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PubMed1978

Neurologic complications of thyroid dysfunction.

Until such time as results of more rigorous studies are available, the morbidity rates for thyroid dysfunction cited here must suffice. The 1955 to 1956 outpatient "incidence" for England and Wales was 1.1 per 1,000 for thyrotoxicosis and 1.7 per 1,000 for myxedema (18). United States in-patient "incidence" for 1971 was 0.16 per 1,000 for thyrotoxicosis and 0.13 per 1,000 for myxedema (25). The 1935 to 1967 average annual incidence of Graves' disease for females in Olmsted County, Minnesota, was 30.5 per 100,000 (10). Well over 50% of hyperthyroid patients have clinical evidence of mild or moderate muscle weakness. Usually this weakness is proximal, and electro-myography and muscle biopsy confirm the existence of myopathic process (Table 11). Severe muscular weakness of acute onset is relatively rare and is encountered in approximately 1% of hyperthyroid patients (11,17,40). Ophthalmoplegia and psychosis are reported 4% and 2% of patients, respectively (17). Myasthenia gravis, although well publicized, is estimated to occur in less than 1% of patients (3,30). TPP is virtually nonexistent in the West; in the Orient it is reported in 2 to 8% of hyperthyroid patients and is 20 to 60 times more frequent in the hyperthyroid male than in the hyperthyroid female (Table 12). The neurologic symptomatology of myxedema is more extensive, and agreement among the various series is poor. The only unselected series addressing itself to neuromuscular manifestations of myxedema that is suitable for citation is that of Scarpalezos et al. (36). This comprehensive study was done without apparent patient selection, and it reported 2% of patients with definite carpal tunnel syndrome, 6% with myopathy, and 18% with polyneuropathy (Table 13). Reported percentages of hypothyroid patients found to have neurologic manifestations of cerebellar dysfunction are extremely diverse: ataxic gait was reported in 5 to 32% (6,7,12,27) of patients and dysdiadochokinesia in 6 to 52% (7,12,27). Psychosis is encountered in 2 to 5% (6,14,17,27,39) of myxedematous patients, memory loss in 23 to 55% (6,14,27), and coma in less than 1% (27).

Adult↗
PubMed1976

Intracellular distribution of phosphate in the underfed rat developing weakness and coma following total parenteral nutrition.

Underfed rats infused intravenously with a glucose-amino acid solution at the rate of 390 kcal/kg/day developed a syndrome of muscular weakness, neuropathy, lethargy and precoma or coma associated with severe hypophosphatemia. The movement of phosphate into the cells was studied to determine where it went and into which organic compounds it was incorporated. All but 8% of the labeled phosphate was found in liver, muscle, bone, and carcass residue. Liver cells took up as much phosphate as bone and twice as much as muscle, on weight basis. About 90% of the labeled phosphate entering liver was found in the acid-soluble fraction. The specific activity of liver phosphate increased in the infused underfed rats compared to uninfused underfed rats. Infusion of the underfed rat until signs of the syndrome appeared was associated with a 2.7- to 5-fold increase over the correspondingly infused normal rat in the labeling of glucose-6-phosphate, glucose-1-phosphate, and 6-phosphogluconate. No increase over the infused normal rat was observed in most of the other sugar phosphate compounds nor in the non-sugar phosphate compounds such as phospholipids, nucleic acids or proteins. he changes in sugar phosphates observed in the underfed rats probably reflect the enzymatic atrophy associated with underfeeding and the consequent inability to respond to the huge glucose load.

Animals↗
PubMed1977

Adult-onset acid maltase deficiency. Case report of an adult with severe respiratory difficulty.

Pompe's disease (acid maltase deficiency) classically affects infants and children, with a few sporadic cases occurring in adults. An adult patient initially have progressive muscular weakness, exertional dyspnea, diaphragmatic paralysis, and objective evidence of restrictive respiratory disease. Muscle biopsy established the diagnosis of acid maltase deficiency. The patient's brother had died at the age of 44 years, after 23 years of a "progressive muscular dystrophy." Acid maltase deficiency should be considered in the differential diagnosis of progressive respiratory insufficiency associated with weakness.

Adult↗
PubMed1979

[Hypothyroid myopathy: histochemical and ultrastructural features with physiopatological correlations (author's transl)].

The Authors describe an adult case of hypothyroid myopathy which occurred after a Hashimoto's thyroiditis. Ultrastructural examination of the deltoid muscle showed two fundamental changes: 1) large collections of mitochondria generally normal in shape, structure and size, especially in the subsarcolemmal sapce of the muscle fibre; 2) glycogen deposits both beneath sarcolemmal membrane and between myofibrils. Histochemical examination reveals an increased activity of mitochondrial oxydative enzymes, such as NADPH and SDH especially in subsarcolemmal regions of many type I fibres. The histogram is normal. It seems that the multiplication of skeletal muscle mitochondria may be compensatory to the slowing down of metabolic activities. This, however, is ineffective because it involves the mitochondria localized more superficially in the fibres with a loosely coupled oxydative phosphorylation. Glycogen accumulations are probably due to deficiency of the thyroid hormone; in fact stimulation of carbohydrate metabolism by thyroxine is well known. The abnormal functioning of the muscular mitochondria and the defective utilisation of glycogen are the most important factors in the pathogenesis of muscular weakness of hypothyroid myopathy.

Adenosine Triphosphatases↗
PubMed1978

[Nemaline myopathy (clinico-morphologic study)].

For the first time in Soviet literature a description of 2 cases is given; both sibs demonstrate a muscular weakness, hypotension, moderately expressed hypotrophy of the body muscles, extremities and face. There were also specific bone anomalies. An electron-microscopic study detected typical "nemaline structures" in the muscular fibres. The disease in both sibs was identical even in details. The authors discuss the possible mechanisms of motor disorders. Besides personal material the paper contains the main facts of modern literature in relation to the clinical picture and pathogenesis of nemaline myopathy.

Asthenia↗
PubMed1978

Weakness, neuropathy, and coma following total parenteral nutrition in underfed or starved rats: relationship to blood hyperosmolarity and brain water loss.

The continuous infusion of a concentrated, high-caloric glucose solution intravenously into underfed or 3-day-starved rats at a rate of 390 kcal/kg/day results in hypophosphatemia, muscular weakness, neuropathy, lethargy, occasional convulsions, and eventual coma and death. This sequence of events is not observed in similarly infused normal rats. It is a model of a fatal parenteral nutrition syndrome which occurs in undernourished patients. Rats in coma had an eightfold increase in the blood glucose level, a 1.6-fold increase in serum osmolarity, a 16% to 20( decrease in brain water content, and normal blood ketones. A lag phase of at least 8 hr and often 12 to 24 hr occurred following the start of the hyperosmotic glucose infusion before the blood glucose began to accumulate progressively and the syndrome developed. The onset of the syndrome could be prevented by the administration of large amounts of insulin required to keep the blood sugar from exceeding 250 mg/dl. Thus the rat model of the fatal hyperalimentation syndrome is a form of hyperglycemic, hyperosmolar, nonketotic coma caused by brain dehydration.

Animals↗
PubMed1979

[Lipidic myopathy with severe cardiomyopathy caused by a generalized carnitine deficiency. Favourable course during carnitine hydrochloride treatment].

The case of a girl who presented with gastrointestinal upsets with nausea, vomiting and occasional hypoglycaemic attacks during childhood is reported. At about 5 years of age generalised muscular weakness with severe amyotrophy, cardiomegaly with a cardiothoracic ratio of 0,63, left ventricular hypertrophy on electrocardiography and left ventricular dilatation with hypokinesis on echocardiography were observed. A few weeks later she developed severe cardiac failure. Muscle biopsy showed muscular dystrophy with lipid infiltration due to carnitine deficiency )serum carnitine 9 nmoles/ml, normal values: 46 +/- 6,9 nmoles/ml; muscle carnitine 0,27 nmoles/mg, normal values: 3,0 +/- 0,79 nmoles/mg fresh frozen weight). She improved rapidly with carnitine chlorhydrate and a diet low in lipids and high in medium chain triglycerides. Regression of muscular symptoms and cardiac failure was observed. After 13 months follow-up with no tonicardiac therapy she is much improved; the signs of heart failure have disappeared, the cardiothoracic ratio is now 0,55 and the electrocardiogramme and echocardiogramme are normal.

Biopsy↗
PubMed1978

[Muscular involvement in osteomalacia: clinical, hystoenzymologic and ultrastructural study in 10 cases].

Osteomalacic myopathies are rare. They can prevail, however, and occur before bone abnormalities. The diagnosis must rest on clinical observation since the histopathologic images are not specific. On the other hand the demonstration of muscular weakness is very frequent during osteomalacia. In fact two types of manifestations correspond to the same anatomopathologic lesions. These are myopathic changes observed also during light microscopy, histoenzymologic and ultrastructural examination in the 10 patients examined. On the basis of these morphologic changes, muscular involvement can be considered to be part of the osteomalacia syndrome. The contribution of various factors including secondary hyperparathyroidism, vitamin D metabolism disorders, and phosphorus depletion is discussed. It is probable that many of them act together, causing reversible changes in muscular fibers. The intimate mechanisms of these changes are unknown.

Apyrase↗
PubMed1979

The otolaryngologic presentation of myasthenia gravis.

Myasthenia gravis is a neuromuscular disease of insidious onset, characterized by weakness and fatigability of voluntary muscles. Most patients present with symptoms relating to the head and neck and thus may be seen first by the otolaryngologist. Predominant symptoms may be ocular (ptosis or diplopia) or related to fatigue of the oropharyngeal or laryngeal musculature (dysarthria, dysphonia, or dysphagia). Alleviation of muscular weakness and fatigability after administration of anticholinesterase drugs is pathognomonic of myasthenia gravis.

Adolescent↗
PubMed1977

Neuromuscular syndromes associated with malignant disease.

Malignant disorders may produce neuromuscular syndromes in a variety of ways, for some of which it is still difficult to determine the exact pathophysiology. In the myopathic and neuropathic disorders, one possible explanation is that they are due to a virus such as is found in the rare "progressive multifocal leukoencephalopathy". This is seen in association with the malignant lymphomas and with other conditions such as sarcoidosis where immune responses may be altered by either the disease or the treatment. No viral material has been found in the nonmetastatic neurological disorders apart from progressive multifocal leukoencephalopathy. An alternative theory is that there may be an autoimmune process, the nervous system sharing some antigenic determinant with the neoplasm (Urich, 1967). The prognosis in the paraneoplastic neurological disorders is usually poor. As well as the direct threat to life posed by the malignant disease, when the neurological disorder is due to destruction of neurones (for instance cerebellar degeneration or sensory neuronopathy) recovery of function is impossible. Spontaneous remissions have been recorded in cases of proximal muscle weakness and sensorimotor neuropathy, but it is difficult to know whether the remissions have been truly spontaneous or related to treatment (excision of the neoplasm or administration of steroids). Further immunological and virological studies will probably reveal the answers to some of the outstanding problems. In the meantime the clinician must continue to investigate patients with muscular weakness for evidence of an occult neoplasm, and to repeat investigations if no other cause for the neurological disorder is found. Also, in patients with known malignant disease, apart from trying to differentiate forms of neuromyopathy from the effects of metastases the various metabolic disorders must be considered because the therapeutic possibilities are a little more promising in the paraneoplastic endocrine disorders. Ross (1975) wisely said that "cancer has replaced syphilis as the great imitator".

Cachexia↗
PubMed1978

[The vessels of the inner ear (author's transl)].

The inner ear as an example of a highly specialized sensory organ also possesses a highly specialized vascularisation. This represents an impressive example for a reasonable adaption of the terminal blood vessels to a specific function of the organ fulfilling more than only the nutrition. In this paper the microvascular bed of the cochlea is examined using both the injection method of the vessels and the biomicroscopic observation in vivo. The combination of these technics supported by histologic and stereoscan microscopic examinations has made it possible to give an account of the functional morphology of the inner ear vessels. As a detailed structural analysis of the vessels morphology with the help of dyes that fill the whole of the vessels space (i.e. Berlin blue) is not possible, perfusion experiments with silver nitrate were performed on the inner ear. After the perfusion the vessels are cleaned again, the silver however imbibes the intercellular reticular substances and after exposure produces a continous and sharp framework of the endothelium and--when present--muscular cells, thus showing the angioarchitectural contours. There is a very clear division of the cochlear vessels in a three dimensional space: The arterial and venous vessels are vividly separated from one another, forming two systems of microvascular units in the lateral wall and the spiral lamina. Each unit begins with special blood vessel convoluts in the modiolus, consisting of loops of arterioles. They are weakly muscularized whereas no muscle structures are seen elsewhere in the other parts of the inner ear vessels. There are no a.-v. anastomoses or sphinkters at all. The function of the vessel loops in the modiolus is to flatten the pulse wave as well as to regulate the blood flow in the microvascular bed by vasomotion. This was proved by statistical examinations of 1200 measurements of the widths of the vessels at several points of the cochlea in a blind study with and without vasoactive drugs. The terminology of the vessels is not standardized. The nomenclature in this paper has regard to the classification of the vessels, the course and the topographic localisation. Silver staining reveals changes in the form of the endothelium cells from the arterial towards the venous end. While the arteries show a long stretched spinle or lancet like form they change over blunt, oval, triangular or rhomboid forms into polygonal cells with spiked border lines at the venules. All experiments together give an account that the blood supply of the inner ear is in close correlation with the blood supply of the brain and too possesses autoregulative mechanisms, which must be localized in the convoluts at the beginning of every microvascular unit of the cochlear vessels.

Arterioles↗
PubMedDate not supplied

The otolaryngologic presentation of amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis is a progressive dengenerative neuromuscular disease of insidious onset. It involves upper and lower motor neurons and causes both spastic and atrophic muscular symptoms. More than one fourth of patients have complaints relating to the head and neck (bulbar palsy); thus, the otolaryngologist may be the first physician to see them. Predominant symptoms are slurred speech, hoarseness, dysphagia, and dyspnea. Muscular weakness, atrophy, and fasciculation are noted on examination. The course is relentless, and only 20% of patients survive five years after diagnosis.

Adult↗
PubMed1975

Remediable neuromuscular disorders.

Generalized muscular weakness may develop from a variety of causes, and in many cases is reversible with appropriate treatment of the underlying disorder.

Adult↗
PubMed1977

Muscle protein synthesis in MED myopathy.

A fatal, rapidly developing progressive muscle disease of delayed onset in mice is produced by the effects of an autosomal recessive gene (MED). We recognize two stages of this disease. The earlier stage, observed between the 11th and 14th postnatal day, is characterized by structurally normal small myofibers, cessation of increase in body weight, and increasing muscular weakness, particularly of the hind limbs. The second stage is characterized by a spheromembranous degeneration of myofibers and almost complete cessation of voluntary movement. Previous studies have revealed neither anatomic abnormalities in neuromuscular junctions nor major changes in oxidative metabolism or electrolyte concentrations in striated myofibers in the early stages of the disease. In this paper we report investigations designed to determine whether the failure of growth of striated muscle in the first stage is due to a defect in muscle protein synthesis or, as has been found in muscular dystrophies, is due to an increased rate of degradation of muscle. We conclude that MED animals demonstrate a different kind of defect than that occurring in dystrophic mice. In MED mice, the failure of growth is primarily due to a diminished rate of protein synthesis.

Animals↗
PubMed1975

Atypical myopathy with myofibrillar aggregates.

An autopsy of a 23-year-old woman with progressive muscular weakness and wasting showed a unique muscle abnormality with segmental involvement of individual fibers by peculiar inclusions. Electron microscopically, these inclusions resembled cytoplasmic bodies, being formed of two concentric zones of filamentous materials. They seemed to arise from filaments of myofibrils that were fragmented and highly disorganized in affected areas.

Adult↗
PubMed1975

Electrolyte disturbances in beer drinkers. A specific "hypo-osmolality syndrome".

A syndrome is described which affects subjects whose consumption of beer is considerable but who take no or little ordinary food. The symptoms include fatigue, dizziness, and muscular weakness; the biochemical changes are hyponatraemia and hypokalaemia. The disorder is rapidly resolved by stay in hospital. Beer is poor in Na (1-2 meq. per litre). Consequently these patients' intake of Na was low, and the production of urea was very low.

Aged↗
PubMed1978

Myoadenylate deaminase deficiency: a new disease of muscle.

Five cases of a new disease presented with muscular weakness or cramping after exercise; three of the cases also had an elevated serum creatine phosphokinase. Muscle biopsies were histologically normal but lacked adenylate deaminase by stain and solution assay, while the erythrocyte isozyme was normal. A clinical diagnostic test has been developed, and the human enzyme was separated by acrylamide-gel electrophoresis.

AMP Deaminase↗
PubMed1979

[Clinical, morphological and biochemical studies on muscle carnitine deficiency (author's transl)].

This report deals with two sisters who died with eight, respectively ten weeks under the signs of respiratory failure caused by progressive muscular weakness. Only an elevated cerebrospinal fluid protein was suspicious of an additional disturbance of the central nervous system. Muscle biopsy revealed a vacuolar myopathy. Histochemistry showed lipid storage, increased mitochondrial enzyme activity, and to a lower degree, glycogen accumulation especially in type I muscle fibers. Electron microscopy confirmed elevated lipid content in combination with increased, enlarged and abnormally structured mitochondria. Biochemical studies on muscle biopsy, in comparison with normal children, showed a significant decrease of carnitine content and an increased activity of carnitine palmityltransferase. Retrospectively from a clinical point of view this disease is suggestive of "systemic carnitine deficiency", even if some symptoms (hepatomegaly, cardiomyopathy) were not present and serum- and liver carnitine was not measured because the children died before the diagnosis of muscle carnitine deficiency was confirmed. The clinical picture of these two fatal cases is compared with another observation of muscle caritine deficiency. This child shows only a mild course of muscle disorder, but very similar morphological changes in muscle biopsy. Biochemically, there was a clear decrease in muscular carnitine, while the serum levels were in the normal range. The activity of muscular carnitine palmityltransferase was also normal.

Biopsy↗