Current opinion in neurology · 2011
Toxic neuropathy.
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Manji Hadi
Аннотация
PURPOSE OF REVIEW: The aim is to review the recent publications highlighting current areas of research on the subject of toxic and drug-related neuropathies.
RECENT FINDINGS: The emphasis in chemotherapy-induced peripheral neuropathy is on trying to elucidate underlying mechanisms using neurophysiological techniques, such as excitability studies. These data are also being used to identify the earliest presymptomatic changes. A large number of papers have been published on chemoprotectants, both in animal models and patients. According to the Cochrane criteria, none of the clinical trials have been shown to be effective. Pharmacogenetic techniques used on tumour and host tissue are now in the embryonic stages of trying to identify genes which may help in predicting individuals at high risk of developing drug-induced neuropathies. A review of alcohol-induced neuropathy provides evidence to suggest reclassification from a nutritional to a toxic neuropathy. Nitrous oxide, which causes myeloneuropathy, is increasingly used as a recreational drug. A red flag has been raised with the triazole antifungal agents, itraconazole and voriconazole, causing neuropathy.
SUMMARY: The introduction of new neurophysiological techniques, such as excitability studies and pharmacogenetics, holds promise in elucidating the underlying mechanisms of drug-induced neuropathies. Furthermore, they will help identify the patients at highest risk of developing drug-induced neuropathies. The hope still remains of identifying chemoprotective agents - the results of animal and human studies suggest there are reasons to be optimistic. Clinicians need to aware of nitrous oxide myeloneuropathy and triazole-induced neuropathy.
RECENT FINDINGS: The emphasis in chemotherapy-induced peripheral neuropathy is on trying to elucidate underlying mechanisms using neurophysiological techniques, such as excitability studies. These data are also being used to identify the earliest presymptomatic changes. A large number of papers have been published on chemoprotectants, both in animal models and patients. According to the Cochrane criteria, none of the clinical trials have been shown to be effective. Pharmacogenetic techniques used on tumour and host tissue are now in the embryonic stages of trying to identify genes which may help in predicting individuals at high risk of developing drug-induced neuropathies. A review of alcohol-induced neuropathy provides evidence to suggest reclassification from a nutritional to a toxic neuropathy. Nitrous oxide, which causes myeloneuropathy, is increasingly used as a recreational drug. A red flag has been raised with the triazole antifungal agents, itraconazole and voriconazole, causing neuropathy.
SUMMARY: The introduction of new neurophysiological techniques, such as excitability studies and pharmacogenetics, holds promise in elucidating the underlying mechanisms of drug-induced neuropathies. Furthermore, they will help identify the patients at highest risk of developing drug-induced neuropathies. The hope still remains of identifying chemoprotective agents - the results of animal and human studies suggest there are reasons to be optimistic. Clinicians need to aware of nitrous oxide myeloneuropathy and triazole-induced neuropathy.