BACKGROUND: Although several studies have been conducted in an attempt to characterize the phenotype and underlying pathophysiology of individuals with early-onset obsessive-compulsive disorder (OCD), the literature on patients who develop OCD later in life remains sparse. OBJECTIVE: To describe clinical outcomes in the 7-year follow-up of a patient with late-onset OCD. METHOD: Single case report. RESULTS: A 64-year-old woman exhibiting a 7-year history of treatment-refractory late-onset OCD developed significant cognitive deterioration. We suggest that the association between late-onset treatment refractory OCD and dementia may stem from at least 3 different scenarios. First, dementia may be an inexorable end-point of some forms of malignant, primary, and late-onset obsessional illness. Second, late-onset OCD and dementia may result from a common pathophysiologic basis, such as in fronto-temporal dementia. Finally, the association between both conditions may result by the interaction between vulnerability toward OCD-type symptoms and the nonspecific effects of a neurodegenerative process. In our case, although subclinical OCD was likely to be "unmasked" by cognitive decline and/or bilateral caudate vascular lesions, ensuing cognitive deterioration could be ascribed to development of Alzheimer dementia. CONCLUSION: Our observation suggests that treatment refractoriness in an individual with late-onset OCD may indicate underlining organicity.
BACKGROUND: Although several studies have been conducted in an attempt to characterize the phenotype and underlying pathophysiology of individuals with early-onset obsessive-compulsive disorder (OCD), the literature on patients who develop OCD later in life remains sparse. OBJECTIVE: To describe clinical outcomes in the 7-year follow-up of a patient with late-onset OCD. METHOD: Single case report. RESULTS: A 64-year-old woman exhibiting a 7-year history of treatment-refractory late-onset OCD developed significant cognitive deterioration. We suggest that the association between late-onset treatment refractory OCD and dementia may stem from at least 3 different scenarios. First, dementia may be an inexorable end-point of some forms of malignant, primary, and late-onset obsessional illness. Second, late-onset OCD and dementia may result from a common pathophysiologic basis, such as in fronto-temporal dementia. Finally, the association between both conditions may result by the interaction between vulnerability toward OCD-type symptoms and the nonspecific effects of a neurodegenerative process. In our case, although subclinical OCD was likely to be "unmasked" by cognitive decline and/or bilateral caudate vascular lesions, ensuing cognitive deterioration could be ascribed to development of Alzheimer dementia. CONCLUSION: Our observation suggests that treatment refractoriness in an individual with late-onset OCD may indicate underlining organicity.