Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case is presented of a 26-year-old male with a 8-day history of fever and back pain, and limb weakness beginning 24 hours before admission. An abscess caused by a staphylococcus aureus was localised in the thoracic paravertebral region with penetration in the subarachnoidal space at T1. Myelography appeared to be superior to CAT-scan and NMRI of the cervico-thoracal region in supporting the diagnosis. Treatment by laminectomy of C7-T3 48 hours after admission did not lead to neurological improvement and an incomplete tetraplegia persisted. The importance and difficulty of early diagnosis is stressed.
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PMID:Epidural abscess causing tetraparesis: case report. 380 47

The authors present three cases where the involuntary, imotivated laughter was a distinct finding. The first patient was a 29-year-old engineer, who had had several bursts of neurologic deficits, either sensitive or motor, which recovered almost completely and was diagnosed as suffering from multiple sclerosis. During and after one of the episodes he presented involuntary laughter and has been like this since then, albeit in much less extension. The second patient was a 35-year-old housewife, who presented several episodes of brain infarction in both hemispheres which were considered as being the result of arteritis. No specific collagen disease was found. The CAT scan showed several hypodense areas in both hemispheres. The third patient was a 52-year-old man of Japanese ancestry who presented three years ago a sudden ischemic stroke with difficulty in the speech and left sided weakness, followed by bursts of imotivated laughter, which persisted since then. Subsequently he had another stroke. He is hypertensive and diabetic. The authors searched the literature for the different causes of involuntary laughter. The occurrence in multiple sclerosis, although reported by several authors is by no means a common finding. In the literature available no case of cerebral arteritis with involuntary laughter could be found. The pathophysiology of this rare symptom was discussed.
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PMID:[Imotivated laughter: report of 3 cases]. 401 40

Postpartum amenorrhea associated with other symptoms and signs of hypopituitarism, such as inability to lactate, weakness, easy fatigability, sexual-hair loss, and clinical evidence of hypothyroidism, were found in two female patients with the antecedent of postpartum hemorrhage. The baseline values of the gonadal, thyroid, and glucocorticoid hormones were all consistently lower than normal. The serum levels of the pituitary hormones were low, and the responses to standard stimulatory tests were either insignificant or blunted. Plane skull films and conventional sella tomography did not reveal any abnormality in the sella turcica. CAT identified hypodensity in the area of the hypophysis with preservation of the pituitary stalk. The combination of the failure of provocative stimuli to affect anterior pituitary hormone release with the radiologic picture compatible with pituitary infarction readily makes the diagnosis of Sheehan's syndrome in vivo and should be used in patients where this syndrome is suspected.
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PMID:Sheehan's syndrome: in vivo diagnosis with the use of computerized axial tomography and pituitary provocative testing. 631 3

Primary amebic meningoencephalitis and granulomatous amebic encephalitis are well recognized clinicopathological entities caused by free-living amebas. Associated arteritis and "mycotic aneurysms" with infiltration of intracranial arteries by lymphocytes, amebic trophozoites and cysts have not been previously reported. A 26-month-old girl had a 3-week history of encephalitis, characterized, initially, by vomiting and low-grade fever. Subsequently, she developed ataxia, generalized weakness, lethargy, and esotropia. The first CSF showed 490 RBC/microliters, 705 WBC/microliters with 90% mononuclears. Her pupils reacted briskly to light. Moderate nuchal rigidity, nystagmus, fixed downward gaze, anisocoria, bilateral 6th nerve palsy, left arm monoparesis and left Babinski were present. CAT scan revealed slight symmetrical dilatation of anterior horns of lateral ventricles and an area of abnormal enhancement above the 3rd ventricle. She died 14 days after admission, 5 weeks after onset of symptoms. The brain showed focal necrotizing encephalopathy, involving thalami, cerebellum, brain stem, and cervical and upper thoracic spinal cord. Numerous free-living amebic trophozoites and cysts were present within a chronic granulomatous encephalitis. There were trombosis of basilar, posterior cerebral, and vertebral arteries with profuse chronic panarteritis, fibrinoid necrosis, and mycotic aneurysms.
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PMID:Granulomatous encephalitis, intracranial arteritis, and mycotic aneurysm due to a free-living ameba. 689 86

The 19 S promoter of cauliflower mosaic virus was analyzed in host protoplasts. In spite of its weakness, it contains a fully functional core promoter. It can be strongly activated by 35 S enhancer elements, even when these elements are located downstream of it, comparable to the situation in the viral genome. The 19 S promoter also contains an element that can strongly enhance expression from a heterologous core promoter. A plasmid expressing the same CAT ORF from two overlapping transcription units, a dicistronic one under control of the 35 S promoter and a monocistronic one under control of the 19 S promoter, was constructed. While in the absence of the virus ORF VI product (pVI, "transactivator") only low levels of CAT activity deriving from the 19 S promoter were observed, in the presence of this protein high levels of CAT activity derived from the 35 S unit were observed in addition. This suggests autocatalytic activation of pVI expression during virus infection.
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PMID:Transcription from the CaMV 19 S promoter and autocatalysis of translation from CaMV RNA. 831 97

Dominant mutations in the copper/zinc superoxide dismutase (SOD1) gene have been observed in 15-20% of familial amyotrophic lateral sclerosis (FALS) cases. The mechanism by which SOD1 mutations result in motor neuron degeneration in FALS mice partly involves oxidative damage and an increased peroxidase activity of the mutant SOD1. A new therapeutic approach designed to eliminate the substrate of this peroxidase activity was examined in two lines of transgenic mice expressing the FALS-linked mutation glycine to alanine (G93A). We investigated the ability of putrescine-modified catalase (PUT-CAT), an antioxidant enzyme that removes hydrogen peroxide and has increased permeability at the blood-brain barrier, to modify the time course of the SOD1 mutation-induced motor neuron disease in these FALS mice. Continuous, subcutaneous administration of PUT-CAT significantly delayed the age at which onset of clinical disease occurred (indicated by loss of splay and/or tremors of hindlimbs) in a high-expressor line of FALS transgenic mice. Intraperitoneal injection of PUT-CAT given two times per week also significantly delayed the onset of clinical disease in a low-expressor line of FALS mice. PUT-CAT also significantly delayed the age at which clinical weakness developed (quantified by measuring the shortening of stride length) in both lines of FALS animals. No significant changes were observed in the survival times of the high-expressor FALS mice in any of the treatment groups. However, a trend toward a prolongation of survival was observed in the PUT-CAT-treated low-expressor FALS mice. These results support the role of free radical-mediated damage in the cascade of events leading to motor neurodegeneration in FALS and indicate that PUT-CAT interacts with a critical step in this cascade to delay the onset of clinical disease as well as the development of clinical weakness in FALS transgenic mice.
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PMID:Therapeutic benefits of putrescine-modified catalase in a transgenic mouse model of familial amyotrophic lateral sclerosis. 1048 88

A 70-year-old man developed pain and functional weakness in the lower limbs with dysesthesia and urinary retention after subarachnoid anesthesia with 0.5% hyperbaric bupivacaine. Neurological and electrophysiological tests and follow-up, as well as diagnostic images (CAT and MR), ruled out spinal cord lesions. The diagnosis was cauda equina syndrome. Cauda equina syndrome is a neurological complication of subarachnoid anesthesia. Associated with use of microcatheters for continuous subarachnoid anesthesia and 5% hyperbaric lidocaine, cauda equina syndrome is rare after a single injection of bupivacaine. Although the pathogenesis of cauda equina syndrome is poorly understood, there is agreement on the neurotoxicity of local anesthetics, particularly of 5% hyperbaric lidocaine.
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PMID:[Cauda equina syndrome after intradural anesthesia with bupivacaine]. 1159 Dec 82

We describe an atypical case of nemaline myopathy with an unusual distribution of muscle weakness who presented at 14 years of age with kyphoscoliosis. In this patient, we demonstrate heterozygosity for a de novo CGT-CAT (Arg167His) mutation in a constitutively expressed exon (exon 5) of slow alpha-tropomyosin (TPM3). This is the first mutation identified in a constitutively expressed exon of TPM3 in a nemaline myopathy patient, but is similar to recently described mutations in beta-tropomyosin (TPM2) associated with nemaline myopathy and mutations in fast alpha-tropomyosin (TPM1) which cause hypertrophic cardiomyopathy.
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PMID:De novo missense mutation in a constitutively expressed exon of the slow alpha-tropomyosin gene TPM3 associated with an atypical, sporadic case of nemaline myopathy. 1246 50

A 78-year-old Caucasian man developed headache, confusion and progressive right-sided weakness following a fall resulting in ecchymosis over the left eye orbit five days prior to admission. A subdural hematoma was diagnosed upon CAT scan. Upon evacuation, a very large left frontoparietal subdural hematoma with the appearance of mixed elements of hemorrhage and older fluid was noted. The finding was chronic subdural hematoma described as "crankcase oil." The patient's only prior medications were lisinopril 20 mg daily and ginkgo biloba 50 mg three times a day. Ginkgo biloba is advocated to augment cerebral blood flow to enhance memory and improve dementia. One of Ginkgo biloba's components is ginkgolide B, a potent inhibitor of platelet activating factor essential for induction of arachidonate-independent platelet aggregation. We believe Ginkgo biloba either caused or predisposed this patient to subdural hematoma and is of concern given ginkgo's widespread use with minimal or no monitoring.
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PMID:Possible subdural hematoma associated with Ginkgo biloba. 1527 97

Hb-M is a very rare hemoglobinopathy in the Indian subcontinent. We report a family with Hb-M with lifelong cyanosis from the Ratnagiri district in western India. The propositus was a 11-year-old female child with a history of increasing cyanosis exacerbated by fever and weakness. Similar complaints were also noted in her mother and five maternal family members. There was no history of cardiac illness or exposure to drugs and chemicals. The methemoglobin level was 39.3% in the propositus and 21.1% in her mother with normal NADH-methemoglobin reductase activity. Abnormal absorption peaks by spectroscopic analysis, presence of hemoglobin instability, and a slow-moving band on starch gel electrophoresis supported the presence of Hb-M. Automated DNA sequence analysis of the beta globin gene showed a C-->T substitution at codon 63. This leads to a substitution of histidine (CAT) by tyrosine (TAT) at the beta 63 (E7) position, similar to Hb-M Saskatoon. We have named this variant as Hb-M(Ratnagiri).
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PMID:Congenital methemoglobinemia caused by Hb-MRatnagiri (beta-63CAT-->TAT, His-->Tyr) in an Indian family. 1592 17


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