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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 74 (1987), S. 354-361 
    ISSN: 1432-0533
    Keywords: Toxic oil syndrome ; Neuromyopathy ; Chromatolysis ; Neurotoxicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Five patients died of a severe neuromyopathy months after the ingestion of adulterated rapessed oil. These patients were selected for this study due to the presence of striking chromatolytic lesions in symmetric and scattered nuclei of the brain stem, including the locus coeruleus, midline raphe, lateral reticular nuclei of the medulla and cuneate nuclei. Two of the five cases, in addition to these topographic levels of involvement, had remarkable chromatolysis, vacuolar degeneration and heavy silver impregnation of the swollen perykarya and proximal dendrites in the nuclei of the basis pontis. In this paper we analyze the features of the chromatolytic lesion and suggest that the neuronal pathology observed in these cases is an example of irreversible chromatolysis involving vacuolization and filamentous proliferation as final events of the chromatolytic process. The cause of the cell degeneration in the toxic oil syndrome (TOS) is yet undetermined. Chromatolysis in this disease may be the result of a neurotoxic action of the toxic factor in the adulterated oil.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 47 (1979), S. 75-79 
    ISSN: 1432-0533
    Keywords: Neurotoxicity ; Cyanate ; Demyelination ; Ultrastructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of sodium cyanate (NaNCO) on the nervous system of Maccaca nemestrina were studied at 2, 4, and 6 months of administration of the drug. The two groups injected with daily doses of 35 and 25 mg/kg/day of Na-cyanate developed a predominantly demyelinating lesion in the pyramidal tracts of the spinal cord. No neuronal changes were observed in the motor cortex, basal ganglia, midbrain, medulla or anterior horn cells of the spinal cord. There was no evidence of peripheral neuropathy. A comparison between the cyanate induced neuropathy in the rat and in the primate was drawn. Ultrastructurally, both species developed a demyelinating process of central or peripheral myelin characterized by vacuolation of the myelin sheath, removal of myelin debris by macrophages and re-myelination. There was little evidence of axoplasmic damage except for an occasional distended fiber containing abundant dense bodies and whorls of neurofilaments. Oligodendrocytes and Schwann cells were electron microscopically intact and participated actively in remyelination. Maccacas maintained at 15 mg/day and sham animals remained normal clinically and anatomically. The predominantly myelinotoxic effect of cyanate is similar to that produced by other myelinotoxic agents and is attributed to a selective modification of myelin proteins by carbamylation.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2307
    Keywords: Toxic-oil syndrome ; Vasculitis ; Inflammatory myopathy ; Perineuritis ; Scleroderma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The Toxic Syndrome (TS) caused by ingestion of adulterated rapeseed oil in Spain is a new disease of multisystemic character whose aetiology and pathogenesis remains unknown. The most prominent pathological feature is a peculiar non-necrotizing vasculitis, that affects mainly the intima and involves vessels of every type and size in practically every organ. The TS begins with an acute clinical picture with pleuropneumopathy, fever, headaches, exanthems and eosinophilia. In these early clinical phases the main pathological findings were observed in the lungs and consisted of intense pulmonary interstitial oedema with scanty inflammatory mononuclear infiltrates. Ultrastructural study revealed hydropic degeneration of pneumocytes types I and II with desquamation of type I. The patients in this phase died of respiratory failure, later deaths were due to thromboembolic complications. Later still the patients developped a neuromuscular syndrome, sclerodermiform skin lesions and severe weight loss and died predominantly of infectious complications and respiratory failure. The anatomopathological picture in the peripheral nerves was that of inflammatory neuropathy with a lymphocytic perineuritis that led to perineural fibrosis with secondary axonal degeneration. The muscle presented an interstitial inflammatory myopathy at first followed by a neurogenic muscular atrophy. The skin lesions in the late phases consisted in dermal or dermal and subdermal fibrosclerosis, with vasculitis of the small arteries in the lower dermis. The salivary glands and pancreas showed vasculitis and interstitial inflammation which progressed to interstitial fibrosis and parenchymal atrophy.
    Type of Medium: Electronic Resource
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