1/7. Subacute central nervous system degeneration in a child: an unusual manifestation of ifosfamide intoxication.A 5-year-old child with desmoplastic small round-cell tumor was treated with a protocol of very-high-dose, short-term chemotherapy, containing HD-CAV (cyclophosphamide, doxorubicin, vincristine, and mesna), ifosfamide, and etoposide. Two days after the initiation of ifosfamide, he exhibited new-onset lethal encephalopathy manifested by subacutely progressive cerebellar and then temporal and frontocortical degeneration leading to a vegetative state and eventually to death. A full work-up, including brain biopsy, was negative, excluding infections and metabolic or vascular causes. ifosfamide is known to be capable of causing acute encephalopathy that can be severe but is generally reversible. This child showed a very atypical progressive, lethal course of ifosfamide toxicity. The possibility of this complication should be considered when high-dose ifosfamide treatment is planned for children.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
2/7. Neuropathy due to podophyllin intoxication.A 22-year-old man developed a severe sensorimotor neuropathy following ingestion of podophyllin, which had been prescribed for genital condylomata. The initial toxic symptoms were vomiting and diarrhoea, followed by peripheral neuropathy. The neuropathy was still present 18 months later. Nerve conduction studies and sural nerve biopsy confirmed the presence of axonal degeneration.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
3/7. phenytoin-related cerebellar degeneration without seizures.Cerebellar changes have been reported in relationship to epilepsy alone as well as to phenytoin therapy for the control of seizures. The cliniconeuropathological correlation between these changes and epilepsy or the anticonvulsant is usually complicated by the presence of both variables. Experimental evidence suggests that phenytoin alone may be sufficient to cause cerebellar changes following intoxication. We report a case of cerebellar degeneration in a patient treated with isoniazid and prophylactically treated wtih phenytoin who never had a seizure.- - - - - - - - - - ranking = 0.25keywords = intoxication (Clic here for more details about this article) |
4/7. Clinical and neuropathological aspects of long-term damage to the central nervous system after lithium medication.A female patient, who died at the age of 61 and had suffered from several manic-depressive psychoses for more than 30 years, developed three phases of intoxication under lithium therapy. There was a 15-year history of electro- and Pentetrazol-induced convulsive therapy prior to lithium medication; neuroleptics were still administered during lithium therapy. The last lithium intoxication, 3 years prior to death was during a low-dosage therapy with normal lithium levels followed by severe lasting impairment: akinesia, rigidity, dysarthria, ataxia, and an organic alteration in character. For the first time, neuropathological findings could be established in such a case: extensive damage to granule and purkinje cells in the cerebellum; gliosis in the dentate nucleus, the inferior olives, and the nucleus ruber; cytoplasmic inclusions in various nerve cells of the cranial nerve nuclei; cytoplasmic vacuoles, especially in the cells of the supra-optic nucleus. Surprisingly little damage could be found in the substantia nigra and in the neostriatum. The clinical course as well as the pattern and intensity of the brain damage oppose an interpretation as a consequence of preceding convulsive shock therapy.- - - - - - - - - - ranking = 0.5keywords = intoxication (Clic here for more details about this article) |
5/7. Chronic thinner intoxication: clinico-pathologic report of a human case.A 27 year old Mexican male addicted for 12 years to glue-sniffing and thinner inhalation developed neurological and behavioural disturbances which led to hospital admission and death. autopsy disclosed diffuse cerebral and cerebellar cortex atrophy and giant axonopathy both central and peripheral. The corpus callosum was atrophic secondarily to neuron loss in the neocortex.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
6/7. germanium intoxication with sensory ataxia.Sensory ataxia in inorganic germanium intoxication is rare. A 63-year-old housewife had taken inorganic germanium preparations at a dosage of 36 mg a day for about 6 years (total dose about 80 g). She subsequently developed difficulty in writing and gait disturbance with peripheral neuropathy and renal involvement. germanium, which is not usually detected in the non-germanium user, was accumulated in her hair and nails, permitting a diagnosis of inorganic germanium intoxication. The peripheral neuropathy and renal injury were not reversible after discontinuing the preparation. pneumonia and sepsis then supervened and the patient died. autopsy findings showed degeneration and loss of the dorsal root ganglion cells and degeneration of the dorsal column of the spinal cord. Two previously reported cases presented with ataxia. These patients took germanium for long periods and/or large quantities like our case. It was supposed that sensory ataxia was induced by chronic and dose dependent toxicity of inorganic germanium.- - - - - - - - - - ranking = 1.5keywords = intoxication (Clic here for more details about this article) |
7/7. carbon disulfide induced polyneuropathy: sural nerve pathology, electrophysiology, and clinical correlation.We report the clinical features, electrophysiological studies, sural nerve pathology and recovery course of carbon disulfide-(CS2) induced polyneuropathy in a 48-year-old man who worked in a viscose rayon plant. sural nerve biopsy 2 years later still showed degeneration of both axon and myelin with a predominant loss of large myelinated fibers and remyelination. Electrophysiologic studies revealed mixed axonal and demyelinating polyneuropathy. To our knowledge, this is the first human report of sural nerve pathology in the recovery stage due to CS2 intoxication. After diagnosis, the patient was removed from the toxic environment. In the following three years, he showed part recovery predominantly in motor function compatible with the serial nerve conduction studies. We conclude that CS2 polyneuropathy may partly recover years after cessation of exposure.- - - - - - - - - - ranking = 0.25keywords = intoxication (Clic here for more details about this article) |