"Cricopharyngeal Muscle Hypertrophy"
927 Cricopharyngeal Muscle Hypertrophy: Radiologic-Anatomic Correlation William E. Torre& There is a divergence of opinion concerning the cncopharyngeal muscle defect James L. Clements, Jr.1 commonly seen in the pharyngoesophageal area on barium esophagram. Some observ- Garth E. Austin2 ers believe this defect is the result of neuromuscular dysfunction with the demonstration of the unrelaxed muscle bundle; however, others believe it is the result of actual Kathryn Knight2 hypertrophy of the cncopharyngeal muscle. Radiologic and pathologic study of 24 unselected autopsy cases revealed cricopharyngeal hypertrophy in 13 cases by radio- logic criteria. Histologic examination revealed that the cncopharyngeal muscle thickness was uniformly greater in these cases than in the radiographically normal cases. The cricopharyngeal muscle defect is associated with actual hypertrophy of the cncophar- yngeal muscle in many cases. A posterior indentation of the esophageal lumen is often observed radiologically at the level of the lower cervical spine. This impression has had several names, including esophageal lip, spasm, hypopharyngeal bar, or hypertrophy of the crico- pharyngeal muscle (fig. i). In our previous clinical study [i ], the cricopharyngeal muscle defect was demonstrated in 1 8% of i 00 unselected patients on barium esophagram. Opinions differ as to the clinicopathologic significance of this posterior indentation on the esophageal lumen. Most authors agree that this esophageal narrowing is caused by contraction of the transverse fibers of the cricopharyngeal muscle. Two main bodies ofthought have emerged: One group postulates that the incoordination of the pharyngoesophageal structures during deglutition may explain this posterior esophageal defect; the second group attributes the cricopharyngeal indentation to muscle hypertrophy. To resolve this question, we examined 24 unselected autopsy specimens for radiographic and pathologic evidence of cricopharyngeal muscle hypertrophy. Materials and Methods En-bloc resection of the cervical esophagus, trachea, and larynx was done during post- mortem examination of 24 unselected patients. The proximal ends of the specimens were closed above the junction of the hypopharynx and the esophagus; barium was introduced into the lumen of the esophagus from below by a catheter passed through its occluded inferior margin. The specimens were then radiographed with the esophageal segment partially Received April 29, 1983; accepted after revision December 29, 1983. and then fully distended with contrast medium (fig. 2). The radiographs from the autopsy 1 Department of Radiology, Emory University specimens were assigned a grade from 0 to 4, determined by the size of the cricopharyngeal Hospital, 1364 Clifton Rd., N.E., Atlanta, GA 30322. muscle in the maximally distended specimen. The defects detected in the specimen radi- Address reprint requests to W. E. Torres. ographed correlated well in both configuration and location with those seen in the living 2 Department of Pathology, Emory University subject. Measurements of the transverse diameter of vertical pharyngeal wall were taken at Hospital, Atlanta, GA 30322. the point of greatest indentation on the posterior pharynx (fig. 3). AJR 141:927-930, May 1984 After this procedure, the specimens were fixed in neutral buffered formalin for gross and 0361 -803x/84/1 425-0927 microscopic study. Pathologic examination was performed without knowledge of the radi- C American Roentgen Ray Society ographic grade of the individual specimens. After gross inspection of the tissue, three vertical 928 TORRES ET AL. AJR:142, May 1984 sections, each 5-6 cm long, were taken through the posterior pha- almost complete correlation between the radiologic and path- ryngeal wall to include the cricopharyngeal muscle. This muscle was ologic grades of the cricopharyngeal muscle hypertrophy. recognized as a collection of oblique and transverse muscle fibers Furthermore, the measured thicknesses of the cricopharyn- located immediately cephalad to the predominantly longitudinal fibers geal muscle for individual specimens correlated well with the of the thinner walled upper esophagus. The degree of hypertrophy radiographic grade. (Examples of the histology of specimens of the cncopharyngeal muscle in each specimen was graded from 0 showing no hypertrophy, 1 + hypertrophy, and 4+ hypertro- to 4+, primarily on the basis of muscle thickness. However, muscle cell size and density of packing of muscle fibers were also taken into phy are shown in fig. 4.) The muscle thickness of the 11 consideration. cases with radiologic grade 0 was 1 .5 ± 0.5 mm (mean ± 1 SD); that of the nine cases graded 1 + or 2+ was 2.9 ± 0.2 Results mm. In cases of radiologic grade greater than 2+, muscle thickness was 4.2 ± i .8 mm. The large standard deviation Table 1 summarizes the radiologic and pathologic changes for the muscle thickness of specimens showing 2+ or greater found in the study of the anatomic specimens. There was hypertrophy was due to one very hypertrophied specimen with a muscle thickness almost twice that of any other spec- imen examined. The mean muscle thickness of the radiologically negative cases was compared with means of those cases showing 1+ hypertrophy or greater using Student’s f-test. The muscle thickness of radiologically negative cases was significantly different from the thickness of 1 + positive cases (p < 0.Oi) and from the 2+ to 3+ positive cases (p < 0.01). Although the mean muscle thickness of the 1 + positive cases was less than that for the 2+ to 3+ positive cases, this difference was not statistically significant (p > 0.10). Discussion There is a great divergence of opinion as to the pathologic and clinical significance of the cricopharyngeal indentation [1- 1. i 1 In our autopsy study, and in a previous clinical study, large cricopharyngeal muscles were identified radiographically in patients with no symptoms of dysphagia. However, Crich- low  has stated, “There is no normal radiologic picture of the cricopharyngeus because the cricopharyngeus is never visualized if the esophagus is acting normally.” Fig. 1 -A, Radiograph of normal cervical esophagus. B, Radiograph of According to Killian , the cricopharyngeal muscle con- patient. Cricopharyngeal impression. sists of two major parts: a pars obliqua and pars fundaforma Fig. 2.-Radiograph of normal ana- tomic specimen distended by liquid bar- ium. No cricopharyngeal muscle impres- sion. Fig. 3.-Radiographs of autopsy spec- imens from two patients. Cricopharyngeal impression. AJR:142, May 1984 CRICOPHARYNGEAL MUSCLE HYPERTROPHY 929 or transverse part (fig. 5). The oblique fibers arise from the goconstrictors and have identical function. The transverse posterior part of the lower third of the lateral surface of the fibers arise from the lateral margin of the cricoid cartilage, cricoid cartilage, extending up and back to insert into the passing backward horizontally without interlinking dorsally in median raphe to the other pharyngeal constrictors. These a raphe, forming a sphincter. This horizontal band of fibers is fibers are intimately fused with those of the inferior pharyn- responsible, along with the uppermost bundle of the esoph- ageal circular muscle, for closure of the mouth of the esoph- agus [4, 5]. TABLE 1 : Correlation of Radiologic and Pathologic Changes in Many observers have concluded that most cricopharyngeal Anatomic Specimens of Cricopharyngeal Muscle diseases cause cervical dysphagia as the main clinical mani- Radiologic Grade: n cncopharyngeMusde festation. However, this has not proved to be true. In 1966, Thkness(mm), Patholoc Grade ness( ) Mean±SD Seaman  postulated that pharyngoesophageal motility in- 0: coordination may be enough to explain this posterior esoph- 0 10 2.0, 1.8, 1.7, 1.5*, ageal defect. He believed that it is not necessary to attribute 1 3*, , *, 0.6 1 .5 ± 0.5 cricopharyngeal muscle indentation to spasm or hypertrophy. 1+ 1 2.3 If the cricopharyngeal muscle fails to open at the correct time 1+: or if it contracts prematurely, a defect would readily be 1+ 6 3.Ot, 2.8, 2.6 apparent in the barium column. This entity has been referred 2+: 2+ 1+ 2 1 3.9, 3.5 2.3 J 2.9 ± 0.2 to as cricopharyngeal achalasia, defined as the failure of the muscle to relax quickly enough during deglutition to permit >2+: 4+ 1 7.9 ‘1 the bolus to pass freely through the hypopharynx into the 3+ 1 4.5 1 4.2±1.8 esophagus. 2+ 2 4.0, 3.4 J In cricopharyngeal muscle dysfunction, the patient seldom . Two cases. complains of difficulty swallowing. The absence of symptoms t Four cases. is an unreliable sign in the evaluation of normalcy of swallow- Fig. 4.-Histologic sections of representative specimens of cricopharyngeal muscle. H and E x45. Bar scale = 0.5 mm. A, No hypertrophy. B, 1 + hypertrophy. C, 4+ hypertrophy (only part of muscle is shown). 930 TORRES ET AL. AJR:142, May 1984 Fig. 5.-Frontal (A) and lateral (B) views of anatomy. Inf. lique Lnsverse pharyngeus jus if Id,ii’z’eL A B ing . Over a long period, patients with abnormal deglutition cerebral vascular accidents, neuritis, thyrotoxicosis, trauma, may become conditioned to swallowing slowly and carefully; or muscle dysfunction. Our autopsy study indicates that they may have unconsciously altered their diet, taking in only anomalies of the cricopharyngeal muscle occur more often small amounts of food at a time. The cricopharyngeal inden- than is detected in the living patient, even when special tation can appear with other forms of esophageal dysfunction attention is directed to this area. in patients with symptoms of dysphagia. A variety of abnor- In a previous clinical study [1 ], we demonstrated the cr1- malities of the swallowing mechanisms may be present, such copharyngeal muscle defect in i 8% of 1 00 unselected pa- as pharyngeal constrictor paresis, dysfunction of the epiglot- tients on barium swallow examination [1 ]. Our autopsy study tis, and aspiration of material into the larynx and laryngeal provides strong evidence that the cricopharyngeal muscle vestibules . When cricopharyngeal dysfunction is present dysfunction in most cases is associated with actual hypertro- in individuals without dysphagia, it is most often a solitary phy of the cricopharyngeal muscle and is not simply due to phenomenon. muscle spasm or pharyngoesophageal incoordination. Many authors have observed variation in the size of the indentation on barium studies and between subsequent REFERENCES esophagrams in the same patient. Often the indentation is only identified for a brief moment during the swallowing phase. 1 Clements . JL, Cox GW, Torres WE, Weens HS. Cervical esoph- Ekberg and Nylander  theorize that the ability to reproduce ageal webs: a roentgen anatomic correlation. AJR 1974; the cricopharyngeal indentation is related to the size of the 121 :221 -231 bolus. Symptomatic patients may make repeated small swal- 2. 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