Saber A.K. Sami

Cortical changes to experimental sensitization of the human esophagus

Topographical organization in the neocortex shows experience-dependent plasticity. We hypothesized that experimental sensitization of the esophagus results in changes of the topographical distribution of the evoked potentials and the corresponding dipole source activities to painful stimulation. An endoscopic method was used to deliver 35 electrical stimuli at the pain threshold to a fixed area of the mucosa in 10 healthy volunteer men and women. The stimulations were repeated after 30 min (reproducibility experiment), and after 60 min following perfusion of 200 ml 0.1 N hydrochloric acid (sensitization experiment). During stimulation the electroencephalogram was recorded from 64 surface electrodes. The sensitization resulted in a decrease in the pain threshold (F=6.2; P=0.004). The topographic distribution of the evoked potentials showed reproducible negative (N1, N2) and positive (P1, P2) components. After acid perfusion a reduced latency and a change in localization was seen for the P1 subdivided into frontal and occipital components (F=29.5, P<0.001; F=53.7, P<0.001). Furthermore the sensitization resulted in a reduction of the latency for P2 (F=6.2, P=0.009). The source analysis showed consistent dipolar activity in the bilateral opercular-insular cortex before and after acid perfusion. For the anterior cingulate dipole there was a reduction in latency (P=0.03) and a posterior shift (P=0.0002) following acid perfusion. The findings indicate that short-term sensitization of the esophagus results in central neuroplastic changes involving the cingulate gyrus, which also showed pathological activation in functional diseases of the gut, thus reflecting the importance of this region in visceral pain and hyperalgesia.

Cerebral processing of painful oesophageal stimulation: a study based on independent component analysis of the EEG

Background and aims: Independent component analysis (ICA) of the electroencephalogram (EEG) overcomes many of the classical problems in EEG analysis. We used ICA to determine the brain responses to painful stimulation of the oesophagus. Methods: Twelve subjects with a median age of 41 years were included. With a nasal endoscope, two series of 35 electrical stimuli at the pain threshold were given to the distal oesophagus and the EEG was subjected to ICA. The sessions were separated by 30 minutes. For each component head models, event related images, spectral perturbation, coherence analysis, and dipoles were extracted. The most valid components were found according to time/frequency information and reliability in both experiments. Results: Reliable components with the most valid dipoles were found in the thalamus, insula, cingulate gyrus, and sensory cortex. Time locked activities were consistent with upstream activation of these areas, and cross coherence analysis of the sources demonstrated dynamic links in the β(14–25 Hz) and γ(25–50 Hz) bands between the suggested networks of neurones. The thalamic components were time and phase locked intermittently, starting around 50 ms. In the cingulate gyrus, the posterior areas were always firstly activated, followed by the middle and anterior regions. Components with dipoles in the sensory cortex were localised in several regions of the somatosensory area. Conclusions: The method gives new information relating to the localisation and dynamics between neuronal networks in the brain to pain evoked from the human oesophagus, and should be used to increase our understanding of clinical pain.

Early Static Pressure-Related Evoked Brain Potentials Indications of Central Middle Ear Pressure Control in Humans

Hypothesis: The aim of this study was to investigate the possibility of afferent subcortical components related to static pressure changes of the human middle ear. Background: The normal middle ear function depends on a proper regulation of middle ear pressure, whereas an inadequate regulation with negative pressures is considered a major pathogenetic factor responsible for a variety of middle ear disorders. However, although studies on middle ear pressure and related clinical problems are common, studies on the role of its central control have been remarkably few. Hence, we attempted recording evoked brain potentials in response to static pressure stimulation of the middle ear in normal adult humans. Methods: The experiments were conducted by stimulating the middle ear in 6 subjects with a novel computer-controlled static pressure triggering system for rapid synchronized pressure loads of +3 kPa. The resulting brain evoked responses were recorded from 64 surface electrodes using a standard electroencephalogram cap. A wide-band electroencephalogram acquisition method was adopted, signals were sampled at 20,000 Hz, and band-pass filtered between 150 and 3,000 Hz. Results: Repeatable pressure evoked brain potentials and topographies were described for the first time. Hence, source localization could be adopted on a realistic head model, which showed the location of these early neural generators in the brainstem, followed by activity generated by the cerebellum. Conclusion: The findings are in agreement with previous animal experiments and provide basic information for further investigations on central components related to static pressure changes of the human middle ear.

Design of a static pressure stimulation system for neurophysiological investigation of human middle ear function

In this work, we describe a rapid, safe and accurate airflow injection method for neurophysiological investigations of the middle ear pressure regulation. The need for such a system arises from new knowledge about a variety of middle ear disorders that could have neurophysiological origins as well as a new understanding about human atmospheric pressure sensitivity. The performance of the system was investigated to confirm its reliability under a set of designated tasks.

FC5.2 The “human visceral homonculus” to pain evoked in the oesophagus, stomach, duodenum and sigmoid colon

patients participated in this study. Patients were instructed to silently read a word immediately after visual presentation of the word. Totally 100 words were presented. Using synthetic aperture magnetometry (SAM), local oscillatory changes were obtained as spatial distribution of Student’s t statistics by comparing 1 s before and after stimulus onset. Language dominance was determined by the laterality index derived from maximum t values of the left and right frontal desynchronization. Language dominance and localization were compared with Wada test (N = 48) and stimulation mapping (N = 12, subdural electrodes: 10, intraoperative cortical stimulation: 2), respectively. Results: Language dominance by SAM was concordant with Wada test in 42 cases (87.5%). Localization of the frontal language areas could be detected in 72 patients (93.5%). Localization of the frontal language areas by SAM was compared with stimulation mapping in eight cases. Estimated frontal language areas were well concordant with stimulation mapping. However, there was a tendency that the anterior part of the frontal language areas was not detected. Discussion: Our method is a noninvasive alternative to Wada test. As for language localization, our method is useful to determine the stimulation sites for invasive mapping. Additional tasks such as sentence reading might improve to detect the anterior part of the frontal language areas.