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

Centronuclear myopathy, which is unusual because of clinical myotonia, is described in two sisters. The diagnosis was established in adult life, but the first symptoms were noticed in infancy. The outstanding points of the clinical picture were mild amyotrophy, paresis, and clinical myotonia.
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PMID:Myotonia in centronuclear myopathy. 15 83

Sixteen cases of juvenile, non-progressive muscular atrophy localized in the hand and forearm were seen at our neurology out-patient clinic for the past 8 years. The analyses of these 16 cases disclosed characteristic features as follows: 1) juvenile onset 2) male preponderance 3) unique distribution of muscular atrophy and weakness in the hand and forearm. 4) insidious onset, initial progressive period and subsequent non-progressive course 5) tendon reflexes of the arms are hypoactive in half of the cases 6) no pathological reflexes 7) cold paresis 8) no definite sensory disturbance 9) no cranial nerve involvement 10) neurogenic patterns on EMG According to these features, this clinical entity carrying good prognosis must be differentiated from several diseases associated with similar muscular atrophy of extremities, especially amyotrophic lateral sclerosis which is notorious as a fetal disease.
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PMID:[Juvenile, non-progressive muscular atrophy localized in the hand and forearm. Report of 16 cases (author's transl)]. 54 13

1. In every case of a vocal cord paresis, its cause should be carefully sought. 2. "Pseudopareses" of the vocal cord can be excluded by electromygraphy. 3. In all cases of neurogneic vocal cord praeses and regardless of aetiology, immediate phoniatric training is indicated for acceleration of nerve regeneration as well as electrostimulation for the prevention of muscular atrophy and ankylosis of the cricoarytenoid joint. 4. If such therapy is neglected, the functional results of spontaneous regeneration, neurolysis and nerve plasty are doubtful. 5. If in cases of mechanical lesions of the recurrent nerve one decides to operate, electromyography of the larynx and a mobility test of the cricoarytenoid joints to be done first. 6. Compression or overstretching of the nerve should be followed by neurolysis after 5 months, unless the nerve has regenerated spontaneously. 7. When the recurrent nerve has had to be served it should be repaired by anastomosis as soon as possible. 8. Judging by our experience in regeneration of the laryngeal nerves, we feel that operations for opening or closure of the glottis are indicated only after 2 years.
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PMID:[Indication and timing of conservative surgery of peripheral neurogenic vocal cord pareses (author's transl)]. 108 85

We reported a 49-year-old mother and her 28-year-old son with autosomal dominantly inherited bulbar spinal muscular atrophy (AD-BSMA). They showed progressive bulbar paresis, muscle wasting and weakness dominant in the proximal groups of limb muscles, and finger tremor. Onset of illness was in adult life. In laboratory examinations, elevated creatine kinase in serum and neurogenic changes either in EMG or muscle biopsy were noted. The son had neither gynecomastia nor abnormal sexual hormone levels which were observed in the sex-linked recessive bulbar spinal muscular atrophy (SR-BSMA). Elongation due to the CAG repeats at the androgen receptor gene of the X chromosome in SR-BSMA was not detected. In conclusion, it is clear that AD-BSMA is different from SR-BSMA on the basis of clinical and genetical aspects.
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PMID:[A mother and her son with autosomal dominant bulbar spinal muscular atrophy]. 130 Feb 63

The authors provide the reported data concerned with differential diagnosis of hereditary and sporadic neuralgic amyotrophy. Describe own observations where members of the same family (mother and son) suffered from neuralgic amyotrophy. Attention is concentrated on the fact that in both cases, the disease started at the preschool age and was of recurrent nature. In the mother, an attack of neuralgic amyotrophy occurred in the postnatal period, in the son, successive exacerbation of the disease occurred in the form of 4 consecutive attacks of neuralgic amyotrophy which provoked deep paresis of the muscles of the shoulder girdle and both hands. After 1.5 years the muscles indicated practically regained their power.
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PMID:[Familial neuralgic amyotrophy]. 133 25

The report describes seven SMA-cases in descendents of crossbreeds of American Brown Swiss x Deutsches Braunvieh. Symptoms and course: After initially normal development of the calves for one to six weeks the disease set in suddenly followed by a rapid lethal course of one to one and a half weeks duration due to asphyxia and/or secondary diseases. Only one case was reported having been sick since birth (?). Characteristic signs were rapidly progressing muscular atrophy, paresis and paralysis of the limbs, the trunk and the diaphragm, usually accompanied by progressive dyspnoea. Signs of congenital neuromyodysplasia (arthrogryposis) of different degree were present in four of the seven calves. Six calves had contracted a secondary pneumonia. Blood gas analysis (6/7) revealed a compensated (1x) or decompensated (4x) respiratory acidosis. Neurohistological findings: Degeneration and loss of motor neurons in the ventral horns of the spinal cord and neurogenic muscular atrophy. Immunohistochemistry revealed a pronounced accumulation of type 200 kD-neurofilaments in perikarya and dendrites of ventral horn motoneurons indicating disturbed mechanisms of the axonal transport. The disease seems to be inherited as a recessive trait.
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PMID:[Spinal muscle atrophy in Brown Swiss x Braunvieh cross calves]. 163 59

Clinical and epidemiologic analyses of PPMA in Japan based on the nation-wide case survey were reported, and differences between PPMA and ALS were discussed. The present survey covering the years from 1984 through 1991 cited 42 PPMA cases (30 male:12 female). The absolute incidence of PPMA is estimated 0.12/10(5) of the Japanese population (about 150 cases in total), which indicates 0.5% of the polio survivors. In Japan an actual increase of patients is noticed in these 10 years, which reflects the big epidemic of polio around 1950-60. The antecedent poliomyelitis occurred at the mean age of 2.6, mostly between 1940 and 1960. Residual paralysis was generally absent or only minimal. Late muscular atrophy and weakness were noticed at age from 16 to 63 y (mean:41.5), with the mean latency of 40.1 years after polio. Both polio-affected and unaffected site of the limb were equally involved by PPMA, but the left leg tends to be predominantly involved. Neurological symptoms were summarized as an asymmetrical proximal muscular atrophy and flaccid motor paresis in one or two limbs with decreased tendon reflexes. Fasciculation in 45.2%, myalgia in 28.6%, and hypesthesia in 28.5% were noticed. Electromyography and muscle CT scan showed marked selective neurogenic changes. In most cases symptoms are stable or slowly progressive, with some recovery by rest or rehabilitation and deterioration by over work and/or trauma. On regarding these clinical features, PPMA is essentially different from classical ALS. Long-term hyperfunction of survived neurons with potential fragility by polio infection is suspected to mediate PPMA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Post-poliomyelitis late progressive muscular atrophy (PPMA)--clinical analyses of Japanese cases]. 181 99

Nine puppies suffered from progressive paresis with muscle wasting, hyporeflexia and extensor rigidity. CK-activity in serum was elevated and electrodiagnostic findings were indicative of lower motor neuron disease. Although lesions were also found in the CNS, additional neurological signs were rare, but CSF examination revealed the presence of inflammatory lesions. On pathologic examination, all animals had a disseminated necrotizing myositis. In addition, a disseminated encephalomyelitis was found as well as, in 2 cases, a neuritis. In the lesions of 6 animals protozoal organisms were found which were immunocytochemically identified as Neospora caninum. Our results show that the protozoal myositis-encephalitis syndrome in puppies can be diagnosed in the clinic with high probability. A clinical differentiation between toxoplasmosis and Neospora caninum infection is presently difficult.
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PMID:[The clinical diagnosis of protozoal myositis syndrome (Neospora caninum) of puppies]. 188 44

Benign, monomelic juvenile amyotrophy of the hand (Hirayama type): new data.--Within the space of a few months a 21-year-old man developed isolated amyotrophy and paresis of the right hand; thirteen years later the clinical picture was unchanged. Medullo-cervical MRI was normal. The EMG confirmed the involvement of the anterior horn. Unilateral chronic distal juvenile amyotrophy located in an upper limb (Hirayama type) was diagnosed on clinical findings. But the spread of electrical abnormalities to the lower limbs suggested a transitional form between this syndrome and other disorders of the anterior horn.
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PMID:[Benign, monomelic juvenile amyotrophy of a hand (Hirayama type): a new case report]. 211 28

In 33 patients, 30 to 64 years old, with spinal amyotrophy and brachial paresis, the sensory symptoms and electrophysiologic signs were analyzed. The paresthesias were felt most often in the ulnar nerve innervation region. The motor conduction velocities, terminal latency quotient, sensory conduction on direct nerve stimulation were within the limits of normal in both median and ulnar nerve. On percutaneous stimulation normal values were obtained for median nerve, and significantly slower for ulnar nerve innervation region. In four cases no nerve potential was obtained over the ulnar nerve with stimulation of the fifth finger. The nerve potential over the ulnar nerve was elicited mostly by stimulation of median nerve innervated fingers. Congenital variations of sensory innervation pattern were considered, which may increase the liability to destruction.
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PMID:Electrophysiologic signs of sensory fiber lesion in spinal amyotrophies and the role of physiologic variations of sensory finger innervation pattern. 222 70


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