A case of Balamuthia mandrillaris meningoencephalitis

Balamuthia mandrillaris is a newly described pathogen that causes granulomatous amebic encephalitis, an extremely rare clinical entity that usually occurs in immunosuppressed individuals. We report a case of pathologically proven Balamuthia encephalitis with unusual laboratory and radiologic findings. A 52-year-old woman with idiopathic seizures and a 2-year history of chronic neutropenia of unknown cause had a subacute illness with progressive lethargy, headaches, and coma and died 3 months after the onset of symptoms. Cerebrospinal fluid (CSF) glucose concentrations were extremely low or unmeasurable, a feature not previously described (to our knowledge). Cranial magnetic resonance imaging scans showed a single large temporal lobe nodule, followed 6 weeks later by the appearance of 18 ring-enhancing lesions in the cerebral hemispheres that disappeared after treatment with antibiotics and high-dose corticosteroids. The initial brain biopsy specimen and analysis of CSF samples did not demonstate amebae, but a second biopsy specimen and the postmortem pathologic examination showed Balamuthia trophozoites surrounded by widespread granulomatous inflammation and vasculitis. The patient's neutropenia and antibiotic use may have caused susceptibility to this organism. Amebic meningoencephalitis should be considered in cases of subacute meningoencephalitis with greatly depressed CSF glucose concentrations and multiple nodular lesions on cerebral imaging. Arch Neurol. 2000;57:1210-1212     

Coxsackievirus B4 myocarditis and meningoencephalitis in newborn twins

Coxsackievirus B4 (CB4) is a picornavirus associated with a variety of human diseases, including neonatal meningoencephalitis, myocarditis and type 1 diabetes. We report the pathological findings in twin newborns who died during an acute infection. The twins were born 1 month premature but were well and neurologically intact at birth. After a week they developed acute lethal neonatal sepsis and seizures. Histopathology demonstrated meningoencephalitis and severe myocarditis, as well as pancreatitis, adrenal medullitis and nephritis. Abundant CB4 sequences were identified in nucleic acid extracted from the brain and heart. In situ hybridization with probes to CB4 demonstrated infection of neurons, myocardiocytes, endocrine pancreas and adrenal medulla. The distribution of infected cells and immune response is consistent with reported clinical symptomatology where systemic and neurological diseases are the result of CB4 infection of select target cells.     

A case of catatonia induced by bacterial meningoencephalitis

A 51-year-old man with renal cell carcinoma developed lethargy, disorientation, and fever; shortly thereafter, he had several episodes of sudden-onset catatonia. He was found to have bacterial meningoencephalitis and frontal lobe EEG abnormalities. Treatment with antibiotic and phenytoin was started, and the catatonic episodes subsided. The authors emphasize the need for a diligent investigation of all possible causes of sudden-onset catatonic syndrome and recommend that bacterial meningoencephalitis be added to the list of differential diagnoses of acute catatonia.     

A case of ischemic stroke secondary to varicella-zoster virus meningoencephalitis

Journal of NeuroVirology - Varicella-zoster virus (VZV) lurks in cranial nerves and other brain ganglias after infection. Because middle cerebral artery (MCA) receives the ipsilateral trigeminal...     

A case of primary HIV infection presenting as meningoencephalitis]

A 23-year-old man presented with disturbance of consciousness and convulsion. Two weeks prior to his admission, he had general arthralgia, retro-orbital pain, and body temperature increase to 40 degrees C. These symptoms persisted for two weeks. He was admitted to the hospital because of general convulsion, followed by disturbance of consciousness. On admission, he was deeply lethargic. Cerebrospinal fluid obtained on admission showed pleocytosis (247/mm3) and an increased level of protein. Electroencephalogram obtained on admission disclosed diffuse slow waves. Enhanced cranial MR image did not show any abnormal lesions in the cerebral parenchyma. The patient was diagnosed as having meningoencephalitis and the treatment consisting of aciclovir, CTRX, and methylprednisolone was undertaken. A test for human immunodeficiency virus (HIV) antibody was found to be positive on the second day of hospitalization. A Western blot was positive with bands at gp160 and P24 confirming HIV infection. Antibody titers of paired acute and convalescent sera including HSV, EBV, CMV, mumps, measles, and Japanese encephalitis did not show any significant increase. The patient became alert on the 3rd day of hospitalization. Electroencephalogram obtained on the 10th day of hospitalization was normal. Western blot, which was obtained 4 months later, was positive with bands at gp120, p68, p55, p52, gp41, p40, p34, p18, including gp160 and P24. He was diagnosed as having primary HIV infection. Meningoencephalitis was attributed to acute primary HIV infection. Acute HIV infection should be considered as an etiology of meningoencephalitis.     

A case of fatal familial insomnia in Africa

Journal of Neurology -     

A case of sarcoid meningoencephalitis with an isolated supratentorial lesion]

A rare case of sarcoid meningoencephalitis with no systemic lesion is reported here. A 58-year old man was admitted experiencing dull headache and speech disturbance. He had never received a diagnosis of systemic sarcoidosis. On admission, neurological examination revealed dysarthria, a defect of the right-side visual field and accelerated right Achilles tendon reflex. A T2-weighted MRI showed a high-intensity signal in the white matter of the left parieto-occipital lobe surrounded by severe brain edema with a mass effect. The meninges around the lesion were enhanced by gadolinium, but no enhancement was observed in the basal portion. Angiotensin-converting enzyme (ACE) activities of cerebrospinal fluid (CSF) and serum were within normal range. The level of interleukin-6 in the CSF was slightly elevated. Chest X ray films and chest CT revealed no abnormal lesions. Whole body gallium scanning showed a hot region only in the intracranial lesion. A brain biopsy was performed. Histological examination revealed typical granuloma of sarcoidosis accompanied by microvasculitis and epithelioid cell granuloma without caseous necrosis. Oral administration of prednisolone improved all symptoms and MRI findings. These observations suggest that release of cytokines from macrophages and epithelioid cells, as well as disruption of the blood-brain barrier due to microvasculitis, are involved in the mechanism responsible for producing lesions of sarcoid meningoencephalitis.     

Acanthameba meningoencephalitis: a case report

A 45 year old lady presented with history of recent surgery for uterovaginal prolapse and retained vaginal tampons following which she developed chronic meningitis due to acanthameba infection. Patient responded to a regimen containing albendazole. She was left with hydrocephalus as a sequelae.     

A case with anti-galactocerebroside antibody-positive Mycoplasma pneumoniae meningoencephalitis presenting secondary hypersomnia

Galactocerebroside (Gal-C) is a major myelin component in the central nervous system. The anti-Gal-C antibody induced by mycoplasma infection may therefore be involved in the pathogenic mechanisms of mycoplasma-associated encephalitis. Here we report an adult case of mycoplasma encephalitis developing excessive daytime sleepiness. Brain MRI suggested that hypothalamic involvement was compatible with hypersomnia. This finding was corroborated by decreased hypocretin-1 in cerebrospinal fluid (CSF) and the manifestation of diabetes insipidus. Screening for anti-glycolipid antibody profiles showed the selective increase of serum anti-Gal-C antibody. After treatment with minocyclin, the patient’s daytime sleepiness was markedly improved and the CSF hypocretin-1 level became almost normal, as well. It is known that CSF hypocretin-1 is decreased in Guillain-Barré syndrome mediated by anti-glycolipid antibody, suggesting a possible mechanistic link between anti-glycolipid antibodies and hypothalamic involvement. The present case further emphasizes the broad spectrum of neurological complications after mycoplasma infection.     

Fulminating cryptococcal meningoencephalitis. An anatomo-clinical case

We report a case of cryptococcal meningoencephalitis in a 52 year-old man. The patient had complained of headache and drowsiness for a few hours before he became comatose with a bilateral sixth cranial nerve palsy. The cerebrospinal fluid contained less than one lymphocyte per cubic millimeter, a low glucose level (0.20 g/l) and numerous Cryptococcus neoformans encapsulated yeasts. A neuropathological study showed that the cortex and midbrain were involved. To our knowledge, such an acute case with death within the first 20 hours has not yet been reported.     

A case of cryptococcal meningoencephalitis and focal cerebral vasculitis with transient immunodeficiency

The AA. report a case of CNS cryptococcosis with vasculopathic complications in a woman in perfect physical conditions. The patient was admitted to hospital after complaining for 20 days of fever, headache and rachialgia. CSF examination revealed hypoglicorrachia (18 mg %), cells 440 mmc (polymorphonuclear leukocytes 90%), brain CT scan negative. During antimycobacterial treatment right hemiparesis appeared; brain CT: hypodense lesion in the posterior brachium of the left inner capsule; at its base the lesion showed a hypodense streak coherent with thromboembolic damage or deep vasculitis. OKT4 lymphocytes were 6% (absolute number: 70). The antimycotic treatment, following the positive reaction of the CSF culture to Cryptococcus Neoformans, entirely cured the hemiparesis and normalized the CSF while OKT4 lymphocytes rapidly grew.     

Monosporium apiospermum meningoencephalitis: a clinico-pathological case.

Twenty nine cases of central nervous system infection due to Monosporium apiospermum have been reported. Six of them occurred after an aspiration pneumonia following a near drowning. The case of a 53 year old man is reported: M apiospermum was isolated from cerebrospinal fluid, sputum, urine and from the mud of the ditch where the patient had fallen. Though the treatment used recommended doses of intravenous, intrathecal and intraventricular amphotericin B, it was ineffective and the patient died 97 days after the near drowning. Necropsy showed that the ventricular infectious process was more prominent distant from the antifungal ventricular source.     

A case of meningoencephalitis caused by persistent Epstein-Barr (E-B) virus infection

A 44-year-old man had several episodes of tingling sensation in his lower extremities, head and face over 1 year and presented mental disturbance 2 months prior to admission. He additionally suffered from dysuria and acute onset of gait disturbance 18 days before admission. Physical and neurological examination revealed marked splenomegaly, stupor, abnormal behavior, spastic tetraparesis and sphincter disturbances, and meningoencephalitis was suspected. There was lymphocytosis in peripheral blood, some of which showed atypical morphology. CSF examination revealed increased protein content and mononuclear pleocytosis. The titers of antibodies against E-B virus were elevated as follows; VCA IgM (X320), VCA IgG (X20,480), EA (X10,240) and EBNA (X10) in serum, and VCA IgM (X4), VCA IgG (X160), EA (X40) and EBNA (less than 1) in CSF. CT and MRI examination revealed ring enhanced lesion adjacent to left lateral ventricle with surrounding diffuse edema. Administration of intravenous glycerol and oral prednisolone induced substantial improvement in sensory, mental and sphincter disturbances and brain CT findings but not in splenomegaly and pyramidal tract signs. Antibody titer against VCA IgM also decreased. After withdrawal of prednisolone, CSF and CT findings worsened, and the antibody titer became elevated again, and CSF and CT findings improved by readministration of prednisolone. From the above signs and laboratory data, especially continuous elevation of antibody titer against E-B VCA IgM for as long as 1 year, this case was considered to be a meningoencephalitis caused by persistent E-B virus infection.