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Bio-Implants Derived from Biocompatible and Biodegradable Biopolymeric Materials
Published in P. Mereena Luke, K. R. Dhanya, Didier Rouxel, Nandakumar Kalarikkal, Sabu Thomas, Advanced Studies in Experimental and Clinical Medicine, 2021
Electrical circuitry is implanted into the nerve cells to activate the parts and structures of the nervous system are called neural implants. Many experiments in the 1960s, material sciences, and the progress in medical and neuroscience lead to advancements in therapies of neurological diseases. This will lead to repair and rehabilitation of lost functions of human systems [80, 81]. Neuromodulation is the process of stimulation of the central nervous system (CNS). These structures which will be modulating the nerve excitability and neurotransmitters release [80]. Patients suffering from Parkinson’s disease (PD) will be cured by suppressing tremor and movement disorders by deep brain stimulation. Similarly, treatment for epilepsy and other psychiatric diseases like depression and obsessive-compulsive disorder are done with the help of vagal nerve stimulation [82, 83]. These treatments are now expanded to psychiatric diseases and many more applications. Some of them are in the development stages in preclinical and clinical trials.
Electrical Stimulation of the Vagus Nerve
Published in Stanley R. Resor, Henn Kutt, The Medical Treatment of Epilepsy, 2020
J. Kiffin Penry, J. Christine Dean
The adverse effects of vagal nerve stimulation were transient and occurred concomitantly with signal on/off vagal nerve stimulation. These were hoarseness and stimulation sensation in the neck. One patient experienced uncontrolled hiccups on one occasion. None of the patients experienced bradycardia or a significant increase in gastric acid due to the device.
Brain stimulation and epilepsy: basic overview and novel approaches
Published in Hans O Lüders, Deep Brain Stimulation and Epilepsy, 2020
Jürgen Lüders, Imad Najm, Hans O Lüders
Controlled studies. Few controlled studies have been performed stimulating the nervous system in humans to treat epilepsy. The results have been disappointing. Two studies have been performed stimulating the cerebellum with no significant change in seizure frequency.27,28 One pilot study has been performed stimulating the centro-median thalamic nucleus which demonstrated no significant change in seizure frequency.40 One controlled study has been performed evaluating the efficacy of vagal nerve stimulation which reported a significant but only relatively small decrease in seizure frequency of approximately 25% with high stimulation parameters.62
Is vagal stimulation or inhibition benefit on the regulation of the stomach brain axis in obesity?
Published in Nutritional Neuroscience, 2022
Işınsu Alkan, Berrin Zuhal Altunkaynak, Elfide Gizem Kivrak, Arife Ahsen Kaplan, Gülay Arslan
Vagus nerve stimulation is generally preferred in the treatment of epileptic disorders. In a 1938 study of Bailey and Bremer on cats, vagal stimulation showed changes in electroencephalogram readings [3]. In another study by Dell and Olson in 1951, it was reported that stimulation of the broken cervical vagus nerve affects the ventroposterior and intralaminar responses of the thalamus [24]. In 1985, Zabara et al. reported that electrical stimulation of the vagus nerve prevents neural processes that can end seizures in dogs and alter the electrical activity of the brain, and as a result of this study, vagus nerve stimulation occurs in various clinical situations [4,5]. Although the use of vagus stimulation usually involves the resolution of epileptic problems, the level of severe weight loss observed in patients supports the hypothesis that it may be effective in food intake [25,26]. In the clinical study of Pardo et al., it was reported that, after the vagus stimulation, the patients lost weight in the 6th and 12th months with amount varying between 7–23 kg [26]. Moreover, the same study found that this weight loss was more pronounced in severely obese patients. Stephens et al. reported that vagus activation caused discomfort in the stomach and decreased the feeling of hunger in healthy or fasting individuals [27].
Endotracheal Tube Electrode Neuromonitoring for Placement of Vagal Nerve Stimulation for Epilepsy: Intraoperative Stimulation Thresholds
Published in The Neurodiagnostic Journal, 2022
Gennadiy A. Katsevman, Darnell T. Josiah, Joseph E. LaNeve, Sanjay Bhatia
Risks for intraoperative vagal nerve stimulation are scarce aside from the standard VNS adverse effects, most of which are transient, stimulation-related, and generally well-tolerated (Heck et al. 2002; Kahlow and Olivecrona 2013; Rychlicki et al. 2006). Given that the electrodes are situated on the ETT, risk of injury to the vocal cords or vocalis muscles is small. Potential surgical complications from VNS implantations include vocal cord palsy and rare cardiovascular events such as bradycardia or asystole, so it is possible that repetitive electrical stimulation of the vagus nerve may cause similar issues, although again the risks are low (Giordano et al. 2017; Heck et al. 2002; Kahlow and Olivecrona 2013). On the contrary, neuromonitoring may help protect vocal cord function by aiding in the localization of the vagus nerve, limiting unnecessary dissection, and allowing for preservation of the blood supply to the area.
Cenobamate for the treatment of focal epilepsies
Published in Expert Opinion on Pharmacotherapy, 2020
Adam Strzelczyk, Catrin Mann, Laurent M. Willems, Felix Rosenow, Sebastian Bauer
In the first study (phase 2, study CO13, NCT01397968 [21]), 222 adult patients (18–65 years of age) with focal epilepsy were treated with either cenobamate (200 mg/d once daily; n = 113) or placebo (n = 109) in addition to a pre-established treatment with 1–3 ASDs, which were not changed during the study. The most frequently used background/concomitant ASDs in the cenobamate arm were levetiracetam (45.1%), followed by lamotrigine (36.3%), carbamazepine (33.6%), lacosamide (23.9%), topiramate (22.1%), and oxcarbazepine (21.2%). Additional vagal nerve stimulation (VNS) treatment was allowed but could not be adjusted during the trial period. Patients recorded their seizure frequency during a 4–8-week baseline period and were eligible if they had ≥3 focal aware motor seizures, focal-impaired awareness seizures, or focal to bilateral tonic-clonic seizures per month. The double-blind treatment period consisted of a 6-week titration phase and a 6-week maintenance phase. Titration of cenobamate began with 50 mg once daily, and the dose was increased by 50 mg every two weeks until 200 mg/d was reached, if tolerated, which was the case in 67% of the patients; 25% tolerated a daily dose of 150 mg/d, 5% tolerated 100 mg/d, and 4% stayed on the initial dose of 50 mg/d.