[Affective disorders and dementia of the frontal lobe type. Hypothesis of a pathogenic relationship]

The evolution of some dysthymic states towards dementia is now rarely considered whereas it was well known at the beginning of the century. In French the final stage of this evolution was known as "démence vésanique". In recent years it has been noted that a proportion of patients with presenile dementia do not have Alzheimer's disease (AD) but a particular type of cognitive impairment., called dementia of the frontal lobe type (DFT), characterised by clinical and neuropsychological signs of frontal lobe disorder as well as an anterior defect of cerebral perfusion or metabolism. The onset of DFT is insiduous and marked by personality changes and inappropriate affect. It has not yet been reported as starting with true dysthymic disorders. PATIENTS AND METHODS. Ten right handed patients (F/M = 9/1) became dysthymic in their fifties (m = 49.8 + 7.6 yr). All initially met the DSM III-R criteria for mood disorders. They were all treated with the standard drugs or ECT. Although initially responsive all the patients relapsed and their dysthymic disorders became less typical in presentation. At a mean age of 63.6 +/- 2.9 yrs a particular type of dementia became evident. None of the patients had a previous history of mood disorder or a family history of dementia. The demented patients received thorough clinical examinations and 8/10 were tested with the Wechsler Adult Intelligence Scale (WAIS). All had XCT and HMPAO-SPECT scans using a rotating gamma camera. Three patients had a MRI Scan. RESULTS. The main symptoms were apathy and a lack of spontaneity as a result of which the patients were no longer able to live alone. HMPAO-SPECT: All the patients had clear hypoperfusion of the frontal and temporal lobes with seven showing a left predominance. XCT: A moderate degree of cortical atrophy, more pronounced in the frontal lobes, was observed in 6 patients. In 3 of them a previous XCT scan had been normal. MRI: Subcortical white matter hyperintensities were seen in the 3 patients examined. DISCUSSION. Although our patients do not probably form, with regard to a etiology a homogeneous group, they share common characteristics which are very similar to those which differentiates DFT from AD. We postulate that some dysthymic disorders of the presenium might represent the initial stage of this type of dementia. This hypothesis relies on the evidence for frontal dysregulation in mood disorders as demonstrated, for example, by PET studies. In these cases the cortical abnormalities usually disappear as the dysthymia improves and are considered functional phenomena. They may correspond to the mechanism of deafferentation (or diaschisis). This implies a primary lesion, presumably located at a subcortical level (for instance a white matter lesion) producing a disruption of function in a distant (initially) intact brain region. As a supplementary hypothesis we propose that with time, and for as yet unknown reasons, the frontal hypoperfusion in our patients lost its reversibility and that, as a result, a particular type of dementia became manifest. In some cases this diaschisis protractiva may lead to secondary cortical atrophy. CONCLUSIONS. A DFT was found in 10 patients who had become dysthymic in their fifties. A pathogenic hypothesis i.e. diaschisis protractiva, is proposed, based on the evidence of neuroimaging studies.