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At least 289 records · Page 16Linked to original sources
PubMedDate not supplied

Tumor-induced hypophosphatemic osteomalacia associated with tertiary hyperparathyroidism: a case report.

BACKGROUND: Tumor-induced hypophosphatemic osteomalacia is a syndrome characterized by urinary phosphate wasting related to the presence of a slowly-growing tumor of mesenchymal origin. The characteristic laboratory findings are normal serum calcium, marked hypophosphatemia, increased serum alkaline phosphatase, markedly reduced renal tubular reabsorption of phosphorus and inappropriately low levels of 1,25-dihydroxyvitamin D [1,25-(OH)2D]. CASE PRESENTATION: A 65-year-old woman presented with a 17-year clinical history of musculoskeletal pain, muscular weakness in the pelvic girdle, spontaneous fractures and difficulty in walking. Over the ensuing years the patient suffered other multiple spontaneous fractures, surgically treated, and the muscular pains worsened until she became bedridden. During the years before hospital admission the patient received treatment with clodronate, oral calcium salts and vitamin D therapy. Standard laboratory, ultrasonography and scintigraphic findings provided a "convenient" diagnosis of primary hyperparathyroidism, but the low plasma level of phosphorus induced to perform an Indium111-octreotide scintigraphy. Scintigraphy visualized an area of pathologic increased signal uptake in the left groin, consistent with a mass containing a high density of somatostatin receptors. After surgery, histologic examination and immunostaining of the resected specimen indicated an hemangiopericytoma. Nevertheless, the persistently low blood phosphorus level, in association with the increased serum calcium and PTH levels, were attributed to the prolonged phosphate therapy the patient underwent over the years, and the persisting abnormal laboratory indexes indicated the development of a tertiary hyperparathyroidism. We performed a subtotal parathyroidectomy and intraoperative assay of serum PTH showed that levels had diminished by more than 80% from preoperative values. Over the ensuing months Ca+2, PTH and serum phosphorus values returned to normal, and the pain symptoms disappeared. CONCLUSIONS: Tumour-induced osteomalacia is a very rare syndrome associated in 5% of cases with tertiary hyperparathyroidism due to long-term therapy with phosphorus and vitamin D. The initial diagnosis of primary hyperparathyroidism, confirmed by the parathyroid MIBI-scintigraphy, would lead us to an inappropriate surgical treatment. Therefore we want to stress the importance of In111-octreotide scintigraphy in detecting tumours, rich in somatostatin receptors, in presence of an hypophosphatemic syndrome.

Aged↗
PubMed2001

Simulations of foot stability during gait characteristic of ankle dorsiflexor weakness in the elderly.

Falls are common among the elderly and often cause injuries. They most frequently occut during walking and are associated with the chronic deterioration in neuromuscular and sensory systems, as well as with ankle dorsiflexor muscular weakness and lowered endurance of these muscles to fatigue. In the present study, a three-dimensional (3-D) finite element model of the structure of the foot was utilized to determine the effects of ankle dorsiflexor muscle weakness on the structural stability of the foot and, consequently, on the risk of falls during gait. The medial-lateral tendency of instability of the foot during gait in such conditions of weakness was analyzed by means of this model to identify the most important muscles used in controlling foot stability in affected individuals. The values of the eccentricity of the center of pressure under the heel during foot placement were used to indicate the degree of foot stability. The computational analysis indicated that it is the tibialis anterior muscle's weakness that dramatically decreases foot stability. Clinical investigation is now needed to correlate the significance of tibialis anterior muscle weakness with other known risk factors affecting the tendency to falls among the elderly, e.g., deterioration of sensory abilities. Rehabilitation practitioners and physical therapists may apply the present analytic approach to evaluate the stability of a foot before treatment and compare the predicted with the actual therapeutic results in terms of optimization of foot-ground pressure.

Accidental Falls↗
PubMed1997

Hypokalaemic myopathy in alcoholism.

We describe the clinical and pathological features of a patient with an acute painless proximal myopathy due to hypokalaemia associated with alcoholism. There was an excellent response to treatment with potassium supplements. The importance of recognition of low potassium states in alcohol-dependent patients with muscular weakness is emphasized.

Adult↗
PubMed1989

[Various problems of the pathogenesis of myopathy in patients with thyrotoxicosis].

In patients with thyrotoxic myopathy, histological investigation showed the decrease in mean diameter of skeletal muscles, and increased collateral branching of distal axons. The percentage of afflicted fibers was not high with focal pathology. The signs of true reinnervation were absent. Electroneuromyographic investigation confirmed mild myopathy. The authors discuss the possible participation of cyclic nucleotide system disorders in muscular weakness in these patients.

Adult↗
PubMedDate not supplied

Childhood progressive spinal muscular atrophy with facioscapulo-humeral predominance, sensory and autonomic involvement and optic atrophy.

A female child of healthy parents developed rotary nystagmus at the age of 15 months. Ophthalmoscopy disclosed incomplete optic atrophy. Blood tests, EEG and CT scans were normal. At 20 months progressive muscular weakness and wasting with limb-girdle distribution commenced, followed later by disturbance of gait. From muscle and nerve biopsy the diagnosis of a peripheral neuropathy with neurogenic muscular atrophy was made. No mental change occurred. At 23 months she sustained cardiac arrest and was resuscitated; thereafter, she remained in a vegetative state and expired 9 months later. Her brain was markedly atrophic and firm. Diffuse old ischemic necroses and neuronal loss with gliosis were found in the cortex, the neostriatum, the thalamus, parts of the lower brainstem, and the cerebellum. Her optic nerves and tracts showed complete atrophy. The spinal cord exhibited degeneration and loss of motor neurons with cervical accentuation. The intermediolateral nuclei, the dorsal nuclei and the spinal ganglia were also involved. There was demyelination of the posterior funiculi, the pyramidal tracts, and the sciatic, peroneal, sural, and superior frontal nerve. The voluntary muscles exhibited large group atrophy with liposclerotic change and limb-girdle predominance. The neck, tongue and ocular muscles were also involved, as were, to a less extent, the lower limbs. Although the loss of motor neurons in the spinal cord and at the bulbar level with the typical pattern of neurogenic muscular atrophy, as well as its distribution, resemble the facioscapulo-humoral type of heredity motor neuropathy (HMN), early onset, rapid course, sensory and autonomic involvement, and atrophy of the optic nerve do not fit this or any one type of HMN.

Atrophy↗
PubMed1997

[A case of spastic tetraplegia with medullo-cervical atrophy].

A 48-year-old man, who had spastic tetraplegia and a marked atrophy of the medulla oblongata and upper cervical cord, was reported. He began to walk in spastic fashion at the age of 12 years, and was diagnosed as spastic paraplegia. His father, whose onset of the disorder was 35 years old and died of pneumonia at the age of 69 years, manifested symptoms and a course, both resembling those of the present patient. Generalized weakness progressed gradually, and the patient was confined to bed in his forties. On admission, he showed markedly increased tendon reflexes and pathological reflexes in all the extremities. Muscular weakness was severe in the neck, trunk and extremities, and mild in the facial muscles. There were neither bulbar sign, significant respiratory failure nor fasciculation of muscles. A needle EMG examination revealed no apparent neuropathic findings. MR imaging showed a marked atrophy of the medulla oblongata and upper cervical cord, which was not considered to be secondary to vascular or infectious diseases. Though sensory evoked potentials showed no response at the latencies of central nervous components, visual evoked potentials, brainstem auditory evoked response and blink reflex were normal. This case might represent an unknown hereditary degenerative disease with autosomal dominant inheritance.

Humans↗
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↗
PubMed1992

[X-ray computed tomographic scans of lower limb and trunk muscles in facioscapulohumeral muscular dystrophy].

X-rays computed tomographic (CT) scans of muscles of the lower limbs and the trunk in 14 patients with facioscapulohumeral muscular dystrophy (FSH) were studied. The CT scans showed that the affected muscles were decreased in density and size. The laterality of muscular involvement was sometimes observed. The muscular lesions in the lower limbs showed proximal distribution. In the thigh, the hamstrings were affected first, the adductor muscles second, and then the muscular involvement progressed to the quadriceps femoris muscle. In the lower leg, the gastrocnemius and soleus muscles were relatively spared as compared with the tibialis anterior muscle. In the lumbar girdle, the abdominal muscles were involved first, the gluteal muscles second, the back muscles third, and the psoas major muscle were relatively spared. The muscular weakness of this distribution exacerbated lumbar lordosis. The neck muscles were less affected than those of the lumbar girdle. The CT scans in FSH demonstrated the characteristic pattern of muscular involvement, which differed from the inherited muscular diseases such as Duchenne muscular dystrophy, myotonic dystrophy, and others.

Adolescent↗
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↗
PubMedDate not supplied

Prolonged neuromuscular blockade in two critically ill patients treated with atracurium.

Recent literature suggests that the risk of prolonged neuromuscular blockade associated with atracurium compared with other nondepolarizing neuromuscular blocking agents may be minimal. Two patients experienced prolonged weakness associated with the administration of atracurium. Both received atracurium 0.5-0.7 mg/kg/hour in combination with methylprednisolone 500-600 mg/day. Electromyographic results and creatine kinase levels were suggestive of muscular weakness in both patients. Despite high-dose corticosteroid therapy, the electromyographic evidence supporting prolonged weakness did not suggest typical corticosteroid myopathy. Although some clinicians advocate routine administration of atracurium in critically ill patients due to the relative lack of reports of prolonged weakness, this may be premature. Although there are fewer reports of atracurium-associated prolonged weakness compared with pancuronium and vecuronium, the patients we describe suggest that it may occur.

Aged↗
PubMedDate not supplied

Mitochondrial changes in muscle phosphoglycerate kinase deficiency.

X-linked phosphoglycerate kinase (PGK) deficiency is a rare disorder which affects the glycolytic pathway and leads to reduced ATP production. Clinically, PGK deficiency is often associated with nonspherocytic hemolytic anemia and symptoms caused by disturbances of the central nervous system. In addition, myopathy characterized by weakness, cramps, intolerance to exercise, and myoglobinuria has been described in a few cases. We here report on a 23-year-old man who presented with episodes of muscular weakness, cramps, rhabdomyolysis, and renal failure induced by intensive physical exercise. Biochemical analysis of muscle specimens disclosed markedly reduced PGK activity (11.5% compared to normal controls). A moderate increase of glycogen was seen in numerous muscle fibers. Mitochondria in muscle fibers and endothelial cells showed accumulations of glycogen. In muscle fibers unusually large matrix granules were present in several mitochondria. A sural nerve biopsy disclosed scattered large hypomyelinated axons without evidence of demyelination and remyelination. These findings indicate involvement of mitochondria in this case of symptomatic PGK deficiency.

Adult↗
PubMed1994

[High dosage intravenous gamma globulin therapy in juvenile dermatomyositis].

In the last few years high-dose intravenous therapy with gammaglobulin in juvenile dermatomyositis with steroid resistant myopathy has been discussed as an alternative to cytostatic therapy. The 12-year-old Filipinogirl suffered from dermatomyositis with pronounced weakness of the limbs and masticatory muscles; creatinine-kinase was increased 22-fold. After 5 weeks of therapy with prednisolone (1.5 mg/kg body/weight/daily), the creatinine kinase decreased to sixfold of its standard value; the muscular weakness, however, progressed to almost complete paralysis of the scapular abductors and rotators and the coxofemoral flectors and rotators. Additional therapy with gammaglobulin at a dose of 1 g/kg body weight on two consecutive days at 4-week intervals led to complete restoration of muscular strength, normalization of muscle enzymes, and stabilization of these results after 12 courses of gammaglobulin and discontinuation of the steroid medication after 8 courses. This observation suggests that high-dose intravenous application of gammaglobulin represents an efficient therapy with minimal side effects in steroid-resistant juvenile dermatomyositis.

Biopsy↗
PubMed2005

[Occurrence of chloroquine-induced myopathy after low-dose treatment of rheumatoid arthritis for seven years].

The myotoxicity of chloroquine and hydroxychloroquine has been known for decades. Limb-girdle weakness due to a vacuolar myopathy may occur occasionally in a dose-dependent manner during the first 24 months on chloroquine. However, we report on a case in which muscular weakness developed after a daily intake of 250 chloroquine phosphate (= 155 mg chloroquine base) for a period of 7 years. Even after long-term and apparently well-tolerated chloroquine treatment, the occurrence of severe side-effects is possible.

Antirheumatic Agents↗
PubMed1999

Amyotrophic lateral sclerosis: Lou Gehrig's disease.

Amyotrophic lateral sclerosis (ALS), commonly called Lou Gehrig's disease, is a progressive neuromuscular condition characterized by weakness, muscle wasting, fasciculations and increased reflexes. Approximately 30,000 Americans currently have the disease. The annual incidence rate is one to two cases per 100,000. The disease is most commonly diagnosed in middle age and affects more men than women. It usually presents with problems in dexterity or gait resulting from muscle weakness. Difficulty in speaking or swallowing is the initial symptom in the bulbar form of the disease. Over a period of months or years, patients with ALS develop severe, progressive muscular weakness and other symptoms caused by loss of function in both upper and lower motor neurons. Sphincter control, sensory function, intellectual abilities and skin integrity are preserved. Patients become completely disabled, often requiring ventilatory support and gastrostomy. Death usually occurs within five years of diagnosis and is attributed to respiratory failure or cachexia. The etiology of the disease is unknown. Current research is focused on abnormalities of neuronal cell metabolism involving glutamate and the role of potential neurotoxins and neurotrophic factors. New drugs are being developed based on these theories. Current management involves aggressive, individualized alleviation of symptoms and complications.

Amyotrophic Lateral Sclerosis↗
PubMed2001

[New trends in neuropathy practice: clinical approach to CIDP].

Our recent study showed that the overall prevalence of CIDP was estimated as 2.2 per 100,000 population in Aomori Prefecture, in Northan Honshu of Japan. In our series of more than 80 cases with CIDP, a chronic acquired inflammatory demyelinating polyneuropathy, nearly 30% showed clear laterality of weakness, and electrophysiologic laterality or multifocality was apparent in almost all cases. Nearly 90% of patients were able to walk without walking aids or other assistance. Sixty% showed distal dominant muscular weakness. In 12 patients with age of onset under 15, pes cavus deformity was seen in 5. Two thirds complained numbness in the extremities during progressive phase. Four cases initially showed severe sensory ataxia associated with motor conduction block. It should be, thus, reminded that clinical spectrum of CIDP is enormously wide: chronic acquired demyelinating multiple mononeuropathy showing asymmetric involvement (Lewis-Summer syndrome) should be put on one side of the clinical presentation of CIDP. Multifocal motor neuropathy (MMN) is, on the other hand, an unique syndrome mimicking amyotrophic lateral sclerosis (ALS). There may be, however, true association syndrome of CIDP and ALS presenting both peripheral nerve demyelination and pyramidal sign with progressive bulbar involvement. Recently, several atypical varieties of CIDP showing only one-limb involvement, upper limb weakness rather than lower limb power loss, or proximal weakness, etc ... have been reported in the literature. To realize such clinical variations of chronic acquired demyelinating neuropathy is important for early diagnosis and commencement of treatment of CIDP. Clinical guideline for suspicion of CIDP could be useful for general physicians and neurologists unfamiliar to peripheral neuropathies.

Chronic Disease↗
PubMed1983

Right ventricular failure in a patient with diabetic neuropathy (myopathy) and central alveolar hypoventilation.

An unusual patient with hypoxemia, hypercapnia, and right ventricular failure is presented. Minimal skeletal muscle weakness, although present, cannot explain hypercapnia. Muscle biopsy revealed diabetic microangiopathy. Carbon dioxide stimulation demonstrated a diminished hypercapnic ventilatory response. The patient benefited from progesterone therapy. In this unusual patient, mild muscular weakness, caused by diabetes, and central alveolar hypoventilation have acted in synergism to cause abnormal ventilation and right ventricular failure.

Diabetic Neuropathies↗
PubMed1999

Mice with IFN-gamma receptor deficiency are less susceptible to experimental autoimmune myasthenia gravis.

IFN-gamma can either adversely or beneficially affect certain experimental autoimmune diseases. To study the role of IFN-gamma in the autoantibody-mediated experimental autoimmune myasthenia gravis (EAMG), an animal model of myasthenia gravis in humans, IFN-gammaR-deficient (IFN-gammaR-/-) mutant C57BL/6 mice and congenic wild-type mice were immunized with Torpedo acetylcholine receptor (AChR) plus CFA. IFN-gammaR-/- mice exhibited significantly lower incidence and severity of muscle weakness, lower anti-AChR IgG Ab levels, and lower Ab affinity to AChR compared with wild-type mice. Passive transfer of serum from IFN-gammaR-/- mice induced less muscular weakness compared with serum from wild-type mice. In contrast, numbers of lymph node cells secreting IFN-gamma and of those expressing IFN-gamma mRNA were strongly augmented in the IFN-gammaR-/- mice, reflecting a failure of negative feedback circuits. Cytokine studies by in situ hybridization revealed lower levels of lymphoid cells expressing AChR-reactive IL-1beta and TNF-alpha mRNA in AChR + CFA-immunized IFN-gammaR-/- mice compared with wild-type mice. No differences were found for AChR-reactive cells expressing IL-4, IL-10, or TGF-beta mRNA. These results indicate that IFN-gamma promotes systemic humoral responses in EAMG by up-regulating the production and the affinity of anti-AChR autoantibodies, thereby contributing to susceptibility to EAMG in C57BL/6-type mice.

Animals↗
PubMed1984

Improvement of muscle strength after treatment for hyperparathyroidism.

Severe muscular weakness and increased fatigability are occasionally encountered in patients with hyperparathyroidism (HPT). An unselected series of 15 HPT patients was studied to assess if subjective fitness could be associated with detectable muscular dysfunction at objective measurements comparing muscle strength before and after surgery. Significant increase in isokinetic strength of knee extension and knee flexion at higher angular velocities was found three months after surgery, suggesting effect predominantly on type II (fast twitch) muscle fibres. The results of the study support the clinical impression that HPT surgery may be beneficial to patients with muscular symptoms.

Aged↗