Neuromodulation : journal of the International Neuromodulation Society
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Substance use disorder (SUD) is characterized by compulsive use of addictive substances with considerable impact on both the medical system and society as a whole. The craving of substances leads to relapse in the majority of patients within one year of traditional treatments. In recent decades, neuromodulation approaches have emerged as potential novel treatments of SUD, but the ideal neural target remains contentious. ⋯ First, we illustrate that the ACC serves as a central "hub" in addiction-related neural networks of cognitive functions, including, but not limited to, decision-making, cognitive inhibition, emotion, and motivation. Then, we summarize the literature targeting the ACC to treat SUDs via available neuromodulation approaches. Finally, we propose potential directions to improve the effect of stimulating the ACC in SUD treatment. We emphasize that the ACC can be divided into at least four sub-regions, which have distinctive functions and connections. Studies focusing on these sub-regions may help to develop more precise and effective ACC stimulation according to patients' symptom profiles and cognitive deficits.
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The ability of noninvasive brain stimulation to modulate corticospinal excitability and plasticity is influenced by genetic predilections such as the coding for brain-derived neurotrophic factor (BDNF). Otherwise healthy individuals presenting with BDNF Val66Met (Val/Met) polymorphism are less susceptible to changes in excitability in response to repetitive transcranial magnetic stimulation (TMS) and paired associative stimulation paradigms, reflecting reduced neuroplasticity, compared to Val homozygotes (Val/Val). In the current study, we investigated whether BDNF polymorphism influences "baseline" excitability under TMS conditions that are not repetitive or plasticity-inducing. Cross-sectional BDNF levels could predict TMS response more generally because of the ongoing plasticity processes. ⋯ The findings should be further substantiated in larger-scale studies. If validated, intrinsic differences by BDNF polymorphism status could index response to TMS prior to implementing plasticity-inducing protocols.
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The evolution of neuromodulation devices in order to enter magnetic resonance imaging (MRI) scanners has been one of understanding limitations, engineering modifications, and the development of a consensus within the community in which the FDA could safely administer labeling for the devices. In the initial decades of neuromodulation, it has been contraindicated for MRI use with implanted devices. In this review, we take a comprehensive approach to address all the major products currently on the market in order to provide physicians with the ability to determine when an MRI can be performed for each type of device implant. ⋯ This is the first comprehensive guideline with regards to various devices in the market and MRI compatibility from the American Society of Pain and Neuroscience.
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Intrathecal baclofen (ITB) pumps are an effective treatment for spasticity; however infection rates have been reported in 3-26% of patients in the literature. The multidisciplinary ITB service has been established at The National Hospital for Neurology and Neurosurgery, UCLH, Queen Square, London for over 20 years. Our study was designed to clarify the rate of infection in our ITB patient cohort and secondly, to formulate and implement best practice guidelines and to determine prospectively, whether they effectively reduced infection rates. ⋯ This study suggests that a straightforward change in clinical practice may lower infection rates in patients undergoing ITB therapy.
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Patients treated with intrathecal therapy frequently require opioid dose increases to maintain analgesia. The kinetics of intrathecal opioid dose escalation are poorly understood. We hypothesized that antidepressant use, antiepileptic use, and lower baseline oral opioid intake prior to intrathecal pump implantation will be protective against intrathecal opioid dose escalation. ⋯ Use of antiepileptics, antidepressants, or low oral opioid doses was not associated with attenuation of intrathecal dose escalation. Intrathecal opioid dose escalation was observed to occur similarly, regardless of baseline oral analgesics concomitantly employed.