Channel interpolation in TMS-EEG: a quantitative study towards an accurate topographical representation.

The co-registration of transcranial magnetic stimulation and electroencephalography (TMS-EEG) is emerging as a successful technique for causally exploring cortical mechanisms and connections. However, various artefacts could affect TMS-EEG signals. Correct artefacted channels reconstruction is crucial to obtain accurate topographical representation and consequently accurate inverse problem solution, in order to map in a proper way the global brain responses after the stimulation of one particular brain region of interest. In this paper, we discuss the problem of artefacted channels interpolation in TMS-EEG signals. Aim of the study was to investigate two different interpolation methods evaluating their performance in two datasets: one constituted by 19 EEG channels montage (low-density spatial resolution) and the other one by 60 EEG channels montage (high-density spatial resolution). In addition, these evaluations took place in two different contexts of application: after the averaging of TMS Evoked Potentials (TEPs) in a time interval to obtain a global information in the considered range, and at fixed latencies 100 ms and 300 ms after the TMS stimulus. The results showed that the global reconstruction error was lower at fixed latencies for the high-density electrodes spatial resolution montage.

Sex-specific trends in 4-year survival in 37 276 men and women with acute myocardial infarction before the age of 55 years in Sweden, 1987-2006: a register-based cohort study.

OBJECTIVE: To examine sex-specific trends in 4-year mortality among young patients with first acute myocardial infarction (AMI), 1987-2006. DESIGN: Prospective cohort study. SETTING: Sweden. PARTICIPANTS: We identified 37 276 cases (19.4% women; age, 25-54 years) from the Swedish Inpatient Register, 1987-2006, who had survived 28 days after an AMI. OUTCOME MEASURES: 4-year mortality from all causes and standard mortality ratio (SMR). RESULTS: From the first to last 5-year period, the absolute excess risk decreased from 1.38 to 0.50 and 1.53 to 0.59 per 100 person-years among men aged 25-44 and 45-54 years, respectively. Corresponding figures for women were a decrease from 2.26 to 1.17 and from 1.93 to 1.45 per 100 person-years, respectively. Trends for women were non-linear, decreasing to the same extent as those for men until the third period, then increasing. For the last 5-year period, the standardised mortality ratio for young survivors of AMI compared with the general population was 4.34 (95% CI 3.04 to 5.87) and 2.43 (95% CI 2.12 to 2.76) for men aged 25-44 and 45-54 years, respectively, and 13.53 (95% CI 8.36 to 19.93) and 6.42 (95% CI 5.24 to 7.73) for women, respectively. Deaths not associated with cardiovascular causes increased from 21.5% to 44.6% in men and 41.5% to 65.9% in women. CONCLUSIONS: Young male survivors of AMI have low absolute long-term mortality rates, but these rates remain twofold to fourfold that of the general population. After favourable development until 2001, women now have higher absolute mortality than men and a 6-fold to 14-fold risk of death compared with women in the general population.

Non-fluent aphasia and neural reorganization after speech therapy: insights from human sleep electrophysiology and functional magnetic resonance imaging.

Stroke is associated with long-term functional deficits. Behavioral interventions are often effective in promoting functional recovery and plastic changes. Recent studies in normal subjects have shown that sleep, and particularly slow wave activity (SWA), is tied to local brain plasticity and may be used as a sensitive marker of local cortical reorganization after stroke. In a pilot study, we assessed the local changes induced by a single exposure to a therapeutic session of IMITATE (Intensive Mouth Imitation and Talking for Aphasia Therapeutic Effects), a behavioral therapy used for recovery in patients with post-stroke aphasia. In addition, we measured brain activity changes with functional magnetic resonance imaging (fMRI) in a language observation task before, during and after the full IMITATE rehabilitative program. Speech production improved both after a single exposure and the full therapy program as measured by the Western Aphasia Battery (WAB) Repetition subscale. We found that IMITATE induced reorganization in functionally-connected, speech-relevant areas in the left hemisphere. These preliminary results suggest that sleep hd-EEGs, and the topographical analysis of SWA parameters, are well suited to investigate brain plastic changes underpinning functional recovery in neurological disorders.

Non-primary motor areas in the human frontal lobe are connected directly to hand muscles.

Structural studies in primates have shown that, in addition to the primary motor cortex (M1), premotor areas are a source of corticospinal tracts. The function of these putative corticospinal neuronal tracts in humans is still unclear. We found frontal non-primary motor areas (NPMAs), which react to targeted non-invasive magnetic pulses and activate peripheral muscles as fast as or even faster than those in M1. Hand muscle movements were observed in all our subjects about 20 ms after transcranial stimulation of the superior frontal gyrus (Brodmann areas 6 and 8). Stimulation of NPMA could activate both proximal and distal upper limb muscles with the same delay as a stimulation of the M1, indicating converging motor representations with direct functional connections to the hand. We suggest that these non-primary cortical motor representations provide additional capacity for the fast execution of movements. Such a capacity may play a role in motor learning and in recovery from motor deficits.

Effect of amlodipine on blood pressure responses in local and whole-body cooling in normotensive men.

The objective of this study was to determine the ability of amlodipine (CAS 88150-42-9, Norvasc) to affect the cold-induced rise of blood pressure and heart rate in normotensive men. Fourteen normotensive men underwent a one-hand cold pressor test (+10 degrees C, 5 min) and a whole-body cold air exposure test (+5 degrees C, 45 min) in a crossover study with and without amlodipine at a seven-day interval. Amlodipine decreased the levels of initial systolic and diastolic blood pressure before both tests, but it had no influence on heart rate. During the cold pressor test, amlodipine lowered the peak diastolic pressure from 96 +/- 10 mmHg (mean +/- SD) to 92 +/- 10 mmHg (p = 0.024). The rise of diastolic blood pressure was 13 +/- 7 mmHg with amlodipine and 16 +/- 8 mmHg without amlodipine (p = 0.138). During the whole-body cold air exposure test, amlodipine decreased the systolic pressure from 135 +/- 2 mmHg to 133 +/- 3 mmHg (p = 0.008) and the diastolic pressure from 88 +/- 2 mmHg to 86 +/- 1 mmHg (p = 0.005). However, the cold-induced rise of blood pressure in whole-body cooling was not affected by amlodipine, because it also decreased the initial values. Amlodipine did not affect the initial or cold-induced changes of heart rate in these tests. In conclusion, in normotensive men amlodipine lowers the peak of diastolic blood pressure in a cold pressor test. In whole-body cold air exposure, amlodipine slightly decreases the levels of both systolic and diastolic pressures, but has no effect on the cold-induced rise of blood pressure. Amlodipine does not prevent the cold-induced physiological responses of blood pressure or heart rate.