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Two cases of peripheral facial paralysis associated with infection by the human immunodeficiency virus in young intravenous drug abuser patients are reported. One patient manifested AIDS-related complex (ARC) and the other fulfilled the Center for Disease Control (CDC) criteria for AIDS. Clinical symptoms and signs occurred as facial paralysis and headache. One patient presented progressive motor slowing and the computerized tomography (CT) of the brain showed a wide hypodense lesion in the left temporal-anterior region and the involvement of the left basal ganglia. In this patient the impairment of the facial nerve was associated with a HIV-related encephalitis. In the second patient the CT did not show cerebral lesions and the etiology of the paralysis was unknown.
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PMID:[Peripheral facial paralysis and HIV infection]. 175 30

Listeriosis occurred in two patients, a 46-year-old woman and a 41-year-old man, in the course of an underlying malignant disease. The woman had a metastasizing pancreatic apudoma, requiring partial pancreas resection with splenectomy. After the end of cytostatic treatment she developed headaches and fever up to 40 degrees C. Listeria monocytogenes was demonstrated in the blood and cerebrospinal fluid. She went into coma on the day after hospital admission and, despite antibiotic administration, she died on the fourth day of treatment. The 41-year-old man was suspected of having an angioimmunoblastic lymphoma. Severe haemolytic anaemia (haemoglobin 4.4 g/dl) was treated with glucocorticoids, massive blood transfusions and splenectomy, at first without success. During immunosuppressive treatment with prednisone and cyclophosphamide the haemoglobin rose. But he was still feverish with nocturnal sweating. Neurological symptoms of motor aphasia, cranial nerve deficits and incomplete hemiparesis rapidly developed. Computed tomography revealed a focus in the internal capsule. Blood culture grew Listeria. The focal encephalitis healed with minor sequelae after antibiotic treatment. Both patients had hypogammaglobulinaemia, but no granulocytopenia. It is stressed that listeriosis should be included in the differential diagnosis in cases of septicaemia or cerebral infection occurring in the course of malignant disease.
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PMID:[Listeriosis in malignant diseases]. 190 99

A case of acute cryptococcal cerebellar encephalitis with CT enhancement confined to the cerebellum is reported. A 46-year-old man with hepatoma was admitted with chief complaints of headache, fever and dizziness. On admission, cerebellar signs (disturbance of finger-to-nose test and of heel-to-knee test, intention tremor, and truncal ataxia) were neurologically noted. However, there were no brainstem signs. Head CT showed swelling and enhancement of the cerebellar cortex and dilatation of the cerebral ventriculi. Cryptococcus neoformans was detected in a culture of the patient's CSF. Clinical symptoms and signs, and enhancement of the cerebellum on CT gradually diminished after administration of anti-fungal drugs, and CSF became negative for cryptococcal antigen 6 months after admission.
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PMID:[A case of acute cerebellar encephalitis due to Cryptococcus neoformans]. 193 83

From 1988 to 1990, we observed five cases of aseptic dural sinus and cerebral venous thrombosis, all in non-smoking women (age 18 to 47 years) receiving low dose oral contraceptives. Treatment consisted of full anticoagulation over 2 to 6 months, over which time the neurologic symptoms disappeared almost completely. Extensive tests of the blood clotting system in 4 patients after 6 to 19 months revealed a reduction of free protein S in 2 patients with a history of contraceptive use over several years, and normal results in 2 patients in which the sinus thrombosis occurred within the first 6 weeks of use of the oral contraceptive. Whether the protein S deficiency was congenital or caused by the oral contraceptive cannot be decided retrospectively. Even modern oral contraceptives seem to lead to an increased incidence of sinus thrombosis. Initial symptoms of sinus thrombosis include headache and somnolence, followed either by focal neurologic deficits (often associated with focal seizures) or by signs of increased intracranial pressure. CT scans show venous infarcts or general brain edema and may specifically show the "empty triangle sign" and "delta sign". The CT scan may also be normal if focal neurologic deficits are absent. MRI is favoured as it can directly show the thrombosed sinus or veins. Differential diagnosis includes arterial stroke, brain tumor, encephalitis or "benign intracranial hypertension", which should only be diagnosed after sinus venous thrombosis has been appropriately ruled out. Recently, full anticoagulation has been recommended as therapy.
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PMID:[Aseptic cerebral sinus thrombosis. 5 cases and a review]. 194 57

Vogt-Koyanagi-Harada syndrome is a rare disease, which probably has a cell-mediated autoimmune pathogenesis, marked by ocular (anterior and/or posterior uveitis), dermatological (poliosis, canities, vitiligo) and neurological (meningo-encephalitis) disorders of variable severity in variable combinations. The clinical pattern in the case reported here showed severe neurological involvement (headache, ataxia and confusional state) followed by anteroposterior uveitis. Instrumental investigations (cerebrospinal fluid, VEPs, BAEPs, EEG, CT and MRI brainscans) confirmed the diagnosis. The response to cortisone therapy was excellent. We emphasize the importance of the neuroradiological investigations, because of their peculiarities, and review the reports of cases with marked meningo-encephalitic impairment, given the dearth of reports in the neurological journals.
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PMID:Vogt-Koyanagi-Harada syndrome: clinical and instrumental contribution. 195 5

We analysed two of our own and 21 patients described in the literature with listeria brainstem encephalitis. The disease was characterised by a prodromal state with fever, nausea and headache followed by severe brainstem dysfunction with multiple cranial nerve palsies, ataxia, respiratory insufficiency and coma. The diagnosis was established by isolation of Listeria monocytogenes from CSF and/or serum. Serological tests are without diagnostic evidence. Cerebrospinal fluid examination may not initially point to a bacterial infection. Computed tomography and magnetic resonance imaging technique might supply evidence of brainstem involvement and contribute to an early diagnosis. There is a high percentage of lethal outcome without early antibiotic therapy.
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PMID:Listeria brainstem encephalitis: two own cases and literature review. 201 6

Mumps virus is one of the most common causes of viral meningitis. Although brain involvement has been observed in a low proportion of children with mumps meningitis, a pure form of mumps encephalitis is extremely uncommon in the adult. A 23 year-old man presented with a rapidly evolving syndrome of cephalalgia , vomiting, mutism, disorders of gait, somnolence and dystonic movements. The electroencephalogram showed a diffusely slowed background activity. The CSF contained no cells, but the total protein concentration was elevated. The patient recovered without sequelae, but severe intellectual and motor disturbances persisted during more than a month. Serological studies showed an increase of blood IgM mumps-specific antibodies. We conclude that mumps encephalitis, although infrequent, should be considered among viral diseases that mimic herpes simplex encephalitis in the adulthood.
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PMID:[Mumps encephalitis in adulthood]. 205

We report two cases of cytomegalovirus (CMV) encephalitis in immunologically normal adults. Patient 1, a 53-year-old man: onset was acute with headache and pyrexia, followed by moderate disturbance of consciousness with meningeal signs. Repeated lumbar puncture revealed 58 CSF cells per microliters and 96 mg protein per dl. On the 11th day after onset, we started treatment with adenine arabinoside (ara-A). He recovered completely. With IgG-ELISA methods, antibody to CMV turned into positive on the third week, and into negative again on the fifth week, and these conversions were concomitant with the symptomatic aggravation and amelioration, respectively. Patient 2, a 78-year-old woman: onset was acute with general fatigue and pyrexia, followed by meningeal signs and mild disturbance of consciousness. Consciousness level was worsened and two courses of acyclovir (Acv) treatment were started on the 59th and on the 93rd day after onset, but consciousness level went down to coma and she died. Repeated lumbar puncture revealed 787 CSF cells per microliters and 229 mg protein per dl. CMV antibody titer (CF) in CSF was 1:32 and antibody index was 58 or more, suggesting antibody production in central nervous system. CMV encephalitis in immunologically normal adults is very rare, only 10 cases having been reported so far. Most patients recover spontaneously, but some may be fatal. In our view ara-A treatment should be taken in consideration in case of acute encephalitis unresponsive to Acv.
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PMID:[Cytomegalovirus encephalitis in immunologically normal adults]. 216 21

All major types of human interferons (IFNs) have been purified and clinically administered as antitumor agents. We summarize here experience to date with toxicity of IFNs in cancer patients. The acute syndrome consists of fever, chills, myalgias, arthralgias, and headache, with some variation according to type of IFN, route of administration, schedule, and dose. Fatigue, perhaps reflecting CNS toxicity, is the most prevalent nonacute symptom. At high doses, IFNs are neurotoxic; the abnormalities seen by EEG resemble those in diffuse encephalitis. Hematologic toxicity consists mainly of leukopenia, but anemia and thrombocytopenia occur in some patients. Nausea, vomiting, and diarrhea are the main gastrointestinal symptoms. Elevation of serum transaminases seems to reflect liver toxicity. Renal function is well preserved, except for rare instances of acute renal failure. Cardiac toxicity remains questionable, although heart failure and arrhythmias have been associated with the administration of IFNs. Most, if not all, of these effects are reversible or can be ameliorated. With IFN alpha, the type most widely used in clinical studies, doses of 1 million to 9 million units (MU) are generally well tolerated, but doses greater than or equal to 18 MU yield moderate to severe toxicity. Doses greater than or equal to 36 MU can induce severe toxicity and significantly alter the performance status of the patient.
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PMID:Clinical toxicity of interferons in cancer patients: a review. 241 69

In the literature there are rare reports on Japanese encephalitis (JE) mimicking poliomyelitis or presenting as respiratory paralysis. A case of JE presenting as respiratory paralysis is described. The 22-year-old male was well until five days earlier, when he experienced the acute onset of headache and fever. Four days after onset he developed dysphagia and respiratory difficulty, and a tracheotomy was performed. The following day he lapsed into semicoma and the respiration had to be maintained by an artificial ventilator. He regained consciousness by the 10th day after onset. He became able to comprehend questions and express himself by gestures. But the respiration was still paralytic, and assisted ventilation via a tracheotomy had to be continued. The case was clinically diagnosed as encephalitis. Bulbar poliomyelitis was initially considered due to the clinical features of aseptic meningitis, respiratory paralysis, pharyngeal paralysis with pooling secretions in the pharynx, tachycardia and elevated blood pressure. But poliovirus culture obtained from stool and appropriate serological studies were negative. The diagnosis of encephalitis due to JE virus was confirmed by hemagglutination inhibition test (acute phase HI titer 1:320; convalescent phase HI titer 1.1280).
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PMID:Respiratory paralysis as a presenting symptom in Japanese encephalitis--a case report. 255 72


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