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At Cambridge, Elliott, and then Langley, speculate that impulses liberate chemicals from nerve endings. Others, including Adrian, believe that nerve endings exert their effects by electric currents flowing through the synapses. In Austria, Otto Loewi dreams of a way to detect any chemical released by the endings of the vagus nerve in the frog heart. The method works and the chemical is later identified as acetylcholine—the first neurotransmitter to be discovered. In London, Henry Dale’s pharmacological experiments lead him to suggest that acetylcholine is also the transmitter in the sympathetic ganglia and at the nerve endings on muscle fibres. His later experiments are aided by Wilhelm Feldberg’s sensitive bioassay for acetylcholine. John Eccles, however, is still convinced that electric currents are responsible for part, or all, of the excitatory and inhibitory effects at synapses. Dale and Loewi share the 1936 Nobel Prize.

Gastric dysrhythmias are abnormal myoelectrical signals originating from the stomach. As recorded from cutaneous or serosal electrodes, bradygastrias range from 0 to 2.5 cycles per minute (cpm). Bradygastrias and mixed gastric dysrhythmias are reviewed in detail in Chapter 8. Tachygastrias range from 3.75 to l0.0cpm. The normal duodenal pacesetter potential ranges from 12 to 14 cpm. In this chapter, tachygastrias are reviewed in detail. Multiple metabolic mechanisms and neural-hormonal pathways influence gastric myoelectrical activity. The normal activities of enteric neurons, smooth muscle, hormones, and extrinsic nerves influence the ongoing activity of the interstitial cells of Cajal (ICCs), the pacemaker cells of the stomach. In healthy subjects, the frequency of gastric myoelectrical activity may vary from approximately 2.5 to 3.7cpm, depending on specific circumstances or provocative tests (Fig. 7.1). Specific diseases and disorders, with their specific pathophysiologies, may adversely affect gastric myoelectrical activity and are associated with gastric dysrhythmias. For example, many patients with type I and II diabetes have gastric dysrhythmias, and in healthy subjects, hyperglycemia itself produces gastric dysrhythmias. Gastric dysrhythmias occur when the ICCs are damaged or dysfunctional or when enteric neurons, circular smooth muscle cells (and perhaps longitudinal muscle activity), and extrinsic nerve activity from the parasympathetic and sympathetic nervous system input to the stomach are abnormal. Endocrine, neurocrine, and paracrine activities may also affect interstitial cells, enteric neurons, and smooth muscle and thereby affect gastric myoelectrical rhythms,21 shifting electrical activity to bradygastrias (0-2.5cpm) or tachygastrias (3.7- l0.0cpm) as shown in Figure 7.1. All of these influences interact to maintain normal gastric myoelectrical activity during baseline periods and in response to meals or other provocative stimuli. Stimuli that provoke stomach neuromuscular activity range from motion and the illusion of motion to emotionally challenging situations (disgust, anger) to the cephalic phase of digestion (vagal activation in the presence of appetizing food) to the relaxation, contraction, and coordination of stomach neuromuscular responses during and after the ingestion of a wide variety of solid and liquid foodstuffs. Thus, there are many gut-brain and brain-gut interactions to consider when evaluating gastric myoelectrical events during EGG recordings at baseline and after provocative stimuli.

Fatigue is a common and disabling symptom for patients with Sjögren’s disease and is best defined as a low-energy state characterized by physical or mental weariness. Fatigue represents one of the main reasons for the diminished quality of life in the Sjögren’s population. Primary factors such as inflammation can be reversible and should be ruled out first. Associated factors such as the side effects of medications and dysfunction of the thyroid gland (present in 20% of patients with Sjögren’s disease) should be taken into consideration as well. Making any needed adjustments in these environmental and psychosocial factors can often ameliorate the fatigue that severely reduces patients’ quality of life.