Progression of Neuropsychiatric Symptoms in FTD

The classical course of FTD is composed of a period of increasing disturbing behaviors, followed by a stage with an apparent improvement due to progression of apathy, before abulia and total dependence occur. Disinhibition usually diminishes over the progression of dementia [35]. Hyperorality remains for a long time, as restlessness does, whereas verbal disinhibition decreases together with the spontaneous and constant reduction of speech evolving toward mutism [71]. The improvement of patients’ behavior that occurs paradoxically at later stages is associated with a lowering of caregivers’ distress [72, 73].

Psychiatric Disorders Preceding FTD

FTLD cases (bvFTD and PPA) due to a GRN mutation have been reported in patients with previous bipolar spectrum disorders [74, 75] or schizophrenia [76, 77]. BvFTD was also described in three patients with previous signs of autistic spectrum disorder, especially Asperger’s syndrome [78]. Whether those cases correspond to a fortuitous association of two pathologies or to a long-lasting prodromal phase of FTD with psychiatric features remains a matter of debate [76, 79]. In our experience, some FTD patients have been described as being original or eccentric throughout their lives.

Links Between bvFTD and Schizophrenia

FTD and schizophrenia share clinical features, especially related to negative symptoms (e.g., blunted affect, apathy, social withdrawal). However, disinhibition, overeating, mutism, or incontinence is not observed in typical schizophrenia, and antipsychotic treatment is not effective in FTD. The morbid risk for schizophrenia in first-degree relatives is higher in relatives of probands with FTD than in relatives of probands with AD. Moreover, in some families with both FTD and schizophrenia, the causal FTD mutation was also present in individuals with schizophrenia. This could indicate a common etiology for both conditions in some families [80]. Vulnerability to psychosis in FTD and schizophrenia might share a common pathophysiology involving alterations in the frontal cortex and thalamus [53].

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