Cases reported "Encephalomyelitis"

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1/5. Encephalo-myelo-radiculo-ganglionitis presenting as pandysautonomia.

    A 68-year-old man developed pandysautonomia with severe orthostatic dysfunction, fixed heart rate, low serum levels of norepinephrine and epinephrine, absent sympathetic skin responses, and pupillary abnormalities. CSF protein was 92 mg/dl. In spite of a good recovery following corticosteroid administration, a relapse occurred, with accompanying sensory symptoms confined to both arms. Fatal sudden cardiac arrest occurred after 4 months. autopsy revealed numerous lymphocytic infiltrates, predominantly in autonomic and sensory ganglia and, to a lesser extent, in the nerve roots, spinal cord, and brainstem without evidence for an underlying tumor. This case provides histopathologic evidence for an inflammatory etiology of panautonomic neuropathy in some patients.
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keywords = ganglion
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2/5. Encephalomyeloneuropathy with ganglionitis of the myenteric plexuses in the absence of cancer.

    A 55-year-old woman presented with rapidly progressive brainstem dysfunction which led to death within a month. She also had constipation for three weeks, and barium enema showed ileus. Subacute encephalomyelitis predominantly involving the medulla and pons correlated with the patient's initial symptoms. In addition, ganglionitis of the myenteric plexuses explained the constipation and ileus. Ganglioradiculoneuropathy was another finding. The presence of abundant neuronophagia in the brainstem, dorsal root ganglia, and myenteric plexuses raised the speculation that a putative virus, toxic agent, or immune reaction possessed special affinity for neurons and ganglion cells. The neuropathological findings were similar to paraneoplastic changes, but no neoplasm was found.
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ranking = 1.5
keywords = ganglion
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3/5. Carcinomatous encephalomyelopathy in conjunction with encephalomyeloradiculitis.

    A man, aged 63, had an illness which lasted 11 months from onset with pain under the left costal margin which radiated to the epigastrium, until his death from cardiac failure. His symptoms consisted principally of parasthesias and proximal weakness of both upper and lower extremities with atrophy of the shoulder and pelvic girdles. He developed pyramidal tract signs, became euphoric, emotionally unstable and mentally retarded. There was no clinical evidence of cerebellar dysfunction. Bronchogenic carcinoma was suspected from a tomograph of the thorax, but, in spite of extensive clinical and laboratory studies, the diagnosis was verified only postmortem. The CSF cell count was high at first but diminished as the disease progressed. Muscle biopsies revealed chronic generalized denervation without signs of myopathy. Neuropathologically, encephalomyeloradiculoneuritis concentrated on the spinal cord was combined with severe rarefaction of the ganglion cells of the anterior horns and with bilateral degeneration of the lateral pyramidal spinocerebellar and posterior tracts. A more diffuse process was obvious in the anterolateral tracts of the lumbar region. Polyneuropathy concentrated in the distal region was accompanied by slight inflammatory reaction in the sciatic nerve. Cerebellocortical degeneration which exceeded physiological age-related rarefaction was also present. The findings are discussed in relation to the literature.
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keywords = ganglion
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4/5. Paraneoplastic encephalo-myelo-ganglionitis: cellular binding sites of the antineuronal antibody.

    The cellular binding sites of an antineuronal antibody were characterized in an autopsy case of the paraneoplastic encephalo-myelo-ganglionitis. A 61 year-old woman developed a subacute sensorimotor polyneuropathy and, later, multiple involvement of cranial nerves, disturbance of consciousness, and generalized seizure. An autopsy revealed a small cell lung carcinoma and neuropathological changes that included disseminated encephalitis, spinal anterior horn lesions, severe loss of dorsal root ganglion neurons, and secondary degeneration and loss of the nerve fibers in the spinal posterior column and peripheral nerves. The serum IgG from the patient contained antineuronal antibody(s) including an antibody to 35- to 37-kDa neuronal antigens called anti-Hu as demonstrated in Western blot. In immunohistochemical studies, the serum IgG immunostained neurons of the brains, spinal cords, and dorsal root ganglia of humans or rats. Confocal laser-scanning microscopy revealed binding of the patient's IgG in the neuronal nuclei and cytoplasm, but not in the nucleoli. In immunoelectron microscopic studies, immunolabelling with the IgG was found diffusely in the karyoplasm, excluding nucleoli, and in the cytoplasmic matrix between the cisternae of the reticulums, golgi apparatus, and mitochondria. Encephalo-myeloganglionitis is a clinicopathological entity frequently associated with the presence of neoplasm and antineuronal antibody, however, the role of the antibody in the pathogenesis remains to be elucidated.
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keywords = ganglion
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5/5. Fatal encephalitis caused by concomitant infection with tick-borne encephalitis virus and borrelia burgdorferi.

    We describe a 38-year-old farmer from the southwestern archipelago of finland where both tick-borne encephalitis (TBE) virus and borrelia burgdorferi are endemic. He presented with fever and headache, developed severe meningoencephalitis in 3 days, and, after 1 month, died without regaining consciousness. High titers of IgG and IgM antibodies to TBE virus were present in both serum and CSF. serology for Borrelia was negative. autopsy revealed necrotizing encephalitis and myelitis with involvement of the dorsal root ganglion. With use of polymerase chain reaction tests, segments of two separate genes of B. burgdorferi were amplified from the patient's CSF. This case demonstrates that the possibility of dual infection should be considered for patients residing in geographic areas where ixodes ticks may carry both the TBE virus and B. burgdorferi. We believe that the most severe damage in this case was caused by TBE virus rather than by B. burgdorferi. Nevertheless, the coinfection might have contributed to the fatal outcome that has not been previously observed in Finnish patients with TBE.
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keywords = ganglion
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