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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After atraumatic birth, three neonates presented with muscle hypotonia and weakness. Flaccid paresis of the upper extremities, spasticity of the lower extremities, dissociate sensory loss and autonomic dysfunction developed later. This ruled out the initial, tentative diagnoses of cerebral palsy, spinal muscular atrophy or hereditary neuropathy. Diagnostic imaging revealed marked thinning of the cervical spinal cord in all patients. The possible aetiology of these lesions is considered. In all cases, an antenatal or perinatal infarction is thought to be the most probable cause. Different clinical pictures following intrauterine spinal cord ischemia are discussed. Spinal cord lesion must be considered even after atraumatic birth.
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PMID:Cervical spinal cord atrophy in the atraumatically born neonate: one form of prenatal or perinatal ischaemic insult? 1269 May 68

Patients with juvenile muscular atrophy of distal upper extremity (Hirayama's disease) often show marked weakness of the fingers occurring with exposure to cold. We term this phenomenon cold paresis. We conducted an original test to induce cold paresis (Cold Paresis Inducement Test) in 11 patients of this disease and 10 normal controls. Cold paresis was induced in 9 of 11 patients, but was not induced in the 2 patients who had the disease longer than 20 years and in all normal controls. We examined the electromyogram of abductor digiti minimi during 5 Hz and 20 Hz rate of ulnar nerve stimulation at cooling. The patients in whom cold paresis was induced exhibited a waning of amplitude of compound muscle action potential (M wave) during 20 Hz stimulation. This waning was aggravated by intravenous administration of anticholinesterase (edrohponium). We found a remarkable conduction delay of M waveform at the waning by means of waveform analysis. These results suggest that cold paresis may be caused by a conduction block of the muscle fiber membrane in re-innervating muscles after active denervation.
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PMID:[Symptomatological and electrophysiological study on cold paresis in juvenile muscular atrophy of distal upper extremity (Hirayama's disease)]. 1271 82

Subacute motor neuropathy involving bulbar nerves is an unusual complication of hyperthyroidism. Clinical and neurophysiologic follow-up of such patients has been rarely reported. We describe a 41-year-old Colombian patient who developed respiratory failure associated with motor neuropathy and severe weight loss. The major clinical features included diffuse amyotrophy, bilateral facial paresis, and fasciculations, suggesting motor neuropathy. Electromyography confirmed the presence of axonal neuropathy, with predominant motor involvement. Goiter with hypervascularization was noticed, associated with pure T3 hyperthyroidism (T3l=26 pg/ml; N<3.8). The patient was given carbimazole which induced a severe skin vasculitis 10 days later. Carbimazole was stopped and replaced by propylthiouracile, which also induced vasculitis with secondary cardiac failure. Total thyroidectomy was then performed. General status improved rapidly as well as motor deficit, amyotrophy and pyramidal syndrome. Electromyographic abnormalities improved significantly within 3 months. This observation demonstrates that hyperthyroidism can produce motor axonal neuropathy, curable with radical surgery.
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PMID:[Subacute motor neuropathy induced by T3 hyperthyroidism]. 1473 39

Schwannomas were diagnosed in twelve dogs and five cats at Massey University Small Animal Clinic and Hospital over a 15-year period (1977-92). A further two feline cases were reported at the Batchelar Animal Health Laboratory. In six dogs, the tumour involved nerves of the brachial plexus. Clinical signs observed in these dogs were forelimb lameness, muscle wasting and pain on movement of the affected limb or neck. Hindlimb paresis was observed in two dogs. Surgical excision of the brachial plexus tumour was attempted in one dog, leading to an 8-month remission of signs. In one dog, the tumour involved the sacral nerves, and in two dogs the cranial nerves were affected. Three dogs had skin nodules. Seven of the twelve affected dogs were destroyed. In five cats, the tumours developed on the carpus, tarsus or interdigital area of a forelimb or hindlimb as a slowly developing nodular lesion. In the other two cats, the site of the tumour was the flank and the lateral thigh respectively. Surgical excision of the tumour was successful in three cats.
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PMID:Nerve sheath tumours in the dog and cat. 1603 48

A growing number of therapeutic agents and exogenous toxins are harmful to structure and function of human skeletal muscle. The clinical syndrome encompasses asymptomatic creatine kinase elevation, myalgia, exercise intolerance, muscle paresis and atrophy, and lastly acute rhabdomyolysis. Toxic myopathies are potentially reversible, hence a prompt recognition is particularly helpful for the early diagnosis and in conclusion elimination of a myopathy inducing toxin. Toxic myopathies may be classified as acute or chronic accordingly to the exposition time to a toxin. Main source of an exogenous induced toxic myopathy is chronic alcohol abuse. Alcohol excess induces acute and/or chronic neuropathy and myopathy, consequently muscle wasting and weakness occurs. Drug-induced myopathies are most frequently seen due to amplified utilization of corticosteroids or lipid lowering agents.
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PMID:[Lipid lowering drug and other toxic myopathies]. 1615 87

We investigated the symptoms, course and prognosis of neuralgic amyotrophy (NA) in a large group of patients with idiopathic neuralgic amyotrophy (INA, n = 199) and hereditary neuralgic amyotrophy (HNA, n = 47) to gain more insight into the broad clinical spectrum of the disorder. Several findings from earlier smaller-scale studies were tested, and for the first time the potential differences between the hereditary and idiopathic phenotypes and between males and females were explored. Generally, the course of the pain manifests itself in three consecutive phases with an initial severe, continuous pain lasting for approximately 4 weeks on average. Sensory involvement was quite common and found in 78.4% of patients but was clinically less impairing than the initial pain and subsequent paresis. As a typically patchy disorder NA can affect almost any nerve in the brachial plexus, although damage in the upper and middle trunk distribution with involvement of the long thoracic and/or suprascapular nerve occurred most frequently (71.1%). We found no correlation between the distribution of motor and sensory symptoms. In INA recurrent attacks were found in 26.1% of the patients during an average 6 year follow-up. HNA patients had an earlier onset (28.4 versus 41.3 years), more attacks (mean 3.5 versus 1.5) and more frequent involvement of nerves outside the brachial plexus (55.8 versus 17.3%) than INA patients, and a more severe maximum paresis, with a subsequent poorer functional outcome. In males the initial pain tended to last longer than it did in females (45 versus 23 days). In females the middle or lower parts of the brachial plexus were involved more frequently (23.1 versus 10.5% in males), and their functional outcome was worse. Overall recovery was less favourable than usually assumed, with persisting pain and paresis in approximately two-thirds of the patients who were followed for 3 years or more.
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PMID:The clinical spectrum of neuralgic amyotrophy in 246 cases. 1637 10

Juvenile muscular atrophy of the distal upper extremity (JMADUE, Hirayama disease) was first reported in 1959 as 'juvenile muscular atrophy of unilateral upper extremity'. Since then, similar patients in their teens or 20s have been described, under a variety of names, not only in Japan, but also in other Asian countries, as well as Europe and North America. Biomechanical abnormalities associated with JMADUE have recently been reported through various imaging examinations, proposing its disease mechanism. Since JMADUE differs from motor neuron disease, or spinal muscular atrophy, this disease entity should be more widely recognized, and early detection and effective treatments should be considered. We report an epidemiological study in Japan. Two nationwide questionnaire-based surveys, conducted in Japan from 1996 to 1998, identified 333 cases. The numbers of patients per year, distribution of ages at onset, mode of onset, time lapse between onset and quiescence, neurological signs and symptoms, imaging findings, and the effects of conservative treatments were analyzed. The peak age was 15 to 17 years, with a marked male preponderance, usually a slow onset and progression, and quiescence six or fewer years after onset. There was a predominantly unilateral hand and forearm involvement with 'cold paresis'. The imaging findings are described.
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PMID:Nationwide survey of juvenile muscular atrophy of distal upper extremity (Hirayama disease) in Japan. 1654 58

A 47-year-old male presented with painful swelling of the right calf. His medical history was negative, except for a herniation of disc LIV-V 5 years before. Physical examination revealed unilateral calf hypertrophy with moderate weakness of plantarflexion, mild paresis of dorsiflexion. Electromyography showed a peripheral neurogenic lesion in the right anterior tibial muscle, but normal findings were obtained from the unaffected quadriceps muscle. Histological examination of the right gastrocnemic muscle showed neurogenic changes with typical targetoid fibers, but no pathological changes were present in the quadriceps muscle. Chronic asymmetric spinal muscular atrophy is an infrequent neuromuscular disease and because of asymmetric appearance, it might be difficult to distinguish from other, acquired neurogenic muscle diseases such as radiculopathy caused by intervertebral disc herniation. Our case confirms that muscular hypertrophy can follow partial denervation in humans.
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PMID:Asymmetric calf hypertrophy of neurogenic origin. 1718 92

Spontaneous and experimental poisoning with the swainsonine-containing and calystegine-containing plant Ipomoea carnea subsp fistulosa is described. Three of 8 goats presenting with emaciation, weakness, symmetrical ataxia, posterior paresis, proprioceptive deficits, abnormal posture, abnormal postural reaction, and muscle hypertonia were necropsied. I fistulosa was suspected to be the cause of the neurologic disease in all cases. An experiment was conducted to confirm the diagnosis using 12 goats and diets containing 3 different concentrations of the plant. All goats fed I fistulosa developed neurological signs that were similar to those observed in the spontaneous intoxication. Muscle atrophy and pallor were the only macroscopic changes observed in spontaneous and in experimental intoxication. Histological lesions of spontaneous and experimental animals were similar. The most prominent lesion was cytoplasmic vacuolation in neurons of the central and the autonomous nervous system, pancreatic acinar cells, hepatocytes, Kupffer cells, follicular epithelial cells of the thyroid gland, and macrophages of the lymphatic tissues. Neuronal necrosis, axonal spheroids formation, and astrogliosis were additionally observed in the brain. Ultrastructurally, the cytoplasmic vacuoles consisted of distended lysosomes surrounded by a single-layered membrane. Nonreduced end-rests or sequence of alpha-Man, alpha-Glc, beta(1-4)-GlcNAc, and NeuNAc on lysosomal membrane were revealed by lectin histochemistry. Samples of plants used in the experimental trial contained swainsonine and calystegine and their intermediary derivate. We conclude that I fistulosa induces a glycoprotein storage disease primarily based on the inhibition of the lysosomal alpha-mannosidase by the alkaloid swainsonine.
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PMID:Spontaneous and experimental glycoprotein storage disease of goats induced by Ipomoea carnea subsp fistulosa (Convolvulaceae). 1731 94

Monomelic amyotrophy (MA) is a rare condition in which neurogenic amyotrophy is restricted to an upper or lower limb. Usually sporadic, it usually has an insidious onset with a mean evolution of 2 to 4 years following first clinical manifestations, which is, in turned, followed by stabilization. We report a case of 20-years-old man who presented slowly progressive amyotrophy associated with proximal paresis of the right upper limb, which was followed by clinical stabilization 4 years later. Eletroneuromyography revealed denervation along with myofasciculations in various muscle groups of the right upper limb. We call attention to this rare location of MA, as well as describe some theories concerning its pathophysiology .
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PMID:Benign monomelic amyotrophy with proximal upper limb involvement: case report. 1766 29


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