Lewy Body disease and suicidality after dopamine agonist withdrawal
Melissa J.Nirenberg, Associate Professor of Neurology
Published October 24, 2016
I read with appreciation the special editorial by Susan Schneider Williams, [1] in which she shares personal details about the tragic death of her husband, Robin Williams, in the face of Lewy body disease. The death of such a talented actor and comedian was a terrible loss to the world. I share my deepest condolences.
In her editorial, Mrs. Williams made one comment of particular importance: "...his medication was switched from Mirapex [pramipexole, a dopamine agonist] to Sinemet [carbidopa/levodopa]..." near the end of July, just before his death on August 11th. This raises the possibility that his suicidality may have been a manifestation of dopamine agonist withdrawal syndrome (DAWS). [2] DAWS is a stereotyped drug withdrawal syndrome that can cause a variety of nonmotor symptoms, including severe and medically-refractory anxiety, panic attacks, depression, dysphoria, fatigue, and suicidality. DAWS does not respond to carbidopa/levodopa or other medications and can be very difficult to recognize because the symptoms are not visible and closely mimic those of a primary psychiatric disorder. [2,3]
Mrs. Williams wrote this piece to "...help make a difference in the lives of others." [1] Her advocacy has undoubtedly raised awareness of Lewy body disease, for which there are currently no adequate treatments. I hope her words and actions will also lead to greater recognition of DAWS and other serious, underrecognized, and preventable complications of dopaminergic therapy. [2-4]
1. Williams SS. The terrorist inside my husband's brain. Neurology 2016;87:1308-1311.
2. Rabinak CA, Nirenberg MJ. Dopamine agonist withdrawal syndrome in Parkinson disease. Arch Neurol 2010;67:58-63.
3. Nirenberg MJ. Dopamine agonist withdrawal syndrome: implications for patient care. Drugs Aging 2013;30:587-592.
4. Weintraub D, Nirenberg MJ. Impulse control and related disorders in Parkinson's disease. Neurodegener Dis 2013;11:63-71.
For disclosures, please contact the editorial office at journal@neurology.org.
I read with appreciation the special editorial by Susan Schneider Williams, [1] in which she shares personal details about the tragic death of her husband, Robin Williams, in the face of Lewy body disease. The death of such a talented actor and comedian was a terrible loss to the world. I share my deepest condolences.
In her editorial, Mrs. Williams made one comment of particular importance: "...his medication was switched from Mirapex [pramipexole, a dopamine agonist] to Sinemet [carbidopa/levodopa]..." near the end of July, just before his death on August 11th. This raises the possibility that his suicidality may have been a manifestation of dopamine agonist withdrawal syndrome (DAWS). [2] DAWS is a stereotyped drug withdrawal syndrome that can cause a variety of nonmotor symptoms, including severe and medically-refractory anxiety, panic attacks, depression, dysphoria, fatigue, and suicidality. DAWS does not respond to carbidopa/levodopa or other medications and can be very difficult to recognize because the symptoms are not visible and closely mimic those of a primary psychiatric disorder. [2,3]
Mrs. Williams wrote this piece to "...help make a difference in the lives of others." [1] Her advocacy has undoubtedly raised awareness of Lewy body disease, for which there are currently no adequate treatments. I hope her words and actions will also lead to greater recognition of DAWS and other serious, underrecognized, and preventable complications of dopaminergic therapy. [2-4]
1. Williams SS. The terrorist inside my husband's brain. Neurology 2016;87:1308-1311.
2. Rabinak CA, Nirenberg MJ. Dopamine agonist withdrawal syndrome in Parkinson disease. Arch Neurol 2010;67:58-63.
3. Nirenberg MJ. Dopamine agonist withdrawal syndrome: implications for patient care. Drugs Aging 2013;30:587-592.
4. Weintraub D, Nirenberg MJ. Impulse control and related disorders in Parkinson's disease. Neurodegener Dis 2013;11:63-71.
For disclosures, please contact the editorial office at journal@neurology.org.