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To The Editor:
Posterior cortical atrophy is a neurodegenerative disease that leads to a dementing syndrome involving distinct neuropsychological deficits of higher visuospatial functions. Although most patients are seen initially with neurological complaints, in some cases, secondary manifestations, such as affective symptoms, might appear in the foreground. Here we report a case of posterior cortical atrophy that initially was diagnosed and treated as a major depressive episode.
Ms. A, a 62-year-old right-handed woman, was referred for psychiatric examination with an approximately 1-year history of depressed mood, poor self-initiative, and anhedonia. She reported appetite reduction and weight loss, worrying most of the time about her health. Her concentration and memory were described as slowly declining within the last few years but were getting worse during the past weeks. Ms. A complained about difficulties reading and writing, noting progressive worsening of her eyesight. However, these symptoms were judged by her relatives as being by far not the most incapacitating of her problems, recognizing her depressive symptoms as being more prominent. Her prior medical history was unremarkable. Before entering our department, these symptoms were interpreted by several general practitioners as well as by a psychiatrist and a neurologist as a major depressive episode. Accompanying complaints of declining cognitive function were interpreted as depressive pseudodementia. However, previous treatment attempts with amitriptyline and citalopram failed to show any beneficial effects.
A psychiatric examination revealed mainly depressive symptoms that fulfilled the diagnostic criteria of a major depressive episode according to DSM-IV. A general neurological examination revealed optic ataxia and dysmetria. Ms. A’s score on the Mini-Mental State Examination was 22 of 30. Her laboratory parameters—including a screening for malignancy, infection, and autoimmune disease—were normal. Analyses of CSF showed increased tau-protein and decreased beta-amyloid levels. Magnetic resonance imaging of her brain revealed bilateral atrophy of the parietal and occipital cortex. Positron emission tomography with 18fluorodeoxyglucose showed decreased brain metabolism in the bilateral parieto-occipital cortex, in line with previously described metabolic deficits in posterior cortical atrophy (1).
Neuropsychological testing demonstrated pronounced visuospatial deficits, including Balint’s syndrome and Gerstmann’s syndrome. Memory and executive functions were relatively less impaired. Ms. A was diagnosed as having posterior cortical atrophy according to currently existing diagnostic criteria (2, 3). Drug therapy with venlafaxine and rivastigmine was initiated. A follow-up exploration after 3 and 6 months revealed progressive worsening of vision but full remission of the depressive symptoms. Within 1 year, Ms. A developed full cortical blindness, which left her memory functions relatively unaffected.
In this case, an atypical dementive syndrome presented with symptoms of a major depressive episode 1 year before the manifestation of dementia-specific symptoms. Cognitive impairment in the elderly requires meticulously exact differential diagnostic consideration of both a major depressive episode and early forms of dementia. Posterior cortical atrophy may initially present with both affective symptoms and deficits of higher visuospatial skills, leaving memory function relatively well preserved at the beginning of the disease. Coexistent depressive symptoms may be a distraction that could lead to a considerable delay of a proper diagnostic investigation. With rapid development of disease-modifying agents, early recognition of atypical variants of dementia in psychiatric practice is crucial for facilitating both early drug therapy as well as adequate health and social care support.
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