1/15. Periodic lateralized epileptiform discharges in influenza B-associated encephalopathy.An 18-year-old woman presented with coma, hemicomvulsions, and transient periodic lateralized epileptiform discharges (PLEDs). Serological tests were positive for influenza B, and cerebrospinal fluid PCR for herpes simplex virus dna was negative. magnetic resonance imaging later showed abnormal signal intensity in the temporal lobe ipsilateral to the PLEDs. Influenza-associated encephalopathy may cause hemiconvulsions and PLEDs, and can mimic herpes simplex encephalitis.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
2/15. Influenza-associated acute encephalopathy in Japanese children in 1994-2002.We addressed the incidence of influenza-associated acute encephalopathy, which is distinct from reye syndrome, in children in japan. Eighty-nine children with a mean age of 3.8 years were reported to have developed this disease during eight influenza seasons (December 1994-April 2002) in Hokkaido, japan. None of them had received aspirin. Most of the patients rapidly became comatose with or without convulsions with a mean interval of 1.7 days from the onset of fever to the onset of central nervous system symptoms. Thirty-three (37.1%) patients died and 17 (19.1%) patients had neurological sequelae. A total of 53 (59.6%) cases were proved to have an influenza virus infection. interleukin-6 and tumor necrosis factor-alpha were markedly elevated in serum and cerebrospinal fluid samples from two patients who died after a rapid, fulminant course. A post-mortem examination of one fatal case revealed vasogenic brain edema with generalized vasculopathy, suggesting that the generalized impairment of vascular endothelial cells caused by highly activated cytokines plays a central role in the pathophysiology of this disease. We conclude that influenza-associated acute encephalopathy may be an underestimated syndrome and is another reason to promote vaccination against influenza in infants and younger children.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
3/15. Fatal avian influenza A (H5N1) in a child presenting with diarrhea followed by coma.In southern vietnam, a four-year-old boy presented with severe diarrhea, followed by seizures, coma, and death. The cerebrospinal fluid contained 1 white cell per cubic millimeter, normal glucose levels, and increased levels of protein (0.81 g per liter). The diagnosis of avian influenza A (H5N1) was established by isolation of the virus from cerebrospinal fluid, fecal, throat, and serum specimens. The patient's nine-year-old sister had died from a similar syndrome two weeks earlier. In both siblings, the clinical diagnosis was acute encephalitis. Neither patient had respiratory symptoms at presentation. These cases suggest that the spectrum of influenza H5N1 is wider than previously thought.- - - - - - - - - - ranking = 5keywords = coma (Clic here for more details about this article) |
4/15. Fatal dengue encephalitis.central nervous system involvement is not an uncommon manifestation of dengue virus infection, but encephalitis is a rare entity. We report the case of a 5-year-old girl with fever and convulsions. She developed coma and shock during the high fever stage without abnormal bleeding.Treatment was supportive and symptomatic. The shock was poorly controlled. High fever persisted for 7.5 days then she expired.cerebrospinal fluid (CSF) and blood dengue-IgM antibody showed dengue infection.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
5/15. Rabies encephalomyelitis: clinical, neuroradiological, and pathological findings in 4 transplant recipients.BACKGROUND: Three patients received solid organ transplants from a common donor and were subsequently discharged from the hospital following an uneventful hospital course. Within 30 days, all 3 organ recipients returned to the hospital with varying symptoms that progressed to rapid neurological deterioration, coma, and death. OBJECTIVE: To describe the clinical, neuroradiological, and pathological findings of rabies virus infection in organ transplant recipients infected from a common donor. DESIGN: Case series involving a common donor and 3 organ recipients ascertained through review of clinical course and autopsy findings. A fourth case was determined by review of pending autopsy cases in which death occurred within the same time interval. Portions of postmortem central nervous system and organ tissues were frozen and formalin-fixed. Fluids and tissues were also collected for cultures, serology, and molecular studies. Postmortem fluids and tissues and antemortem fluids and tissues from all 4 transplant recipients and serum and banked lymphocyte or spleen cells from the donors were sent to the Centers for disease Control and Prevention for further evaluation. SETTING: Transplant unit of an urban teaching hospital. RESULTS: Antemortem cerebrospinal fluid analysis for 3 of the 4 recipients was consistent with a viral etiology. neuroimaging and electroencephalogram studies were suggestive of an infectious encephalitis or a toxic encephalopathy. Initial laboratory testing did not demonstrate an infectious etiology. Postmortem histologic analysis, immunohistochemistry, electron microscopy, and direct fluorescence antibody testing revealed rabies virus infection. Serological testing done postmortem confirmed rabies virus infection in the common donor. CONCLUSIONS: These cases demonstrate a risk for transmitting rabies virus infection through solid organ and tissue transplantation, and this diagnosis should be considered in any rapidly progressing neurological disease.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
6/15. Human herpesvirus-6 encephalitis after unrelated cord blood transplantation.Here we describe 2 patients with acute leukemia in whom human herpesvirus-6 (HHV-6) encephalitis developed after cord blood transplantation. In patients 1 and 2, generalized seizure and coma developed on day 62 and day 15, respectively, after cord blood transplantation, which failed to engraft in patient 1. Magnetic resonance imaging (MRI) of patient 1's brain showed low-intensity signals at the gyri of the bilateral lateral lobes on T1-weighted images and high-intensity signals on T2-weighted images. MRI of patient 2's brain showed high-intensity signals in bilateral white matter on T2-weighted images and on fluid-attenuated inversion recovery (FLAIR) images. cerebrospinal fluid examination revealed an increased protein level with pleocytosis in patient 1 and a normal protein level without pleocytosis in patient 2. polymerase chain reaction analysis detected HHV-6 dna in the cerebrospinal fluid of both patients. Patient 1 recovered after administration of gancyclovir for 3 weeks. However, she again suffered from encephalitis after discontinuation of gancyclovir, and died of sepsis. Patient 2 died from an anoxic brain caused by generalized seizure. When neurological symptoms and signs appear in hematopoietic stem cell transplantation recipients, we should consider HHV-6 encephalitis and promptly and empirically treat them with gancyclovir or foscarnet.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
7/15. MRI findings from a case of fulminating adult-onset measles encephalitis.We report a rare case of fulminating adult-onset measles encephalitis. A 34-year-old man developed a comatose state after measles eruptions and ultimately akinetic mutism. Titers of anti-measles IgM antibodies were elevated in both serum and cerebrospinal fluid. Brain magnetic resonance imaging (MRI) 3 months after onset revealed widespread hyperintense lesions in the periventricular white matter and marginal hyperintense lesions in the brainstem on fluid-attenuated inversion recovery and diffusion-weighted images. The marginal lesions in the brainstem are similar to subpial demyelinating lesions seen in postinfectious encephalomyelitis. This case of encephalitis may be related to an autoimmune-mediated process triggered by measles infection.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
8/15. Persistent Coxsackie B encephalitis: Report of a case and review of the literature.Although the diagnosis is rarely confirmed, enteroviruses are a common cause of meningitis. Coxsackie B is responsible for more than half of the cases of aseptic meningitis in infants less than 3 months old, but is less common as a cause of neurological disease in older persons. In addition to aseptic meningitis, Coxsackie B has been reported to cause a wide range of other neurological disorders, albeit rarely. The authors report a young adult with persistent Coxsackie B encephalitis that was heralded by focal seizures and evolved to intractable coma with multifocal myoclonus. The diagnosis was established by immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR) on tissue obtained at brain biopsy. cerebrospinal fluid (CSF) viral cultures and PCR were negative for enteroviruses. This case highlights unusual features of a persistent infection that could easily have been mistaken for a neurodegenerative or other noninfectious process. It also emphasizes the importance of performing brain biopsy on individuals with neurological disease of obscure nature.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
9/15. Operculum syndrome: unusual feature of herpes simplex encephalitis.herpes simplex encephalitis in adults and young patients carries a high mortality and morbidity. Its presentation may be nonspecific, sometimes hampering early diagnosis. Two young children are reported with herpes simplex encephalitis in whom the operculum syndrome was an outstanding feature. This syndrome is caused by focal, bilateral cortical damage to the anterior opercular regions resulting in anarthria and impairment of mastication and swallowing. After initiation of treatment with acyclovir in the early stage of the disease, the outcomes in both patients were characterized by good general recovery with persistence of deficits of speech, mastication, and swallowing, more pronounced in the patient who was comatose during the illness. Early recognition of the operculum syndrome as a presenting feature of herpes simplex encephalitis may expedite the diagnosis and thereby improve the prognosis.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
10/15. Neurogenic diabetes insipidus in a child with fatal Coxsackie virus B1 encephalitis.A 5 year-old boy presented with fever, sore throat, diarrhea, and general soreness which evolved into encephalitis. His cerebrospinal fluid showed a cell count of 3 mononuclear cells/microliters, protein 2800 mg/l, and growth of Coxsackie virus B1. Cardiorespiratory arrest was noted after a convulsion and infusion of diazepam. Although he was immediately resuscitated, he remained unconscious with a modified Glasgow coma score of 4 or 3. He developed neurogenic diabetes insipidus 169 hours after the convulsion and died the next day. We conclude that although Coxsackie virus infection is usually benign it may become overwhelming and be complicated with neurogenic diabetes insipidus. It is important to recognize this potential sequel by regularly monitoring weight, intake and output, plasma sodium level, and urine specific gravity.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
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