Electrogastrography for suspected gastroparesis

Normal 3 cpm gastric slow waves: Pacemaker cells of the stomach

The stomach is a complex neuromuscular organ ( Fig. 15.1 ). Contractions and relaxations of the gastric fundus, corpus, antrum, and pylorus are neuromuscular events under myoelectrical, neurological, and hormonal control . Gastric peristaltic contractions are coordinated by the pacesetter potential or slow wave activity of the stomach. The term gastric slow waves will be used in this chapter. Gastric slow waves originate in the pacemaker region on the greater curvature of the stomach, between the fundus and the corpus ( Fig. 15.1 ). Slow waves are electrical depolarization and repolarizations travel circumferentially and migrate distally with increasing velocity and amplitude at a rate of approximately 3 cpm in humans . The slow waves control the frequency and propagation of velocity of the normal 3 per minute gastric peristaltic contractions. The fundus of the stomach has little or no intrinsic slow wave activity.

Gastric slow waves are generated by the ICCs. The ICC networks within the circular muscle control the frequency of depolarization of the circular smooth muscle cells . In the normal stomach with normal numbers of ICCs, the slow wave frequency ranges from 2.5 to 3.7 cpm or approximately 3 cpm . The density of ICCs is greater in the distal antrum than the corpus. GMA amplitude and velocity are greatest in the terminal 3–4 cm of the antrum . The ICCs also form synapses with the enteric neurons of the intrinsic nervous system of the stomach. Inputs from the enteric nervous system and the parasympathetic and sympathetic nervous systems to the stomach are transmitted to the ICCs and affect the slow waves and thus modulate contraction and relaxation of the circular muscle cells through these relationships that inhibit or promote gastric peristaltic contractions .

Gastric action potentials, plateau potentials, and circular muscle contractions

Circular muscle contractions of the stomach wall occur during action potential or plateau potential activity . Action potential activity and plateau potential activities are linked to the slow waves that bring the circular smooth muscle membrane to the threshold of depolarization and contraction. Thus, normal 3 per minute gastric peristaltic waves are composed of electrical components—the 3 cpm slow waves linked with the action potential or plateau potential activity ( Fig. 15.2 ). These two electrical components produce the GMA recorded in the EGG. Consequently, the increase in amplitude of the GMA waves (20-second duration) after meals reflects the slow wave linked with plateau/action potentials that occurs every 20 s during the postprandial 3 per minute gastric peristaltic contractions ( Fig. 15.2 ) . The GMA recorded noninvasively with EGG in waves of 20-second duration methods accurately reflects GMA recorded simultaneously with serosal electrodes .

Thus, slow waves and plateau/spike potentials generate changes in cellular myoelectrical activity, all of which are summed in GMA and measured in the EGG. During the fasted state, the GMA from the stomach reflects predominantly the gastric slow wave activity and additional myoelectrical activity from intermittent gastric contractions. Thus, the EGG activity during fasting may be relatively unstable. In contrast, after a homogenous meal such as water, barium, or soup, the 3 per minute gastric peristaltic contractions empty these stomach contents; and, the corresponding GMA shows increased amplitude and regularity of 3 cpm waves as recorded in the EGG from healthy subjects . Studies using dozens of electrodes positioned on the corpus-antrum show that the slow waves propagate circumferentially and distally to form an elegant electrical ring that originates in the proximal corpus, migrates to the proximal antrum, and accelerates and gains amplitude in the terminal antrum, the 3–4 cm of the prepyloric antrum ( Fig. 15.2 ). Thus, the rhythmicity and amplitude of the EGG signal measures the integrity of the GMA and ICCs in the mid and distal antrum.

Gastric dysrhythmias

Gastric dysrhythmias are abnormal frequencies that include bradygastrias (1–2.5 cpm), tachygastrias (3.7–10 cpm), and mixed gastric dysrhythmias (combinations of tachygastrias and bradygastrias) . These dysrhythmias are recorded using electrogastrography methods ( Fig. 15.3 ) . In patients with chronic nausea conditions, gastric dysrhythmias represent a pathophysiological abnormality related to several known mechanisms. First, gastric dysrhythmias are related to depletion of the ICCs. ICCs are severely depleted (0–2 ICCs per high power field) in patients with gastric dysrhythmias and gastroparesis . In contrast, subjects with normal 3 cpm GMA have 5 or more ICCs per high power field . Interestingly, less severe ICC depletion (3–4 ICCs per high power field) has been reported in patients with unexplained nausea, gastric dysrhythmias, and normal gastric emptying . Thus, gastric dysrhythmias are present in both gastroparesis and in patients with gastroparesis-like symptoms (functional dyspepsia, chronic unexplained nausea) and appear to be a biomarker for nausea .

Second, chronic mesenteric ischemia is associated with nausea and vomiting and gastroparesis with gastric dysrhythmias . Gastric dysrhythmias resolved when stents or grafts were placed in the arteries and normal blood flow and oxygenation to the stomach was restored. Thus, chronic hypoxemia and oxidative stress may be a mechanism affecting GMA. Gastric dysrhythmias were eradicated and 3 cpm GMA was restored after treatment and indicate that depletion of ICCs may not be the only mechanism for developing gastric dysrhythmias.

Third, drugs such as domperidone and cisapride that have actions on enteric neurons eradicate gastric dysrhythmias in some patient groups, indicating that enteric neural dysfunction is another potential mechanism underlying gastric dysrhythmias in some patients . In full-thickness biopsies of the stomach from patients with gastroparesis, the smooth muscle cells appear to be intact, but enteric neurons have deformed cell processes and ICCs are depleted to various extents as described above . Thus, gastric dysrhythmias appear to be due to several pathophysiological pathways that include but are not limited to Cajalopathy, enteric neuropathy, autonomic nervous system dysfunction, or combinations of all. Fig. 15.3 shows examples of normal 3 cpm GMA and bradygastria and tachygastria.

Electrogastrography in patients with suspected gastroparesis

Clinical electrogastrography is indicated in the comprehensive evaluation of patients with symptoms suggesting upper GI motility disorders such as unexplained early satiety, nausea and vomiting, bloating, and abdominal discomfort. Symptoms are unexplained because gallbladder and pancreas imaging studies, upper endoscopy, and routine laboratory tests are normal in these patients. Thus, standard structural disorders are excluded and gastric neuromuscular disorders should be considered.

Gastric emptying scintigraphy and electrogastrography are noninvasive diagnostic tests that define objective gastric neuromuscular disorders. Solid-phase gastric emptying tests using scintigraphy or wireless motility capsule may indicate normal, rapid, or delayed gastric emptying of test meals . The EGG test provides further diagnostic precision for these patients by determining the presence or absence of normal 3 cpm GMA (the presence of normal numbers of ICCs) in response to the WLST.

Recording high quality EGGs

EGGs are recorded by placing fresh EKG-type electrodes in standard positions on the surface of the epigastrium. The skin should be prepared by gentle abrasion before placement of the electrodes to reduce impedance. The amplitude of the EGG signal ranges from 100 to 500 µV and the signal must be properly amplified and filtered. A 0.016 Hz high-pass filter and a 0.25 Hz low-pass filter are used. These filters create a window from approximately 1 to 15 cpm through which myoelectrical signals pass during the EGG recording . The normal EGG rhythm is approximately 3 cpm (2.5–3.7 cpm) . Bradygastrias range from 1.0 to 2.5 cpm and tachygastrias from 3.7 to 10.0 cpm. The duodenal pacesetter potential frequency is approximately 10–12 cpm. Occasionally, the respiration rate is less than 15 breaths per minute, may be seen in the EGG signal, and may be confused with tachygastria or duodenal slow wave frequencies .

The recording of high quality, artifact-free EGG signals is essential to facilitate visual analysis and ensure accurate computer analysis of the signal . To avoid movement artifact and to obtain high quality EGG recordings, the test must be performed in a quiet, warm room with the subject seated in a comfortable recliner with the back tilted to 30–45 degrees. The main source of artifact in the EGG signal is created by the subjects coughing, talking, or creating body movements during the recording. The EGG signal is reviewed visually for frequencies in the signal and for movement artifact that disrupts the EGG signal. These minutes of movement-induced artifact must be marked by the assistant who is always monitoring both the patient and the recording so that the artifact events are not used for computer analysis. The digitized EGG signals are subjected to fast Fourier transform to extract the frequency information present in the signal. The frequency data are presented as running spectral analyzes. Computer analysis allows for quantitative expression of the EGG signal as described below.

Provocative test meals and EGG recordings