Depression and Devic’s Syndrome
To the Editor: Devic’s syndrome (neuromyelitis optica) is a rare neurological condition (<5 per 100,000 individuals) that involves optic neuritis and transverse myelitis, usually without involvement of the CNS (1). Devic’s shares certain properties with multiple sclerosis; however, the relationship between them is controversial (1). Although an autoimmune etiology is speculated, the exact cause of Devic’s is unknown (1), and the primary treatment involves corticosteroids. A review of the literature (MEDLINE/MeSH terms: “neuromyelitis optica,” “Devic.mp,” “Devic’s.mp,” “depression,” “affect,” “mental disorders”) revealed no previous report of depression secondary to Devic’s syndrome. To our knowledge, we report the first case of depression secondary to Devic’s syndrome.
Ms. A, a 40-year-old woman of West Indian descent, had a history of depression. She was successfully treated with fluoxetine, 50 mg/day, at age 16 for mood symptoms related to body image. She experienced another episode of decreased mood and was treated successfully with citalopram, 20 mg/day. Later she experienced shoulder pain and leg paresthesia that progressed to debilitating generalized myalgia and optic neuritis. Then a diagnosis of Devic’s syndrome was confirmed on the basis of magnetic resonance imaging findings.
After the onset of Devic’s symptoms, Ms. A’s mood deteriorated, and she fulfilled criteria for major depression, which was treated with an increase in citalopram to 40 mg/day. Subsequent to treatment with intravenous corticosteroids and a course of plasmapheresis, her neurological symptoms gradually improved, and her mood improved with the increased antidepressant dose and remission of the disease.
Ms. A then relapsed acutely, with increased pain in addition to nausea, vomiting, vertigo, weakness, and light flashes in one eye. She experienced increased depressive symptoms concomitant with her acute neurological symptoms. Her most recent symptoms were treated with intravenous corticosteroids and plasmapheresis, and her regular medications included 1200 mg t.i.d. of gabapentin, 200 mg/day of carbamazepine, 40 mg/day of citalopram, 0.5 mg b.i.d. of clonazepam, 1–2 mg every 4 hours as needed of lorazepam, and morphine (patient-controlled analgesia). Upon review, these medications were determined to be justifiable, with no dependence on pain medication. Results of a review of her systems was negative for substance use, somatoform disorder, mania, anxiety, psychosis, dementia, delirium, and a current eating disorder. Her past medical history included various cosmetic surgeries, a cholecystectomy, an appendectomy, a tonsillectomy, an ovarian wedge resection, a gastrectomy, a tubal ligation, and bilateral glaucoma.
The temporal sequence of depressive symptoms and history of improved mood with improved neurological conditions allowed the patient’s current depression to meet partial criteria for a mood disorder secondary to a general medical condition. Although there may well have been some functional element to this depression, there was likely a pathophysiological underpinning. This may be similar to the pattern of depression in multiple sclerosis, in which the functional contribution to depression is as yet unclear (2).
1. O’Riordan JI, Gallagher HL, Thompson AJ, Howard RS, Wingsley DP, Thompson EJ, McDonald WI, Miller DH: Clinical, CSF, and MRI findings in Devic’s neuromyelitis optica. J Neurol Neurosurg Psychiatry 1996; 60:382–387Crossref, Medline, Google Scholar
2. Lynch SG, Kroencke DC, Denny DR: The relationship between disability and depression in multiple sclerosis: the role of uncertainty, coping, and hope. Mult Scler 2001; 7:411–416Crossref, Medline, Google Scholar
