Electrophysiology as a tool to unravel the origin of pancreatic pain

Table 1 Summary of findings of electroencephalography studies in chronic pancreatitis to date

Ref.	Methods	Results
Dimcevski et al[8],	64-channel EPs; 12 HV and 10 CPP	Decreased latencies of the early EP components
Gastroenterology, 2007	Electrical stimulation of the oesophagus, stomach, and duodenum	The bilateral insular sources localized more medial after stimulation of all 3 gut segments
	Amplitudes, latencies, and brain sources of the EPs were analysed	The cingulate source localized more posterior after stimulation of oesophagus
Drewes et al[26], World J Gastroenterol, 2008	62-channel EPs; 12 HV and 8 CPP	Higher activity in theta band
	Electrical stimulation of the oesophagus	The main theta components oscillated with 4.4 Hz in the patients and 5.5 Hz in the controls
Olesen et al[27], Pancreatology, 2010	Topographic matching pursuit was used to extract the EEG information in the early brain activation after stimulation	The energy in the delta band was higher in healthy volunteers
	62-channel EPs; 14 HV and 24 CPP	EP latencies at frontal electrodes were prolonged
	Electrical stimulation of the sigmoid	The insular dipoles were localised more posterior
	Patients’ daily pain experience was recorded in a pain diary	The shift of insular dipole localisation was negatively correlated with the patients’ clinical pain scores
	Amplitudes, latencies, and brain sources of the EPs were analysed
	Correlation analysis was done between patients’ pain scores and the changes in brain sources
Olesen et al[9], Clin Gastroenterol Hepatol, 2010	62-channel EPs; 15 HV and 25 CPP	Increased latency of P1
Olesen et al[21], Eur J Gastroenterol Hepatol, 2011	Electrical stimulation of the sigmoid	Increased activity in delta, theta and alpha bands, and decreased beta band activity
	Amplitudes and latencies of the EPs were analysed
	62-channel spontaneous EEG; 15 HV and 31 CPP
	Wavelet frequency analysis was used to retrieve amplitude strengths of the EEG	Differences in theta activity were located over centro-frontal brain regions, whereas differences in other frequency bands were located over frontal regions
	The amplitude strengths were summarized in frequency bands with corresponding topographies
Olesen et al[28], Aliment Pharmacol Ther, 2011	62-channel EPs	No differences in any of the EP characteristics between pregabalin and placebo groups
	31 CPP randomly assigned to receive increasing doses of placebo or pregabalin over 3 wk
	Electrical stimulation of the sigmoid
	Amplitudes, latencies, and brain sources of the EPs were analysed
Olesen et al[7], Eur J Pain, 2013	Three sequences of 62-channel CHEPs; 15 HV and 15 CPP	During successive stimulation of the pancreatic area, N2/P2 amplitude increased 25% in CP patients, while it decreased 20% in healthy volunteers
	Upper abdominal region (pancreatic ”viscerotome”) and the right forearm (heterologous area) were stimulated.	After stimulation of the forearm, N2/P2 amplitudes increased 3% in CP patients compared to a decrease of 20% in healthy volunteers
	Habituation was calculated as the relative change in CHEPs amplitudes between the first and the third stimulation sequence

EPs: Evoked potentials; HV: Healthy volunteers; CP: Chronic pancreatitis; CPP: Chronic pancreatitis patients; EEG: Electroencephalography; CHEPs: Contact heat evoked potentials.