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A Myopathy Presenting in Adult Life with Features Suggestive of Glycogen Storage Disease by J

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A Myopathy Presenting in Adult Life with Features Suggestive of Glycogen Storage Disease by J J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.23.4.302 on 1 November 1960. Downloaded from J. Neurol. Neurosurg. Psychiat., 1960, 23, 302. A MYOPATHY PRESENTING IN ADULT LIFE WITH FEATURES SUGGESTIVE OF GLYCOGEN STORAGE DISEASE BY J. MACDONALD HOLMES, C. R. HOUGHTON, and A. L. WOOLF* From the Midland Centre for Neurosurgery, Smethwick Following von Gierke's (1929) description of the Thus the case we are about to report, if due to hepatonephromegalic form of glycogen storage glycogen storage disease, appears to be unique in disease, Pompe (1932, 1933) and Kimmelstiel (1933) that the patient presented at the age of 21 with published reports of a cardiomegalic form (see symptoms of a myopathy and did not die until the Table I). Kimmelstiel's case was the first in which age of 31 years. It will be seen that the histological deposition of glycogen within the cells of the nervous findings differed considerably from those in the system was noted, and the two cases were the first in infantile cases, and although evidence of the disease which glycogen deposition in skeletal muscle had was in fact present in repeated muscle biopsies carried out the dramatic lesions were been mentioned. Neither of these cases showed any during life, guest. Protected by copyright. clinical evidence of muscular involvement. In 1936, misinterpreted as indicating a parasitic infection and Wolff reported a case in which the muscles were prevented us from undertaking appropriate bio- described as poorly developed. In 1939, Gunther chemical investigations. reported a case of an infant, 11 months old at the We are, therefore, making this report in the hope time of death, in whom widespread flaccid paralysis that subsequent cases may be recognized during was a striking feature. Childs, Crosse, and Hen- life and appropriate studies made. derson (1952) reported a brother and sister who both died within the first two years of life from glycogen Case Report storage disease affecting the liver, heart, nervous Clinical History.-The patient was a young woman system, and skeletal muscles, in whom progressive aged 31 years who was first seen by one of us in March, weakness was among the presenting symptoms. 1958, for investigation of weakness of the legs. Krivit, Polglase, Gunn, and Tyler (1953) described She had noticed a difficulty in climbing stairs nine two further similar cases. More recently Zellweger years before and at about the same time found difficulty (1956) and Zellweger, Dark, and Abu Haidar (1955) in rising from a chair. The weakness progressed very have reported three cases presenting with a clinical slowly and the next symptom was difficulty in rising picture suggestive of Werdnig-Hoffmann disease in from a lying position. She noticed that the muscular whom a storage disease was weakness was worse in very cold or hot weather, but diagnosis of glycogen there was no variation throughout the day. In the past established by chemical estimation of glycogen in three or four years the weakness of the legs had become biopsy specimens of muscle. Within the last two much worse and the knees would often give way, years Schnabel (1958) has reported a further case of especially the right. http://jnnp.bmj.com/ hepato - cardio - neuromuscular glycogen storage In 1950, she attended the neurological clinic in another disease in which the patient at 51 months of age hospital, where myasthenia gravis was suspected, but showed scarcely any active movement. No case of there was no response to neostigmine. The reason for glycogen storage disease has ever been reported as suspecting myasthenia seems to have been the occasional presenting clinically with symptoms of muscular failure of her voice to a faint whisper, but she said that involvement except in infancy, and although there is this had occurred since adolescence and it appears to have been a functional aphonia. She had also had on record a single report (Antopol, Boas, Levison, bilateral for in childhood and Tuchman, 1940) in which two brothers aged operations dacryocystitis which had produced an appearance of her eyelids suggesting on October 1, 2021 by 11 years and 15 years were shown to have been slight ptosis. A later diagnosis made in the same hospital suffering from the cardiomegalic form of the disease, was thyrotoxic myopathy, but at no time was there there was no suggestion of muscular weakness. convincing evidence of thyrotoxicosis. She was said to have had meningitis at the age of * In receipt of a grant from the Muscular Dystrophy Association 5 years, but this left no sequelae. In 1954, she had of America Inc. pneumonia and came under observation at a chest clinic. 302 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.23.4.302 on 1 November 1960. Downloaded from ADULT MYOPATHY SUGGESTING GLYCOGEN STORAGE DISEASE 303 TABLE I SUMMARY OF REPORTED CASES OF GLYCOGEN STORAGE DISEASE AFFECTING MUSCLE Age of Nervous Author Date Patient Liver Heart Muscles System Pompe 1932 7/12 Not enlarged Enlarged 6 x 9-39 % glycogen Kimmelstiel 1933 5/52 Greatly enlarged Frosted appear- Droplets of glycogen Glycogen in (1,600 g.) ance, vacuolate uider sarcolemma nerve cells muscle fibres Abundant glycogen in lymph spaces Humphreys and Kato 1934 5/12 Enlarged, hepatic Enlarged 5 x Vacuolated muscle cells, pale foamy Hypertrophy and fibres cytoplasm vacuolation of muscle fibres Wolff 1936 5/12 Enlarged Left ventricular Vacuolated muscle Poorly developed wall 1-4 cm. fibres in tongue muscles thick Skeletal muscle not examined 35-3 % of dry wt. glycogen Hertz and Jeckeln 1936 5/52 Ufpper border of Enlarged 2 x Round cell foci, Picture of cretinism normal weight Large amounts vacuolated muscle of glycogen in fibres muscle fibres (vacuoles in formalin-fixed tissues) Gunther 1939 11/12 Enlarged (325 g.) Enlarged (75 g.) Vacuolated, haema- Paralysis and Vacuolated paren- Vacuolated toxylin and eosin, atonia chymal cells muscle fibres blue-stained granules in muscle fibres Antopol et al. 1940 15 yr. Large (1,850 g.) Enlarged 3 x Basophilic masses in Parenchymal cells, Vacuolated mus- centre of muscle foamy cytoplasm cle fibres, baso- fibres staining posi- guest. Protected by copyright. philic substance tively with Best's carmine stain Clement and Godman 1950 6/12 Enlarged, vacuola- Enlarged 3 x Vacuolation, baso- Nerve cells Resembled cretin- tion, glycogen in Glycogen in philic substance contain ism, mongolism, liver cells muscle fibres, glycogen and finally amyo- vacuolation tonia congenita Childs et al. 1952 11/12 Enlarged, liver cells Enlarged 3 x Granular or fibrillar Glycogen in Atonia, areflexia (1) vacuolated, glyco- Perinuclear eosinophilic or baso- nerve cells gen in vacuoles clear spaces con- philic material in taining eosino- muscle fibres phil material, glycogen in sar- coplasm (2) 17/12 Half normal size Enlarged 4 x As Case 1 but less Glycogen in Weak, atonia, (as Case 1) (as Case 1) basophilic material nerve cells areflexia Krivit et al. 1953 19/12 Enlarged, foamy Enlarged, vacuo- Vacuolation, fine Retarded motor (1) parenchymal cells lation of muscle granules and amor- development, fibres phous solid masses marked hyptonia, staining strongly with reduced muscle P.A.S. and Best's bulk stain material (2) 12/12 Enlarged as Case 1 Enlarged 3 x as As Case I Motor retardation, Case I hyptonia, hypore- flexia, muscles soft and reduced in bulk Zellweger 1956 3 10/12 Biopsy, no histology Weakness, absent (1) but glycogen content reflexes, atrophy 20 x normal (2) 5/12 No histology but Weakness, promi- glycogen content nent muscles 13x normal (3) 18/12 Vacuolated muscles Weakness and fibres with basophilic hypotonia substance http://jnnp.bmj.com/ Schnabel 1958 5X/12 Enlarged (275 g.) Enlarged 4 x Vacuolated muscle Nerve cell Scarcely any active Vacuolated mus- fibres and basophilic contains movement cle fibres substance glycogen Tuberculosis was suspected, but not confirmed. She quadriceps of both sides, which were extremely weak. lost a good deal of weight after this respiratory illness. She could not rise from a chair without using her arms. In 1957, she had another respiratory infection with a There was also bilateral weakness of dorsiflexion of the slight haemoptysis and tuberculosis was again suspected ankles. The posterior part of the left deltoid was notice- on October 1, 2021 by from the radiological appearances of the chest. In ably wasted and the erectores spinae were very weak. March, 1958, she had a right-sided pleurisy and was Upper limbs.-There was bilateral weakness of abduc- referred to one of us by Dr. T. M. Curran who had tion; tremor of outstretched hands; no fasciculation or noticed her muscular weakness and wasting. fibrillary twitching; no sensory disturbance, supinator, On examination she was very thin, with generalized biceps, and tricepsjerks present but very weak; abdominal muscular wasting, but this was most pronounced in the reflexes present. J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.23.4.302 on 1 November 1960. Downloaded from 304 J. MACDONALD HOLMES, C. R. HOUGHTON, AND A. L. WOOLF o Q d2 42 (W I d 9 d.67 d434 drowned 70 d34 0 d23 0 56 0 d67 killed drowned 56 I I, I I I 1- I r,I I ZLX d ddcfQ QQQgdkilled killed 9 47 0o43 d4 dg d.> d31 d31 30 e '12 Died in mancy or eary adult life of pneumonia disease. 16 21 17 13 9 14 10 Q or*heart The patient. guest. Protected by copyright. Genealogical table of the patient's family. It will be noted that the patient's mother married Examined. twice. 9 Other members of family. Lower Limbs.-There was gross weakness and wasting Muscle biopsies were performed on the right palmaris of both quadriceps; marked weakness of dorsiflexion of longus and vastus internus on April 11, 1958.
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