Cases reported "Myelitis"

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1/11. Radiculomyelitis following acute haemorrhagic conjunctivitis.

    The clinical manifestations and natural history of radiculomyelitis following a newly reported disease--acute haemorrhagic conjunctivitis (AHC)--have been studied in 33 patients in taiwan, and the following observations made: All the patients in this series were adults at ages ranging from 21 to 55 years; the salient initial neurological manifestations were radicular pains and acute flaccid paralysis which developed from five to thirty-seven days after the onset of AHC. In some patients, signs and symptoms indicating involvement of the meninges, cranial nerves and the white matter of the cord were observed; motor paralysis was the most striking feature during the whole clinical course; it consisted of flaccid asymmetrical weakness in one or more limbs, usually being more severe in the lower limbs than in the upper, and often more proximal than distal. Atrophy in the severely affected muscles usually became apparent in the second or third week of the weakness; the prognosis regarding the return of function in the affected muscles was dependent on the severity of the involvement. Permanent incapacitation due to paralysis and muscular atrophy in the affected proximal muscles of lower limbs was the main sequel in severe cases. The pattern and prognosis of flaccid motor paralysis were reminiscent of acute poliomyelitis in which the anterior horn cells of the spinal cord are mainly involved. Pleocytosis ranging from 11 to 270 per mm3 was noted in the majority of the patients when the cerebrospinal fluid was examined within the first three weeks from the onset of neurological symptoms; the total protein level was raised invariably from the second week onwards in all specimens, and remained so throughout the subsequent course as long as the seventh week or later. Tissue culture neutralization tests were performed on the sera from 9 patients; significant rises in the antibody titres (greater than or equal to 1:16) to AHC virus antigens were found in 8 cases, and in 2 of them a fourfold rise in the paired sera was noted. The differentiation of this syndrome from poliomyelitis and from guillain-barre syndrome, the relative freedom of children from neurological complications of AHC and the aetiological relationship of AHC virus to the syndrome have been discussed. It is concluded that this unusual neurological syndrome is caused by the neurovirulent properties of the AHC virus.
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2/11. 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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3/11. Multifocal relapsing-remitting myelitis in a patient with atopic dermatitis: multiple sclerosis or atopic myelitis?

    We describe a patient with multifocal relapsing-remitting myelitis. This case had abnormal high intensity lesions in the spinal cord at the cervical and thoracic levels on magnetic resonance imaging (MRI). She had complicated atopic dermatitis and high serum IgE levels, which showed strong sensitivity to mite antigen. These features closely resemble those of atopic myelitis, suggesting that atopic myelitis may develop a relapse with multifocal involvement of the spinal cord, which can mimic multiple sclerosis.
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4/11. Post-transplantation HTLV-1 myelopathy in three recipients from a single donor.

    OBJECTIVES: This paper reports for the first time three cases of infection by HTLV-I via organ transplantation; all the organs coming from the same asymptomatic infected donor. The need is considered for the implementation of compulsory screenings for HTLV antibodies on organ donors and on blood banks. methods: The determination of antibodies for HTLV-I/II on samples of serum and cerebral spinal fluid from the patients and the donor was performed by enzyme immunoassay and western blot. Analysis of proviral dna was performed by polymerase chain reaction. To detect changes in the sequence of amino acids, the tax gene was sequentiated, amplified, and compared with ATK prototype stocks. spinal cord magnetic resonance imaging, cerebral spinal fluid, and somatosensory evoked potential studies were carried out in all patients. RESULTS: All three transplanted patients developed a myelopathy within a very short period of time. In all three patients and donor the virus belonged to the Cosmopolitan A subtype. The homology of HTLV-I sequences recovered from the patients and donor was 100% in all four cases. Proviral load was high in all three patients. The factors that certainly contributed to the infection in the first place, and the development of the disease later, were on the one hand the high proviral load and their immunosuppressed condition, and on the other the virus genotype, which proved to be an aggressive variant. However, the analysis of the histocompatibility antigen showed that two of the patients carried an haplotype that has been associated with a lower risk of developing this disease. CONCLUSIONS: It is argued that, although in spain and other European countries there is not compulsory screening for HTLV antibodies because of the studies that show a low seroprevalence, in view of the cases here reported, and to avoid the serious consequences that such infection has on transplanted patients, compulsory screenings, both on organ donors and on blood banks, should be implemented.
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5/11. Multifocal multinucleated giant cell myelitis in an AIDS patient.

    A 19-year-old male intravenous drug abuser, was admitted to hospital with a one-week history of lower limb weakness and urinary retention. He was known to have been HIV-seropositive for 3 years and had been treated for cerebral toxoplasmosis. Neurological examination confirmed flaccid paraparesis with weak ankle jerks and bilateral extensor plantar responses. There was no obvious sensory deficit. Neurological examination was otherwise normal. CSF contained 63 mg/dl protein and 10 leucocytes/mm3. myelography was normal. He died 1 month later from septic peritonitis. Neuropathological examination showed chronic lesions of toxoplasmosis in brain. Small necrotic foci with myelin loss, proliferation of microglia, macrophages and multinucleated giant cells (MGC) were disseminated in the whole spinal cord, mostly in the white matter, but the brain was spared. immunohistochemistry demonstrated p24 and p17 hiv antigens in macrophages, MGC and microglial cells. These lesions resemble those of so called 'multifocal giant cell encephalitis'. The present case demonstrates that HIV-related multifocal inflammatory changes may be restricted to the spinal cord and may be a cause of myelopathy in AIDS patients.
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6/11. Acute ascending necrotizing myelitis in Okinawa caused by herpes simplex virus type 2.

    A case of rapidly progressing ascending myelitis was necropsied. necrosis was present throughout the whole length of the spinal cord and involved both the grey and white matter randomly. The perivascular lymphocytic infiltration in the spinal cord in the present case was more pronounced than that in the previously reported two cases of necrotizing myelopathy associated with malignancy. Using immunoperoxidase staining the presence of herpes simplex virus type 2 (HSV 2) antigen was demonstrated. Electron microscopic examinations revealed large numbers of HSV particles in the spinal cord. HSV 2 may be a common aetiological agent of necrotizing myelopathy and myelitis in Okinawa, an HSV 2 endemic area. In the present case, the necrosis was mainly found in the spinal cord but was also observed, to a very limited extent, in the brain.
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7/11. Eosinophilic meningoradiculomyelitis caused by gnathostoma spinigerum. A case report.

    A 51-year-old man had excruciating pains in the left arm and chest approximately four weeks after ingestion of live loaches. eosinophilia, eosinophilic pleocytosis in the CSF, and a high serum IgE level were noted. skin tests and antigen-antibody reactions were positive for gnathostoma infection. His clinical signs and symptoms ameliorated with symptomatic treatment within six months. Only 34 cases of gnathostomiasis involving the CNS have been reported in the English literature, and ours is the first Japanese case, to the best of our knowledge, of eosinophilic meningoradiculomyelitis caused by gnathostoma spinigerum.
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8/11. 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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9/11. Vogt-Koyanagi-Harada syndrome with focal neurologic signs.

    The Vogt-Koyanagi-Harada syndrome includes inflammation of the uveal tract, retina, and meninges. Integumentary and auditory signs are common. Neurologic involvement has been reported. We studied two patients who manifested many of the varied clinical signs of Vogt-Koyanagi-Harada syndrome, but who also showed focal neurologic involvement, including acute transverse myelitis and ciliary ganglionitis. Both patients responded well to corticosteroid therapy. The findings in these patients and the results of previous studies suggest that Vogt-Koyanagi-Harada syndrome is a cell-mediated autoimmune disorder in which a component of myelin acts as an inciting antigen.
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10/11. radiation therapy of midline granuloma.

    During a 15-year period, 10 patients with well-documented midline granuloma were treated with high-dose, deep local irradiation and followed for extended periods of time. Long-term remissions were achieved in 7 patients, with a mean ( /- SEM) survival postirradiation of 7.4 ( /- 1.4) years in the 6 patients still alive. True midline granuloma, which is a localized, destructive, inflammatory process of the upper airways, can be distinguished from Wegener's granulomatosis and neoplasms of the upper respiratory tract by several clinicopathologic criteria. The cause of midline granuloma is unknown, but it most likely represents an abnormal accelerated hypersensitivity reaction to an unknown antigen(s). Although serious complications of high-dose local irradiation to the upper airways can occur, the risk is warranted because of the high, long-term remission rate in this previously uniformly fatal disease.
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