NOTE ON THE PATHOLOGY OF MORTON'S METATARSALGIA MAJOR LESTER S. KING, M.C., A.U.S. From the Laboratory Service of the William Beaumont General Hospital, El Paso, Texas Until relatively recently, the immediate cause of Morton's metatarsalgia ; first described by Thomas G. Morton in 1876 under the title "A peculiar and painful affection of the fourth metatarso-phalangeal joint," was unknown. The earlier authors dealing with the subject 1 ' 2 ' 3-4 recommended specially fitting shoes and other palliative devices as conservative treatment; or amputation of the toe or resection of the metatarso-phalangeal joint if the pain was intractable. Recent authors, 6 ' 6 ' ' 8 however, have shown conclusively that some affection of the lateral branch of the medial plantar nerve is at fault. Neurectomy offers complete permanent cure, and may now be definitively considered as the proper treatment. Nevertheless there is no agreement concerning the pathologic changes in the resected nerve. Betts 6 speaks of a neuritis, with increase of fibrous tissue. Swart 7 in his one case mentions merely "fibrous tissue with regressive changes." In McElvenny's 12 tumors, only five were examined microscopically. 8 He considers the lesion to be a neurofibroma or angioneurofibroma. He mentions further that there was no agreement among a number of pathologists who studied the sections. Baker and Kuhn 8 in 14 operations on 11 patients, describe the pathology in a single paragraph. They make three approximate subdivisions, but state, "All specimens showed collagenous connective tissue proliferation, degeneration of the nerve elements and focal neuromatous proliferation. In general, the microscopic picture is not unlike that of amputation neuroma." In view of the wide differences of opinion and of the complete absence of photomicrographic evidence in the literature, it seems worth while to describe the pathology in five cases observed in the past two years. Our observations in the main fully confirm the brief description of Baker and Kuhn. Of our five cases three were in women, and two in men. The ages ranged from 25 to 62. The gross specimens were all essentially similar, consisting of portions of tissue from ten to twenty millimeters in length, and varying frcm 3 to 8 mm. in other dimensions. They were all cf firm glistening fibrous character cutting with definitely more resistence than is found in normal nerves. Grossly recognizable nerve bundles could be seen in seme specimens, and not in others. The microscopic pieparations, although exhibiting variation frcm case to case, form a generally characteristic picture. The characteristic feature, present in all cases, is the occurrence of nerve bundles cf varying size, separated from the surrounding dense connective tissue by a very thick collagenous capsule, representing a greatly thickened perineurium. This sheath is generally mere compact than the surrounding fibrous tissue and is composed cf dense collagen bundles sometimes hyalinized and with few nuclei, tut mere often containing numerous oval or flattened nuclei. Small relatively thick-walled arterioles are frequently found within the sheaths. This perineurium generally has a lamellated appearance toward the periphery, formed by concentric strands cf looser connective tissue which merge imperceptibly with the surrounding stroma. 124
PATHOLOGY O F M O R T O N ' S M E T A T A R S A L G I A 125 The tissue within the perineurium is sometimes scarcely recognizable as nervous in origin. In extreme cases there is a very loose fibrous matrix which may or may not exhibit a myxomatous character. Scattered longitudinallyrunning strands of slightly wavy appearance run through this matrix, representing persisting nerve fibrils and connective tissue bundles. More often the tissue within the perineurium is relatively compact. It consists of clearly recognizable nerve fibrils mingled with collagenous strands. In some bundles F I G. 1. T H R E E L A R G E N E R V E B U N D L E S, S H O W I N G S E V E R E L Y T H I C K E N E D P E R I N E U R I U M, D I M I N U T I O N O F C O N T A I N E D N E R V E F I B E R S, AND I N C R E A S E OF C O N T A I N E D CONNECTIVE T I S S U E, P R I N C I P A L L Y OF L O O S E CHARACTER this collagenous component takes the form cf hyalinized masses. Frequently small blood vessel lumens are surrounded by dense acellular hyalin tissue. Considering the size of the nerve bundles and the striking thickness of the perineurium, the total number of contained nerve fibers appears sharply diminished, in comparison with bundles of similar size seen in other types of neuroma. The amount of contained connective tissue is greatly increased. Attempts Avere made to exhibit axis cylinders en paraffin sections by the Bodian stain. The impregnation was successful only in the larger nerve trunks
126 LESTER S. KING F I G. 2. S I N G L E N E R V E B U N D L E S, W I T H M A R K E D L Y T H I C K E N E D P E R I N E U R I U M W i t h i n t h e bundle there is an increased number of blood vessels, with thick hyaline walls, and small masses of hyalin connective tissue. F I G. 3. N E R V E B U N D L E C U T L O N G I T U D I N A L L Y There is severe loss of nerve fibers, and replacement by loose myxomatous connective tissue.
PATHOLOGY OF MORTON'S METATARSALGIA 127 least affected by fibrosis. In these larger trunks the preserved axis cylinders are frequently separated by an excess of fibrous tissue which can be demonstrated by counterstaining with van Gieson stain. Where the perineurium is thickest, and large amounts of collagen are present within the nerve bundles, the silver stain fails to exhibit nerve fibrils, although some may be present among the slightly impregnated connective tissue fibrils. But silver stains on these tissues form a marked contrast with similar impregnations on simple neuromas or normal nerve bundles, in which abundant axis cylinders, both thick and thin, are readily demonstrable. Attempts to demonstrate myelin sheaths on paraffin sections by specific stains were not successful. Nevertheless in the largest nerve bundles, with the best preserved axis cylinders, scattered fibers could be seen with a delicately reticulated sheath that is characteristic of myelin in hematoxylin-eosin preparations. Such sheaths, however, were infrequently seen. In none of our cases was there any trace of inflammatory reaction. Within the nerve bundles all the nuclei are of fibroblastic or of the neurilemmal type. In the surrounding stroma the connective tissue was relatively dense, and poor in cells. Lymphocytes and polymorphonuclear leucocytes were entirely absent. The separate nerve bundles may be characterized by a markedly thickened perineurium; sharp reduction of the number of contained nerve fibers and corresponding increase in connective tissue, either loose or dense, with similar increase in number of blood vessels; and a complete absence of inflammatory change. These changes are sufficient to demarcate this group of neuromas from the usual amputation or traumatic neuroma. In the latter, occasional perineuria may show considerable thickening, while other bundles may show slight edema and myxoid change; but the overall picture does not lead to any confusion. As a further difference our five cases of Morton's metatarsalgia showed only relatively few nerve bundles, compared to the considerable number generally seen in other neuromas. In addition no small bundles with or without perineurium, and no diffuse proliferation of nerve fibers in nonfasciculated form, were present in our cases. The five cases described here seem to form a separate and special group, readily distinguishable from other types of neuroma. We propose the name "sclerosing neuroma" to describe this condition. The etiology is obscure. These tumors cannot be considered as a true neoplasm, as are neurofibromas or neurinomas. Rather should they be considered as a type of reactive hyperplasia with sclerosing and degenerating changes. We choose to consider most neuromas as analogous, perhaps, to keloids. Some long continued traumatic factor is probably partly responsible for the characteristic appearance seen in cases of Morton's metatarsalgia. SUMMARY The nerve tumors in five cases of Morton's metatarsalgia were investigated histologically. They showed, within an increased mass of connective tissue,
128 LESTER S. KING relatively few nerve bundles, but most of them with very markedly thickened perineurium. There was sharp reduction in the number of nerve fibers, with corresponding increase in loose or dense connective tissue within the bundles, and increase in number of blood vessels. There was no inflammatory change. The term "sclerosing neuroma" is proposed to distinguish this group from the usual amputation or traumatic neuroma. REFERENCES 1. MORTON, THOMAS G.: A peculiar and painful affection of the metatarso-phalangeal articulation. Am. J. M. Sc, 71: 37, 1876. 2. MORTON, THOMAS S. K.: Metatarsalgia (Morton's Painful Affection of the Foot). Am. J. Surg. & Gynec, 3: 204, 1892. 3. TUBBY, A. H.: Metatarsal neuralgia or Morton's Disease, with four cases. Lancet, 2: 1217, 1896. 4. TYRRELL, J. B.: A consideration of Morton's neuralgia or metatarsalgia. Cleveland M. J., 13: 639,1914. 5. BBTTS, L. O.: Morton's Metatarsalgia: Neuritis of fourth digital nerve. M. J. Australia, 1:514, 1940. 6. MCELVENNY, R. T.: The etiology and surgical treatment of intractable pain about the fourth metatarso-phalangeal joint (Morton's Toe). J. Bone & Joint Surg., 25: 675, 1943. 7. SWART, H. A.: A new cause of metatarsalgia. West Virginia M. J., 40: 12, 1944. 8. BAKER, LENOX D. AND KUHN, HAROLD H.: Morton's Metatarsalgia. South. M. J., 37: 123, 1944.