J. Neurol. Neurosurg. Psychiat., 1970, 33, 431-437

Myasthenia gravis in the dogD. C. FRASER, A. C. PALMER, AND J. E. B. SENIOR

From the Department of Veterinary Clinical Studies, School of Veterinary Medicine, Cambridge

J. D. PARKES AND M. F. T. YEALLAND

From the Department of Neurology, Addenbrooke's Hospital, Cambridge

SUMMARY An account is given of four cases of myasthenia gravis in the dog. All animals showedfatigue, and considerably reduced tolerance to exercise. Recovery followed rest or treatment withneostigmine. Three animals, two of which are still alive, had dilatation of the oesophagus. Thefourth eventually died from an aortic body tumour. The occurrence of myasthenia in the dog may beof value in elucidating the cause of the disease in man.

Recent case reports suggest that myasthenia occursin the dog as well as man (Ormrod, 1961; Hall andWalker, 1962; Zacks, Shields and Steinberg, 1966).This paper describes four further cases in the dogwhich appear to fulfil the necessary criteria forsucha diagnosis. The occurrence of myasthenia in the dogas well as in man is important in relation to possiblecommon causative factors.

CASE 1

This 6-year-old alsatian bitch collapsed after a half milewalk on 20 October 1965 and had to be carried home.Thereafter it developed a progressively reduced exercisetolerance. Heart tonic tablets (Astra-Hewlett) containingglyceryl trinitrate, digitalis, strophanthin, and atropinewere given, although no abnormality of heart sound washeard; vitamin E was also prescribed. The owner kept a60-acre orchard and the dog was reported to be in thehabit of eating unripe pears. The animal was sent to theSchool of Veterinary Medicine in Cambridge, with thepossibility that the illness arose from the ingestion oftoxic orchard spray.The dog was admitted on 10 November 1965 (day 1)

and was found to be in good general condition; its heartwas normal. Stance was normal, but exercise toleranceconsiderably reduced. The animal would walk about20 yards (18-3 m), and then drag back on its lead, refusingto walk. It took shorter and shorter strides with its fore-legs, falling forwards on to its nose if forced to go on.Seconds before collapsing there appeared to be normalstrength in the hind-legs and the gluteal muscles felt hard.Recovery followed a few minutes' rest, the dog pickingitselfup. There was no visible muscle wasting in the limbs,and resistance to passive movement felt normal. Tricepsand patellar reflexes were equal and brisk. There was nosign of sensory or motor deficit ascribable to a lesion of

the spinal cord. Ptosis was not present, and no abnorm-ality ofthe cranial nerves was seen.

Haematological examination, blood glucose, serumcalcium, sodium, and potassium were all within normallimits. An electrocardiograph was normal.The animal's exercise tolerance remained limited to

20 yards (18 m) for the subsequent five days. On day 6,0 65 mg atropine sulphate and 2-5 mg neostigminemethylsulphate were injected intramuscularly. Twentyminutes later, the animal walked and trotted 900 yards(823 m).On day 16, at a time of clinical improvement, electro-

myographic studies were carried out under generalanaesthesia before and after edrophonium chloride(Tensilon: Roche). No convincing evidence of abnormalskeletal muscle 'fatigue' was seen. A muscle biopsy fromthe rectus abdominis was taken. The histological appear-ances were normal in sections stained with haematoxylinand eosin.The alsatian was discharged on day 23 without it

having been necessary to give further neostigmine. Theowner kept a diary of the animal's progress, and found itnecessary to give atotal of four 15mg tablets neostigminebromide between days 29 and 33. Increased salivationfor several days accompanied neostigmine medication.On day 68 the owner reported that there had been noweakness or distress for five weeks and that exercise hadincluded two mile runs. A year later the animal had shownno relapse.

Nineteen months after the original illness, the animalwent off its food, showing signs of respiratory distress.Anticholinesterase injections had no effect on the con-dition. There was pyrexia, abdominal breathing, andincreased pulse rate, and pleural effusions were seen onradiographs of the chest. Transient improvement accom-panied antibiotic treatment but a relapse occurred oneweek later and the animal was readmitted. Under generalanaesthesia, 3 1. of fluid were removed from the chest,

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with immediate relief of respiratory distress. However,two days later the owner decided to have the animalput down.

POST-MORTEM EXAMINATION The animal appeared wellnourished with no enlargement of the superficial lymphglands or obvious neoplasm of mammary glands ortonsils. The thyroid was macroscopically normal; noabnormalities were seen in the abdominal cavity. Kidney,pancreas, and liver tissue samples were taken. A bloodstained watery fluid was present in the pleural cavity andmasses of hard grape-like substance were felt in themediastinum, both anterior and posterior to the heart. Asmall similar lesion was present in a diaphragmatic lobeof the lung.On histological examination abnormalities were con-

fined to the tumour mass in the mediastinum, and tothat in the lung. Both consisted of an aggregation of cells,separated by connective tissue trabeculae. Cell nucleiwere of two types; small round nuclei with a moderateamount of chromatin, and larger vesicular oval nuclei(Fig. 1). The latter cells showed considerable palisadingaround the trabeculae which contained blood vesselswhereas the dark nuclei were more widely scattered. Insome areas both types were mixed at random; mitoseswere not seen. The position of this tumour and its mor-phology indicated a heart base or carotid body tumour,described by Jubb and Kennedy (1963) as a cardio-aortictumour. Further tissue samples and skeletal musclesections showed no histological abnormality.

CASE 2

This male golden retriever was purchased as an 8-week-old puppy. It was vaccinated against distemper andappeared quite normal until 8 months of age. It then hadperiodic bouts of diarrhoea and vomiting sometimeswith a slight temperature rise. When the dog was firstseen at the age of 10 months, it showed symptoms ofocular congestion and was vomiting frothy mucus.Temperature was normal. Two days later it had difficultyin rising as though it had hind-leg cramp, and showedweakness after minimal exercise. The dog was treatedwith the same proprietary heart tablets as the previouscase. However, these were stopped four days later becauseof the onset of haemorrhagic gastroenteritis, and anti-biotics were given. During the next three weeks the animalcollapsed for a brief period when excited or after walking20 to 30 yards (18 to 24 m).On first examination at the School of Veterinary

Medicine, the animal was in good condition, but haddifficulty in rising to its feet. The favoured posture wasprone with limbs widely abducted (Fig. 2). When helpedto its feet it could walk with unduly short steps, butcollapsed after about 20 yards. Strides became shorterand shorter, the animal then refusing to move its forelegs.After a rest, the dog would get up and resume walking fora short distance only to collapse again. No musclewasting was seen, muscle tone felt normal, and deeptendon reflexes were unremarkable. There was no ptosisor deviation of the eyes, but a passive blowing in and out

FIG. 1. Case 1. Photomicrograph ofmediastinal tumour, showing the differentiation into two primary cell types. HandE x1,000 (approx.).

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FIG. 2. Case 2. From a cine film, showing posture of dogwhenfatigued.

of the cheeks accompanied respiration. Hip radiographswere normal. After a barium meal, the oesophagus wasseen to be widely dilated, being 4 cm in diameter. Thebarium bolus took over 10 minutes to reach the stomach(Fig. 3).Blood samples on the second day after admission

showed a normal haematological picture. On severalsubsequent samplings, blood glucose and urea, serumsodium, potassium, calcium, magnesium, and phosphoruswere found to be normal.The day after admission, the dog was led from its kennel

but soon collapsed. Neostigmine, 1 mg, with 1P3 mgatropine were injected intramuscularly. Four minuteslater, the dog rose to its feet and after a further threeminutes walked round wagging its tail. Improvementcontinued; it looked alert, the gait becoming springy.Three hours later it was still standing normally. The next

FIG. 3. Case 2. Dilatedoesophagus outlinedby barium meal.

day the dog had reverted to its collapsed condition, butrecovery again followed neostigmine injection. Duringthe subsequent 10 days, intermittent muscle 'fatigue' wasseen, which was again relieved by either oral or intra-muscular neostigmine. Even during drug-induced im-provement, however, a barium swallow still showed theoesophagus to be dilated. On the eighth day after ad-mission 15 mg neostigmine orally led to improvement, sothat five hours later it walked half a mile. The oral treat-ment was repeated two days later with beneficial resultslasting 24 hours. Satisfactory control of muscle fatiguewas gained from the twelfth day after admission withoral neostigmine. However in the subsequent 10 days, theanimal had repeated bouts of diarrhoea and vomiting,and excessive salivation only poorly controlled by atro-pine. The treatment was complicated by a purulent nasaldischarge, probably caused by infection from vomituslodged in the nasal cavities. The infection was controlledby tetracycline.

Electromyographic studies were performed undergeneral anaesthesia. After acepromazine and atropinepremedication, anaesthesia was induced with thiopentonesodium (Pentothal: Abbot) and after intubation, wasmaintained on nitrous oxide, oxygen, and methoxyflurane(Penthrane: Abbot). Induced action potentials wererecorded from the right tibialis anterior muscle with aconcentric needle electrode, the peroneal nerve in theregion of the fibular head being stimulated via surfaceelectrodes at a frequency of 17 c/s, with supramaximalpulses. This repetition rate was kept constant for oneminute, and the cycle repeated after injection of edro-phonium chloride 10 mg (Tensilon: Roche). Results areshown in Fig. 4. Induced action potentials in the tibialisanterior declined five-fold in voltage during the initial30 seconds of nerve stimulation. After Tensilon, thisdecline was twofold. Motor conduction velocity in theright peroneal nerve was within normal limits at 52 m/sec.The owner was supplied with tablets of neostigmine

and atropine, but had difficulty in dose regulation.However, the animal appeared to make a spontaneousrecovery, so that at the end of two months it was able towalk a mile.Twenty-seven months after the original episode, the

animal was reported in the best of health, with noevidence of relapse.

CASE 3

This animal was an 8i-month-old male labrador, referredto us from the same veterinary practice as case 2. The doghad been vaccinated against distemper and had beenboarded out temporarily in kennels. Three days after itsreturn, the owners noticed the animal had a hoarse-sounding bark and on the fifth day it started to vomit andhad diarrhoea. Symptomatic treatment was given. A weekafter coming out of kennels the dog was seen to fall down,and over a period of time it became unable to walk at all.Treatment with neostigmine tablets I to 1 tablet twicedaily and atropine was reported to result in improvement,but later this improvement was not maintained. Radio-graphy showed a dilated oesophagus.

Seventeen days after the onset of the condition the

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, 0o

% MUSCLE ACTIONPOTENTIAL VOLTAGE

so

0

VA

_*Aa

A

A

A

.

m a

A A

* U

I II I

3 0

TIME (SECONDS)* - BEFORE TENSILON

*- AFTER TENSILON

60

NERVE STIMULUS RATE. I' SEC

FIG. 4. Case 2. Induced action potentials in the anterior tibial muscle. Nerve stimulus rate =17 c/s. Results are expressed as apercentage ofthe original summated action potential voltage.

animal was admitted to the School ofVeterinary Medicine.On examination, there was drooling of saliva, persistentbouts of vomiting (mostly of mucus), and minimaltolerance to exercise. When attempting to walk thepattern of behaviour was similar to that in cases 1 and 2:it would begin to take progressively shorter and shorterstrides with the forelegs and eventually would lie down,refusing to move. The cheeks puffed in and out with eachrespiration and the animal looked dejected. During theonset of such an episode, the head was held stiffly, straightforward. After a period of rest, the dog tended to regainits strength, and this happened especially overnight.Levels of serum calcium, sodium, and potassium werewithin the normal range. Dilatation of the oesophaguswas visible on radiographs, a contrast medium not beingrequired.Treatment consisted of intramuscular injections of

1-8 mg neostigmine and 065 mg atropine. Within fiveminutes the animal looked alert, wagged its tail, and fourminutes later got up and walked about i mile, pullingstrongly on the lead. The next day the animal was againin a collapsed state with slight respiratory distress andpyrexia (treated with penicillin). Subsequently the dosesof neostigmine were reduced to 1 25 mg which controlledthe muscle weakness, occasionally for up to two days.However, sometimes a second dose was required within24 hours. Despite agood appetite, salivation and vomitingpersisted. A total of nine doses of neostigmine was given,eight of which resulted in dramatic improvement ofstrength and ability to walk. Unfortunately, pneumoniadeveloped which could not be controlled with antibiotictreatment and the animal became dehydrated. An intra-

venous drip of 1/5 N saline dextrose had little effect and inview of the animal's distress it was decided to put it down.

POST-MORTEM EXAMINATION The only macroscopic ab-normalities observed were severe pneumonia and dila-tation of the oesophagus throughout its length (Fig. 5).There was no evidence of neoplasia or of myopathy. Atotal of 36 tissues was subjected to histological exam-ination. There was severe inhalation type pneumonia, butthe morphological appearance of the oesophageal musclewas normal in sections stained with haematoxylin andeosin. There were no significant abnormalities of themyocardium, skeletal muscle, central nervous system orsciatic nerve. The thymus was showing normal regressivechanges. Thoracic lymph nodes showed some hyperplasia.All other organs appeared normal.

CASE 4

This 16-months-old male alsatian showed clinical signssimilar to the previous cases. The presenting manifesta-tions were those of obstruction of the oesophagus-namely, retching and gagging. A probang was passed intothe stomach, with the animal under general anaesthesia,but the symptoms returned within three days. The dogwas referred to the Cambridge Veterinary School on 21March 1969, 11 days after the operation.The owner remarked that during the previous few days

the dog's exercise tolerance had become reduced and thatafter walking 20 yards (18 m), it sat down for a rest.Dilatation of the oesophagus was confirmed by radio-graphy after a barium meal (although, in radiographs

A A A

* a . U * *

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FIG. 5. Case 3. Post-mortem specimen showing severe

dilatation of the oesophagus.

taken at a later date, this dilatation could be seen withoutcontrast medium). When exercised the animal could run

for about 50 to 60 yards (45 to 54 m), and then began totake short strides with the forelegs and gradually sankinto a sitting position, refusing to go further. After a 30second period of rest it was able to resume walking, onlyto collapse again after a much shorter period of exercise.The animal was taken into the hospital and observed

for the next three weeks. During this time the reducedtolerance to exercise was demonstrated many times, butrest overnight was usually followed by marked improve-ment. Haematological results showed no abnormality andblood glucose was within normal limits. When fatiguedby exercise, there appeared to be a tremor of the forelegsand increased tone. The animal salivated and pantedexcessively and frequently vomited, especially overnight.A biopsy was taken from the intercostal muscles undergeneral anaesthesia.

Injection of 1-75 mg neostigmine and 06 mg atropineintramuscularly effectively controlled the muscularweakness but the treatment had to be repeated every

three to four days. The dog was discharged, but withinfour days the owner reported collapse after exercise.Neostigmine was given intramuscularly, but this treatmentwas replaced by ls mgpyridostigmine bromide (Mestinon:Roche) given daily in tablet form. However, the animal

could not be maintained satisfactorily on this preparationand so neostigmine therapy was reinstituted, in tabletform, dosage being related to the severity of signs.

DISCUSSION

The cardinal clinical features of human myastheniaare abnormal skeletal muscle fatigue after exertionand recovery with rest together with response toanticholinesterase drugs. The four animals describedshowed these features. Human myasthenia gravis iscommonly punctuated by remissions and relapses;remissions were not seen in three of these four dogs.In man, the muscles of the upper limbs are slightlymore frequently affected than those of the lower(Simpson, 1960); the forelimbs of the dogs seem tohave been primarily affected. The dog's oesophaguscontains a large proportion of striated muscle fibres(Trautmann and Fiebiger, 1952; Mann and Shorter,1964) and this is probably significant in relation tothe mega-oesophagus described. This dilatation, aprominent feature in three of our cases, and in thatreported by Zacks et al. (1966) may thus well be afeature of myasthenia in this species. Hereditarydilatation of the oesophagus, with or withoutachalasia, has frequently been recorded in the dog(Clifford and Gyorkey, 1967), but concomitant signsof myasthenia apparently have not been observed.A myasthenicsyndrome in man has been described

in association with carcinoma, polymyositis, andseveral other conditions. There was no histologicalevidence of primary muscle disease in any of theanimals described. Prolonged good health, in thesecond, makes a carcinoma unlikely and, in the third,no signs of neoplasia were found at necropsy. Theexcellent responseto neostigmine favoursmyastheniagravis rather than a myasthenic syndrome. However,individual species show marked differences in res-ponse to anticholinesterases. The electromyographicfeatures described, closely resemble those in the dogdescribed by Zacks et al., and mimic those seen inhuman myasthenia gravis rather than those in themyasthenic syndrome accompanying carcinoma.Evidence has been given to show that there was noconcomitant hypoglycaemia or electrolyte imbalancewhich might have been responsible for similarclinical features.The previously reported cases in the dog have

several features in common. The cocker spanielreported by Ormrod (1961) responded to neostigmine.Through the kindness of the late Mr. Ormrod, acine film of this animal was made available to us,and shows clearly the animal's reluctance to walk,taking the characteristic short strides, with improve-ment after anticholinesterase. The case in a chowbitch reported by Hall and Walker was somewhat

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different. The disease was unmasked by suxameth-onium chloride before hysterectomy, the animalbecoming-quadriplegic for three days after operation.The only movement possible was a reflex closure ofthe eyelids when the eyes were threatened; the limbsflaccid, and deep reflexes depressed. Restoration ofmuscle power followed the giving of neostigmine.There was suggestive evidence of respiratory in-fection before the onset of myasthenia in Ormrod'scase and this is a noteworthy feature commonlydescribed before onset in man. Respiratory infectionmay precipitate the onset or exacerbation of thedisease in man.The third case (Zacks et al., 1966) was a male

8-month-old mongrel. This puppy was from a litterof seven, six of which died between 3 and 4 weeks ofage from unknown causes. At 5 weeks of age thepuppy was vomiting every other day about one hourafter feeding. At 3 months the bark was abnormallyhigh pitched, and the dog limped, and the hind-legsoccasionally collapsed. There was difficulty in risingfrom the lying position and the animal fell downafter taking a few steps. A mega-oesophagus wasshown. Eventually the animal could stand only formicturition and defaecation. Good recovery followedthe administration of anticholinesterases. Electronmicroscopy showed end-plate changes comparableto those in human myasthenia gravis. The dogrecovered well following a Heller-Ranstedt operationto relieve the mega-oesophagus, and one year later,showed no recurrence of signs.During the last 11 years, three other animals have

been seen at the Cambridge Veterinary Schoolshowing signs suggestive of myasthenia. All werelabradors (two being litter mates) but the diagnosiswas not confirmed by neostigmine. One other con-dition in the dog is worthy of mention because of thesimilarity of clinical presentation. A 2-year-old JackRussell terrier ate between 70 to 80 g thyroid. Afortnight later all limbs became progressively weak;sensation was unaffected. There was some atrophy ofmasseters and limb musculature, with no significantresponse to 0-5 mg neostigmine intramuscularly. Thisperhaps represented a thyrotoxic myopathy.

In the animals described here, anticholinesteraseshad a more prolonged action than is seen in man.After the first neostigmine injection, the first alsatiannever relapsed to its previous state. In the goldenretriever, relapsesbecame less marked after successivetreatment. This may indicate a natural recovery or,alternatively, a cumulative drug effect. The dog, ascompared with man, shows a different sensitivity toneuromuscular blocking agents. Thus a basicallysimilar pharmacological defect at end-plate level indog and man shows slight differences in behaviourin the two -species.

The first alsatian's habit of eating unripe pears hasbeen reported, and the possibility arises of the dog'scondition being provoked by ingestion of toxicinsecticide. Insecticides of the organophosphorusgroup are potent cholinesterase inhibitors provokingacetylcholine accumulation. Neostigmine could onlyprecipitate further deterioration. The owner hadseveral other dogs thatateunripepears, none of whichshowed signs of muscle weakness. Myasthenia hasbeen reported three times in association with trimeth-adione (Booker, Chun, and Sanguino, 1968) andcarbamates, sometimes used as insecticides, have avery similar chemical structure. However, otherinsecticides, those of natural origin such as pyreth-rum, chlorinated hydrocarbons, and organophos-phorus compounds do not show any chemicalrelation to the oxazolidine nucleus or side chains oftrimethadione (3,5,5,-trimethyloxazolidine-2-4-dione).The occurrence of the aortic body tumour in the

first alsatian suggests some possible relationship tothe muscle fatigue. However, symptoms provokeddirectly by the tumour were not seen for over oneyear after the onset of myasthenia, and review ofother cases of aortic body tumour in the dog doesnot give any evidence of similar clinical signs. On theother hand, it is perhaps noteworthy that the aorticbody in man develops from a mesodermal in-pouching of the third pharyngeal cleft, the thymusdeveloping from the third and fourth clefts. Thesmall round cell of the aortic body tumour bears asuperficial resemblance to the thymocyte. If relevantto the cause of human myasthenia, reports of myoidfibres withinthe thymus (Strauss, Kemp, and Douglas1966) may be paralleled by such inclusions withinaortic body tissues.While our cases do not mimic exactly all the

clinical features of human myasthenia gravis, thereseems to be sufficient evidence suggestive that asimilar disease, and not solely a myasthenic syn-drome, occurs in the dog. Identification of furthercases and study of possible precipitating causes willbe of considerable value in the search for a primecause of this disease.

In the diagnosis of the type of tumour we gratefullyacknowledge the help of Dr. A. R. Jennings, Dr. L.Mawdsley-Thomas and Professor S. Nielsen. We wish tothank Miss M. Hall and Mr. J. E. Payne for technicalhelp.

REFERENCES

Booker, H. E., Chun, R. W. M., and Sanguino, M. (1968).Myasthenic syndrome associated with trimethadione.Neurology (Minneap.), 18, 274.

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Clifford, D. H., and Gyorkey, F. (1967). Myenteric ganglialcells in dogs with and without achalasia of the esophagus.J. Amer. vet. med. Ass., 150, 205-210.

Hall, L. W., and Walker, R. G. (1962). Suspected myastheniagravis in a dog. Vet. Rec., 74, 501-503.

Jubb, K. V. F., and Kennedy, P. C. (1963). Pathology ofDomestic Animals. Vol. 1, p. 340. Academic Press:London.

Mann, C. V., and Shorter, R. G. (1964). Structure of thecanine esophagus and its sphincters. J. surg. Res., 4,160-163.

Ormrod, A. N. (1961). Myasthenia gravis in a cocker spaniel.Vet. Rec., 73, 489-490.

Simpson, J. A. (1960). Myasthenia gravis: a new hypothesis.Scot. med. J., 5, 419-436.

Strauss, A. J. L., Kemp, P. G., Jr., and Douglas, S. D. (1966).Myasthenia gravis. Lancet, 1, 772.

Trautmann, A., and Fiebiger, J. (1952). The Fundamentals ofthe Histology of Domestic Animals. Comstock Pub.Associates, Cornell Univ. Press: Ithaca, N.Y.

Zacks, S. I., Shields, D. R., and Steinberg, S. A. (1966). Amyasthenic syndrome in the dog: a case report withelectron microscopic observations on motor end platesand comparisons with the fine structure of end plates inmyasthenia gravis. Ann. N. Y. Acad. Sci., 135, 79-97.

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