Normal smooth muscle contraction in the esophagus requires a balance between excitatory and inhibitory influences on esophageal motor function [13]. When control of smooth muscle contraction is abnormal, the contraction wave can be premature, non-peristaltic, and exaggerated (Fig. 4.1). The duration of the contraction wave can be prolonged, and the contraction at individual amplitudes can be double peaked or multiple peaked [13]. The correlate for multiple peaked waves on HRM consists of overlapping smooth muscle contraction segments (Fig. 4.1), rather than the normal sequential segmental architecture where the third contraction segment follows the second segment [14]. Using balloon distension in conjunction with pressure measurements, Sifrim et al. demonstrated abnormal esophageal inhibition in patients with contraction wave abnormalities (CWA) and simultaneous contractions fulfilling criteria for diffuse esophageal spasm (DES) [15]. In these studies, there was an inverse relationship between the degree of inhibition and the propagation velocity of deglutitive contraction, as well as an absence of inhibition in simultaneous contractions [13]. With HRM, however, individual smooth muscle contraction segments are not separately evaluated; instead, vigor of the entire smooth muscle contraction is evaluated using DCI, thereby overriding specific contraction abnormalities to obtain an overview of adequacy of smooth muscle contraction [16]. Similarly, timing of peristalsis is assessed using DL, which measures timing of contraction in relationship to initiation of peristalsis, but does not assess simultaneity in the smooth muscle contraction [17]. Use of these two HRM metrics identifies motor disorders that are well developed (i.e., hypercontractile disorder, diffuse esophageal spasm), but may miss individual contraction wave abnormalities (CWA) if DCI or DL is normal [9].

There is increasing evidence suggesting a relationship between esophageal perception and CWA. For instance, Borjesson et al. demonstrated using intraesophageal balloon distension that increased visceral perception (i.e., lowered thresholds for esophageal pain perception) correlated with higher amplitude and duration of esophageal peristaltic waves [18]. Further evidence for increased esophageal perception is provided by the fact that patients with these nonspecific changes in the contraction wave are more likely to have residual perceptive esophageal symptoms such as heartburn, and an increased need for medication usage following adequate antireflux therapy, when compared with patients without these abnormalities [19]. There is a higher likelihood of acid sensitivity (where esophageal acid exposure time is physiologic, but a statistical correlation is identified between symptoms and reflux events) in patients with exaggerated contraction patterns in the esophageal smooth muscle [20].

Provocative study of nonobstructive dysphagia and noncardiac chest pain has provided insights into the relevance of contraction wave abnormalities. Some CWA can be induced by provocative balloon testing in patients with nonobstructive dysphagia [21, 22]. While normal volunteers are not symptomatic and only develop secondary peristalsis during sustained balloon distension in the esophagus, patients with nonobstructive dysphagia develop simultaneous contractions and other CWA during balloon distension, and the majority develop their characteristic symptom [21, 23]. Further, automated impedance manometry (AIM) analysis has suggested that nadir esophageal impedance (indicating peak bolus content) is closer to peak contraction pressures with nonobstructive dysphagia in contrast to healthy controls, where nadir impedance and peak contraction are further apart [24]. While the exact pathophysiology is not known, asynchrony between contraction of the esophageal circular and longitudinal muscles may explain these findings. This has been demonstrated in patients with noncardiac chest pain, which could provide insights into how CWA might be associated with perceptive symptoms. In a normal patient, circular muscle contraction, as assessed by increase in intraluminal pressure, is synchronized with longitudinal muscle contraction, as measured by cross-sectional area on high-frequency ultrasound images [25]. In contrast, in patients with nutcracker esophagus, the pressure peak follows increase in cross-sectional area, suggesting that the two muscle groups are not in synchrony with exaggerated contraction, which represents a CWA.

In fact, these abnormal perception concepts are borne out on functional magnetoencephalography [26]. Normal subjects demonstrate symmetrical activation of the sensorimotor cortex with swallowing. Patients with functional dysphagia not only have abnormal activation of these areas, but also demonstrate activation of areas depicting vigilance and self-monitoring. These in turn may interfere with downstream sensorimotor control of deglutition [26]. Therefore, both abnormal motor function and abnormal perception or increased vigilance may participate in functional esophageal symptoms. It is possible that abnormal peristalsis, possibly in the form of contraction wave abnormalities, could be epiphenomena of the increased vigilance that is seen with these disorders. There is limited data suggesting that contraction wave abnormalities can also be seen as a consequence of distal esophageal obstruction [27], or from respiration-induced motion artifact in esophageal pressure phenomena [28]. In assessing symptom burden in the context of contraction wave abnormalities, these different CWA may have similar relationships to esophageal symptom burden.

Characteristics of contraction wave abnormalities:

Contraction wave abnormalities not identified with HRM software tools include the following (Fig. 4.1):

Integrity of the peristaltic wave relies on adequate formation of esophageal body contraction segments. In particular, the second segment, which is the proximal of the two smooth muscle contraction segments, can form poorly in hypomotility disorders, resulting in prominence of the trough between skeletal and smooth muscle contraction segments [35, 36]. This trough, which has been termed intersegmental trough or a transition-zone defect, has been linked to dysphagia, and indeed, bolus retention has been identified at this location using HRM with impedance [35, 37–39]. Studies using HRM with impedance suggests that breaks of >2 cm in the 20 mm Hg isobaric contour may be variably associated with impaired bolus clearance, while breaks >5 cm are uniformly associated with bolus escape [38, 40]. However, the association with dysphagia is not perfect, and the trough can be identified in healthy normal individuals, suggesting that the mere presence of a trough is not abnormal [38]. For this reason, focus has shifted to measurement of vigor of remaining contraction segments when such troughs are present, using DCI. The Chicago Classification v 3.0 currently recognizes >5 cm breaks as abnormal, if DCI is within the “intact” range (i.e., >450 mm Hg cm s)—these sequences are termed “fragmented.”