In this study we examined the phenomenology of depression in PD patients. In particular, we analyzed the depressive profile of PD patients compared with that of patients affected by non-neurological medical illnesses, in order to control for the confounding effect of having a disabling illness.
Our results, after correction for multiple comparisons, showed that PD patients and CS as whole groups did not differ for severity of depressive symptomatology as measured by both the HDRS and BDI total score and PSY and SOM subscores. When we considered the frequency of specific symptoms of depression using the inclusive approach recommended by the NINDS/NIMH Work Group13
we found that PD patients experienced lower rates of worthlessness/guilt and changes in appetite than CS. Our results are in line with previous papers describing reduced negative affective feelings of guilt and worthlessness,11
but are discordant with regard to changes in appetite.21
In fact, in PD patients, changes in appetite associated with weight loss had been previously described even before the onset of the illness or at the very early stage. Moreover, depression had been proposed as a contributor to appetite loss. In our PD sample we found reduced rates of loss of appetite, and one of the explanations we propose could be the effect of L-dopa treatment on the hypothalamus,33
a region associated with appetite regulation. 35
In fact, it is reported that dopamine in the ventromedial hypothalamus is associated with stimulation of food intake.36
The L-dopa administration could increase the extracellular dopamine in the ventromedial hypothalamus with a restoration of food intake,37
thus contributing to maintain this aspect in equilibrium.
Results found in PD patients with MDD are sometimes different because they showed reduced severity of psychic depressive symptomatology using the HDRS (with a trend using the BDI), indicating that in well-structured and more severe clinical depression, such as MDD, the psychic dimension of depression may be less severe in PD patients when compared with CS. This finding is also reinforced by the fewer depressive symptoms of DSM-IV-TR found in PD patients with MDD in comparison with CS with MDD. On the other hand, in MIND patients we did not find any significant difference between PD and CS, probably because this diagnostic category of depression is less homogeneous and stable than MDD, thus impeding the capture of specific differences between these two groups of patients. Finally, only NODEP PD patients consistently reported increased severity of psychic, somatic, and total depressive symptoms in comparison with NODEP CS. In line with this, NODEP PD patients suffered from a greater number of DSM-IV-TR depressive symptoms compared with NODEP CS. These results support the idea that in PD patients with subtle depressive symptoms but without formal diagnosis of mood disorder, the neurological symptoms could overlap the depressive phenomenology, leading to a more severe symptom expression. 13
Accordingly, severity of motor symptoms measured by UPDRS-III was found to be associated with the somatic symptoms of depression, highlighting a relationship between the somatic symptoms of the neurological illness and the somatic symptoms of depression.
When we focused on groups with MDD, MIND, and NODEP separately, the frequency of the nine depressive symptoms listed in Criterion A of the DSM-IV-TR did not differ between the two groups of PD and CS.
Furthermore, our findings are not consistent with previous research about the somatic subtype of depression in PD, not only due to the differences in the clinical characteristics of the employed controls group and measures of depression used, but also because in our study we analyzed PD patients under stable dopaminergic therapy and during an “on” state. In fact, our results revealed that depressed PD patients did not exhibit a different somatic depressive profile compared with CS. In particular, depressed PD patients in our study did not report more somatic depressive symptoms, such as sleep disturbances and difficulty of concentration, as previously referred,9
rejecting the hypothesis that somatic depression in PD may be primarily related to the neurobiological mechanism of the disorder.
Strengths of our study are the stable dopaminergic therapy and assessment during the “on” phase. Moreover, the current study successfully addressed previous flaws in methodology by the addition of a relevant control group (ie, controlling for the impact of non-neurological chronic illnesses) that may be more comparable with PD in physical and psychological experiences. Another strength of our study is the thorough evaluation of both diagnosis and symptoms of depression using specific and validated scales, as well as a structured interview for diagnostic criteria.
One may criticize our study because we compared an unbalanced number of subjects in each category of depression: ie, MDD, MIND, and NODEP. This methodological confound could have resulted in weak statistical control. However, using this procedure we recruited a consecutive sample of individuals with depression, leaving preserved the clinical impact of depression in this population of individuals. Moreover, we employed a control group with different non-neurological medical illnesses in which the comorbidity could play an important role in depression prevalence, but, at the same time, this sample provides a clear picture of depression characteristics in elderly patients without neurological diseases. Nevertheless, future research should be dedicated to definitively confirm the hypotheses derived by our results.