Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Esophagogastric  Junction

  Browse by Author
  Browse by Movies
Volume: Primary Motility Disorders of the Esophagus
Chapter: Diffuse esophageal spasms (Corkscrew esophagus)

How to avoid overlap between disordered motor activity and secondary reflux damage ?

J. M. Suduca, M. Delvaux J. Frexinos (Toulouse)

Esophageal motor disorders (HMD) are frequently observed in patients with gastroesophageal reflux (GER): lower esophageal sphincter (LES) dysfunction and esophageal peristalsis alterations may facilitate the reflux or dramatically delay the esophageal acid clearance. On the contrary, the reflux itself has been reported to induce motility disorders. In spite of the numerous studies available in this field, the main question remains to know whether these motility disorders are primary or secondarily induced in patients with GER.

LES function and GER

Several features are consistent with the reality of EMD in GER : 1. the most common abnormalities of LES function in GER are a decrease in the resting pressure and an inappropriate relaxation (relaxation not preceded by an esophageal peristaltic sequence) [3, 13]; 2. similar alterations are observed in patients with scleroderma, diabetes mellitus, presbyesophagus, that are conditions associated with an increased risk of GER [15] ; 3. the severity of the mucosal damage due to GER has been correlated to the decrease in the LES pressure [1, 5, 6, 9, 17, 23].

Nevertheless, it remains unknown whether this LES dysfunction is the cause or the consequence of esophagitis[19]. Experimental studies in animals have shown that induction of esophagitis by long-term perfusion of acid into the esophagus results in a transient LES pressure decrease which returned to normal values after acid infusion had been stopped since several weeks [12]. In humans, clinical studies have demonstrated that the LES pressure was decreased in esophagitis patients, and that the LES function improved after medical or surgical healing of the esophagitis [2, 4, 8, 22]. These features suggesting that impairment of the LES function in reflux esophagitis would be induced by the presence of esophageal lesions.

Effects of reflux on the esophageal motility (figure I)

The peristaltic contractions of the esophageal muscle play a major role in enhancing esophageal clearance and thereby in decreasing the contact-time of the refluxate with the esophageal mucosa. In healthy subjects, the response of the esophagus to an experimental intraesophageal infusion of HC1 0.1 N has been studied by manometry and by measuring the esophageal acid clearance in the absence of any swallowing [7, 18]. The results have shown that the presence of acid in the esophagus provokes an increase in the motor activity (physiological secondary waves) and an accelerated emptying of the esophageal content. In patients with non cardiac chest pain, the same acid infusion tests may induce motility disorders that could stimulate the mechanoreceptors and thereby be responsible for chest pain [24].

In patients with evolutive esophagitis, the primary as well as the secondary peristaltic activities may be altered : decrease in the amplitude, duration and propagation rate of the peristaltic waves, absence of peristaltic contractions following a swallowing [16, 17]. Moreover, the presence of tertiary waves (unpropagated, small amplitude waves with a « dome » shape) suggesting an injury of the esophageal mucosa and have been observed in patients with severe GER. The EMD observed in patients with erosive esophagitis are not specific. However, these EMD may lead to delayed acid clearance and thus worsen the esophagitis lesions. The presence of EMD in such patients is an indicator of severity of GER disease and may impair the results of antireflux surgery [1, 6]. These assumptions have been assessed by clinical studies: 25 p. cent of patients with mild esophagitis and 48 p. cent of patients with severe esophagitis show motor abnormalities [17]. Some features support the primarity of EMD in the pathogenesis of GER : 1. intensive care patients with severe esophagitis have a significant decrease of


Figure 1. Esophageal manometry. A: Normal esophageal motility. B: Instillation of HC1. Increased amplitude and duration of peristaltic waves. C : Esophagitis. LES : Hypotension ; CO : Non propagated waves of decreased amplitude.

the secondary peristaltic waves as shown by acid clearance tests in the absence of swallowing [25]; 2. the solid bolus transit test shows that there is no correlation between clinical or endoscopic severity of the GER and the transit time of food [11];

3. both medical and surgical treatment of GER allowed healing of the mucosal lesions but dit not modify the esophageal motor activity in several clinical studies [2,

4, 10, 20, 21] On the contrary, many observations suggest that EMD are secondary induced by GER : 1. the inflammatory changes around esophagitis lesions may also damage esophageal muscle and nerves and thereby be responsible for EMD [12]; 2. several studies showed that EMD are improved after antireflux surgery [4, 14].

In conclusion, experimental and clinical observations remain contradictory and thereby the actual relationship between EMD and GER, still unclear. It seems true that abnormalities of the LES and of the esophageal peristalsis exist in patients with GER and that their severity increases at the same time as to that of the esophagitis. The lack of a definite physiological pathway for EMD in GER does not signify that EMD are devoid of any clinical relevance. In case of reflux esophagitis, the complete healing of the mucosal damage must be obtained before to investigate into the possibility of EMD responsible for the reflux. On the other side, before to take EMD into account as the cause of chest pain, one will actively search for a non typical GER, namely by performing a 24-hour pH monitoring. Finally, the preoperative evaluation of patients with GER will certainly include an esophageal manometry in order to better assess the prognosis of the further surgical procedure.


1. Ahtaridis G, Snape WJ, Cohen S (1979) Clinical and manometric findings in benign peptic stricture of the esophagus. Dig Dis Sci 24 : 858-861.

2. Baldi F, Ferrarini F, Longanesi AM, Angeloni M, Ragazzini M, Miglioli M, Barbara L (1988) Esophageal function before, during and after healing of erosive esophagitis. Gut 29 : 157-160.

3. Baldi F, Ferrarini F, Balestra R, Borioni D, Longanesi AM, Miglioli M, Barbara L (1985) Esophageal motor events at the occurrence of acid reflux and during endogenous acid exposure in healthy subjects and patients with esophagitis. Gut 26: 336-341.

4. Bancewicz J, Osugi H, Marples M (1987) Clinical implications of abnormal esophageal motility. Br J Surg 74: 416-419.

5. Brand W, Shay S, Peura D, Oliver G, Johnson L (1986) A comparison of reflux test parameters and patient demographics in different patient groups defined by the severity of endoscopic esophagitis. Gastroenterology 90: 1353 A.

6. Bruley des Varannes S, Touchais JY, Weber J, Desechalliers JP, Sauger F, Denis P, Galmiche JP (1986) Esophagite de reflux : roles respectifs des facteurs pathogeniques esophagiens et gastriques. Gastroenterol Clin Biol 10 : 662-668.

7. Corazziari E, Pozzessere C, Dani S, Anzini F, Torsoli A (1978) Intraluminal pH and esophageal motility. Gastroenterology 75 (2): 275-277.

8. DeMeester TR, Bonavina L, Albertucci M (1986) Nissen fundoplication for gastroesophageal reflux disease. Evaluation of primary repair in 100 consecutive patients. Ann Surg 204 : 9-20.

9. Denis P, Le Bihan M, Galmiche JP, Hecketsweiler P, Colin R, Pasquis P (1980) Syndrome du reflux gastrooesophagien. Exploration fonctionnelle de 1'oesophage chez 55 malades. Nouv Presse Med 9: 2125-2127.

10. Eckardt VF (1988) Does healing of esophagitis improve esophageal motor function? Dig Dis Sci 33: 161-165.

11. Eriksen CA, Sadek SA, Cranford C, Sutton D, Kennedy N, Cuschieri A (1988) Reflux esophagitis and esophageal transit: evidence for a primary esophageal motor disorder. Gut 29 : 448-452.

12. Eastwood GL, Castell DO, Higgs RH (1975) Experimental esophagitis in cats impairs lower esophageal sphincter pressure. Gastroenterology 69: 146-153.

13. Galmiche JP, Denis P, Desechalliers JP (1981) Valeur diagnostique des examens complementaires au cours du reflux gastro-oesophagien chez 1'adulte. Gastroenterol Clin Biol 5 : 1014-1025.

14. Gill RC, Bowes KL, Murphy PD, Kingma YJ (1986) Esophageal motor abnormalities in gastroesophageal reflux and the effects of fundoplication. Gastroenterology 91 : 364-369.

15. Gosselin A, Friguet JL (1987) Troubles moteurs de 1'oesophage au cours de la sclerodermie et autres collagenoses. In : Troubles de la motricite de 1'oesophage, reflux gastro-oesophagien. Progres en hepato-gastro-enterologie 2 Doin Ed p 53-64.

16. Gosselin A, Gosselin M, Gastard J, Paulet G (1982) Troubles moteurs de 1'oesophage au cours des oesophagites peptiques ? Gastroenterol Clin Biol 6 (2 bis): 86 A.

17. Kahrilas PJ, Dodds WJ, Hogan WJ, Kern M, Arndorfer RC, Reece A (1986) Esophageal peristaltic dysfunction in peptic esophagitis. Gastroenterology 91 : 897-904.

18. Leveque AM, Lambert R, Minaire Y (1980) La clairance acide de 1'oesophage au cours du reflux gastro-oesophagien et chez les temoins etudies par deux methodes dont une originale. Gastroenterol Clin Biol 4 (2 bis): 226 A.

19. Pope CE (1976) Is LES enough ? Gastroenterology 71 : 328-329.

20. Robertson DAF, Aldersley MA, Shepherd H, Lloyd RS, Smith CL (1987) H2 antagonists in the treatment of reflux esophagitis ; can physiological studies predict the response ? Gut 28 : 946-949.

21. Russel COH, Pope CE, Gannan RM, Allen FD, Velasco N, Hill LD (1981) Does surgery correct esophageal motor dysfunction in gastroesophageal reflux? Ann Surg 194: 290-296.

22. Segol P, Baptiste P, L'Hirondel C, Marchand P, Gignoux M (1982) Effets de la fundoplicature sur le sphincter inferieur de 1'oesophage. Gastroenterol Clin Biol 6: 222-228.

23. Sontag S, Schnell T, O'Connell S, Serlovsky R, Nenchausky B, Miller T (1986) Esophageal acid reflux profiles correlate with status of esophageal mucosa in gastro esophageal reflux and Barrett's. Gastroenterology 90 : 1643 A.

24. Vantrappen G, Janssens J (1988) What is irritable esophagus? Another point of view. Gastroenterology 94 (4): 1092-1093.

25. Veyrac M, Bories P, Chardon P, Du Cailar J, Balmes JL, Michel H (1982) (Esophagite et soins intensifs : role des troubles moteurs de 1'oesophage. Gastroenterol Clin Bio] 6 (2 bis): 86 A.

Publication date: May 1991 OESO©2015