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OESO©2015
 
Volume: Primary Motility Disorders of the Esophagus
Chapter: Diffuse esophageal spasms (Corkscrew esophagus)
 

Is the LES always normal in diffuse esophageal spasm ?

E. Tiomny, P. Rozen (Tel Aviv)

Is is important to define diffuse esophageal spasm (DES) and to recognize that the literature on this subject, in the past decade, is not always comparable because of changing techniques. For this reason, we will define DES as a motor disorder of the esophagus clinically presenting mainly with dysphagia and, or, chest pain. Various authors suggested the following manometric criteria : basal esophageal body manometry demonstrating at least 10 p. cent of simultaneous contractions after wet swallows, intermittent with normal peristalsis. In addition, repetitive contractions (more than 3 peaks), prolonged contractions (more than 6 seconds), spontaneous contractions and high amplitude contractions in the esophageal body could also be found [1-4].

Review of large published series demonstrates that LES function in DES is normal in less than 75 p. cent of the patients [2, 5]. But some authors could demonstrate a hypertensive and, or, partially non-relaxing LES in approximately 1/3 of the DES patients [5-7]. Some of those series are summarized in table I.

It has already been described as early as 1964 by Barrett [11], that if some patients with DES were followed over a period of time, typical achalasia appeared [6, 12]. The possible common mediator, in both diseases, could be postganglionic denervation of the LES. That may be shown by provocative tests using CCK-OP or pentagastrin or mecholyl, all of them giving a hypersensitive type of reaction with

Table 1. Selected series, demonstrating abnormal LES function in DES patients

Authors

Number

Number of patients

of patients

with abnormal LES (%)*

Orlando & Bozymski 1973 [8]

1

1 (100%)

DiMarino & Cohen 1974 [5]

27

10 (37 %)

Swamy 1977 [9]

12

3 (25 %)

Davies et al. 1982 [7]

12

5(42%)

Mellow 1982 [10]

5

2 (40 %)

* High LES pressure and/or, abnormal relaxation

increase in LES pressure [13, 14]. As in achalasia, the most consistent pathological finding could be identified in the LES and in the absence or decrease in ganglionic cells in the myenteric (Auerbach's) plexus [15].

In achalasia, this loss of ganglionic cells is probably progressive, proportional to the duration of the disease [16]. The intrinsic nerves of the LES were also shown to be disturbed. There was a marked decrease in VIP containing fibers in the achalasia LES smooth muscle strips. In DES the pathology differs somewhat: there were generalized degenerative changes in vagal nerves, especially the afferent fibers [17].

Also, minimal focal smooth muscle changes were shown as well and esophageal muscle hypertrophy was demonstrated in the lower esophagus [17, 18]. These could represent progressive changes from one pathological state (DES) to another (achalasia), but this is still speculative, and no clear cut evidence exists.

Conclusion

In general, the majority of DES patients have normal LES function with an abnormality mainly demonstrated in the esophageal body. One-third of the patients show a hypertensive, non-relaxing LES.

References

1. Henderson RD (1983) Diffuse esophageal spasm. Surg Clin North Am 63 : 951-962.

2. Richter JE, Castell DO (1984) Diffuse esophageal spasm : a reappraisal. Ann Intern Med 100 : 242-245.

3. Nelson JB, Castell DO (1988) Esophageal motility disorders. DM 34 : 297-389.

4. Benjamin SB, Richter JE, Cordova CM, Knuff TE, Castell DO (1983) Prospective manometric evaluation with pharmacologic provocation of patients with suspected esophageal motility dysfunction. Gastroenterology 84: 893-901.

5. DiMarino AJ Jr, Cohen S (1974) Characteristics of lower esophageal sphincter function in symptomatic esophageal spasm. Gastroenterology 66 : 1-6.

6. Vantrappen G, Janssens J, Hellemans J, Coremans G (1979) Achalasia, diffuse esophageal spasm, and related motility disorders. Gastroenterology 76 : 450-457.

7. Davies HA, Kaye MD, Rhodes J, Dart AM, Henderson AH (1982) Diagnosis of esophageal spasm by ergometrine provocation. Gut 23 : 89-97.

8. Orlando RC, Bozymski EM (1973) Clinical and manometric effects of nitroglycerin in diffuse esophageal spasm. N Engl J Med 289: 23-25.

9. Swamy N (1977) Esophageal spasm: clinical and manometric response to nitroglycerin and long acting nitrites. Gastroenterology 72 : 23-27.

10. Mellow MH (1982) Effect of isosorbide and hydralazine in painful primary esophageal motility disorders. Gastroenterology 83 : 364-370.

11. Barrett NR (1964) Achalasia of the cardia: Reflections upon a clinical study of over 100 cases. Br Med J I : 1135-1140.

12. Kramer P, Harris LD, Donaldson RM Jr (1967) Transition from symptomatic diffuse spasm to cardiospasm. Gut 8 : 115-119.

13. Ippoliti AF, Varner AA (1980) Does denervation of the lower esophageal sphincter occur in diffuse esophageal spasm? Gastrointestinal Motility ; J. Christensen Ed, Raven Press, New York, pp. 79-85.

14. Holloway RH, Dodds WJ, Helm JF et al. (1986) Integrity of cholinergic innervation to the lower esophageal sphincter in achalasia. Gastroenterology 90 : 924-929.

15. Cassella RR, Brown AL Jr, Sayre GP, Ellis FH Jr (1964) Achalasia of the esophagus: pathological and etiologic considerations. Ann Surg 160: 474-485.

16. Csendes A, Smok G, Braghetto 1, et al. (1985) Gastroesophageal sphincter pressure and histological changes in distal esophagus in patients with achalasia of the esophagus. Dig Dis Sci 30: 941-945.

17. Cassella RR, Ellis FH Jr, Brown AL Jr (1965) Diffuse spasm of the lower part of the esophagus. J Am Med Assoc 191 : 379-382.

18. Sloper JC (1956) Idiopathic diffuse muscular hypertrophy of the lower esophagus. Thorax 9 : 136-146.


Publication date: May 1991 OESO©2015