क्रेग चेपके डॉ, खाजगी सराव मानसोपचारतज्ज्ञ आणि मानसोपचार सहाय्यक सहायक प्राध्यापक, नॉर्थ कॅरोलिना स्कूल ऑफ मेडिसिन विद्यापीठ, CURESZ बोर्ड सदस्य

टार्डिव्ह डायस्किनेशिया (टीडी) हा विलंबाने सुरू झालेला न्यूरोलॉजिकल सिंड्रोम आहे जो अँटीसायकोटिक औषधांच्या दीर्घकाळापर्यंत वापराचा दुष्परिणाम म्हणून होऊ शकतो. टीडी विकसित करणार्‍या लोकांमध्ये पुनरावृत्ती होणार्‍या अनैच्छिक हालचाली असू शकतात ज्या सामान्यत: मंद आणि कुरकुरीत असतात किंवा नृत्यासारख्या असतात. हालचाली सामान्यतः चेहरा, तोंड आणि जीभ यांच्या स्नायूंमध्ये होतात, परंतु हात, पाय किंवा धड मध्ये देखील दिसू शकतात. TD च्या वारंवारतेचा अंदाज भिन्न असतो परंतु दीर्घ कालावधीसाठी अँटीसायकोटिक्स घेणार्‍या लोकांच्या 7%-30% पर्यंत असतो.1 टीडी विकसित होण्यासाठी लागणाऱ्या एक्सपोजरची लांबी बदलू शकते, परंतु अँटीसायकोटिक उपचार सुरू केल्यानंतर काही महिने किंवा वर्षांनंतरही हे होऊ शकते. एकदा TD प्रकट झाल्यानंतर, ते अपरिवर्तनीय होऊ शकते. त्यामुळे, लवकर ओळखणे आणि टार्डिव्ह डायस्किनेशियाचे उपचार महत्वाचे आहेत.

CURESZ चा भाग होण्याचा मला सन्मान आहे टार्डिव्ह डायस्किनेशिया तज्ञ पॅनेल, 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.

संदर्भ: 1. कार्बन आणि इतर. जे क्लिन मानसोपचार 2017;78(3):e264–e278.