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Psychosomatics 47:361-363, August 2006
doi: 10.1176/appi.psy.47.4.361
© 2006 Academy of Psychosomatic Medicine
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Letter

A Case of Multiple Sclerosis Masked by Depression and Diabetic Neuropathy

M. Schilling, M.D., Corinna Brueckner-Totonji, M.D., V. Arolt, M.D., and Bernhard T. Baune, M.D., M.P.H., Univ. of Muenster, Germany

TO THE EDITOR: There is considerable overlap between symptoms of depression and multiple sclerosis (MS).1,2 Four of nine core symptoms of depression in the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM–IV) of the American Psychiatric Association also occur in MS: fatigue, psychomotor retardation, decreased concentration, and sleep disturbance.3 We report the case of a woman whose long-term symptoms that were initially attributed to depression and diabetic neuropathy were finally explained by a complex clinical picture of MS, depression, and diabetic neuropathy.

Case Report

Ms. A, a 40-year-old woman, was admitted to our department of psychiatry in 2005 with the diagnosis of major depressive episode (MDE) and a history of an insulin-dependent juvenile diabetes mellitus (since age 13). Ms. A presented with poor self-care and personal hygiene. Speech was slow, and concentration was poor. Her mood was low and sad, with feelings of worthlessness and indecisiveness. Ms. A showed irritability, reduced energy and drive, anhedonia, loss of interest in normal activities, and broken sleep. Social isolation, pessimistic thoughts concerning the future, and recurrent thoughts of death were present over time. The first depressive symptoms had occurred at the age of 13, with first MDE at the age of 20, followed by several MDEs. Her first psychiatric treatment started after a suicide attempt with insulin (at age 30). Ms A discontinued psychiatric care, which led to a hospital admission in 2005.

Neurologically, Ms. A showed a saccadic ocular motility, a decreased light reaction, and a reduction of visual acuity to 20% for the right eye, an atrophy of the small muscles of her feet, an ataxia of finger-to-nose and heel–knee tests, a reduction of vibratory sense (3/8) at both ankles, increased patellar reflexes but decreased Achilles tendon reflexes, non-obtainable abdominal reflexes, and ataxic gait. A first reduction in visual functioning at the age of 21 was attributed to diabetic retinopathy. At age 24, a retro-bulbar neuritis was diagnosed after the sudden onset of a rapid reduction of visual acuity of the right eye. A progressive formication in both feet since the age of 29 was attributed to diabetic neuropathy.

Investigations

Blood tests showed increased HbA1c, at 7.8% (normal: 4.4–5.7). Cerebrospinal fluid (CSF) had normal cell count; total protein was slightly elevated (516 mg/l; reference: <450 mg/l). A pathological intrathecal IgG production and 21 oligoclonal bands in the CSF, versus 2 bands in the serum probe, indicated a CNS inflammatory disease. Cranial MRI revealed MS-typical lesions in the periventricular medullary layer, the corpus callosum, and the cerebellum (Figure 1). Visual evoked potentials were normal (right: 107.0 msec; left: 91.3 msec), but the abnormal difference between sides (normal: <10 msec) was compatible with a retro-bulbar neuritis, a typical early manifestation of MS. Pathological somatosensory and magnetic evoked potentials of both arms and legs indicated peripheral and central nervous system impairment consistent with diabetic neuropathy and MS.


Figure 1
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FIGURE 1.  Cranial MRI

The saggital FLAIR [A] sequence shows typical lesions in the corpus callosum, the axial FLAIR [B], periventricular and subcortical lesions.



Diagnoses and Therapy

Ms. A was diagnosed with an MDE (DSM-IV-TR),3 which was treated with 20 mg of fluoxetine and cognitive-behavioral therapy.2,4 A diagnosis of MS was based on at least two clinical attacks, more than two MRI-detected lesions consistent with MS, and typical CSF manifestations.5 Because of her only partial recovery from previous MS episodes, intrathecal IgG synthesis, and the number of MRI lesions (>6), we started prophylactic therapy with Glatirameracetate 20 mg/day as an immunomodulatory agent, because of the contraindication of interferons in depressive disorders. Optimized insulin therapy led to improved serum glucose levels.

Follow-Up

A 4-week outpatient follow-up showed improved gait in Ms. A, longer walking distances, and improved color perception. Ms. A appeared well-dressed and friendly. Her mood was euthymic; tension had reduced markedly, and sleep patterns had normalized. Her drive and energy had improved, as well as self-care and concentration. Ms. A was optimistic about the future.

Discussion

This case raises a few clinically relevant points for psychiatric patients. First, symptoms of MS can be masked by a complex clinical picture of depression and diabetic neuropathy. The immunologic alterations responsible for the onset and course of MS are likely to induce symptoms similar to signs of MDE.6 Second, the novel aspect to this report is the psychiatric perspective on this case of MS, given that previous literature has addressed the prevalence, diagnosis, and treatment of depression among patients primarily diagnosed with MS.4,7 Third, we should consider a wide spectrum of differential diagnoses in psychiatric patients presenting with predominantly somatic symptoms. The diagnostic process of MS involves clinical and technical investigations5 that are essential for starting adequate treatment of MS. Last, the choice of MS treatment options such as immunomodulatory agents should take into account their well-known potentially depressive side effects.8

REFERENCES

  1. Mohr DC, Goodkin DE, Likosky W, et al: Identification of Beck Depression items related to multiple sclerosis. J Behav Med 1997; 20:407–414[CrossRef][Medline]
  2. Ehde, DM, Bombardier CH: Depression in persons with multiple sclerosis. Phys Med Rehabil Clin N Am 2005; 16:437–448[Medline]
  3. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR). Washington, DC, American Psychiatric Association, 2000
  4. Goldman Consensus Group: The Goldman Consensus Statement on Depression in Multiple Sclerosis. Mult Scler 2005; 11:328–337[Abstract/Free Full Text]
  5. McDonald WI, Compston A, Edan G: Recommended diagnostic criteria for multiple sclerosis: guidelines from The International Panel on the Diagnosis of Multiple Sclerosis. Ann Neurol 2001; 50:121–127[CrossRef][Medline]
  6. Yirmiya R: Behavioral and psychological effects of immune activation: implications for depression due to general-medical condition. Curr Opin Psychiatry 1997; 10:470–476[CrossRef]
  7. Siegert RJ, Abernethy DA: Depression in multiple sclerosis: a review. J Neurol Neurosurg Psychiatry 2005; 76:469–475[Abstract/Free Full Text]
  8. Beratis S, Katrivanou A, Georgiou S, et al: Major depression and risk of depressive symptomatology associated with short-term and low-dose interferon-{alpha} treatment. J Psychosom Res 2005; 58:15–18[Medline]




This Article
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Related Collections
* Depression
* Syndromes Secondary to General Medical Disorders


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