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Late-Onset Obsessive-Compulsive Disorder Without Evidence of Focal Cerebral Lesions: A Case Report

Key Words: late-onset OCD • cerebral lesions • orbitofrontal area • basal ganglia

SIR: Obsessive-compulsive disorder (OCD) belongs to a rapidly evolving field of psychopathology that goes beyond classical nosological conceptions to meet a broad spectrum of disorders concerning impulse control as a result of structural or biochemical neuronal modifications. Such disorders appear in conditions as Tourette's Syndrome, autism, body dysmorphic disorder, pathological gambling, trichotillomania, hypochondriasis, etc.¹ The concept of spectrum is justified by similarities in symptomatology, prognosis, psychiatric comorbidity, family history, neurobiological overlaps and response to SSRI's.²

OCD is a disabling disease with onset usually in adolescence and early adulthood. According to Weissman et al, the symptoms appear before age 25 in about 2/3 of affected persons,³ and Rasmussen et al state that only in 15% of patients do symptoms begin after age 35.⁴ In late-onset OCD, especially in cases with onset after age 40, Koran stresses that the possibility of an underlying medical condition should be investigated.⁵

Cerebral areas, lesions of which have been related to the appearance of OCD, are the frontal lobe and basal ganglia. The same areas have been implicated in the neuropathology of "idiopathic" OCD⁶; the first such proof came with the work of Lewis Baxter, who demonstrated in 1987 with the use of radioactively labeled glucose that patients suffering from OCD present hyperactivity in the orbitofrontal areas and the caudate nuclei.⁷

In this report, we describe the rare case of a patient with late-onset OCD without any specific underlying cerebral lesions.

Case report:
Mr. L., a 68-year-old married white man, presented himself at the Center of Mental Health Services with obsessive-compulsive symptoms that had appeared two years before. He had then visited a psychiatrist, but had not complied with the prescribed treatment. His symptoms, whose pathological nature he was fully conscious of, consisted of excessive worries of infection. For fear of contamination, he would avoid handshakes; he found it difficult to touch money, he would wash his hands over 30 times a day, he would not touch furniture or doorknobs, and he would meticulously disinfect his clothes. His Yale-Brown OC Scale (Y-BOCS) score was 27 (maximal score 40—for the diagnosis of OCD a score of more than 16 is required). Head scans with computed tomography (CT) and magnetic resonance imaging (MRI) did not reveal any abnormalities. Mr. L. was started on a treatment with paroxetine, whose dose was gradually raised to 40 mg/day. His symptoms resolved after 3 weeks of treatment. Ten months later, Mr. L. continues his treatment and remains asymptomatic.

Comment:
OCD usually occurs in the second and third decade of life. The participation of frontal lobe and basal ganglia is well known in this disorder, but focal cerebral lesions are usually not found except in the late-onset forms. Although such cases are uncommon, two reports have recently been published concerning the development of OCD after the age of 65, where, however, the majority of cases concerned women.^6,8 According to a recent epidemiological study by Nestadt et al,⁹ the incidence of OCD is bimodal in men and women, both peaks occurring later in women; the second peak concerns the age spectrum between 30–44 years in men, whereas in women it appears after the age of 65.

The uniqueness of the presented case consists in the fact that it concerns a late-onset, after the age of 65, occurrence of OCD in a man; moreover, no signs of underlying cerebral pathology could be detected, as it usually is the case in late-onset OCD. Interestingly, from the 10 cases described by Weiss et al⁶ and Chacko et al,⁸ only one patient did not show evidence of specific cerebral abnormalities. Our patient's response to medication was excellent, something rather unusual in the "late" forms of OCD.

ACKNOWLEDGMENTS

This work was presented at the 16^th Hellenic Congress of Psychiatry, April 19–23, 2002, Chalkidiki, Greece

REFERENCES

1. Stein DJ: Neurobiology of the obsessive-compulsive disorders. Biol Psychiatry 2000; 47:296–304[CrossRef][Medline]
2. Hollander E, Wong CM: Obsessive-compulsive spectrum disorders. J Clin Psychiatry 1995; 56(suppl 4):3–6
3. Weissman MM, Bland RC, Canino GL, et al: The cross national epidemiology of obsessive compulsive disorder. The Cross National Collaborative Group. J Clin Psychiatry 1994; 55(suppl):5–10
4. Rasmussen SA, Eisen JL: The epidemiology and clinical features of obsessive-compulsive disorder. Psychiatr Clin North Am 1992; 15:743–759[Medline]
5. Koran ML: Obsessive-compulsive and related disorders in adults. Cambridge University Press, 2000, 119–132.
6. Weiss AP, Jenike MA: Late-onset obsessive-compulsive disorder: a case series. J Neuropsychiatry Clin Neurosci 2000; 12:265–268[Abstract/Free Full Text]
7. Baxter LR, Phelps ME, Mazziota JC, et al: Local cerebral glucose metabolic rates in obsessive-compulsive disorder. A comparison with rates in unipolar depression and in normal controls. Arch Gen Psychiatry 1987; 44:211–218[Abstract/Free Full Text]
8. Chacko RC, Corbin MA, Harper RG: Acquired obsessive-compulsive disorder associated with basal ganglia lesions. J Neuropsychiatry Clin Neurosci 2000; 12:269–272[Abstract/Free Full Text]
9. Nestadt G, Bienvenue J, Guojun Cai MB, et al: Incidence of obsessive-compulsive disorder in adults. J Nerv Ment Dis 1998; 186:401–406[CrossRef][Medline]

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