Cases reported "Myelitis"

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1/4. Spinal cord lesions of myelitis with hyperIgEemia and mite antigen specific IgE (atopic myelitis) manifest eosinophilic inflammation.

    We report the neuropathological findings of spinal cord specimens obtained from two patients who had localized myelitis with hyperIgEemia and mite antigen specific IgE (atopic myelitis). Both cases showed mild spinal cord dysfunction, and the gadolinium-enhanced area of the isolated spinal cord lesion observed on MRI was biopsied, respectively. Neuropathologically, both cases showed many perivascular lymphocyte cuffings associated with disrupted vessels, and the infiltration of eosinophils in the spinal cord lesions. Both myelin and axons were lost in the lesions, which were associated with astrogliosis. These findings suggest that an allergic mechanism may play a role in this condition.
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2/4. vascular malformations of the spinal cord (angiodysgenetic myelomalacia): a critique on its pathogenesis.

    Two cases of angiodysgenetic myelomalacia are presented. Both patients had progressive weakness and sensory deficits in the lower extremities and vascular malformations of their spinal cords. The lesions were located on the dorsum of the spinal cord and the dorso-spinal roots. We believe the symptoms that developed later in life were due to spinal cord ischemia resulting from late degenerative changes in the vessels of the malformation and an ever increasing spinal "steal".
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3/4. endotoxemia-induced diffuse myelitis and extensive patchy necrosis of the liver.

    An autopsy case with endotoxemia-induced diffuse myelitis and extensive, grossly patchy necrosis of the liver occurring in a 70-year-old female was examined histopathologically and electron microscopically. Leucopenia with prominent leukemoid reaction (myeloblasts 20%) preceded the terminal fulminant hepatitis by two weeks. Soon after the terminal event, bacteremia and endotoxemia were detected and negativity for HB antigen was proved. Diffuse myelitis was characterized by devastation of hyperplastic bone marrow structure mottled with destructed sinus architecture and scattered exudative necrosis, resulting in the loss of mature granulocytes and erythropoiesis. Regenerative clusters of myeloblasts and prominent increase of megakaryocytes were observed. Electron microscopically, the bone marrow contained fibrin and platelets within the exudate of the marrow stroma. Extensive, grossly patchy necrosis of the liver microscopically consisted of well demarcated coagulation necrosis of hepatic parenchyma with scattered fibrin thrombi in the sinusoids at the boundary. There were no definite thrombi but occasional fibrin accumulation in the small blood vessels of the liver. Both extensive diffuse myelitis and extensive, patchy necrosis of the liver seemed to be quite rare in incidence. The pathogenesis of these combined lesions was discussed in relation with endotoxemia.
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4/4. paraplegia following surgery in Foix and Alajouanine syndrome. (Arteriovenous malformation of the spinal cord).

    Two patients with spinal cord arteriovenous malformation became paraplegic after removal of the abnormal vessels from the dorsal surface of the thoracolumbar spinal cord. Surgical exposure of a spinal cord arteriovenous malformation without an attempt at removal accelerated the pace of progressive paraparesis in two other patients. The poor outcome of our cases is, however, not representative of modern surgical techniques, since selective spinal angiography and the operating microscope were not used. We propose that the intramedullary vascular changes in this condition are an integral component of the arteriovenous malformation. Additionally, the phenomenon of nocturnal seminal ejaculation in spite of progressing impotence may be a clinical feature unique to spinal cord arteriovenous malformations.
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