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Tardive dyskinesia: The role of targeted therapy
Tardive dyskinesia is a movement disorder characterized by involuntary and repetitive movements of the tongue, lips, face, trunk, and extremities. It is caused by the use of dopamine receptor-blocking drugs, most often antipsychotics, but has also been associated with treatments for some gastrointestinal disorders.
Dr. Peter LeWitt, Sastry Foundation Endowed Chair in Neurology at Wayne State University School of Medicine in Detroit, MI, walks through some of the known causes of tardive dyskinesia as well as steps physicians can take in making a differential diagnosis.
Next, Dr. LeWitt dives into the role of targeted therapy in the management of tardive dyskinesia. VMAT2 (vesicular monoamine transporter type 2) inhibitors are emerging as a treatment class of choice that help suppress tardive dyskinesia symptoms by depleting presynaptic dopamine, while other patients may benefit more from benzodiazepines, botulinum toxin, or deep brain stimulation.
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Dr. Peter LeWitt, Sastry Foundation Endowed Chair in Neurology at Wayne State University School of Medicine in Detroit, MI.
Peter A. LeWitt reports advisory roles for: Abide, Acorda Therapeutics, Adamas, Biogen, Cavion, Denali, Intec Pharma, Jazz Pharmaceuticals, Lundbeck, Neurocrine, Mitsubishi NeuroDerm Ltd, Prexton, Revance, Sage, and US WorldMeds.
Lecture fees from: Acorda, American Academy of Neurology, Kyowa Hakko Kirin, and US WorldMeds.
Research grant support from: Abide, Acorda, Amneal, Lundbeck, Michael J. Fox Foundation for Parkinson's Research, Mitsubishi NeuroDerm Ltd, Parkinson Study Group; Pharma 2B, Revance, Hoffmann-La Roche; Sunovion, Sun Pharma, and US WorldMeds.
Tardive dyskinesia is a movement disorder characterized by involuntary and repetitive movements of the tongue, lips, face, trunk, and extremities. It is caused by the use of dopamine receptor-blocking drugs, most often antipsychotics, but has also been associated with treatments for some gastrointestinal disorders.
Dr. Peter LeWitt, Sastry Foundation Endowed Chair in Neurology at Wayne State University School of Medicine in Detroit, MI, walks through some of the known causes of tardive dyskinesia as well as steps physicians can take in making a differential diagnosis.
Next, Dr. LeWitt dives into the role of targeted therapy in the management of tardive dyskinesia. VMAT2 (vesicular monoamine transporter type 2) inhibitors are emerging as a treatment class of choice that help suppress tardive dyskinesia symptoms by depleting presynaptic dopamine, while other patients may benefit more from benzodiazepines, botulinum toxin, or deep brain stimulation.
--
Dr. Peter LeWitt, Sastry Foundation Endowed Chair in Neurology at Wayne State University School of Medicine in Detroit, MI.
Peter A. LeWitt reports advisory roles for: Abide, Acorda Therapeutics, Adamas, Biogen, Cavion, Denali, Intec Pharma, Jazz Pharmaceuticals, Lundbeck, Neurocrine, Mitsubishi NeuroDerm Ltd, Prexton, Revance, Sage, and US WorldMeds.
Lecture fees from: Acorda, American Academy of Neurology, Kyowa Hakko Kirin, and US WorldMeds.
Research grant support from: Abide, Acorda, Amneal, Lundbeck, Michael J. Fox Foundation for Parkinson's Research, Mitsubishi NeuroDerm Ltd, Parkinson Study Group; Pharma 2B, Revance, Hoffmann-La Roche; Sunovion, Sun Pharma, and US WorldMeds.
Tardive dyskinesia is a movement disorder characterized by involuntary and repetitive movements of the tongue, lips, face, trunk, and extremities. It is caused by the use of dopamine receptor-blocking drugs, most often antipsychotics, but has also been associated with treatments for some gastrointestinal disorders.
Dr. Peter LeWitt, Sastry Foundation Endowed Chair in Neurology at Wayne State University School of Medicine in Detroit, MI, walks through some of the known causes of tardive dyskinesia as well as steps physicians can take in making a differential diagnosis.
Next, Dr. LeWitt dives into the role of targeted therapy in the management of tardive dyskinesia. VMAT2 (vesicular monoamine transporter type 2) inhibitors are emerging as a treatment class of choice that help suppress tardive dyskinesia symptoms by depleting presynaptic dopamine, while other patients may benefit more from benzodiazepines, botulinum toxin, or deep brain stimulation.
--
Dr. Peter LeWitt, Sastry Foundation Endowed Chair in Neurology at Wayne State University School of Medicine in Detroit, MI.
Peter A. LeWitt reports advisory roles for: Abide, Acorda Therapeutics, Adamas, Biogen, Cavion, Denali, Intec Pharma, Jazz Pharmaceuticals, Lundbeck, Neurocrine, Mitsubishi NeuroDerm Ltd, Prexton, Revance, Sage, and US WorldMeds.
Lecture fees from: Acorda, American Academy of Neurology, Kyowa Hakko Kirin, and US WorldMeds.
Research grant support from: Abide, Acorda, Amneal, Lundbeck, Michael J. Fox Foundation for Parkinson's Research, Mitsubishi NeuroDerm Ltd, Parkinson Study Group; Pharma 2B, Revance, Hoffmann-La Roche; Sunovion, Sun Pharma, and US WorldMeds.
