1/13. Long-term psychological and neurological complications of lindane poisoning.A thin, healthy, partial-vegetarian, white female, who was exposed to three doses of lindane (through the application of Kwell), developed a severe case of long-term lindane poisoning. review of the literature suggests that her toxicity was so severe because of the repetitive nature of her exposure and the fact that she was partly protein restricted when first exposed. She developed profound central nervous system toxicity, as well as skin and gastrointestinal changes, that persisted for 20 months. She was treated with high doses of Valium. It was noted that every time her Valium was diminished below a critical level, her symptoms tended to recur until she had adequately cleared the lindane from her system. We believe this is the longest term of poisoning reported following exposure to an organochloride insecticide. Her symptoms are well explained by the physiology of these compounds as described in the literature. The case is important, for it represents the longest persistence of symptoms clearly associated with poisoning by the potent gamma isomer of BHC-lindane.- - - - - - - - - - ranking = 1keywords = organ (Clic here for more details about this article) |
2/13. multiple chemical sensitivity (MCS)--differential diagnosis in clinical neurotoxicology: a German perspective.The multiple chemical sensitivity syndrome (MCS) is a new cluster of environmental symptoms which have been described and commented on for more than 15 years now in the USA. In the meantime it has also been observed in European countries. The main features of this syndrome are: multiple symptoms in multiple organ systems, precipitated by a variety of chemical substances with relapses and exacerbation under certain conditions when exposed to very low levels which do not affect the population at large. There are no lab markers or specific investigative findings. In our view, MCS is not a separate clinical syndrome but a collective term. A very small part of the patients in question may actually exhibit a somatic or psychosomatic response to low levels of a variety of chemicals in the environment. For another part, even if the MCS symptoms are induced by chemical substances in the environment, the basic hypersensitivity is a psychological stress reaction. In the third and largest group, the patients have been misdiagnosed, i.e. a somatic or psychiatric disease has been overlooked. There is a fourth group of patients in whom there is no evidence of any exposure at all but instead a belief system installed by certain physicians, the media and other groups in society. This paper tries to describe the neurological and neurotoxic aspects of MCS problems and to illustrate it with examples of an alleged outbreak of chronic neurotoxic disease caused by pyrethroids in germany. research strategy should establish clearly determined diagnostic criteria, agreement on the use of specific questionnaires as well as clinical and technical diagnostic procedures, prospective clinical studies of MCS patients and comparative groups as well as experimental approaches.- - - - - - - - - - ranking = 1keywords = organ (Clic here for more details about this article) |
3/13. muromonab-cd3-induced neurotoxicity: report of two siblings, one of whom had subsequent cyclosporin-induced neurotoxicity.muromonab-cd3 is widely used for immunosuppression in patients undergoing solid organ transplant. We report two siblings with oligomeganephronia and end-stage renal disease who developed encephalopathy and seizures from muromonab-cd3 following renal transplant. The first case is a 13-year-old girl who developed encephalopathy, seizure, and triparesis following renal transplant while muromonab-cd3 was used for immunosuppression. The second case was the 6-year-old sister of the first case, who also developed recurrent focal seizures while she was on muromonab-cd3 for renal transplant immunosuppression. In both cases, a sequential brain magnetic resonance image (MRI) showed progression of abnormalities from the cerebral cortex to the white matter. In the first case, the MRI normalized after muromonab-cd3 was discontinued. In the second case, the patient developed a leukoencephalopathy following cyclosporin administration. The pathophysiology of muromonab-cd3 encephalopathy is believed to be a disturbance to the blood-brain barrier mediated by cytokine release from lymphocyte stimulation by muromonab-cd3. Because the major histocompatibility complex genes are known to regulate cytokine responses, it is possible that the excessive production of cytokines that causes encephalopathy may occur in patients who share close major histocompatibility complex genes. muromonab-cd3 in a patient whose sibling has developed cerebral complications from its use should be administered with caution. The second case suggests that muromonab-cd3 encephalopathy predisposes patients to develop cyclosporin neurotoxicity. Because the pathogenesis of muromonab-cd3 encephalopathy and cyclosporin-related cerebral complications are both potentially mediated through a disturbance of the blood-brain barrier, it is possible that one agent may predispose a patient to the complication of the other.- - - - - - - - - - ranking = 1keywords = organ (Clic here for more details about this article) |
4/13. Enhanced vincristine neurotoxicity from drug interactions: case report and review of literature.This study reports observed toxicity in a child with acute lymphocytic leukemia who had received vincristine (VCR) with nifedipine and itraconazole. A 5-year-old-child with leukemia developed bilateral cranial nerve palsies, severe peripheral neuropathy involving upper and lower extremities, seizures, hypertension, heart failure, and syndrome of inappropriate antidiuretic hormone secretion after being treated with VCR, nifedipine, and itraconazole. Appropriate management of the above problems including discontinuation of VCR resulted in recovery from neurotoxic manifestations. Concurrent administration of VCR with nifedipine and itraconazole may enhance its neurotoxicity.- - - - - - - - - - ranking = 3.1583644731181keywords = nerve (Clic here for more details about this article) |
5/13. A case of neurotoxicity following 5-fluorouracil-based chemotherapy.5-fluorouracil (5-FU) is a commonly used chemotherapeutic agent. However, its neurotoxicity is rare and not well recognized. We report a case of 5-FU neurotoxicity with organic brain syndrome and progression to multifocal leukoencephalopathy in a 44-year-old male patient having malignant gastrointestinal stromal tumor. 5-FU-induced neurotoxicity should, therefore, be considered as an important differential diagnosis in cancer patients with neurological abnormality and history of chemotherapy.- - - - - - - - - - ranking = 1keywords = organ (Clic here for more details about this article) |
6/13. Neuropathy in an artist exposed to organic solvents in paints: a case study.A 61-year-old artist in israel had been painting for 30 years in his home studio. He had been healthy until he reached the age of 59.5 years, at which time he began complaining of weakness and paresthesia in both hands and legs. He also complained that he had difficulty concentrating, and his memory was impaired. His work was unusual in that he painted large posters (i.e., 2 x 3 m) with different mixtures of organic solvents, including toluene, xylene, benzene, methyl ethyl ketone, toluene diisocyanate, acetone, and thinner. He did not use any protective gloves and did not wear a mask. He was evaluated with several methods and was diagnosed as having peripheral and central neuropathy, including ototoxic hearing loss as a result of long exposures to organic solvents. The authors were unable to find any similar case report in the literature.- - - - - - - - - - ranking = 6keywords = organ (Clic here for more details about this article) |
7/13. autopsy case of aluminum encephalopathy.We report the case of a 59-year-old female aluminum encephalopathy patient who had chronic renal failure and took 3.0 g hydroxy-aluminum gel per day for the control of serum phosphorus level during a 15-year period. Nine months before her death she developed disorientation, memory disturbance, emotional incontinence, general convulsions and consciousness disturbance. Neuropathologically, the brain showed nerve cell atrophy and mild loss with stromal spongiosis, proliferation of astrocytes and microglia in the cerebral cortex, basal ganglia and thalamus. Some nerve cells were stained immunohistochemically by phosphorylated neurofilament, but apparent neurofibrillary tangles were not observed. aluminum was detected in the nerve cells of the cerebral cortex by X-ray microanalysis. Despite the long-term intake of aluminum, there were no neuropathological findings of Alzheimer's disease. The findings in our case suggested that aluminum alone might not develop Alzheimer's disease.- - - - - - - - - - ranking = 9.4750934193542keywords = nerve (Clic here for more details about this article) |
8/13. thalidomide-induced neuropathy.BACKGROUND: thalidomide is effective for the treatment of some refractory dermatologic and oncologic diseases. Toxic neuropathy limits its use, as embryopathy can be avoided by contraceptive measures. OBJECTIVE: To describe the clinical, electrophysiologic, and pathologic features of thalidomide-induced peripheral neuropathy. methods: Clinical and electrophysiologic examinations were performed in seven patients with thalidomide-induced peripheral neuropathy. thalidomide was used for graft-vs-host disease, pyoderma gangrenosum, and discoid lupus with dosages ranging from 100 to 1,200 mg/day for 5 to 16 months (cumulative dosages of 24 to 384 g). RESULTS: All seven patients had clinical and electrophysiologic evidence of a sensory more than motor, axonal, length-dependent polyneuropathy that presented as painful paresthesias or numbness. sural nerve biopsies, done in three patients, showed evidence of wallerian degeneration and loss of myelinated fibers. The symptoms, signs, and electrophysiologic data correlated with total cumulative dose of thalidomide. CONCLUSIONS: thalidomide induces a dose-dependent sensorimotor length-dependent axonal neuropathy; it should be judiciously used with close neurologic monitoring.- - - - - - - - - - ranking = 3.1583644731181keywords = nerve (Clic here for more details about this article) |
9/13. health effects of diazinon on a family.There is increasing evidence of permanent sequalae from acute organophosphate poisoning. We report on accidental diazinon overexposure with acute organophosphate poisoning through cutaneous absorption and inhalation followed by persistent neurological effects. In addition, we observed skeletal and endocrine effects likely attributable to the diazinon poisoning. A family of seven was exposed to diazinon in June 1999 over a two-day period. The pesticide company mistakenly used diazinon to heavily spray the inside of the home instead of permethrin. The applicator applied the pesticide over the entire surface of the floor, carpeting, furniture, and clothing in closets to eradicate an infestation of fleas. Acute symptoms in the family members included headaches, nausea, skin irritation, runny nose, and vomiting. The family was first evaluated at 3 months and then 3 years after the acute poisoning. There were persisting neurological symptoms of memory loss, decreased concentration, irritability, and personality changes of varying degrees in all family members. Objective neurological findings of impaired balance, reaction time, color vision, slotted pegboards and trials making were present in the three older children who could be tested. Neuropsychological evaluation revealed evidence of organic brain dysfunction in all seven family members. Bone growth difficulties are present in four of five children. One child has delayed menarche.- - - - - - - - - - ranking = 3keywords = organ (Clic here for more details about this article) |
10/13. Acute methyl iodide exposure with delayed neuropsychiatric sequelae: report of a case.BACKGROUND: Methyl iodide is a monohalomethane used as an analytic and organic chemistry reagent, as a methylating agent in organic chemical synthesis, and as a fumigant. In an acute exposure, methyl iodide is a pulmonary and dermal irritant. Chronic neurotoxicity has been reported in survivors of acute exposure. methods: A review of the 11 case reports of methyl iodide poisoning in the medical literature of the 20th century found that six of the patients experienced a chronic neurological syndrome characterized primarily by delayed psychiatric, behavioral, and cognitive sequelae. RESULTS: The case patient experienced a massive exposure to methyl iodide with resulting life-threatening burns. During convalescence, various cognitive and behavioral deficits became apparent. The results of a comprehensive evaluation at our occupational toxicology clinic, which included sequential neuropsychometric testing, are described. CONCLUSION: The findings in the case patient may advance our understanding of the mechanisms and clinical manifestations of chronic neurotoxicity after exposure to methyl iodide.- - - - - - - - - - ranking = 2keywords = organ (Clic here for more details about this article) |
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