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  • 1
    Electronic Resource
    Electronic Resource
    Granulomatous Amebic Encephalitis presenting as a cerebral mass lesion (1980)
    Springer
    Acta neuropathologica 51 (1980), S. 85-91 
    Details
    ISSN: 1432-0533
    Keywords: Acanthamoeba ; Amebic encephalitis ; Corticosteroids ; Free-living amebas ; Immunosuppression ; Intracranial mass ; Naegleria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Clinical and brain biopsy or autopsy findings in six patients with Granulomatous Amebic Encephalitis (GAE) due toAcanthamoeba sp. were characterized by focal neurological symptoms, increased intracranial pressure, and focal neuroradiological findings. Craniotomies were performed because of the diagnostic possibility of a mass lesion such as a brain tumor or abscess. In four patients, frozen sections demonstrated free-living amebas. GAE may present as an acute or subacute intracerebral mass lesion with signs and symptoms of focal brain disease and should be differentiated from viral, bacterial, fungal, and other protozoal encephalitides.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690448
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  • 2
    Electronic Resource
    Electronic Resource
    Granulomatous encephalitis, intracranial arteritis, and mycotic aneurysm due to a free-living ameba (1980)
    Springer
    Acta neuropathologica 49 (1980), S. 7-12 
    Details
    ISSN: 1432-0533
    Keywords: Free-living amebas ; Encephalitis ; Granuloma ; Acanthamoeba ; Naegleria ; “Mycotic aneurysm”
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Primary amebic meningoencephalitis and granulomatous amebic encephalitis are well recognized clinicopathological entities caused by free-living amebas. Associated arteritis and “mycotic aneurysms” with infiltration of intracranial arteries by lymphocytes, amebic trophozoites and cysts have not been previously reported. A 26-month-old girl had a 3-week history of encephalitis, characterized, initially, by vomiting and lowgrade fever. Subsequently, she developed ataxia, generalized weakness, lethargy, and esotropia. The first CSF showed 490 RBC/μl, 705 WBC/μl with 90% mononuclears. Her pupils reacted briskly to light. Moderate nuchal rigidity, nystagmus, fixed downward gaze, anisocoria, bilateral 6th nerve palsy, left arm monoparesis and left Babinski were present. CAT scan revealed slight symmetrical dilatation of anterior horns of lateral ventricles and an area of abnormal enhancement above the 3rd ventricle. She died 14 days after admission, 5 weeks after onset of symptoms. The brain showed focal necrotizing encephalopathy, involving thalami, cerebellum, brain stem, and cervical and upper thoracic spinal cord. Numerous free-living amebic trophozoites and cysts were present within a chronic granulomatous encephalitis. There were thrombosis of basilar, posterior cerebral, and vertebral arteries with profuse chronic panarteritis, fibrinoid necrosis, and mycotic aneurysms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00692213
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Progressive multifocal leukoencephalopathy with paramyxovirus-like structures, Hirano bodies and neurofibrillary tangles (1974)
    Springer
    Acta neuropathologica 27 (1974), S. 277-288 
    Details
    ISSN: 1432-0533
    Keywords: Progressive Multifocal Leukoencephalopathy ; Hirano Bodies ; Papova Virus ; Paramyxovirus-like ; Nuclear Bodies ; Electron Microscopy ; Neurofibrillary Tangles
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have identified three structures that have not previously been reported in electron microscopic examinations of brain from patients with PML: 1. coiled nuclear bodies that may possibly represent tubular paramyxovirus nucleocapsids, 2. Hirano bodies and 3. Neurofibrillary tangles. The paramyxovirus-like material is interesting in view of reports of a transition between nuclear bodies and tubular paramyxovirus nucleocapsids and because of a possible interaction between syncytiogenic paramyxoviruses and Papova viruses in the pathogenesis of SSPE and PML. A study of the Hirano bodies in this case, taken in conjunction with the findings of others leads us to believe that these structures are formed from an overgrowth of neurofilaments. The presence of tangled masses of neurofilaments in the processes of neurons also seen in the present case is consistent with this hypothesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690693
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  • 4
    Electronic Resource
    Electronic Resource
    Acute hexachlorophene encephalopathy: Clinico-neuropathological correlation (1974)
    Springer
    Acta neuropathologica 28 (1974), S. 93-103 
    Details
    ISSN: 1432-0533
    Keywords: Hexachlorophene Intoxication ; Toxic Encephalopathy ; Optic Nerve Necrosis ; Cerebral Edema ; Status Spongiosus ; Electron Microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This is the first report of neuropathologic findings following oral ingestion of hexachlorophene in the human. The patient was a 7 year old boy who accidentally ingested 45 ml (approx.) of pHisoHex (hexachlorophene).Toxic reactions included nausea, vomiting, anorexia, diarrhea, decrease in visual acuity, blurred vision blindness, somnolence and disorientation. He developed cardiac arrhythmia, fever, isoelectric EEG and finally respiratory and cardiac arrest 61 h after admission. Autopsy findings showed interstitial myocarditis, pneumonitis and acute bronchiolitis. The brain was edematous. Light microscopy revealed mild diffuse vacuolization of white matter, occasional neuronal degeneration, most prominent on deepest layers of the visual cortex. Disintegration of myelin sheaths and necrosis of axon cylinders were present throughoutoptic pathways. Electron microscopy revealed large, empty extracellular and intramyelinic spaces formed by splitting and separation of the myelin lamellae. These changes are known to occur in experimental animals intoxicated with hexachlorophene, triethyltin, isonicotinic acid hydrazide and cuprizone. However, with respect to hexachlorophene, the localization of lesions to be optic pathways appears to be dependent upon an oral route of administration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00710320
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  • 5
    Electronic Resource
    Electronic Resource
    Meningoencephalitis due to acanthamoeba SP (1977)
    Springer
    Acta neuropathologica 37 (1977), S. 183-191 
    Details
    ISSN: 1432-0533
    Keywords: Acanthamoeba ; Naegleria ; Meningoencephalitis ; Granulomatous ; Free-living amebas ; Cysts ; Trophozoites
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Amebic Meningoencephalitis (AM) and Primary Amebic Meningoencephalitis (PAM) are infectious diseases essentially confined to the Central Nervous System (CNS) and caused by free-living amebas of the genusAcanthamoeba (A.) andNaegleria (N.) respectively. AM due toA. sp. (Acanthamoeba castellanii andAcanthamoeba culbertsoni) have been reported in chronically ill debilitated individuals, some of them under immunosuppressive therapy, or in immunologically impaired patients without a history of recent swimming in contrast to cases due toN.sp. which usually occurs in healthy, young individuals with a recent history of swimming in man-made lakes or heated swimming pools. AM due toA.sp. is characterized by a subacute or chronic granulomatous meningoencephalitis involving mainly the midbrain, basal areas of the temporal and occipital lobes and posterior fossa structures. CNS lesions in AM are perhaps secondary and the portal of entry in humans is probably from the lower respiratory tract, genitourinary system or skin reaching the CNS by hematogenous spread. The predominant host reaction is usually composed of lymphocytes, plasma cells, monocytes and multinucleated foreign body giant cells. Necrosis is moderate and hemorrhage scant or absent. Cysts as well as trophozoites may be seen within the CNS lesions. PAM is due toNaegleria fowleri and is characterized by an hemorrhagic necrotizing meningoencephalities with an acute inflammatory response. Only trophozoites are found in lesions. The portal of entry is through the olfactory neuroepithelium. CNS tissues fixed in formalin may be used for further identification and taxonomical classification of the causative protoza using immunofluorescent antibody techniques (IFAT) and electron microscopic methods.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00686877
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  • 6
    Electronic Resource
    Electronic Resource
    Aseptic meningitis due to atheromatous material in the subarachnoid space (1974)
    Springer
    Acta neuropathologica 30 (1974), S. 145-154 
    Details
    ISSN: 1432-0533
    Keywords: Aseptic Meningitis ; Atheromatous Material ; Hypersensitivity ; Electron Microscopy ; Macrophages ; Pia-Arachnoid ; Granuloma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 500 mg of sterile pooled human atheromatous material was injected into the cisterna magna of 6 mongrel dogs. Repeated cisternal punctures were done at various intervals until sacrifice from 1 day to 28 days following injection. CSF was obtained for cell count, sugar, protein and analysis in the Technicon 6/60 which measured 14 additional chemical and enzymatic variables. All 6 animals showed a prompt cerebrospinal fluid (CSF) pleocytosis which largely subsided during the first 2 weeks after injection. Increased CSF protein content developed more slowly, but was more prolonged than the pleocytosis. There was a variable decrease in CSF sugar and increase in CSF lactate dehydrogenase, calcium and inorganic phosphorous. Light and electron microscopic studies showed an intense acute inflammatory reaction with marked phagocytosis of the foregin material, probably by arachnoidal cells and moderate edematous changes in the astrocytic processes at the site of injection. During the first 2 weeks after the injection the inflammatory reaction became chronic and the edematous changes in the medulla subsided.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685439
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