Ann. rheum. Dis. (1968), 27, 590

MYOPATHY OF HYPOTHYROIDISMBY

W. J. FESSEL*Assistant Clinical Professor of Medicine, University of California School of Medicine, San Francisco, and Department

of Medicine, The Permanente Medical Group, Kaiser Foundation Hospital, San Francisco, California, USA

Few present-day physicians, aside from endo-crinologists, know that hypothyroidism may causea profound myopathy. Past generations of clini-cians, however, were well aware of this. As longago as 1880, Ord described a patient as follows:

"Her strength failed, her activity, bodily and mental,declined; her movements became slower and slower;and the muscles of the neck in particular were from timeto time affected with remarkable weakness. Of lateshe could not keep her head erect; in spite of all herefforts to the contrary it would fall forward, and the chin,resting on the lower part of the neck, would hinderswallowing and even embarrass her breathing. She hadbecome unable to raise herself from a stooping position.Her gait was staggering like that of a drunken person;she often fell down by reason of the knees giving way . . "

Necropsy showed that all organs, including mus-cle, had a massive increase in connective tissue.Years later, Tatum (1913) made complete thyroid-ectomies on rabbits and observed that striatedmuscle had a serous infiltration, atrophy, and fattydegeneration. Some fibres contained vacuoles andothers were hyaline.

There are many reports, particularly in theliterature of the first half of the 20th century, thatdescribe myopathy in patients with clinically-established hypothyroidism. Muscular symptomsas the earliest feature of hypothyroidism werestressed by Wilson and Walton (1959). The presentpaper reports three patients with hypothyroidismin whom the muscular symptoms were the first tobe observed. These three patients represented5'6 per cent. of all patients with acquired myo-pathic disorders seen during the past 2 years.

Case ReportsCase 1, a 45-year-old woman, had had pain in the entirespine for the previous 7 years and, for the past year, inthe thighs, calves, arms, hands, and fingers. The painwas in the muscles rather than in the joints and wasespecially bad at night, awakening her three or four times.She had not noticed any specific weakness, although shehad felt generally exhausted for about 8 months. Forabout a year she had had symptoms suggesting carpaltunnel syndrome, the lateral three fingers of the righthand becoming numb as often as a dozen times per day.She had been quite depressed during the previous year.She had noted no hair fall or change in her voice.

Examination.-The thyroid was not enlarged and thepulse rate was within normal range. The joints were allnormal. The patient was able to hold her neck off thecouch for only 45 seconds (normal time> 60), and couldarise from the supine position only with the greatestdifficulty unless she used her hands. She was able toperform deep knee bends only very awkwardly. Therewas definite weakness of the deltoid and the iliopsoasmuscles. When lying supine, she was able to hold thestraight lower limb at 45° to the horizontal only for35 seconds on the right and 20 seconds on the left(normal time> 60).

Laboratory Findings.-Creatine phosphokinase (CPK)99 units (normal value< 12); protein-bound iodine (PBI)4 - 2 jug./I00 ml.; red blood cell uptake of triiodothyronine(T3) 31 per cent. (normal values 25-35); and 24-hr.radioactive iodine uptake 16 per cent. (normal> 20 percent.). The photomotogram ("one half of the relaxa-tion time" of the Achilles reflex) was 280 msec. (normalvalue< 380). The electromyogram was normal.

Muscle Biopsy.-There was an increase in numbers ofsarcolemmal nuclei, many of which were hyperplastic andmany of which were centrally located. An occasionalarteriole was infiltrated by lymphocytes.

Treatment.-It was believed that this patient hadidiopathic polymyositis and it was decided to observeher for a short while before starting any definitive therapy.After 6 weeks the thyroid function tests were repeated;now the radioactive iodine uptake was 5 per cent. in

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* Please address correspondence to 2200 O'Farrell Street, SanFrancisco, California. 94115

MYOPATHY OF HYPOTHYROIDISM

24 hours; and the PBI 2-5 ,ug./100 ml. Red blood celluptake of T3 was 29 per cent. The patient then men-tioned that previous tests had shown low thyroid func-tion; we learned from her former doctor that 2 years

ago her PBI had been 25 ,ug./100 ml., and that she hadtaken a small dose of thyroid for approximately 6 months.The patient was started on thyroxine, 0 2 mg. daily,

which was later increased to 0 3 mg. daily. She wasnow found unable to arise from the supine positionwithout the aid of her arms; 3 months later she felt nobetter, and muscle testing showed no improvement.Thyroxine was stopped and triiodothyronine started,gradually reaching a dose of 25 jug. four times daily.A month later, when there was still no improvement,prednisone (7 * 5 mg. daily) was added.

After 3 months on the combined therapy, musclestrength remained unchanged, and the prednisonedosage was increased to 40 mg. daily; 4 months afterstarting the high dose of prednisone she felt more ener-getic, and muscle pain was abating, and there wasmarked objective improvement in muscle strength.The prednisone was gradually withdrawn over the follow-ing 2 months and when she was last seen she was withoutsymptoms or signs.

Case 2, a 65-year-old man, complained that for the past2 years he had experienced severe muscle cramps thatrecently had become disabling. They affected the mus-cles of the four limbs, the trunk, and the face. Theywere so severe that they had enforced his temporaryretirement, and so prolonged that they caused contractionof the neighbouring joints. The cramps were precipi-tated by cold in particular, and by sudden changes ofposture. Some observers had thought that he hadmyotonia.The patient had been bald since the age of 21, and there

was a family history of baldness. The family historywas further significant in that one brother and a sisterexperienced severe muscle cramps.

Examination.-There was slight weakness of the shoul-der girdle and of both iliopsoas muscles. The pulse ratewas within the normal range. The thyroid gland wasslightly enlarged and contained several small nodules.

Laboratory Findings.-Raised CPK levels 198 and240 units; PBI 1 -6, 1 9, and 2-0 ,ug./100 ml.; serumthyroxine iodine< 1 0 ,tg. (normal value> 3 4); redblood cell uptake of T3 23, 25, and 27 per cent.; 24-hr.radioactive iodine uptake 21 per cent.

Muscle Biopsy (Fig. 1).-Definite variation in musclefibre size, a mild increase in the numbers of sarcolemmalnuclei, and a solitary focus of chronic interstitial in-filtrate. Electromyography was normal.

Treatment.-It was considered that this patient hadhypothyroid myopathy and he was started on thyroxine,gradually increasing to a dose of 0 -2 mg./day. Seen 2months later he was without symptoms and the musclestrength was considered to be normal.

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Case 3, a 28-year-old woman, complained of aching inthe calves, thighs, buttocks, and arms. The pain in thelower limbs was constant but occurred in the arms onlywith exertion. This myalgia had been present for 1 yearand was becoming progressively worse. There was anassociated feeling of exhaustion and lethargy that wasworse just after her menstrual periods.The family history was significant in that her aunt

had suffered from similar muscle pains for several years.

Examination.-There was neither enlargement nortenderness of the thyroid gland and the pulse rate waswithin the range of normal. The muscles showed mildweakness of external rotation of both shoulders, and ofextension and adduction of both hips, difficulty in arisingfrom the supine position with the arms crossed over thechest, and considerable tenderness of the thighs andbuttocks.

Findings.-These were initially unhelpful apart fromthe presence of a slight rise in serum aldolase, to 2 -7m. units/mi. serum (normal value<2 5). Electromyogram

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ANNALS OF THE RHEUMATIC DISEASES

normal. PBI 5 -2 and 8 -0 ,ug./100 ml.; red blood celluptake of T3 20 per cent.; 24-hr. radioactive iodine up-take 20 per cent. Photomotogram 280 msec.

Muscle Biopsy (Fig. 2). A rare muscle cell had a mildincrease of basophilic staining and several nucleilocated centrally.

.. *.*Fig. 2.-Muscle biopsy (Patient 3). A single fibre shows increasedbasophilia, and four hyperplastic centrally-located nuclei (the numberof nuclei is more convincingly seen in the original preparation).

Haematoxylin and eosin. x 1,000.

muscles, pain in the chest, soreness in the jaws, alternat-ing diarrhoea and constipation, palpitations of the heart,trembling of the extremities, dizziness, a feeling of lackof oxygen, and poor circulation. Examination nowshowed that the thyroid gland was mildly but diffuselyenlarged. All muscle groups were now considered tobe normally strong. The radioactive iodine uptake was15 per cent. Further thyroid function studies showedPBI 6-1 ,tg./100 ml.; red blood cell uptake of T3 23 percent., and photomotogram in the hypothyroid range(420 msec.). The radioactive iodine uptake, repeated1 month later, was only II per cent.

Treatment.-Hypothyroid myopathy was now diag-nosed and the patient started on thyroxine, but aftertaking 0 * 2 mg. of the hormone daily for 3 weeks she notedno improvement at all; her muscle aches and pains andthe complaints of weakness were as severe as before andexamination showed weakness of both iliopsoas muscles.The thyroxine was then increased to 0 3 mg./day, and3 months after starting the drug she began to feel muchless tired than before, but discomfort in the joints of thefingers and knees appeared; 6 months after starting thethyroid hormone, however, most of the symptoms haddisappeared. She estimated that her muscles wereabout 75 per cent. better, but objective testing showedresidual weakness of both iliopsoas muscles. CPK atthis time was raised to 35 units. She has not been seensince.

Special StudiesANTIBODIES TO MUSCLE were looked for, as re-

ported in detail elsewhere (Fessel and Raas, inpress), using direct and indirect fluorescent anti-body methods, complement-fixation with muscleantigen, and double diffusion in agar with a salineextract of muscle.

THYROID ANTIBODIES were looked for by the tannedred-cell method.

Progress. It was considered that this patient probablyhad low-grade chronic polymyositis. During the nextfew months, however, she saw several doctors includingtwo general physicians, an endocrinologist, and a

neurologist, whose consensus was that she probably was

psychoneurotic and had no significant endocrine or

muscle disease. Studies during this time showed normalvalues for serum aldolase, serum hydroxybutyric dehy-drogenase, CPK, and serum glutamic oxalacetic tran-saminase (SGOT). The PBI was 5 4 ,ug./100 ml., andthe photomotogram 340 msec.

Second Consultation.-When seen 9 months after thefirst consultation, the patient complained of generalweakness, spells of drowsiness, aching and twitching of

GLYCOGEN AND PHOSPHORYLASE LEVELS weremeasured in the muscles of all patients.

It was not possible to demonstrate the presenceof antibodies to muscle in the patients' serum ormuscles by the above methods. Thyroid antibodieswere present in only one serum (Patient 2), in thelow titre of 1:140. The phosphorylase levels werelow in two of the muscles studied. In one musclewith low phosphorylase levels, glycogen synthetasewas present in normal amounts. Glycogen levelswere normal in two of the muscles; there wasinsufficient tissue for this estimation in one musclethat contained a low phosphorylase level. Theseobservations are being pursued.

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DiscussionThe three patients were each referred for the

diagnosis of their muscle complaints; in none wasthere clinically obvious hypothyroidism. This ex-perience re-emphasizes the statement by Wilson andWalton (1959) that muscular symptoms may be thefirst manifestations of hypothyroidism. Thosephysicians who have experience in treating hyper-thyroidism with radioactive iodine know thatcomplaints of myalgia and cramps may portendhypothyroidism. But the observation came as asurprise that among 53 patients seen in a communityhospital for various acquired disorders (Table),three (5 * 6 per cent.) had unexpected hypothyroidism.It is worth stressing that the thyroid function testswere normal when two of the three patients werefirst seen. In one subject, the thyroid functiontests fell to within the hypothyroid range only after10 months. Bergouignan, Vital, and Bataille (1967)reported the case of a patient with muscle pains for4 years, during which he made diverses peregrina-tions medicales, before the diagnosis of hypothy-roidism was reached. Presumably, in some patients,the tissue response is a more sensitive indicator ofthyroid deficiency than the laboratory tests. Itwould seem worthwhile, therefore, to make repeatedtests of thyroid function in patients with so-calledidiopathic polymyositis while that they are underobservation. This experience is reminiscent of thatof Jellinek and Kelly (1960) with cases of cerebellardegeneration in association with myxoedema; theypointed out that the features of myxoedema wereby no means clinically obvious in some, and thatthree of their six patients had been seen by generalphysicians who failed to recognize the myxoedema.

In my Patients 1 and 3 the muscular symptomswere not totally reversed after several months ofreplacement therapy with thyroid hormone. Thismight be thought to demonstrate that these werenot true cases of hypothyroid myopathy. Yet thesame irreversibility by treatment with thyroidhormone was seen by Astrom, Kugelberg, andMuller (1961) in two of their eight patients, and byRimbaud and Passouant (1947) in one of theirs.The two patients reported by Bergouignan and others(1967) each had a symptomatic recovery after thy-roid therapy, but a second biopsy showed persistentabnormalities-sarcoplasmic masses and ringed-fibres were prominent both before and after treat-ment. Wilson and Walton (1959) presented apatient whose strength recovered with thyroxinebut who relapsed when thyroid extract was substit-uted. They suggested the possibility of a defect inthe breakdown of thyroid to thyroxine. Rimbaud

and Passouant (1947) wondered whether the musclefibres under certain circumstances might becomeunresponsive to thyroid hormone. On the otherhand, this may have to do with the length of timenecessary for complete recovery; it took 3 monthsfor strength to return in one patient of Nickel,Frame, Bebin, Tourtellotte, Parker, and Hughes(1961), 5 and 6 months in two of the cases reportedby Norris (1966), and 6 months in my Patient 3.Lambert and Sayre (1955) studied the effect ofthyroidectomy on rabbits and observed that whilstthe electromyographic abnormalities quite rapidlydisappeared after replacement therapy with thy-roxine, the resolution of the structural changes inthe muscles took a great deal longer. Analogoussituations are those in which the colonic abnorma-lity (Kelley and Stewart, 1964), cerebellar disorder(Jellinek and Kelly, 1960), and renal lesion (DiScala,Salomon, Grishman, and Churg, 1967) associatedwith myxoedema did not recover after adequatereplacement with thyroid hormones; the thyrotoxicmyopathy progressed despite proper treatment ofhyperthyroidism (Schwarz and Rose, 1963), and themyopathy seen in hyperparathyroidism had notbeen completely reversed one year after parathy-roidectomy (Bischoff and Esslen, 1965).

The various sorts of muscular disorder that maybe seen in hypothyroidism include:

(1) Hypertrophy of muscle with or withoutmyotonia, both in acquired myxoedema (the so-called Hoffman syndrome) and, also, in congenitalhypothyroidism (the so-called Debre-Semelaignesyndrome);

(2) Atrophy of muscles described by Alajouanineand Nick (1945), and seen by Rimbaud and Passou-ant (1947) in a case that progressed despite the useof thyroid replacement.

Severe pain, a prominent feature in one of mypatients, has not usually been reported as a majorproblem of hypothyroid myopathy. Pain was notemphasized by Rimbaud and Passouant (1947) intheir review, or by Nickel and coworkers (1961)who studied 25 patients with known myxoedema.Although Nickel and others (1961) found thatmuscle cramps were present in fourteen of theirpatients, they did not see persistent pain. Ala-jouanine and Nick (1945) and Bergouignan andothers (1967), however, emphasized the presence ofpain in their four patients.Each of my three patients had features that would

entitle one to diagnose polymyositis according tothe usual criteria: namely, the presence of musclepain or weakness, increase in those serum enzymes

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ANNALS OF THE RHEUMATIC DISEASES

considered to reflect muscle damage, and abnorma-lities in the muscle biopsy. Although only oneshowed a slight cellular infiltrate in the biopsy,other authors have seen considerable infiltrates inthe muscles of hypothyroid patients. Garcin andBertrand (1935) reported a patient who not onlyhad degenerative and regenerative changes in themuscles, but also massive infiltration of histiocytes.Rimbaud and Passouant (1947) indicated that in oneof their cases there was a marked cellular infiltratewith lymphocytes. Astrom and others (1961)reported on eight patients, of whom one showedsevere acute degeneration of muscle fibres togetherwith invasion by macrophages and lymphocytes.This sort of histopathological appearance in con-junction with the clinical picture of muscle pain andweakness raises the question of the diagnosticsignificance of the term polymyositis; although it isnot the purpose of this paper to discuss this in anydetail, it is worth pointing out how unspecific thisterm is and how important is the pursuit of possibleunderlying aetiologies in patients diagnosed ashaving polymyositis. Not only may polymyositisbe part of an underlying connective tissue disease or aremote effect of a neoplasm, but it may also reflectan underlying endocrine disorder; hypothyroidism,hyperthyroidism, Cushing's syndrome, and hyper-parathyroidism must always be considered.

The prevalence of hypothyroidism in patients withmyopathy is difficult to estimate, but as shown in theTable, among my 53 patients with acquired musclediseases seen in a community practice, there werethree (5 6 per cent.) with hypothyroidism. Eachcase of hypothyroid myopathy was at one timethought to be polymyositis: if these two groups,i.e. those with polymyositis and those with hypo-thyroidism, are added together, it is seen that three(9 1 per cent.) of 33 patients with polymyositishad hypothyroidism. Whether myopathy trulyresults from hypothyroidism in an individual patientor is coincidental is difficult to state with certainty;

TABLEDIAGNOSES IN 53 PATIENTS WITH ACQUIRED MUSCLE

DISEASES SEEN DURING 2 YEARS IN ACOMMUNITY HOSPITAL

Diagnosis Number ofPatients

Idiopathic 21Polymyositis 30Secondary to cancer } 30

or collagen disease 9

Hypothyroid myopathy 3

Others (including five endocrinopathies) 20

this is so even if there is an improvement aftertreatment with thyroid because idiopathic poly-myositis may undergo spontaneous remission. Yetit seems extremely improbable that among 53patients with miscellaneous disorders there wouldbe three with hypothyroidism; this high prevalenceof hypothyroidism in a group of patients withmyopathies makes it seem likely that there is acausal relationship between the two conditions.

Contrariwise, the prevalence of myopathy inhypothyroidism is easier to estimate. Nickel andothers (1961) performed biopsies in twelve patientsand found myopathic changes in all of them.Saito, Hibi, Kawazura, and Fukuyama (1963) andEkbom, Hed, Herdenstam, and Nygren (1966) sawraised serum levels of creatine phosphokinase in allpatients with hypothyroidism. In their 75 patients,Collins, Zimmer, Johnson, and Kough (1964)recorded neuromuscular complaints in 54 (72 percent.), complaints of weakness in 33 (44 per cent.),and muscle cramps or stiffness in fifteen (20 percent.). Thus, although the precise prevalencedepends upon the mode of detection, a muscledisorder is extremely common in hypothyroidism.

Possible mechanisms for the myopathy seen inhypothyroidism include an autoimmune reactionaffecting the muscle, infiltration by "myxoedema",or a disorder of the muscle membrane. An auto-immune reaction might independently cause chronicthyroiditis and hypothyroidism, and polymoysitis.Two facts are against this idea: only one patient'sserum contained thyroid antibodies, which are al-most always seen in chronic thyroiditis; and noantibodies against muscle were demonstrated in anypatient (Fessel and Raas, in press). It seems mostlikely that thyroid deficiency affects the musclecells directly. A serous infiltration of muscle wasseen in experimental cretinism by Tatum (1913),although this finding in human myxoedema ismentioned in only occasional case reports and wasnot seen in the biopsies of the three patients reportedhere. Thyroxine is well known to have importanteffects on the cell membranes. For example,Gustafsson, Tata, Lindberg, and Ernster (1965)observed that thyroidectomy led to an increase inthe total amount of mitochondria in muscle and thatthe ratio of cristae to matrix within the mitochondriawas increased. Norris and Panner (1966) sawimportant changes in the mitochondria by electronmicroscopy in their case of hypothyroid myopathy.The serum enzymes may rise to high levels in hypo-thyroidism, presumably because thyroid deficiencypermits leakage across muscle membranes and,possibly, actual muscle necrosis (Saito and others,

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MYOPATHY OF HYPOTHYROIDISM

1963; Griffiths, 1965; Ekbom and others, 1966).The evidence suggests that thyroid deficiency has adirect action on muscle, most likely on the variouscell membranes.

SummaryThree patients with hypothyroidism whose pre-

senting symptoms were in the muscles were seenamong 53 patients with acquired myopathy observedduring a 2-year period. Pain was a prominentfeature. Two of the patients required prolongedreplacement of thyroid hormone for reversal of the

muscle reaction, and in one prednisone was alsonecessary. Evidence suggests that the relationshipbetween hypothyroidism and a muscle disorder maybe causal rather than coincidental. The mechanismis unexplained.

This work was supported in part by a grant from theKaiser Foundation.

Dr. Hibbard Williams estimated the muscle phos-phorylase and glycogen levels; Dr. Hugh H. Fudenbergmade the thyroid antibody titrations; Dr. Alvin Glassperformed and interpreted the electromyograms.Patients 2 and 3 were referred by Drs. Alvin Glass andW. H. Tu.

REFERENCESAlajouanine, T., and Nick, J. (1945). Paris mid., 35, No. 32 (10 Nov), p. 346 (De l'existence d'une

myopathie d'origine hypothyroldienne).Astrom, K.-E., Kugelberg, E., and Muller, R. (1961). Arch. Neurol. (Chicago), 5, 472 (Hypothyroid

myopathy).Bergouignan, M., Vital, C., and Bataille, J.-M. (1967). Presse mid., 75, 1551 (Les myopathies

hypothyroldiennes: aspects cliniques et histopathologiques).Bischoff, A., and Esslen, E. (1965). Neurology (Minneap.), 15, 64 (Myopathy with primary hyper-

parathyroidism).Collins, J. A., Jr., Zimmer, F. E., Johnson, W. J., and Kough, R. H. (1964). Postgrad. Med., 36,

371 (The many faces of hypothyroidism).DiScala, V. A., Salomon, M., Grishman, E., and Churg, J. (1967). Arch. Path. (Chicago), 84,

474 (Renal structure in myxedema).Ekbom, K., Hed, R., Herdenstam, C.-G. P., and Nygren, A. (1966). Acta med scand., 179, 433 (The

serum creatine phosphokinase activity and the Achilles reflex in hyperthyroidism and hypo-thyroidism).

Fessel, W. J., and Raas, M. C. (1968). Neurology (Minneap.) In press (Autoimmunity in the patho-genesis of muscle disease).

Garcin, R., and Bertrand, I. (1935). Rev. Neurol., 64,82(Syndromethomsenienetsyndromemyxo-edemateux cliniquement associes Debut simultan6. Evolution parall'ele (3e Memoire).Etude anatomique et conclusions).

Griffiths, P. D. (1965). J. clin. Path., 18, 660 (Serum enzymes in diseases of the thyroid gland).Gustafsson, R., Tata, J. R., Lindberg, O., and Ernster, L. (1965). J. Cell. Biol., 26, 555 (The relation-

ship between the structure and activity of rat skeletal muscle mitochondria after thyroidec-tomy and thyroid hormone treatment).

Jellinek, E. H., and Kelly, R. E. (1960). Lancet, 2, 225 (Cerebellar syndrome in myxoedema).Kelley, M. L., Jr., and Stewart, J. M. (1964). Amer. J. dig. Dis., n.s. 9, 79 (Myxedema and intestinal

malabsorption (nontropical sprue?) with severe hypomotility of the gastrointestinal tract:report of a case).

Lambert, E. H., and Sayre, G. P. (1955). Amer. J. Physiol., 183, 636 (Myopathy in rabbits followingthyroidectomy tabstract]).

Nickel, S. N., Frame, B., Bebin, J., Tourtellotte, W. W., Parker, J. A., and Hughes, B. R. (1961).Neurology (Minneap.), 11, 125 (Myxedema neuropathy and myopathy: a clinical and pathologicstudy).

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ANNALS OF THE RHEUMATIC DISEASES

Norris, F. H., Jr., (1966). Ann. intern. Med., 64, 81 (Neuromuscular transmission in thyroid disease).

Norris, F. H., Jr., and Panner, B. J. (1966). Arch. Neurol. (Chicago), 14, 574 (Hypothyroid myo-

pathy: clinical, electromyographical, and ultrastructural observations).

Ord, W. M. (1880). Trans. clin. Soc. Lond., 13, 15 (Cases of myxoedema).

Rimbaud, L., and Passouant, P. (1947). Rev. neurol. (Paris), 79, 81 (Les dystrophies musculairesdes hypothyrcl liens).

Saito, M., Hibi, l., Kawazura, M., and Fukuyama, Y. (1963). Lancet, 2, 252 (Creatinephosphokinaselevels in hypothyroidism).

Schwarz, G. A., and Rose, E. (1963). Arch. intern. Med. (Chicago), 112, 555 (Neuromyopathies andthyroid dysfunction: some unusual associations).

Tatum, A. L. (1913). J. exp. Med., 17, 636 (Morphological studies in experimental cretinism).Wilson, J., and Walton, J. N. (1959). J. Neurol. Neurosurg. Psychiat., 22, 320 (Some muscular mani-

festations of hypothyroidism).

Myopathie hypothyroidienne

RESUMEParmi 53 malades atteints de myopathie acquise et

observes pendant 2 ans on a trouve trois cas d'hypothy-roidisme se manifestant par des symt6mes musculaires,et principalement par la douleur. Une therapie pro-longee de remplacement par l'hormone thyroidienne pourrenverser la reaction musculaire etait neeessaire chezdeux d'entre eux et le traitement par la prednisone chezun. Les donnees existantes suggerent que le rapportentre l'hypothyroidisme et l'atteinte musculaire n'est pasfortuit, mais le meeanisme de ce rapport n'est pas connu.

Miopatia hipotiroidea

SUMARIOEntre 53 enfermos con miopatia adquirida, observados

durante dos afios, se encontraron tres casos de hipotiroi-dismo con sintomas reveladores en los musculos, particu-larmente el dolor. Una terapia prolongada de substitu-ci6n por la hormona tiroidea para invertir la reaccionmuscular fue necesaria en dos de ellos y el tratamientopor la prednisona en uno. Los datos sugieren que larelaci6n entre el hipotiroidismo y la sintomatologiamuscular no es casual, pero el mecanismo de esta relaci6nno es conocido.

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