésie tardive sont essentiels.

Je suis honoré de faire partie du CURESZ Groupe d'experts sur la dyskinésie tardive, but I haven’t always been adept at diagnosing TD. For years, no one in my current practice seemed to have “obvious” symptoms of TD, so I came to assume that it was more of a historical problem associated with the older first-generation antipsychotics that I rarely prescribe. In 2016, however, I began working with a young man with schizophrenia whose TD was unmistakable. With no FDA-approved medications at the time, the best I could offer was to remove or reduce one of the two antipsychotics he was taking. He and his father wouldn’t consider any change, because that combination was the only thing that had ever worked for him. When his father suddenly passed away months later, his grief inspired me to learn as much as I could about treating TD. I couldn’t give him his father back, but I could at least try to give him the dignity of control over his body.

I studied neurology journals and textbooks for months and realized that I had unconsciously set my bar for diagnosing TD at only the highest severity level. I had inadvertently become blind to detecting mild to moderate TD. Reading the numerous failed clinical trials of medications and supplements for treating TD, I gained an appreciation of the decades of powerlessness clinicians had felt in trying to treat it. It seemed that recognition of TD was gradually overshadowed by increased screening for other potential side effects of antipsychotics, such as blood sugar and cholesterol elevations– perhaps because the latter are problems for which we have long had good treatment options. In 2017, the FDA approved the first two medications for TD, and treating my patient with one of them benefitted him in profound ways I didn’t expect.

Every psychiatric provider trained in an era in which there was little or nothing we could do to address TD, so many didn’t have enough urgency looking for it. Our diagnostic skills withered, and many newer clinicians never established proficiency in the first place. Now that approved treatments exist, the mental health field will eventually enhance its recognition of TD, but if I didn’t have this unique experience when I did, it might have been years before I stepped up my screening. Until every provider makes a thorough examination for TD a standard part of their appointments, I urge everyone taking an antipsychotic, especially anyone experiencing unusual or unexpected movement problems, to be your own advocate and take the lead in discussing tardive dyskinesia treatment with your provider.

Référence : 1. Carbon et al. J Clin Psychiatry 2017;78(3):e264–e278.