Bipolar disorder and multiple sclerosis: comorbidity and risk factors

Transtorno bipolar e esclerose múltipla: comorbidade e fatores de risco

LETTERS TO THE EDITORS

Bipolar disorder and multiple sclerosis: comorbidity and risk factors

Transtorno bipolar e esclerose múltipla: comorbidade e fatores de risco

Ana Claudia Rodrigues de Cerqueira^I,II; Antônio Egídio Nardi^I,II; Fabiana Souza-Lima^III; José Maurício Godoy-Barreiros^III

^ILaboratory of Panic and Respiration, Institute of Psychiatry, Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro, RJ, Brazil

^IINational Institute for Translational Medicine (INCT-TM)

^IIIDepartment of Neurology, Universidade do Estado do Rio de Janeiro (UERJ), Rio de Janeiro, RJ, Brazil

Dear Editor,

Multiple sclerosis (MS) is a demyelinating central nervous system (CNS) disease that affects mainly young adults. The disease course is unpredictable, and clinical manifestations include motor deficits, sensory changes, bladder and bowel dysfunction, uni- optical neuritis, diplopia, and cerebellar signs. Rarely, MS may initially present itself as a manic syndrome, similar to that observed in bipolar disorder (BD).¹ We report a patient diagnosed with BD who was later diagnosed with MS. The possibility of mania as a symptom or comorbidity of MS was examined in this case report to assess possible risk factors.

Case report

The patient, JPS, is a 50-year-old divorced female. In 1999, she developed euphoria, irritability, impulsivity, and grandiose delusions. For example, she started taking various classes to achieve grandiose goals, pursuing unrealistic business ideas, acquired several debts that she could not repay, requested dismissal from her employment because she believed she would become a millionaire, exhibited inappropriate seductive behavior, and placed an advertisement in a newspaper offering call girl services that resulted in the termination of her marriage. At that time, her relatives noticed that she was experiencing psychomotor agitation, aggressiveness, auditory hallucinations and delirious ideas; she was admitted to a psychiatric clinic for treatment, and her psychotic symptoms subsequently went into remission with the use of haloperidol plus promethazine. After six months, she presented with daily sadness, anhedonia, psychomotor retardation and fatigue; these symptoms were resolved with 20mg/day of fluoxetine. In 2000, she developed a subacute motor deficit on her left side and gait impairment, both of which partially improved spontaneously. At that time, her CT scan was normal. In 2001, she developed urinary incontinence and was referred for neurological assessment. A clinical examination revealed left hemiparesis, spasticity, and tendon reflexes that were brisk on the left side, and normal on the right side. Her cutaneous-plantar reflex was equivocal on the left side and resulted in toe flexion on the right side, and her gait was hemiparetic on the left side. The remainder of the neurological examination was normal. Magnetic resonance imaging (MRI) of her brain showed demyelinating periventricular lesions (Figure 1). An MRI scan of her cervical cord also showed demyelinating lesions. Autoantibody (anti-Ro, anti-LA, anti-Sm, ANA, anti-DNA and anticardiolipin) and serology (syphilis, hepatitis B and C, HIV and HTLV) tests were negative. Analysis of the cerebrospinal fluid (CSF) detected the presence of oligoclonal bands. Visual evoked potentials showed increased latencies and reduced amplitudes. Based on these findings, the patient was diagnosed with MS, and treatment was initiated with interferon beta-1A. During the nine years of follow-up, the patient did not present any episodes suggestive of a mood disorder despite treatment with interferon beta, but she experienced worsening symptoms of her neurological disease. Neuroimaging studies revealed subsequent appearance of new lesions, mainly in the corpus callosum and in the callous-septal interface. Treatment with interferon was discontinued due to the severity of her disability.

Discussion

The association between mood disorders and MS has been described by several studies. There is evidence that this population is more susceptible to BD. An epidemiological study conducted by Schiffer et al. showed that BD is twice as common in patients with MS than in the general population.² Joffe et al. showed that 13% of an outpatient sample of patients with MS were diagnosed with BD.³ In these two studies, patients with a history of hypomania/mania episodes due to corticosteroid use were excluded. Using MRI, Lyoo et al. systematically evaluated 2,783 individuals who had been referred for psychiatric hospitalization and found changes in white matter that were compatible with the neuroradiological criteria of MS in 23 patients (0.83%).⁴ The mechanisms underlying these associations are unknown and have been poorly investigated to date. Family studies investigating the involvement of HLA (human leukocyte antigen) genes have demonstrated a common genetic susceptibility among patients with BD and MS.⁵

We described a patient diagnosed with BD according to the DSM-IV-TR who was later diagnosed with MS according to the MacDonald criteria. Because a detailed neurological examination was not available at the onset of this case, it is impossible to assert that the patient's mania was a symptom of MS. However, the absence of a personal or family history of BD and the late onset of symptoms raises this possibility.

Ana Claudia Rodrigues de Cerqueira,

Antônio Egídio Nardi

Laboratory of Panic and Respiration, Institute of Psychiatry,

Universidade Federal do Rio de Janeiro (UFRJ),

Rio de Janeiro, RJ, Brazil

National Institute for Translational Medicine (INCT-TM)

Fabiana Souza-Lima, José Maurício Godoy-Barreiros

Department of Neurology, Universidade do Estado do

Rio de Janeiro (UERJ), Rio de Janeiro, RJ, Brazil

• 1. Asghar-Ali AA, Taber KH, Hurley RA, Hayman LA. Pure neuropsychiatric presentation of multiple sclerosis. Am J Psychiatry 2004;161(2):226-31.
• 2. Schiffer RB, Wineman NM, Weitkamp LR. Association between bipolar affective disorder and multiple sclerosis. Am J Psychiatry 1986;143(1):94-5.
• 3. Joffe RT, Lippert GP, Gray TA, Sawa G, Horvath Z. Mood disorders and multiple sclerosis. Arch Neurol 1987;44(4):376-8.
• 4. Lyoo IK, Seol HY, Byun HS, Renshaw PF. Unsuspected multiple sclerosis in patients with psychiatric disorders: a magnetic resonance imaging study. J Neuropsychiatry Clin Neurosci. 1996;8(1):54-9.
• 5. Schiffer RB, Weitkamp LR, Wineman NM , Guttornsem S. Multiple sclerosis and affective disorder: family history, sex, and HLA-DR antigens. Arch Neurol 1988;45(12):1345-8.

Publication Dates

• Publication in this collection
  07 Feb 2011
• Date of issue
  Dec 2010