Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cervical radiculopathy unaccompanied by pain or sensory disorder but manifested only by paresis, atrophy, fasciculation, and reflex loss is unusual. Three such cases are presented. Considerable diagnostic difficulty may arise in distinguishing patients presenting with these features from those who have primary motor neuron disease. Two additional case reports demonstrate that this distinction is not always possible. Diagnosis, management, and prognosis are discussed. Differentiation between motor neuron disease and spondylosis will avert needless surgery in the former group and will result in beneficial, sometimes curative surgery in the latter group.
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PMID:Cervical spondylotic radiculopathy producing motor manifestations mimicking primary muscular atrophy. 53 45

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

Clinical analysis of 378 acute cases of Malathion insecticide intoxication and pathological and histochemical investigation of skeletal muscles in 7 autopsied victims of acute poisoning have revealed the pronounced neuromuscular disorders. Generalized paresis and paralysis of muscles were observed in trunk and limbs. Muscular fasciculation, hypotonia and hyporeflexia were also generalized. Multiple foci of muscular fibers necrosis and necrobiosis were found with intermuscular nerves and motor endings degenerated, neuromuscular junctions cholinesterase sharply inactivated.
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PMID:[Clinico-morphologic and histochemical changes in the neuromuscular apparatus in acute carbophos poisoning]. 318 79

A case of intracranial hypoglossal neurinoma is reported. A 32-year-old man with a history of unsteady gait and headache for one and a half years was admitted to our hospital on September 23, 1983. Neurological findings on admission were nystagmus toward the left, left IXth and Xth cranial nerve paresis, left cerebellar signs, paresthesia of the left upper and lower extremities on neck flexion, and left pyramidal signs. Atrophy or fasciculation of the tongue was not noted. Computed tomography demonstrated a large isodensity and partially low density mass in the posterior fossa which was markedly enhanced and sharply margined with contrast medium. The tumor extended 45 mm over the edge of the foramen magnum. The maximum size was 45 mm X 40 mm. The coronal and sagittal reconstruction CT scan clearly demonstrated the attachment and extension of the tumor. Enlargement of the hypoglossal canal was clarified by changing the window level, window width and using 2 mm slice CT scan. Anterior-posterior x-ray view of the skull tomography showed enlargement of the hypoglossal canal, as indicated by the CT scan. The left hypoglossal canal was 7 mm and right was 3 mm in diameter. Vertebral angiography demonstrated that the tumor was located in the left posterior fossa, but no tumor stain appeared. This patient did not have XIIth cranial nerve palsy, but the neuroradiological findings strongly suggested a hypoglossal neurinoma, especially the findings of the CT scan and the anterior-posterior x-ray view of the skull tomography. On October 5, suboccipital craniotomy with Cl laminectomy was performed in prone position.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of intracranial hypoglossal neurinoma]. 380 8

Gracile axonal dystrophy (GAD) is an inherited neurodegenerative disease in the mouse with progressive sensory ataxia and motor paresis. Electromyographic examination was conducted in 25 unanaesthetized GAD mice and 24 controls of the same strain during 6, 9 and 12 wk of postnatal life. Among 9 and 12 wk old mice, about 75% showed resting spontaneous activities--either fibrillation or fasciculation or both. On stimulation of the tibial nerve at ankle, with single pulse, the EMG showed repetitive muscle potentials of large amplitude, following "M" response. The frequency and duration of the train of these stimulus--induced repetitive muscle potentials (SIRMP) were almost constant in a given animal. The SIRMP failed to reappear in response to the second stimulus within 5 s when twin pulses were applied or within 5 min when tetanic stimuli were applied, indicating their fatigability. It is concluded that the SIRMP originate from immature, supplementary motor endplates that develop at ultraterminal nerve sproutings induced by denervation and reinnervation and possibly are due to hyperexcitable trigger points in the peripheral nerve endings. The EMG abnormalities in the GAD mouse are very much similar to those observed in human syndromes with hyperexcitable peripheral nerves that result in sustained muscle activity like neurotonia and hence the GAD mouse is a good model of such motor abnormalities in man.
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PMID:Stimulus induced repetitive muscle potentials in the gracile axonal dystrophy (GAD) mouse. 755 27

We report a 54-year-old man with progressive generalized muscle atrophy and ophthalmoparesis in the terminal stage. He was well until 44 years of age (1982) when he noted weakness in his right hand and muscle atrophy; in May of 1985, he noted weakness in his left hand and in both legs. His weakness had become progressively worse, and he became unable to walk in November of 1985. He noted dysarthria one month later, and dysphagia in March of 1986. His difficulty in swallowing had also become worse; he regurgitated foods into the trachea in September of that year, and he developed a low grade fever on the same day. He was admitted to our service on September 24, 1987. On physical examination, general findings were unremarkable, except for low grade fever (37.3 degrees C). On neurologic examination, he was alert and mentally sound. He had normal vision and visual fields; ocular movements were normal. He had moderate weakness in facial muscles, dysarthria, dysphagia, and atrophy in his tongue. He had marked generalized muscle atrophy with fasciculation. He was unable to stand or walk. His muscle strength was not more than 1/6 in any part. The lower extremities were spastic. Deep reflexes were exaggerated in both lower extremities but were normal in upper extremities. Sensation was intact. Laboratory examination was unremarkable, and so was the cranial CT scan. He was treated with nasogastric feeding. He was able to communicate smoothly using his eyes, but a restriction in the vertical gaze was noted in February of 1989. The range of ocular movement was better in the oculocephalic reflex compared with his spontaneous vertical eye movements. In April of 1990, his horizontal gaze also had become slow, and he was complicated by bronchial asthma. He was treated with 20 mg/day of prednisolone; after the institution of prednisolone, his horizontal eye movement showed much improvement. In the terminal stage, he was able to move his eyes only very slowly; vertical gaze was impossible. His subsequent course was complicated by respiratory tract infection and septicemia, and he expired on July 15, 1992. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that this patient had amyotrophic lateral sclerosis with oculomotor paresis. Post-mortem examination revealed spongy change involving the posterior column and the posterior spinocerebellar tract, in addition to severe degenerative change in the upper and the lower motoneurons, which were consistent with amyotrophic lateral sclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 54-year-old man with generalized muscle atrophy and oculomotor paresis]. 799 50

A 22-year-old female noted a low grade fever and swelling of the cervical lymph nodes in May 1997, and later developed a dry cough. She was diagnosed to have interstitial pneumonitis, and then administration of corticosteroids alleviated her symptoms. On February 6, 1998, however, a high fever recurred and her swollen cervical lymph node on the right side was biopsied on February 9, 1998. A histological examination revealed an increased number of histiocytes and karyorrhexis of the lymphocytes in the paracortical areas, and she was therefore diagnosed to have histiocytic necrotizing lymphadenitis. She could not fully elevate her arm on February 16, 1998. On admission, her cervical lymph node was swollen on the left side. A neurological examination revealed a marked weakness of the right deltoid muscle, moderate weakness of the right latissimus dorsi, triceps and brachioradialis muscles and also a mild weakness of the serratus anterior, supra- and infra-spinatus, and biceps brachii muscles. The muscle power of the other muscles were normal and no muscle atrophy was evident. Winging of the right scapula was observed. The deep tendon reflexes were normal in all four limbs, and her sensation was also normal. No cerebellar sign was found. The Jackson, Spurling, Allen, Morley and Adson tests were all negative. ESR was mildly elevated to 18 mm/hr, but CRP was negative. RF, ANA and anti-SS-A and SS-B antibodies were positive, whereas LE-test, direct and indirect Coombs tests and other autoantibodies were negative. Needle EMG disclosed fasciculation potentials in the right triceps muscle and polyphasic waves in the right deltoid muscle. MRI showed gadolinium-enhancement of the right brachial plexus. Although an abnormal accumulation of gallium was detected in the right parotid and bilateral submandibular glands, no sicca symptoms were found and the Schirmer test findings were normal. Oral prednisolone (50 mg/day with gradual tapering) alleviated both her symptoms and the gadolinium-enhancement of the right brachial plexus. As a result, her right upper limb paresis was thus considered to have been caused by right brachial plexus neuritis, which was probably associated with histocytic necrotizing lymphadentis. Although acute cerebellar ataxia and meningitis have previously been reported to be complicated with histiocytic necrotizing lymphadenitis, this is the first report to describe the complication of peripheral neuritis with this condition.
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PMID:[A case of subacute necrotizing lymphadenitis complicated with brachial plexus neuritis]. 1020 79

A 34-year-old woman presented with numbness in both lower limbs and weakness of right lower limb twenty six days after a primary varicella infection (chickenpox) associated with fever and rash. Neurological examination revealed numbness of both lower limbs, more severe on the right side, mild paresis of the right lower limb, particularly in the tibialis anterior muscle, and absent ankle jerk on the right. After admission, hyperalgesia appeared at the thoracic 10-12 levels. The T2-weighted MRI of the spinal cord revealed a high signal intensity lesion at the Th 9 level and gadolinium enhancement was seen in that lesion as well as in the bilateral posterior radicles and the left anterior radix at the Th 9 level. On needle electromyography, fasciculation was found in the right tibialis anterior and gastrocnemius muscles. The temporal dispersion of F-wave was seen in the right peroneal nerve. We diagnosed the patient suffered from radiculomyelitis following the primary varicella infection. The secondary immunological mechanism rather than direct viral invasion is most likely in our patient, because (1) neither VZV DNA, nor anti-VZV antibody was positive in the CSF, and (2) the duration was relatively long between the development of skin rash and that of neurological symptoms.
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PMID:[A case of radiculomyelitis following chickenpox in adulthood]. 1058 25

X-linked spinal and bulbar muscular atrophy or Kennedy's disease is an adult-onset motor neuronopathy caused by a CAG repeat expansion within the first exon of an androgen receptor gene. We report the case of a 66-year-old man, previously diagnosed with motor neuron disease (MND), who presented acute and reversible left vocal fold (dysphonia) and pharyngeal paresis, followed by a slowly progressive weakness and also bouts of weakness, wasting and fasciculation on tongue, masseter, face, pharyngeal, and some proximal more than distal upper limb muscles, associated to bilateral hand tremor and mild gynecomastia. There were 5 electroneuromyography exams between 1989 and 2003 that revealed chronic reinnervation, some fasciculations (less than clinically observed) and rare fibrillation potentials, and slowly progressive sensory nerve action potentials (SNAP) abnormality, leading to absent/low amplitude potentials. PCR techniques of DNA analysis showed an abnormal number of CAG repeats, found to be 44 (normal 11-34). Our case revealed an acute and asymmetric clinical presentation related to bulbar motoneurons; low amplitude/absent SNAP with mild asymmetry; a sub-clinical or subtle involvement of proximal/distal muscles of both upper and lower limbs; and a probable evolution with bouts of acute dennervation, followed by an efficient reinnervation.
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PMID:X-linked spinal and bulbar muscular atrophy (Kennedy's disease) with long-term electrophysiological evaluation: case report. 1583 83

We report a rare case of multiple cranial nerve palsy associated with pregnancy, the cause of which remained to be clarified despite of extensive inspections. A 28-year-old woman with type 1 diabetes on insulin therapy developed left oculomotor nerve palsy in the fourth month of pregnancy. Her symptoms improved after one month's administration of vitamins B1 and B12. Numbness appeared in the left side of the face in the 8th month of pregnancy, and then moved to the right side in two weeks. Dysarthria and dysphagia occurred one month later. Bulbar symptoms were worsened, and she became unable to eat or drink. Neurological examination revealed disturbance of sensation in the right side of the face, soft palate paresis, and bilateral atrophy and fasciculation of the tongue. Extensive laboratory examinations including immunological and endocrinological studies, cerebrospinal fluid examination and brain magnetic resonance imaging were unremarkable. These symptoms remitted spontaneously after delivery, and the methylprednisolone pulse therapy accelerated the improvement. Neurological examination done one year after delivery showed complete recovery of the symptoms except for persistent tongue atrophy.
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PMID:[Recurrent multiple cranial nerve palsy in a gravida with type 1 diabetes, that remitted after delivery and with steroid therapy]. 1893 78


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