Alpha and beta EEG power reflects L-dopa acute administration in parkinsonian patients.

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.

1-Hz repetitive transcranial magnetic stimulation increases cerebral vasomotor reactivity: a possible autonomic nervous system modulation.

BACKGROUND: Neuromodulation techniques, i.e. repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS), can modify cerebral hemodynamics. High frequency rTMS appeared to decrease cerebral vasomotor reactivity (VMR), while there is still poor evidence about the effect of low frequency (LF) rTMS on cerebral blood flow (CBF) and VMR. HYPOTHESIS: The present study aimed to test if LF rTMS decreases CBF and increases cerebral VMR. Monolateral or bilateral hemispheric involvement and duration of the effect were considered. A possible role of autonomic nervous system in CBF and VMR modulation was also investigated. METHODS: Twenty-four right-handed healthy subjects underwent randomly real (12) or sham (12) 20-min 1-Hz rTMS on left primary motor cortex. Mean flow velocity and VMR of middle cerebral arteries were evaluated by means of transcranial Doppler before (T0), after 10 min (T1) and after 2 (T2), 5 (T3) and 24 h (T4) from rTMS. Heart rate variability (HRV) was studied within the same timing interval, assessing low frequency/high frequency (LF/HF) ratio as index of autonomic balance. RESULTS: After real rTMS compared with sham stimulation, MFV decreased bilaterally at T1 (F = 3.240, P = .030) while VMR increased bilaterally (F = 5.116, P = .002) for at least 5 h (T3). LF/HF ratio decreased early after real rTMS (F = 2.881, P = .040). CONCLUSION: 1-Hz rTMS may induce a bilateral long-lasting increase of VMR, while its effect on MFV is short-lasting. Moreover, HRV changes induced by rTMS suggest a possible autonomic nervous system modulation.

Mobile phone emission modulates interhemispheric functional coupling of EEG alpha rhythms.

We tested the working hypothesis that electromagnetic fields from mobile phones (EMFs) affect interhemispheric synchronization of cerebral rhythms, an important physiological feature of information transfer into the brain. Ten subjects underwent two electroencephalographic (EEG) recordings, separated by 1 week, following a crossover double-blind paradigm in which they were exposed to a mobile phone signal (global system for mobile communications; GSM). The mobile phone was held on the left side of the subject head by a modified helmet, and orientated in the normal position for use over the ear. The microphone was orientated towards the corner of the mouth, and the antenna was near the head in the parietotemporal area. In addition, we positioned another similar phone (but without battery) on the right side of the helmet, to balance the weight and to prevent the subject localizing the side of GSM stimulation (and consequently lateralizing attention). In one session the exposure was real (GSM) while in the other it was Sham; both sessions lasted 45 min. Functional interhemispheric connectivity was modelled using the analysis of EEG spectral coherence between frontal, central and parietal electrode pairs. Individual EEG rhythms of interest were delta (about 2-4 Hz), theta (about 4-6 Hz), alpha 1 (about 6-8 Hz), alpha 2 (about 8-10 Hz) and alpha 3 (about 10-12 Hz). Results showed that, compared to Sham stimulation, GSM stimulation modulated the interhemispheric frontal and temporal coherence at alpha 2 and alpha 3 bands. The present results suggest that prolonged mobile phone emission affects not only the cortical activity but also the spread of neural synchronization conveyed by interhemispherical functional coupling of EEG rhythms.

Mobile phone emissions and human brain excitability.

OBJECTIVE: To test-via Transcranial Magnetic Stimulation (TMS)-the excitability of each brain hemisphere after 'real' or 'sham' exposure to the electromagnetic field (EMF) generated by a mobile phone operating in the Global System for Mobile Communication (GSM). METHODS: Fifteen male volunteers attended two experimental sessions, one week apart, in a cross-over, double-blind paradigm. In one session the signal was turned ON (EMF-on, real exposure), in the other it was turned OFF (EMF-off, sham exposure), for 45 minutes. Motor Evoked Potentials (MEPs) were recorded using a paired-pulse paradigm (testing intracortical excitability with 1 to 17 ms interstimulus intervals), both before and at different times after exposure to the EMF. Short Intracortical Inhibition (SICI) and Facilitation (ICF) curves were evaluated both on the exposed and non-exposed hemispheres. Tympanic temperature was collected during each session. RESULTS: The intracortical excitability curve becomes significantly modified during real exposure, with SICI being reduced and ICF enhanced in the acutely exposed brain hemisphere as compared to the contralateral, non-exposed hemisphere or to sham exposure. Tympanic temperature showed no significant main effect or interactions. INTERPRETATION: These results demonstrate that GSM-EMFs modify brain excitability. Possible implications and applications are discussed.

Motor cortex excitability in Alzheimer's disease: a transcranial magnetic stimulation study.

Motor deficits affect patients with Alzheimer's disease only at later stages. Recent studies demonstrate that the primary motor cortex is affected by neuronal degeneration accompanied by the formation of amyloid plaques and neurofibrillary tangles. It is conceivable that neuronal loss is compensated by reorganization of the neural circuitries occurring along the natural course of the disease, thereby maintaining motor performances in daily living. Cortical motor output to upper limbs was tested via motor-evoked potentials from forearm and hand muscles elicited by transcranial magnetic stimulation of motor cortex in 16 patients with mild Alzheimer's disease without motor deficits. Motor cortex excitability was increased, and the center of gravity of motor cortical output, as represented by excitable scalp sites, showed a frontal and medial shift, without correlated changes in the site of maximal excitability (hot-spot). This may indicate functional reorganization, possibly after the neuronal loss in motor areas. Hyperexcitability might be caused by a dysregulation of the intracortical GABAergic inhibitory circuitries and selective alteration of glutamatergic neurotransmission. Such findings suggest that motor cortex hyperexcitability and reorganization allows prolonged preservation of motor function during the clinical course of Alzheimer's disease.