[Clinical aspects of meningoencephalitis of unknown etiology (the so-called viral meningoencephalitis) in Western Europe].
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We report three patients presented with meningoencephalitis associated with polyradiculoneuropathy with increased HSV IgG antibody titer. The first patient was a 27-year-old woman with meningoencephalitis who developed status epilepticus. The CSF showed pleocytosis and increase in HSV IgG antibody titer. Herpes encephalitis was suspected, and she was treated with acyclovir. The symptoms of meningoencephalitis improved, but she developed flaccid tetraplegia. The NCV study was compatible with polyradiculoneuropathy. About two months later from the onset, muscle atrophy appeared in her all limbs. The second patient was a 23-year-old woman with meningoencephalitis, which was followed by ascending motor paralysis. The CSF showed pleocytosis and increase in HSV IgG antibody titer. The symptoms of meningoencephalitis improved by administration of acyclovir, but paralysis didn't improve. About two months later from the onset, muscle atrophy of all limbs appeared. The NCV study was compatible with polyradiculoneuropathy. The third patient was a 43-year-old man presenting somnolence, neck stiffness and ascending motor paralysis developing into flaccid tetraplegia. The CSF showed pleocytosis and increase in HSV IgG antibody titer. Somnolence and neck stiffness improved by administration of acyclovir but tetraplegia didn't improve. The NCV study was compatible with polyradiculoneuropathy. Immuno-absorption therapy and administration of prednisolone were performed. Meningoencephalitis associated with increased HSV IgG antibody titer is rare. Auto-allergic process which is initiated by HSV infection may be involved in the pathogenesis of polyradiculoneuropathy in these patients.
OBJECTIVE: To review reported cases of anthrax meningoencephalitis and describe the clinical findings, diagnostic test results, treatment, and outcome over the past 50 years. METHODS: Retrospective review of English language articles published since Haight's (1952) review. RESULTS: Thirty-four core articles were identified, describing 70 patients with cutaneous (29%), gastrointestinal (17%), inhalational (39%), and unknown (16%) sources of infection. Clinical signs on presentation included fever, malaise, meningeal signs, hyperreflexia, and delirium, stupor, or coma. CSF analyses demonstrated hemorrhagic meningitis, with positive Gram's stains and CSF cultures. Many patients presented in extremis following a prodromal period of 1 to 6 days, and 75% died within 24 hours of presentation. Despite aggressive treatment in many cases, only 6% (4 of 70) survived, none of whom had pulmonary anthrax. Surviving patients generally had a cutaneous portal of entry, were younger, and had less severely abnormal initial CSF results than patients who died. Most of the survivors recovered fully. Pathologic findings included hemorrhagic meningitis, multifocal subarachnoid and intraparenchymal hemorrhages, vasculitis, and cerebral edema. CONCLUSIONS: Anthrax meningoencephalitis has a high case-fatality rate, even with aggressive antibiotic treatment and supportive therapy. Hemorrhagic meningitis should raise suspicion of anthrax infection, particularly if gram-positive rods are demonstrated on Gram's stain. Anthrax meningoencephalitis can develop from any primary focus, but survival appears to be most likely if meningoencephalitis develops from cutaneous anthrax. Treatment of surviving patients was generally begun before signs and symptoms of meningoencephalitis were present.
INTRODUCTION: Eosinophilic meningoencephalitis is characterized by a meningeal syndrome and an eosinophilic reaction of the cerebrospinal fluid (CSF). When these symptoms persist for more than four weeks, it is said to be chronic. Both eosinophilic meningoencephalitis and chronic meningoencephalitis are of multiple aetiologies, including fungi. CLINICAL CASE: We report a case in which chronic meningoencephalitis occurred, with persistence of leukocytes, mainly eosinophils, in the CSF. The patient complained of intense, generalized headache and a temperature of 37 degrees C. On physical examination, the only unusual finding was slight neck stiffness. During the clinical course there were focal motor signs and evidence of intracranial hypertension. On CSF culture Candida guillermondii was grown. Treatment with amphotericin B was given, and the neurological disorder remitted completely. CONCLUSION: Candida guillermondii may be the etiological agent in chronic eosinophilic meningoencephalitis.
Since the advent of pandemic of the human immunodeficiency virus infection, the possible pathogens responsible for acute meningoencephalitis have broadened. Human immunodeficiency virus itself can cause acute meningoencephalitis, and the immunocompromise associated with human immunodeficiency virus infection predisposes the infected patients to acute meningoencephalitis caused by a variety of other infectious or non-infectious etiologies. Here reported are 2 cases of acute meningoencephalitis with history of blood transfusion and travel to southeast Asia; both are positive for screening tests of human immunodeficiency virus infection. One of the pathogen causing central nervous system infection, Mycobacterium tuberculosis, was identified by polymerase chain reaction; the other left undiagnosed. It is known that patients of human immunodeficiency virus infection or acquired immunodeficiency syndrome can present with acute central nervous system infection. The need for routine screening of human immunodeficiency virus antibody is currently under debate; nevertheless, the possibility of human immunodeficiency virus infection has to be kept in mind in patients with acute meningoencephalitis.
Nationally synthesized chemopreparations: phosphonoacetic (PAA), phosphonoformic (PFA) acids and acycloguanosine (Acg) exhibit a marked antiherpetic effect in cell cultures and marked protective effect in herpes meningoencephalitis in mice induced by intraperitoneal inoculation of herpes simplex virus type 1 (HSV-1) (43% PFA, 33% PAA, 25% Acg). Both in vitro and in vivo (mouse meningoencephalitis), PFA (its trisodium salt) on the whole proved to be less toxic than PAA but exerted a higher or similar antiherpetic effect. The combined use of pyrophosphate analogues (PAA, PFA) with Acg is more effective that their use separately both in vitro and in herpes meningoencephalitis in mice an produces an additive effect or one similar to it. Systemic inoculation of interferon inducers, lafarine or ridostine, is effective in herpes meningoencephalitis in mice induced by intraperitoneal inoculation of HSV-1 (the protective effect 33% and 26%, respectively). The combined use of ridostine and PAA in herpes meningoencephalitis in mice led to synergistic effect.
PURPOSE: Our purpose was to investigate cerebral blood flow disturbances in patients with bacterial and viral meningoencephalitis. METHODS: Forty-two patients with acute bacterial and viral meningoencephalitis and 14 control subjects were studied using 99mTc-hexamethylpropyleneamine oxime (HMPAO) single-photon emission computed tomography (SPECT). SPECT images were evaluated semiquantitatively. The results were compared with clinical severity of the meningoencephalitis assessed at the time of the SPECT study with the Hunt and Hess scale, with separately recorded focal clinical signs, and with the Glasgow outcome scale (GOS) after 3 weeks. RESULTS: Count density values were significantly reduced in patients with bacterial meningoencephalitis as compared with the control subjects. Inhomogeneous tracer accumulation assessed by asymmetry indexes was significantly greater in patients than in the control group. With increasing Hunt and Hess scores, the count density values decreased and the asymmetry indexes increased. Patients with a poor outcome (GOS 1 to 3) had significantly higher asymmetry indexes and lower CDV values than did patients with a good outcome. CONCLUSION: Global and focal alterations of cerebral perfusion are frequent in bacterial and viral meningoencephalitis and correlate with acute clinical state.
BACKGROUND: The number of children with AIDS in Africa is high. Such children may be at risk for cryptococcal meningoencephalitis, but data are scarce regarding this disease in our population. METHODS: We examined records of HIV-infected children (< or =16 years) diagnosed with cryptococcal meningoencephalitis in Harare, Zimbabwe, between 1995 and 2000. To elucidate features unique to pediatric disease, the children were compared with adult patients with HIV-associated cryptococcal meningoencephalitis. RESULTS: Thirteen children presented to our institution with headache (85%), nuchal rigidity (69%), vomiting (46%), impaired mental status (38%), convulsions (38%) and focal neurologic signs (23%). The mean duration of symptoms before diagnosis was 9 days. Cerebrospinal fluid examination revealed normal white blood cell counts in 64%, protein value in 67% and glucose concentration in 57% of patients. Children were more likely than adults to have seizures (38% vs. 11%, P = 0.02) and normal cerebrospinal fluid protein (67% vs. 10%, P < 0.01). The in-hospital mortality was 43%. Convulsions (P = 0.05) and impaired mental status (P < 0.01) were associated with increased mortality CONCLUSIONS: Cryptococcal meningoencephalitis in African children presents acutely or subacutely, can have a fulminant picture and is consistent with progressive meningoencephalitis.