1/11. Echovirus 7 associated encephalomyelitis.BACKGROUND: hand, foot, and mouth disease (HFMD) is endemic in malaysia. In 1997, a large outbreak of enterovirus 71 (EV-71) associated HFMD resulted in 41 deaths due to severe left ventricular dysfunction and central nervous system infection with extensive damage to the medulla and pons. The clinical presentation in all these patients were rapid cardio-respiratory decompensation leading to cardiac arrest. Another large outbreak of HFMD with 55 fatal cases and a similar clinical picture was reported in taiwan in 1998. In 2000, an outbreak of HFMD resulted in the deaths of three children who had rapid cardio-respiratory decompensation and one child who survived a central nervous system infection. OBJECTIVES: We set out to study the etiologic agent and mechanism involved in three children who presented to our hospital, two of whom died and one survived a central nervous system infection. STUDY DESIGN: The clinical course of the disease was described. Throat, rectal swab and cerebrospinal fluid samples were subjected to viral isolation and viral isolates were identified by immunofluorescence, micro-neutralisation using human rhabdomyosarcoma (RD) cells, and reverse transcritpase polymerase chain reaction. magnetic resonance imaging was performed on two of the patients. RESULTS: Echovirus 7 was the sole pathogen isolated from three cases of acute encephalomyelitis, two of which were fatal due to severe left ventricular dysfunction resistant to inotropic support. The survivor had residual bulbar palsy, but is considered to have had a good neurological outcome. CONCLUSION: Echovirus 7 infection associated with encephalomyelitis could be fatal due to indirect involvement of the heart resulting in severe left ventricular dysfunction. In addition one of the children presented with hand, foot, and mouth disease, a syndrome that has not been previously associated with echovirus 7 infection.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
2/11. role of plasmapheresis in acute disseminated (postinfectious) encephalomyelitis.Acute disseminated encephalomyelitis (ADEM) is a demyelinating central nervous system disease that is associated with high morbidity and mortality. Although the recognition of ADEM may be facilitated by newer imaging techniques, the optimal treatment of this disease remains uncertain. We describe 4 patients with severe ADEM who responded to treatment that included intensive plasmapheresis. Two of the patients were in coma at the time that plasmapheresis was instituted, and all 4 patients made an excellent recovery. Immunologic studies revealed increased serum IgA levels, increased circulating immune complex levels as measured by the Raji cell assay, and decreased numbers of T and B cells prior to treatment of ADEM. These abnormalities improved following plasma exchange. plasmapheresis appears to be effective in reversing the neuropathologic process in ADEM. The role of this treatment modality in ADEM requires further evaluation in controlled clinical trials.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
3/11. Acute severe combined demyelination.We present a second case in which guillain-barre syndrome (GBS) and acute disseminated encephalomyelitis (ADEM) appeared simultaneously, both in acute and fulminant form. The patient, a 10-year-old girl, presented with acute onset of coma and flaccid, are-flexic quadriparesis. The elevated CSF protein levels and delayed F waves fulfilled the criteria of GBS and an MRI study revealed extensive multifocal demyelination compatible with a diagnosis of ADEM. Prompt clinical response followed by complete recovery was achieved by treatment with corticosteroids. It is suggested that acute severe combined demyelination might constitute a separate entity in which the demyelinating process, involving simultaneously the central and the peripheral nervous systems, indicates immune response against a component of the myelin of one system carrying cross-antigenicity with the other.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
4/11. Fatal acute encephalomyelitis after a single dose of intrathecal methotrexate.A 40-year-old Hispanic man with acute lymphoblastic leukemia was treated with a single dose of intrathecal methotrexate 12 mg for prophylaxis against leptomeningeal spread of tumor. The day after methotrexate administration, the patient complained of severe back pain and urinary retention. The diagnosis of encephalomyelitis was made on day 3 after methotrexate administration, and by day 6 mechanical ventilation was begun secondary to ascending paralysis. By day 8 the patient was comatose, with minimal signs of brain activity and little hope for recovery; on day 12 he died. Although neurotoxicity is a frequent complication of methotrexate therapy, fatal acute neurotoxicity is extremely uncommon, especially in adults. The mechanisms of methotrexate toxicity remain unclear, and no effective treatment exists to prevent its occurrence. This patient rapidly progressed from mild neurotoxicity to fatal encephalopathy after one dose of intrathecal methotrexate during his third cycle of chemotherapy. Clinicians should be aware of the signs and symptoms of neurotoxicity during treatment, as well as predisposing factors that put patients receiving methotrexate at risk for neurotoxic effects.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
5/11. Acute disseminated encephalomyelitis associated with hepatitis a virus infection.We describe the case of a 30-month-old boy who developed acute disseminated encephalomyelitis (ADEM) after hepatitis a virus (HAV) infection and ultimately died. As far as we know, this is only the second case of HAV-associated ADEM to be reported in the literature. The child was brought to hospital with fever, lethargy and weakness of 2 days duration. He had developed jaundice, abdominal pain and malaise 2 weeks beforehand and these problems had resolved within 2 days. Neurological examination revealed lethargy, generalised weakness and positive Babinski's signs bilaterally. cerebrospinal fluid examination showed mild lymphocytic pleocytosis, increased protein and elevated anti-HAV IgM and IgG titres. serum HAV IgM and IgG titres were also elevated. Despite aggressive treatment with ceftriaxone, acyclovir and anti-oedema measures, he developed papilloedema and coma within 24 hours of admission. magnetic resonance imaging of the brain revealed diffuse cerebral oedema and multifocal hyperintensities on T2-weighted images, with most lesions in the white matter of both cerebral hemispheres. The diagnosis of ADEM was established and high-dose steroids and intravenous immunoglobulin were added to the treatment regimen. However, his clinical condition continued to deteriorate and he died on the 20th day in hospital. This case shows that HAV infection can be linked with ADEM. patients with HAV infection should be examined carefully for central nervous system symptoms during follow-up. Likewise, the possibility of HAV infection should be investigated in cases of ADEM.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
6/11. Paraneoplastic coma and acquired central alveolar hypoventilation as a manifestation of brainstem encephalitis in a patient with ANNA-1 antibody and small-cell lung cancer.INTRODUCTION: Paraneoplastic neurological disorders are a well recognized complication of malignancy. methods: A case report to expand the currently described clinical manifestations of type 1 antineuronal antibody (ANNA-1)-associated paraneoplastic encephalomyelitis to include coma. RESULTS: We present an unusual case of fluctuating coma and rapid fulminant progression to acute respiratory failure from central alveolar hypoventilation caused by ANNA-1 paraneoplastic encephalomyelitis associated with small-cell lung carcinoma. Paraneoplastic infiltration of the brainstem and cerebellum, including respiratory and arousal centers, was documented on autopsy. CONCLUSIONS: Paraneoplastic encephalomyelitis should be considered as a possible cause of coma and central alveolar hypoventilation.- - - - - - - - - - ranking = 7keywords = coma (Clic here for more details about this article) |
7/11. encephalomyelitis associated with leukemia in a child.A case of an encephalomyelitis in a child with acute lymphoblastic leukemia is reported. The patient was a 5-year-old boy who developed seizures, progressive confusion, and coma after radiation and intrathecal methotrexate therapy. Computed tomography (CT) of the brain showed bilateral hypodensities in the posterior parietal and temporal regions. At autopsy, perivascular inflammation, microglial nodules without intranuclear viral inclusions, and bilateral necrosis of the temporoparietal and hippocampal regions were seen in the brain and spinal cord. Paraneoplastic encephalomyelitis is generally recognized in adult patients with underlying malignancy but, to our knowledge, has not been reported in children with leukemia. This report should alert the clinicians to an entity that must be included in the differential diagnosis of leukemic children with progressive neurologic disorder.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
8/11. MRI in children with postinfectious disseminated encephalomyelitis.Acute disseminated encephalomyelitis, an inflammatory and demyelinating disorder of central nervous system white matter, typically occurs following childhood viral infections. Although CT may demonstrate abnormalities, many children have normal CT studies in spite of widespread neurologic abnormalities. We report a series of five patients with the typical clinical presentation of disseminated encephalomyelitis who were studied using magnetic resonance imaging (MRI). In each case the children presented with progressive subacute neurologic abnormalities including headache, diplopia, ataxia, hemiparesis, seizures, dysarthria, and/or coma. CT was nondiagnostic. MRI clearly demonstrated multifocal white matter lesions of the cerebrum, brainstem, and cerebellum which corresponded to clinical signs. The patients improved dramatically with corticosteroid therapy. MRI showed progressive resolution of multifocal lesions in conjunction with clinical improvement.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
9/11. Eosinophilic radiculomyeloencephalitis: an angiostrongyliasis outbreak in american samoa related to ingestion of Achatina fulica snails.For the first time in american samoa an outbreak of eosinophilic radiculomyeloencephalitis was related to eating giant African snails (Achatina fulica) infected with angiostrongylus cantonensis. Among 24 Korean fisherman sharing the same infective meal, 16 who ate raw or partially cooked snails became ill; five who ate boiled snails and three who ate none remained well. The ensuing illnesses began within 1-6 days, persisted up to 10 weeks, and were characterized by both peripheral blood and spinal fluid eosinophilia, severe pains, weakness and hyporeflexia of the legs, and dysfunction of the bladder and bowels. Eight patients also had transient hypertension and/or lethargy, and three became comatose. One man died 17 days after eating the infected snails, and maturing larvae of A. cantonensis were found in his spinal cord. enzyme-linked immunosorbent assay titers for antigens of A. cantonensis were elevated to 1:64 or greater (mean 1:128) in all 10 patients tested. Treatment with thiabendazole had no appreciable effect on the clinical course of the illness.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
10/11. Bilateral, reversible, selective thalamic involvement demonstrated by brain MR and acute severe neurological dysfunction with favorable outcome.We report on two children who presented acute, severe, neurological dysfunction with bilateral, reversible, selective thalamic lesions demonstrated by brain MRI. In both children neurological symptoms appeared two weeks after a febrile respiratory illness. Clinical conditions worsened in a few days to a stuporous state and tetraplegia in one and to coma with decerebrate posturing in the other. Three weeks after the onset, both children improved and recovered within one month. During the acute phase, brain MRI showed in both children bilateral hyperintense areas on T2-weighted sequences limited to both thalamic regions. During the follow-up, repeated brain MRI showed complete disappearance of abnormalities in one patient and a small residual left thalamic lesion in the other. In both patients hematological routine exams were normal. Bacterial and viral studies of serum and CSF were negative. CSF findings showed elevated white blood cell count and protein levels, with no oligoclonal IgG bands. urine and CSF organic acids by GC/MS and plasma as well as CSF amino acids were normal. We believe that the benign evolution of this disorder and CSF findings strongly suggest a postinfectious process of the central nervous system.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
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