Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Penile erections are a characteristic phenomenon of paradoxical sleep (PS), or rapid eye movement sleep. Although the neural mechanisms of PS-related erections are unknown, the forebrain likely plays a critical role (Schmidt et al., 1999). The preoptic area is implicated in both sleep generation and copulatory mechanisms, suggesting it may be a primary candidate in PS erectile control. Continuous recordings of penile erections, body temperature, and sleep-wake states were performed before and up to 3 weeks after ibotenic acid lesions of the preoptic forebrain in three groups of rats. Neurotoxic lesions involving the medial preoptic area (MPOA) and anterior hypothalamus (n = 5) had no significant effects on either erectile activity or sleep-wake architecture. In contrast, bilateral lesions of the lateral preoptic region, with (n = 4) or without (n = 5) MPOA involvement, resulted in a significant decrease in the number of erections per hour of PS, number of PS-related erections, and PS phases exhibiting an erection. Lesion analysis revealed that the candidate structures for PS erectile control include both the lateral preoptic area (LPOA) and ventral division of the bed nucleus of the stria terminalis; however, lesions of the LPOA were the most effective in disrupting PS erectile activity. LPOA lesioning also resulted in a long-lasting insomnia, characterized by the significant increase in wakefulness and decrease in slow wave sleep (SWS). PS architecture and waking-state erections remained unchanged after lesion in all groups. These data identify an essential role of the LPOA in both PS-related erectile mechanisms and SWS generation. Moreover, higher erectile mechanisms appear to be context-specific because LPOA lesioning selectively disrupted PS-related erections while leaving waking-state erections intact.
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PMID:Role of the lateral preoptic area in sleep-related erectile mechanisms and sleep generation in the rat. 1096 69

Neurotoxic anticancer drugs, such as platinum-based anticancer drugs, taxanes, vinca alkaloids, and proteasome/angiogenesis inhibitors are responsible for chemotherapy-induced peripheral neuropathy (CIPN). The health consequences of CIPN remain worrying as it is associated with several comorbidities and affects a specific population of patients already impacted by cancer, a strong driver for declines in older adults. The purpose of this review is to present a comprehensive overview of the long-term effects of CIPN in cancer patients and survivors. Pathophysiological mechanisms and risk factors are also presented. Neurotoxic mechanisms leading to CIPNs are not yet fully understood but involve neuronopathy and/or axonopathy, mainly associated with DNA damage, oxidative stress, mitochondria toxicity, and ion channel remodeling in the neurons of the peripheral nervous system. Classical symptoms of CIPNs are peripheral neuropathy with a "stocking and glove" distribution characterized by sensory loss, paresthesia, dysesthesia and numbness, sometimes associated with neuropathic pain in the most serious cases. Several risk factors can promote CIPN as a function of the anticancer drug considered, such as cumulative dose, treatment duration, history of neuropathy, combination of therapies and genetic polymorphisms. CIPNs are frequent in cancer patients with an overall incidence of approximately 38% (possibly up to 90% of patients treated with oxaliplatin). Finally, the long-term reversibility of these CIPNs remain questionable, notably in the case of platinum-based anticancer drugs and taxanes, for which CIPN may last several years after the end of anticancer chemotherapies. These long-term effects are associated with comorbidities such as depression, insomnia, falls and decreases of health-related quality of life in cancer patients and survivors. However, it is noteworthy that these long-term effects remain poorly studied, and only limited data are available such as in the case of bortezomib and thalidomide-induced peripheral neuropathy.
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PMID:Long-Term Effects, Pathophysiological Mechanisms, and Risk Factors of Chemotherapy-Induced Peripheral Neuropathies: A Comprehensive Literature Review. 2828 83