Discussion
Our findings of the EEG waves slowing in frontal lobe areas and the
association of this phenomenon with the executive function decline in PD
patients (revealed with neuropsychological assessment using TMT-A and
TMT-B) is in line with the previous literature data describing the
mechanisms of PD-specific frontal dysfunction.1,7,8Furthermore, lower values of putamen and caudate nuclei
[18F]Fluorodopa PET/CT uptake ratios in our PD
patients are consistent with the current state of knowledge and describe
PD-related dopaminergic deficits.4–8,19,20 Thus,
taking into account the concept of the “dual
hypothesis”,8 which assumes the dopaminergic-mediated
striatofrontal executive dysfunction in early-stage PD (and
cholinergic-based cognitive impairment, especially in later demented PD
patients), we hypothesized a significant correlation of the frontal lobe
EEG waves slowing with the dopaminergic deficiency and the executive
dysfunction measures in mild non-demented PD patients tested in the
present study. Indeed, our results confirmed almost completely this
hypothesis as for the negative correlation between the PSD-EEG and
striatal [18F]Fluorodopa PET/CT uptake ratios.
However, with regard to consideration on the associations of the EEG
waves slowing in frontal lobe and striatal dopaminergic deficiency with
neuropsychological outcomes describing the executive dysfunction (i.e.
TMT and and ST), one should point out that in majority of our results
these associations were confirmed only with the Trail Making Test but
not with the Stroop Test. The TMT consists of two parts (TMT-A and
TMT-B). In TMT-A part a subject connects (by drawing a line) numbers in
sequential order, but in the TMT-B the subject alternates between
numbers and letters (1, A, 2, B, etc.). The former is used to examine
cognitive processing speed, while the latter assesses executive
function.15,16 The ST also consists of two parts:
ST-I, in which a subject reads a list of 40 words, which are names of
colors printed in the color itself; and ST-II, where color names are
printed in an incongruent color and the subject is required to ignore
the word and correctly name the ink color. The former is used as a
measure of processing speed and the latter to test selective attention
and inhibition.17,18 Thus, both of these tests (TMT
and ST) evaluate an executive function, but the TMT is more related to
motor skills (due to line’s hand drawing task), and therefore a
disordered performance of this test in PD patients might be partly
related to pathological neural networks causing bradykinesia. According
to the triadic subdivision of the parallel striatal projections in the
dopaminergic system (mesostriatal, mesocortical and mesolimbic pathways)
the mesostriatal component is responsible for the bradykinesia in the
hypodopaminergic conditions 21 as in our PD patients.
At the same time, it is important to note that the mesocortical system
is responsible for executive function.21 It is
necessary take into account that the mesostriatal dopaminergic circuit
is most prominently affected, also on the early stage of PD, whereas the
mesocortical and mesolimbic dopaminergic circuits are relatively
preserved in the early stage of the disease.22,23Therefore in our mild PD patients (being on early stage of disease) the
mesostriatal component of the triadic striatal projections in the
dopaminergic system might be more affected by stated in our study
dopaminergic deficiency. In consequence, this may be a reason of stated
by us significant correlations of the PD-specific slowing of brain waves
and dopaminergic deficiency with the Trail Making Test, with
simultaneous lack of significant correlations with the Stroop Test.
Our diagnostic accuracy analyses showed that some of the PSD-EEG
parameters might be potentially a good alternative for expensive PET/CT
diagnostics in PD. Particularly, the PSD-EEG theta-alpha maximal peak
and lower-alpha band for the SMA and PFC regions seemed to be promising
PD-related executive dysfunction biomarkers, since they presented high
diagnostic sensitivity and specificity, significantly differentiated
mild PD patients from healthy controls, as well as they were correlated
with dopaminergic deficiency and executive dysfunction parameters.