Abstract
Aim: To evaluate the effect of an acute L-dopa administration on eye-closed resting state electroencephalographic (EEG) activity of cognitively preserved Parkinsonian patients.Methods: We examined 24 right-handed patients diagnosed as uncomplicated probable Parkinson’s disease (PD). Each patient underwent Unified Parkinson’s Disease Rating Scale (UPDRS)-part-III evaluation before and 60 min after an oral load of L-dopa-methyl-ester/carbidopa 250/25 mg. Resting condition eyes-closed EEG data were recorded both pre- and post L-dopa load. Absolute EEG power values were calculated at each scalp derivation for Delta, Theta, Alpha and Beta frequency bands. UPDRS scores (both global and subscale scores) and EEG data (power values of different frequency bands for each scalp derivation) were submitted to a statistical analysis to compare Pre and Post L-Dopa conditions. Finally, a correlation analysis was carried out between EEG spectral content and UPDRS scores.Results: Considering EEG power spectral analysis, no statistically significant differences arose on Delta and Theta bands after L-dopa intake. Conversely, Alpha and Beta rhythms significantly increased on centro-parietal scalp derivations, as a function of L-dopa administration. Correlation analysis indicated a significant negative correlation between Beta power increase on centro-parietal areas and UPDRS subscores (Rigidity of arms and Bradykinesia). A minor significant negative correlation was also found between Alpha band increase and resting tremor.Conclusions: Assuming that a significant change in EEG power spectrum after L-dopa intake may be related to dopaminergic mechanisms, our findings are consistent with the hypothesis that dopaminergic defective networks are implicated in cortical oscillatory abnormalities at rest in non-demented PD patients.
Highlights
Parkinson’s disease (PD) is a movement disorder finding its origin from the degeneration of pigmented dopaminergic neurons within the substantia nigra pars compacta and their striatal projections (Rodriguez-Oroz et al, 2009)
Assuming that a significant change in EEG power spectrum after L-dopa intake may be related to dopaminergic mechanisms, our findings are consistent with the hypothesis that dopaminergic defective networks are implicated in cortical oscillatory abnormalities at rest in non-demented PD patients
The progressive deterioration of the nigrostriatal dopaminergic system in PD leads to a secondary disruption in looping circuits constituted by cortico-basal ganglia-thalamo-cortical connections (Rodriguez-Oroz et al, 2009)
Summary
Parkinson’s disease (PD) is a movement disorder finding its origin from the degeneration of pigmented dopaminergic neurons within the substantia nigra pars compacta and their striatal projections (Rodriguez-Oroz et al, 2009). Otherwise, according to Braak’s neuropathological staging system for PD (Braak et al, 2003), degeneration of nondopaminergic nuclei (i.e., noradrenergic neurons in the locus coeruleus and serotoninergic neurons in the dorsal raphe nuclei) is a neuropathological hallmark that characterizes the earliest stages of PD. Since all these non-dopaminergic neurotransmitter systems are linked to corticopetal projections and regulate synaptic properties at cortical levels, they might play a role in modifications of post-synaptic pyramidal cells membrane potentials, which represent the source of brain oscillatory electroencephalographic (EEG) activity
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