RESUMO
We describe a patient with the sudden onset of a painful, purely sensory, mononeuritis multiplex. Investigations showed no evidence for any underlying systemic condition. A nerve biopsy showed fascicular wallerian degeneration with perineurial thickening, inflammatory cells, and immunoglobulin G (IgG) deposition. His painful sensory deficits persisted, with no improvement after treatment with prednisone. The clinical characteristics in this case were very similar to those originally described by Wartenberg, and subsequently by other investigators. The investigations in our case strongly suggest that there may be an underlying immune pathogenesis for cases of Wartenberg's migrant sensory neuritis.
Assuntos
Neurite do Plexo Braquial/patologia , Neurite (Inflamação)/patologia , Adulto , Biópsia , Plexo Braquial/patologia , Plexo Braquial/ultraestrutura , Neurite do Plexo Braquial/imunologia , Humanos , Linfócitos/patologia , Masculino , Microscopia Eletrônica , Neurite (Inflamação)/imunologia , Nervos Periféricos/patologiaRESUMO
We present the MR imaging findings in an autopsy-proven case of selective neuronal necrosis involving the entire left cerebral hemispheric cortex, left thalamus, and contralateral cerebellum following a period of status epilepticus. Imaging findings include diffusion abnormality on diffusion-weighted images and increased intensity on T2-weighted images in the above-mentioned regions of the brain.
Assuntos
Encéfalo/patologia , Imageamento por Ressonância Magnética , Neurônios/patologia , Estado Epiléptico/patologia , Adulto , Evolução Fatal , Humanos , Masculino , Necrose , Estado Epiléptico/complicaçõesRESUMO
Whereas plasminogen activator of the tissue-type (t-PA) is present in extracts of kidney parenchyma, only small amounts of the enzyme can be detected in normal urine where the major plasminogen activator is of the urokinase-type (u-PA). These observations suggest the existence of physiological or anatomical barriers that effectively confine t-PA to renal tissue and exclude it from the urine. We examined the notion that disease might breach these barriers and so lead to the appearance of abnormal amounts of t-PA in the urine. Under the conditions of the simple fibrinolytic assay that we have developed, urine samples from 30 normal subjects did not contain detectable amounts of t-PA whereas we were able to demonstrate t-PA in samples from 43 of 65 patients with various forms of renal disease. When positive, therefore, tests for the presence of t-PA in human urine provide evidence for renal disease that may not otherwise be apparent.
