: Depression is a frequent non-motor symptom of Parkinson’s disease (PD), and may even precede the onset of motor symptoms of parkinsonism. Beyond its negative influence on mood, depression in PD is frequently associated with other neuropsychiatric symptoms and with late-stage complications such as dementia. Despite its profound impact on the quality of life and cognitive functioning in PD, depression in PD is often under-recognized and poorly treated. : Pathophysiological studies demonstrated that depression in PD is associated with global dysfunction of interactions between discrete brain areas rather than focal structural or functional abnormalities, and that it is sustained by pathological changes of several neurotransmitter/receptor complexes. : In general, all traditional antidepressants and some dopamine agonists have been found to be safe and well-tolerated to treat depressive symptoms in PD, despite initial warning on worsening of parkinsonism. Available data suggest that the time-course of response differs among antidepressants. Efficacy results from clinical trials with antidepressant in PD are, however, rather uncertain, although pooled analysis suggests a moderate benefit. Several issues may critically impact the results of clinical trials with antidepressants in PD, including the correct psychiatric diagnosis, the overlap of symptoms between depression and PD, and the selection of appropriate end-points and rating scales.
IntroductionPhenotypic variants of progressive supranuclear palsy (PSP) are all characterized by the combination of motor symptoms of parkinsonism with a number of neuropsychiatric and cognitive disorders. Despite the strong effort in characterizing these features in PSP, alexithymia and anhedonia have not been investigated at present. Here, we aimed at investigating the qualitative and quantitative differences of alexithymia and anhedonia in the two more frequent variants of PSP, Richardson's syndrome (PSP‐RS) and PSP with predominant parkinsonism (PSP‐P) compared to Parkinson's disease (PD) patients recruited within 24 months after the onset of motor symptoms.MethodsOne hundred fifty‐five PD, 11 PSP‐P, and 14 PSP‐RS patients underwent clinical, neuropsychiatric, and neuropsychological evaluations. Alexithymia was assessed using the Toronto Alexithymia Scale‐20 item (TAS‐20), and hedonic tone was measured by the Snaith–Hamilton Pleasure Scale (SHAPS).ResultsIn PSP‐P and PSP‐RS patients, the frequency of alexithymia diagnosis was higher than in PD. On the TAS‐20 scores, PSP‐RS performed worse in the total score and in F2 sub‐scale when compared to PD. Among patients with diagnosis of depression, PSP‐RS showed higher scores in TAS‐20 total and TAS‐20 F2 than PD. No significant differences in TAS‐20 scores were found in nondepressed patients. Finally, we did not find significant differences among PD, PSP‐P, and PSP‐RS groups in the SHAPS scores.ConclusionsAlexithymia is identifiable very early in PSP‐P and PSP‐RS patients. Alexithymic symptoms differentiate PSP‐RS group from PD group but not between the two subtypes of PSP. Further, alexithymia in PSP seems to be predicted by the presence of depression. Altered emotional capability could be related to specific neurophysiological dysfunction occurring precociously in PSP; therefore, its identification could orient the diagnosis toward PSP cases.
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