Esophageal Hypomotility and Spastic Motor Disorders: Current Diagnosis and Treatment

Abstract

Esophageal hypomotility (EH) is characterized by abnormal esophageal peristalsis, either from a reduction or absence of contractions, whereas spastic motor disorders (SMD) are characterized by an increase in the vigor and/or propagation velocity of esophageal body contractions. Their pathophysiology is not clearly known. The reduced excitation of the smooth muscle contraction mediated by cholinergic neurons and the impairment of inhibitory ganglion neuronal function mediated by nitric oxide are likely mechanisms of the peristaltic abnormalities seen in EH and SMD, respectively. Dysphagia and chest pain are the most frequent clinical manifestations for both of these dysfunctions, and gastroesophageal reflux disease (GERD) is commonly associated with these motor disorders. The introduction of high-resolution manometry (HRM) and esophageal pressure topography (EPT) has significantly enhanced the ability to diagnose EH and SMD. Novel EPT metrics in particular the development of the Chicago Classification of esophageal motor disorders has enabled improved characterization of these abnormalities. The first step in the management of EH and SMD is to treat GERD, especially when esophageal testing shows pathologic reflux. Smooth muscle relaxants (nitrates, calcium channel blockers, 5-phosphodiesterase inhibitors) and pain modulators may be useful in the management of dysphagia or pain in SMD. Endoscopic Botox injection and pneumatic dilation are the second-line therapies. Extended myotomy of the esophageal body or peroral endoscopic myotomy (POEM) may be considered in highly selected cases but lack evidence.

Markedly Effective Steroid Treatment of Three Patients with Allergy-related Jackhammer Esophagus

“…Within at least one month after the onset of GERD symptoms, a choking sensation on food ingestion, dysphagia, and chest pain appeared, and JHE was diagnosed based on HRM findings. Furthermore, in cases 1 and 2, in which EoE was diagnosed with JHE as the causal factor, longitudinal furrows and vitiligo (characteristic endoscopic findings of EoE) and luminal compression exhibiting esophageal dysmotility were seen (12). Although case 3 was attributed to EGD, luminal compression was not seen, and an esophageal biopsy revealed no invasion of eosinophils, which is a definitive diagnostic criterion of EoE.…”

“…Although the optimal treatment for JHE has not yet been established, cases of spontaneous remission have been reported (11). A calcium-channel blocker or nitrous acid agent is administered to relax the smooth muscles, and balloon dilatation and a muscle layer incision are performed (12). There are also cases in which a lengthy incision of the muscle layer from the middle to lower esophagus is required.…”

Phosphodiesterase inhibitors are viable options for treating esophageal motility disorders: A case report and literature review

“…The precise physiology behind distal esophageal spasm is unclear. It may be due to degeneration or the loss of distal esophageal inhibitory ganglion neurons . There is also evidence that nitric oxide deficiency is associated with these abnormal inhibitory neurons, as inhibition of nitric oxide leads to simultaneous distal esophageal contractions while the addition of nitric oxide reverses this pattern .…”

Current treatment options for esophageal diseases

“…Because of this, the first step in the management of DES is a therapeutic trial with a PPI, especially if functional testing or endoscopic examination suggest pathologic GER. If PPIs are not effective, smooth muscle relaxants (nitrates, calcium channel blockers, 5‐phosphodiesterase inhibitors) and pain modulators may be given to alleviate both pain and dysphagia, although the data do not show a clear benefit . The administration of low‐dose antidepressants (such as trazodone) was assessed in patients with abnormal esophageal contractility in a double‐blind, placebo‐controlled trial in which the authors observed symptomatic but not manometric improvement.…”

“…If PPIs are not effective, smooth muscle relaxants (nitrates, calcium channel blockers, 5-phosphodiesterase inhibitors) and pain modulators may be given to alleviate both pain and dysphagia, although the data do not show a clear benefit. [25][26][27] The administration of low-dose antidepressants (such as trazodone) was assessed in patients with abnormal esophageal contractility in a double-blind, placebo-controlled trial 28 in which the authors observed symptomatic but not manometric improvement. Antidepressants are not recommended to treat patients with DES, despite some studies having demonstrated a possible benefit in patients with hypercontractile (or hypersensitive) esophagus.…”