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)

A 34-year-old patient was treated four weeks before his death for a recurrent binocular iritis. He died with clinical symptoms of a cerebral respiratory paresis. The diagnosis of epithilial cells sarcoidosis was made only after histological post mortem examination. It was a cerebral form of chronic disseminated encephalomeningitis with a vascular component. Typical granulomes were found in several organs and also in conjunctiva, ciliary body, choroid and optic nerve.
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PMID:[Generalized sarcoidosis with brain and eye participation]. 115 64

6-Aminonicotinamide, an antimetabolite of nicotinamide, given by intraperitoneal injection produced diarrhea, ascending paresis/paralysis, death, and bilateral ocular alterations in both sexes of New Zealand white and Dutch belted rabbits. Ocular vascular lesions consisted of iridal congestion with iridal hemorrhage and associated acute iritis and aqueous flare in some rabbits. Cytoplasmic swelling, vacuolation, and loss of staining affinity that represented hydropic change were present in both layers of ciliary epithelium and the inner layer of iridal epithelium. Cells in the outer layer of the iridal processes and the ciliary ridge, were most severely affected. Vacuoles were also present in the retinal pigment epithelium and scattered throughout the outer plexiform layer of the retina with a few in the inner and outer nuclear layers. Ocular alterations were prevented by simultaneous administration of nicotinamide and their development appeared related to nicotinamide deficiency. No ocular alterations were caused by nicotinamide administration alone.
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PMID:Ocular lesions of 6-aminonicotinamide toxicosis in rabbits. 315 43

We report two siblings with sarcoidosis; the younger sister had symptoms of central nervous system, and both sisters had subcutaneous mass lesions in the gluteal region. Case 1. A 30-year-old woman presented with two episodes of right leg paresis. On admission, neurological examination revealed right leg weakness, spasticity of both legs, increased deep tendon reflexes in all extremities, urinary disturbance and hearing loss of the right ear, but she had no meningeal signs. Serological studies were normal including angiotensin converting enzyme. Cerebrospinal fluid revealed elevated protein to 340 mg/dl, mild pleocytosis, decreased glucose. CSF culture was negative, and cytology showed no malignant cells. Enhanced MR imaging showed diffuse leptomeningeal enhancement in both the brain around basal meninges and the whole spinal cord. Case 2. A 34-year-old woman (the elder sister of Case 1) presented with visual disturbance. She had been diagnosed to have bilateral iritis at Hiroshima Red Cross Hospital before visiting our hospital. Neurological examination and serological studies were normal. In both cases, left gluteal subcutaneous mass was detected and its biopsy revealed characteristic sarcoid nodules and confirmed the diagnosis of sarcoidosis. A tendency of familial occurrence and positive associations of the specific HLA antigens in sarcoidosis have been reported. Though the diagnosis of neurosarcoidosis has been difficult without extraneurological signs, sarcoidosis should be considered as a differential diagnosis in all the patients with myelopathy, and enhanced MRI and measure of CSF angiotensin converting enzyme seem to be useful for diagnosis and evaluation of drug effect during the course of steroid therapy.
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PMID:[Two siblings with sarcoidosis diagnosed by younger sister's central nervous symptoms]. 904 58