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dennis100
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« Reply #60 on: August 13, 2013, 06:18:37 AM »

J Neurosurg Pediatr. 2010 Jun;5(6):595-602. doi: 10.3171/2010.3.PEDS09153.
Vagus nerve stimulation therapy in patients with autism spectrum disorder and intractable epilepsy: results from the vagus nerve stimulation therapy patient outcome registry.
Levy ML, Levy KM, Hoff D, Amar AP, Park MS, Conklin JM, Baird L, Apuzzo ML.
Source
Division of Pediatric Neurosurgery, Children's Hospital of San Diego, University of California, San Diego, California, USA. mlevy@chsd.org

Abstract
OBJECT: The purpose of this study was to determine the effectiveness of vagus nerve stimulation (VNS) therapy on quality-of-life (QOL) variables among patients with both autism spectrum disorder (ASD) and persistent or recurrent intractable epilepsy.

METHODS: Data were obtained from the VNS therapy patient outcome registry, which was established after US FDA approval of the VNS device in 1997 as a means of capturing open-label clinical data outside of protocol. The integrity of the systems for collecting and processing registry data was authenticated by an independent auditing agency. The effect of potential selection bias, however, remains uncertain.

RESULTS: Two cohorts were compared: 1) patients with epilepsy but without ASD (non-ASD [NASD] Group, 315 patients) who were being tracked in the registry (this cohort, which was controlled for age, included patients 20 years of age or younger); and 2) patients with a diagnosis of ASD who underwent implantation of the VNS device (ASD Group, 77 patients). Differences between the ASD and NASD groups were noted in the following categories: sex (male preponderance in ASD); normal imaging results (MR imaging results normal in ASD); depression (less common in ASD); behavioral problems (more common in ASD); neurological deficit (more common in ASD); mental retardation (more common in ASD); and developmental delay. The only QOL difference between the ASD and NASD groups was noted in mood at 12 months postimplant (mood was improved in ASD) (p = 0.04). There were no other differences in the QOL variables.

CONCLUSIONS: Patients with ASD and intractable epilepsy respond as favorably as all other patients receiving VNS therapy. In addition, they may experience a number of QOL improvements, some of which exceed those classically observed following placement of a VNS device.

PMID:20515333[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/20515333
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« Reply #61 on: August 13, 2013, 06:21:10 AM »

Neuromodulation. 2012 Nov-Dec;15(6):527-36. doi: 10.1111/j.1525-1403.2012.00454.x. Epub 2012 May 2.
Low voltage vagal nerve stimulation reduces bronchoconstriction in guinea pigs through catecholamine release.
Hoffmann TJ, Simon BJ, Zhang Y, Emala CW.
Source
ElectroCore LLC, Morris Plains, NJ, USA; and Department of Anesthesiology, Columbia University, New York, NY, USA.

Abstract
OBJECTIVE: Electrical stimulation of the vagus nerve at relatively high voltages (e.g., >10 V) can induce bronchoconstriction. However, low voltage (≤2 V) vagus nerve stimulation (VNS) can attenuate histamine-invoked bronchoconstriction. Here, we identify the mechanism for this inhibition.
 
METHODS: In urethanea-nesthetized guinea pigs, bipolar electrodes were attached to both vagus nerves and changes in pulmonary inflation pressure were recorded in response to i.v. histamine and during VNS. The attenuation of the histamine response by low-voltage VNS was then examined in the presence of pharmacologic inhibitors or nerve ligation.

RESULTS: Low-voltage VNS attenuated histamine-induced bronchoconstriction (4.4 ± 0.3 vs. 3.2 ± 0.2 cm H(2) O, p < 0.01) and remained effective following administration of a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester, and after sympathetic nerve depletion with guanethidine, but not after the β-adrenoceptor antagonist propranolol. Nerve ligation caudal to the electrodes did not block the inhibition but cephalic nerve ligation did. Low-voltage VNS increased circulating epinephrine and norepinephrine without but not with cephalic nerve ligation.

CONCLUSION: These results indicate that low-voltage VNS attenuates histamine-induced bronchoconstriction via activation of afferent nerves, resulting in a systemic increase in catecholamines likely arising from the adrenal medulla.

© 2012 International Neuromodulation Society.

PMID:22551486 [PubMed - indexed for MEDLINE] PMCID PMC3710689 [Available on 2013/11/1]

http://www.ncbi.nlm.nih.gov/pubmed/22551486
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« Reply #62 on: August 13, 2013, 06:23:55 AM »

J Affect Disord. 2006 May;92(1):79-90. Epub 2006 Mar 3.
Evidence for a vagal pathophysiology for bulimia nervosa and the accompanying depressive symptoms.
Faris PL, Eckert ED, Kim SW, Meller WH, Pardo JV, Goodale RL, Hartman BK.
Source
Department of Psychiatry, Fairview-University Medical School, Minneapolis, MN 55455, USA.

Abstract
BACKGROUND: The bilateral vagus nerves (Cranial X) provide both afferent and efferent connections between the viscera and the caudal medulla. The afferent branches increasingly are being recognized as providing significant input to the central nervous system for modulation of complex behaviors. In this paper, we review evidence from our laboratory that increases in vagal afferent activity are involved in perpetuating binge-eating and vomiting in bulimia nervosa. Preliminary findings are also presented which suggest that a subgroup of depressions may have a similar pathophysiology.

METHODS: Two main approaches were used to study the role of vagal afferents. Ondansetron (ONDAN), a 5-HT3 antagonist, was used as a pharmacological tool for inhibiting or reducing vagal afferent neurotransmission. Second, somatic pain detection thresholds were assessed for monitoring a physiological process known to be modulated by vagal afferents, including the gastric branches involved in meal termination and satiety. High levels of vagal activity result in an increase in pain detection thresholds. Depressive symptoms were assessed using the Beck Depression Inventory (BDI). Positron Emission Tomography (PET) was used to identify higher cortical brain areas activated by vagal stimulation produced by proximal gastric distention in normal eating subjects.

RESULTS: Double-blind treatment of severe bulimia nervosa subjects with ONDAN resulted in a rapid and significant decrease in binge-eating and vomiting compared to placebo controls. The decrease in abnormal eating episodes was accompanied by a return of normal satiety. Pain detection thresholds measured weekly over the course of the treatment protocol were found to dynamically fluctuate in association with bulimic episodes. Thresholds were the most elevated during periods of short-term abstinence from the behaviors, suggesting that not engaging in a binge/vomit episode is accompanied by an increase in vagal activity. ONDAN also resulted in abolition of the fluctuations in pain thresholds. Depressive symptoms in these subjects also were reduced by ONDAN. Like pain thresholds, depressive symptoms varied dynamically with the bulimic behaviors, with BDI scores increasing (more depressed) as more time elapsed since the last bulimic episode. PET studies indicated that mechanical distention of the stomach with a balloon (a non-nutritive stimulus) was associated with the activation of several brain loci, including those associated with vagal activation (parabrachial nucleus), emotive aspects of eating (lateral inferior frontal and orbitofrontal), and depressive symptoms (anterior cingulate).
 
CONCLUSIONS: The results of the ONDAN study in bulimia nervosa subjects suggest that cyclic increases in vagal activity drive the urge to binge-eat and vomit. The alterations in vagal firing patterns are possibly a physiological adaptation to the high levels of vagal stimulation initially provided by voluntarily binge-eating and vomiting for weight control. The depressive symptoms that occur in association with the urge to binge-eat are also likely due to the cyclic increase in vagal activity. This suggestion is supported by the reduction of depressive symptoms during ONDAN treatment in bulimia subjects and PET imaging studies in normal eating subjects showing that brain loci classically involved in depression are activated by vagal stimulation administered by mechanical gastric distention. In normal eating individuals, depressions accompanying visceral diseases may also be vagally mediated. Ondansetron and other drugs known to modulate vagal activity may be helpful in treating depressions of this origin.

PMID:16516303 [PubMed - indexed for MEDLINE]

 http://www.ncbi.nlm.nih.gov/pubmed/16516303

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« Reply #63 on: August 13, 2013, 06:26:24 AM »

Burns. 2009 Sep;35(6):783-9. doi: 10.1016/j.burns.2008.08.023. Epub 2009 May 30.
Burn-induced organ dysfunction: vagus nerve stimulation attenuates organ and serum cytokine levels.
Niederbichler AD, Papst S, Claassen L, Jokuszies A, Steinstraesser L, Hirsch T, Altintas MA, Ipaktchi KR, Reimers K, Kraft T, Vogt PM.
Source
Department of Plastic, Hand and Reconstructive Surgery, Burn Center, Medizinische Hochschule Hannover, Germany. niederbichler.andreas@mh-hannover.de

Abstract
INTRODUCTION: The interaction of the CNS and the immune system is well known. A parasympathetic anti-inflammatory pathway has recently been described. Both electrical and pharmacological parasympathetic stimulation attenuate proinflammatory mediator generation. Burn induces abacterial cytokine generation and we sought to evaluate whether parasympathetic stimulation after experimental burn decreases cardiodepressive mediator generation.

MATERIAL AND METHODS: A 30% TBSA full-thickness rat burn model was used. After microsurgical preparation of the cervical portion of the vagus nerve, we performed electric vagus nerve stimulation. Serum was harvested and organ samples of heart and liver were homogenized. Samples were subjected to sandwich-ELISA specific for TNF-alpha, IL-1beta and IL-6. Heart rate measurements were done using left ventricular microcatheterization. Statistical analysis was done using Student's t-tests and analysis of variance (ANOVA).

RESULTS: Burn induced a significant rise of TNF-alpha, IL-1beta and IL-6 in organ homogenates and serum. After cervical vagal electrostimulation, serum and organ homogenate levels of proinflammatory cytokines were markedly reduced compared to burn controls. Left ventricular microcatheter assessment demonstrated no cardiodepressive effect of the vagal stimulation itself.

CONCLUSION: Our results encourage further research regarding the neuroimmunologic background of burn, possibly leading to the development of a novel therapeutic approach to burn-induced organ dysfunction and immunodysregulation.

PMID:19482432 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/19482432
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« Reply #64 on: August 13, 2013, 06:31:51 AM »

Nat Rev Cardiol. 2013 Feb;10(2):98-110. doi: 10.1038/nrcardio.2012.178. Epub 2012 Dec 11.
Devices in the management of advanced, chronic heart failure.
Abraham WT, Smith SA.
Source
Division of Cardiovascular Medicine, The Ohio State University, 473 West 12th Avenue, Room 110P, Columbus, OH 43210-1252, USA. william.abraham@osumc.edu

Abstract
Heart failure (HF) is a global phenomenon, and the overall incidence and prevalence of the condition are steadily increasing. Medical therapies have proven efficacious, but only a small number of pharmacological options are in development. When patients cease to respond adequately to optimal medical therapy, cardiac resynchronization therapy has been shown to improve symptoms, reduce hospitalizations, promote reverse remodelling, and decrease mortality. However, challenges remain in identifying the ideal recipients for this therapy. The field of mechanical circulatory support has seen immense growth since the early 2000s, and left ventricular assist devices (LVADs) have transitioned over the past decade from large, pulsatile devices to smaller, more-compact, continuous-flow devices. Infections and haematological issues are still important areas that need to be addressed. Whereas LVADs were once approved only for 'bridge to transplantation', these devices are now used as destination therapy for critically ill patients with HF, allowing these individuals to return to the community. A host of novel strategies, including cardiac contractility modulation, implantable haemodynamic-monitoring devices, and phrenic and vagus nerve stimulation, are under investigation and might have an impact on the future care of patients with chronic HF.

PMID:23229137[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/23229137
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« Reply #65 on: August 13, 2013, 06:33:32 AM »

Seizure. 2006 Jun;15(4):259-63. Epub 2006 May 2.
Vagus nerve stimulation and cognition.
Boon P, Moors I, De Herdt V, Vonck K.
Source
Reference Centre for Refractory Epilepsy, Laboratory for Clinical and Experimental Neurophysiology (LCEN), Department of Neurology, Ghent University Hospital, De Pintelaan 185, B-9000 Gent, Belgium. Paul.Boon@UGent.be

Abstract
Vagus nerve stimulation (VNS) has been developed as an add-on treatment for patients with refractory epilepsy. Based on the clinical observation of improved cognition in many epilepsy patients who received VNS, we reviewed the recent literature for evidence concerning the cognitive effects of this treatment. From most of these studies it seems that, with currently used stimulation parameters, the effects on memory are only of theoretical importance. However, some animal studies suggest positive effects on specific modalities of memory function. In studies in epilepsy patients, there is no evidence of adverse effects on cognition but clear-cut positive effects cannot be expected either. Preliminary results of VNS in the treatment of diseases associated with cognitive decline such as Alzheimer's disease seem promising but need to be further investigated.

PMID:16651013[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/16651013

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« Reply #66 on: August 13, 2013, 06:37:34 AM »

Vagal neurostimulation in patients with coronary artery disease   (Citations: 14)
A. V Zamotrinsky, B Kondratiev, J. W de Jong

We tested the hypotheses that (1) progression of coronary artery disease (CAD) increases sympathetic inflow to the heart, thus impairing cardiac blood supply, and (2) reduced sympathetic tone improves cardiac microcirculation and ameliorates severity of anginal symptoms. Electrical irritation of the nerve auricularis—a sensitive ramus of the vagus nerve—provides a central sympatholytic action. Using this technique, we studied the effects of vagal neurostimulation (VNS) on hemodynamics, the content of atrial noradrenergic nerves and the microcirculatory bed of CAD patients. VNS was performed in the preoperative period of CAD patients with severe angina pectoris. The comparison groups consisted of untreated patients with CAD or Wolff–Parkinson–White syndrome. Atrial tissue of patients with this syndrome (n=6); with effort angina (n=14); with angina at rest (n=10); and with severe angina treated with VNS (n=8) contained the following volume percentages of noradrenergic nerves: 1.7±0.1%, 1.3±0.3%, 0.5±0.1% (p<0.05 vs. the other groups) and 1.3±0.2%, respectively. In these groups, cardiac microcirculatory vessels (diameter, 10–20 μm) had the following densities: 2.7±0.2%, 3.4±0.2%, 2.0±0.4% (p<0.05 vs. the other groups) and 3.3±0.3%, respectively. VNS treatment abolished angina at rest, decreased heart rate and blood pressure. It improved left ventricular ejection fraction from 50±1.5% to 58±1.0% (p<0.05), also changing left ventricular diastolic filling. The ratio of time velocity integrals of the early (Ei) to late (Ai) waves increased from 1.07±0.12 to 1.65±0.17 after VNS (p<0.05). In electrocardiograms of VNS-treated patients, QRS- and QT-duration were shortened, the PQ-interval did not change, but T-wave configuration improved. In the postoperative period, heart failure occurred in 90% of the control group, vs. 12% in patients treated with VNS (p<0.05). We conclude that CAD is characterized by overactivity of sympathetic cardiac tone. Vagal stimulation reduced sympathetic inflow to the heart, seemingly via an inhibition of norepinephrine release from sympathetic nerves. VNS' sympatholytic/vagotonic action dilated cardiac microcirculatory vessels and improved left ventricular contractility in patients with severe CAD.

Journal: Autonomic Neuroscience-basic & Clinical - AUTON NEUROSCI-BASIC CLIN , vol. 88, no. 1, pp. 109-116, 2001
DOI: 10.1016/S1566-0702(01)00227-2

http://academic.research.microsoft.com/Publication/35509092/vagal-neurostimulation-in-patients-with-coronary-artery-disease


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« Reply #67 on: August 13, 2013, 06:39:11 AM »

Semin Pediatr Neurol. 2010 Mar;17(1):54-7. doi: 10.1016/j.spen.2010.02.009.
Dramatic first words spoken in 2 children after vagus nerve stimulation.
Grill MF, Ng YT.
Source
Department of Neurology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ 85013, USA.

Abstract
Vagus nerve stimulation has become an accepted adjunctive treatment for refractory epilepsy with more recent FDA approval in the treatment of depression. Many "positive" effects have been noted in patients with epilepsy namely increased alertness, improved cognition, behavior and mood. These changes appear to be independent of seizure reduction and antiepileptic drug decrease. We present two children (aged 8 and 9 years) who were non-verbal and spoke their first words shortly after vagus nerve stimulators were implanted. The mechanism is unclear although vagus nerve stimulation has been clearly shown to induce neuronal, chemical and perfusion changes in both subcortical and cortical regions of the brain. There is likely a combined effect on primary speech areas as well subcortical and mamillothalamic tracts, and possibly even stimulation and changes at the local vocal cord level contributing to this phenomenon. Our observation has important implications in encephalopathic patients both with and without epilepsy.

Copyright 2010 Elsevier Inc. All rights reserved.
Comment in
Editorial Comment: can VNS therapy influence language and other cognitive functions? [Semin Pediatr Neurol. 2010]
PMID:20434697 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/20434697
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« Reply #68 on: August 13, 2013, 06:44:06 AM »

Seizure. 2011 Jul;20(6):468-74. doi: 10.1016/j.seizure.2011.02.011. Epub 2011 Mar 10.
Effectiveness of vagal nerve stimulation (VNS) in patients with drop-attacks and different epileptic syndromes.
Zamponi N, Passamonti C, Cesaroni E, Trignani R, Rychlicki F.
Source
Pediatric Neurology Department, Ospedali Riuniti, Ancona, Italy.

Abstract
PURPOSE: The effectiveness of VNS was evaluated in thirty-nine encephalopatic patients with drug-resistant epilepsy characterized by multiple seizures and drop attacks. Twenty-five patients were affected by severe epilepsy with multiple independent spike foci (SE-MISF) and fourteen patients by Lennox-Gastaut syndrome (LGS).

METHOD: Changes in seizure frequency, cognition, adaptive behaviour and quality of life were assessed before and after VNS implant until three years. Outcome assessment for all seizure types included the number of seizures/month and the reduction in seizure frequency rate at each follow-up. Moreover, the effect of VNS on frequency, duration and intensity of drop attacks was separately addressed by a modification of McHugh scale.

RESULTS: VNS produced a mean seizure rate reduction of 41% at six months, 50% at twelve months, and 54% at thirty-six months. After one year of stimulation, thirteen patients with SE-MISF (52%) and three patients with LGS (21%) showed a reduction above 50% in all seizures' frequency rate. As for drop attacks, eight patients (20%) gained a reduction above 50%, while seven patients (17%) showed a reduction only in intensity and duration. Cognitive level and adaptive behaviour were unchanged, while a better quality of life was reported in half out of the patients.

CONCLUSIONS: VNS had a greater effect in reducing seizures frequency and drop attacks' intensity and duration in SE-MISF patients than LGS patients. An improved quality of life was observed also in those patients who only reduced the intensity and duration of drop attacks.

Copyright © 2011 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved.
PMID: 21396833 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/21396833

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« Reply #69 on: August 13, 2013, 06:45:39 AM »

Epigee Women's Health

Vagus Nerve Stimulation (VNS) Treatment
Latest medical research suggests that a treatment that is proving useful for epilepsy and depression may also help people with eating disorders.

What Is It?

The Vagus Nerve Stimulator is a device that produces intermittent electrical stimulation of the vagus nerve. For people with eating disorders it is used to interrupt the normal communication between the brain and the digestive system. This stimulation seems to either fool the stomach into thinking it is full, and therefore people naturally eat less, or enables people who have a medical condition that prevents them recognizing when they are they are full to do so.
How Does It Work?

Electrodes are implanted on the nerves around the esophagus and then a small generator device, similar to a pacemaker, is placed just under the skin in the chest or trunk area.

This stimulator then sends small bursts of low-level electric impulses to the nerves and this interferes with the brain’s ability to communicate with the stomach and stop it expanding. It may also affect the hormones involved with appetite.
Weight Loss

Patients participating in trials have naturally reduced their calorie intake by more than 30% in a month, and therefore lost weight, without any special diets or exercise programs.

Doctors are able to adjust and individualize the frequency of the VNS treatment for each patient and can switch it on and off as required. In some versions of the device, the VNS is automatic and in others, the patient can be given the control, by use of a magnet, to increase or decrease the intensity of the stimulation.

The operation is much less invasive than gastric by-pass surgery and may even be possible to do as a day patient procedure. When the patient has lost the necessary weight, the device can be removed or it can be turned off, left in the body, and turned on again later if necessary.

It appears that it is important that the nerve stimulation is intermittent, as otherwise, the brain is able to learn a different way of communicating with the digestive system, and therefore override the VNS device.
Helping Bulimics

This VNS treatment seems to be particularly effective for people suffering from bulimia as it can help reduce the symptoms of binge eating and purging.

It seems that long-term bulimics have damaged their vagus nerve, and the nerve ends up operating in overdrive. This nerve then seems to create the compulsion to binge and vomit, making the disorder physiological rather than purely physiological. The VNS enables the nerve surges to be controlled, in the same sort of way a heart pace-maker controls erratic heart beats.
Availability

Although VNS is a promising new therapy for people with obesity and eating disorders, it is not yet widely available. You should consult with your health practitioner to see if it is a suitable treatment for you, if it is available in your area, and covered under your HMO health plan.

http://www.epigee.org/vagus-nerve-stimulation-treatment-eating-disorders

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« Reply #70 on: August 13, 2013, 06:48:16 AM »

Pain Med. 2011 Sep;12(9):1406-13. doi: 10.1111/j.1526-4637.2011.01203.x. Epub 2011 Aug 3.
Safety and efficacy of vagus nerve stimulation in fibromyalgia: a phase I/II proof of concept trial.
Lange G, Janal MN, Maniker A, Fitzgibbons J, Fobler M, Cook D, Natelson BH.
Source
Department of Radiology, UMDNJ-New Jersey Medical School, Newark, New Jersey, USA.

Abstract
OBJECTIVE: We performed an open-label Phase I/II trial to evaluate the safety and tolerability of vagus nerve stimulation (VNS) in patients with treatment-resistant fibromyalgia (FM) as well as to determine preliminary measures of efficacy in these patients.

METHODS: Of 14 patients implanted with the VNS stimulator, 12 patients completed the initial 3-month study of VNS; 11 patients returned for follow-up visits 5, 8, and 11 months after start of stimulation. Therapeutic efficacy was assessed with a composite measure requiring improvement in pain, overall wellness, and physical function. Loss of both pain and tenderness criteria for the diagnosis of FM was added as a secondary outcome measure because of results found at the end of 3 months of stimulation.

RESULTS: Side effects were similar to those reported in patients treated with VNS for epilepsy or depression and, in addition, dry mouth and fatigue were reported. Two patients did not tolerate stimulation. At 3 months, five patients had attained efficacy criteria; of these, two patients no longer met widespread pain or tenderness criteria for the diagnosis of FM. The therapeutic effect seemed to increase over time in that additional participants attained both criteria at 11 months.

CONCLUSIONS: Side effects and tolerability were similar to those found in disorders currently treated with VNS. Preliminary outcome measures suggested that VNS may be a useful adjunct treatment for FM patients resistant to conventional therapeutic management, but further research is required to better understand its actual role in the treatment of FM.

Wiley Periodicals, Inc.
PMID: 21812908 [PubMed - indexed for MEDLINE] PMCID:PMC3173600 Free PMC Article

http://www.ncbi.nlm.nih.gov/pubmed/21812908
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« Reply #71 on: August 13, 2013, 06:56:07 AM »

J Trauma Acute Care Surg. 2012 Aug;73(2):338-42; discussion 342. doi: 10.1097/TA.0b013e31825debd3.
Vagal nerve stimulation modulates gut injury and lung permeability in trauma-hemorrhagic shock.
Levy G, Fishman JE, Xu DZ, Dong W, Palange D, Vida G, Mohr A, Ulloa L, Deitch EA.
Source
Department of Surgery, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, New Jersey, USA. levyga@umdnj.edu

Abstract
BACKGROUND: Hemorrhagic shock is known to disrupt the gut barrier leading to end-organ dysfunction. The vagus nerve can inhibit detrimental immune responses that contribute to organ damage in hemorrhagic shock. Therefore, we explored whether stimulation of the vagus nerve can protect the gut and recover lung permeability in trauma-hemorrhagic shock (THS).

METHODS: Male Sprague-Dawley rats were subjected to left cervical vagus nerve stimulation at 5 V for 10 minutes. The right internal jugular and femoral artery were cannulated for blood withdrawal and blood pressure monitoring, respectively. Animals were then subjected to hemorrhagic shock to a mean arterial pressure between 30 mm Hg and 35 mm Hg for 90 minutes then reperfused with their own whole blood. After observation for 3 hours, gut permeability was assessed with fluorescein dextran 4 in vivo injections in a ligated portion of distal ileum followed by Evans blue dye injection to assess lung permeability. Pulmonary myeloperoxidase levels were measured and compared.

RESULTS: Vagal nerve stimulation abrogated THS-induced lung injury (mean [SD], 8.46 [0.36] vs. 4.87 [0.78]; p < 0.05) and neutrophil sequestration (19.39 [1.01] vs. 12.83 [1.16]; p < 0.05). Likewise, THS gut permeability was reduced to sham levels.

CONCLUSION: Neuromodulation decreases injury in the THS model as evidenced by decreased gut permeability as well as decreased lung permeability and pulmonary neutrophil sequestration in a rat model.

PMID:22846937[PubMed - indexed for MEDLINE] PMCID:PMC3683843 Free PMC Article

http://www.ncbi.nlm.nih.gov/pubmed/22846937
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« Reply #72 on: August 13, 2013, 06:59:33 AM »

PLoS One. 2013;8(2):e56728. doi: 10.1371/journal.pone.0056728. Epub 2013 Feb 12.
Electrical vagus nerve stimulation attenuates systemic inflammation and improves survival in a rat heatstroke model.
Yamakawa K, Matsumoto N, Imamura Y, Muroya T, Yamada T, Nakagawa J, Shimazaki J, Ogura H, Kuwagata Y, Shimazu T.
Source
Department of Traumatology and Acute Critical Medicine, Osaka University Graduate School of Medicine, Osaka, Japan. k.yamakawa0911@gmail.com

Abstract

This study was performed to gain insights into novel therapeutic approaches for the treatment of heatstroke. The central nervous system regulates peripheral immune responses via the vagus nerve, the primary neural component of the cholinergic anti-inflammatory pathway. Electrical vagus nerve stimulation (VNS) reportedly suppresses pro-inflammatory cytokine release in several models of inflammatory disease. Here, we evaluated whether electrical VNS attenuates severe heatstroke, which induces a systemic inflammatory response. Anesthetized rats were subjected to heat stress (41.5°C for 30 minutes) with/without electrical VNS. In the VNS-treated group, the cervical vagus nerve was stimulated with constant voltage (10 V, 2 ms, 5 Hz) for 20 minutes immediately after completion of heat stress. Sham-operated animals underwent the same procedure without stimulation under a normothermic condition. Seven-day mortality improved significantly in the VNS-treated group versus control group. Electrical VNS significantly suppressed induction of pro-inflammatory cytokines such as tumor necrosis factor-α and interleukin-6 in the serum 6 hours after heat stress. Simultaneously, the increase of soluble thrombomodulin and E-selectin following heat stress was also suppressed by VNS treatment, suggesting its protective effect on endothelium. Immunohistochemical analysis using tissue preparations obtained 6 hours after heat stress revealed that VNS treatment attenuated infiltration of inflammatory (CD11b-positive) cells in lung and spleen. Interestingly, most cells with increased CD11b positivity in response to heat stress did not express α7 nicotinic acetylcholine receptor in the spleen. These data indicate that electrical VNS modulated cholinergic anti-inflammatory pathway abnormalities induced by heat stress, and this protective effect was associated with improved mortality. These findings may provide a novel therapeutic strategy to combat severe heatstroke in the critical care setting.

PMID:23424673 [PubMed - indexed for MEDLINE] PMCID: PMC3570456 Free PMC Article

http://www.ncbi.nlm.nih.gov/pubmed/23424673
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« Reply #73 on: August 13, 2013, 07:01:06 AM »

Neurosci Lett. 2011 Apr 20;494(1):70-4. doi: 10.1016/j.neulet.2011.02.059. Epub 2011 Mar 6.
Vagus nerve stimulation inhibits heroin-seeking behavior induced by heroin priming or heroin-associated cues in rats.
Liu H, Liu Y, Yu J, Lai M, Zhu H, Sun A, Chen W, Zhou W.
Source
Laboratory of Behavioral Neuroscience, Ningbo Addiction Research and Treatment Center, School of Medicine, Ningbo University, 42 Xibei Str., Ningbo 315010, Zhejiang Province, PR China.

Abstract
Vagus nerve stimulation has been used for the treatment of neuropsychiatric disorders, such as epilepsy. However, little is known whether it is also effective for the treatment of heroin dependence, in particular for relapse to heroin seeking. In the present study, we investigated the effects of vagus nerve stimulation on reinstatement (relapse) of heroin-seeking behavior induced by heroin priming or heroin-associated cues. The rats were trained for heroin self-administration for 14days and followed by extinction training in which heroin was replaced by saline and heroin-associated cues were turned off. In addition, animals were also received daily electric stimulation of vagus nerve (30Hz, pulse width of 0.5ms, 0.5mA (low-intensity) or 1mA (high-intensity); 30s on, 5min off; 10 continuous cycle per day) or false stimulation during extinction training. We found that such vagus nerve stimulation significantly inhibited heroin priming (0.25mg/kg, s.c.) - or heroin-associated conditioned cue-induced reinstatement of drug-seeking behavior, when compared to false stimulation control. Further, such a behavioral inhibition was correlated to a reduction in the expression of FosB and an increase in the expression of phosphorylation of cAMP response element binding protein (p-CREB) in nucleus accumbens. The data suggest that vagus nerve stimulation may inhibit heroin- or heroin cue-induced relapse, possibly by regulation of the expression of Fos and CREB in nucleus accumbens.

Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
PMID:21362452[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/21362452
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« Reply #74 on: August 13, 2013, 07:02:28 AM »

J Neurosurg. 2005 May;102(5):935-7.
Vagus nerve stimulation for chronic intractable hiccups. Case report.
Payne BR, Tiel RL, Payne MS, Fisch B.
Source
Department of Neurosurgery, Louisiana State University Medical School, New Orleans, Louisiana 70112, USA. bpayne1@lsuhsc.edu

Abstract
Intractable hiccups are debilitating and usually a result of some underlying disease. Initial management includes vagal maneuvers and pharmacotherapy. When hiccups persist despite medical therapy, surgical intervention rarely is pursued. Cases described in the literature cite successful phrenic nerve blockade, crush injury, or percutaneous phrenic nerve pacing. The authors report on a case of intractable hiccups occurring after a posterior fossa stroke, Complete resolution of the spasms has been achieved to date following the placement of a vagus nerve stimulator.

PMID:15926725[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/15926725
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« Reply #75 on: August 13, 2013, 07:04:28 AM »

J Trauma. 2011 May;70(5):1168-75; discussion 1175-6. doi: 10.1097/TA.0b013e318216f754.
Postinjury vagal nerve stimulation protects against intestinal epithelial barrier breakdown.
Krzyzaniak M, Peterson C, Loomis W, Hageny AM, Wolf P, Reys L, Putnam J, Eliceiri B, Baird A, Bansal V, Coimbra R.
Source
Division of Trauma, Surgical Critical Care, and Burns, Department of Surgery, University of California, San Diego School of Medicine, San Diego, California 92103-8896, USA.

Abstract
BACKGROUND: Vagal nerve stimulation (VNS) can have a marked anti-inflammatory effect. We have previously shown that preinjury VNS prevented intestinal barrier breakdown and preserved epithelial tight junction protein expression. However, a pretreatment model has little clinical relevance for the care of the trauma patient. Therefore, we postulated that VNS conducted postinjury would also have a similar protective effect on maintaining gut epithelial barrier integrity.

METHODS: Male balb/c mice were subjected to a 30% total body surface area, full-thickness steam burn followed by right cervical VNS at 15, 30, 60, 90, 120, and 150 minutes postinjury. Intestinal barrier dysfunction was quantified by permeability to 4 kDa fluorescein isothiocyanate-Dextran, histologic evaluation, gut tumor necrosis factor-alpha (TNF-α) enzyme-linked immunosorbent assay, and expression of tight junction proteins (myosin light chain kinase, occludin, and ZO-1) using immunoblot and immunoflourescence.

RESULTS: Histologic examination documented intestinal villi appearance similar to sham if cervical VNS was performed within 90 minutes of burn insult. VNS done after injury decreased intestinal permeability to fluorescein isothiocyanate-Dextran when VNS was ≤90 minutes after injury. Burn injury caused a marked increase in intestinal TNF-α levels. VNS-treated animals had TNF-α levels similar to sham when VNS was performed within 90 minutes of injury. Tight junction protein expression was maintained at near sham values if VNS was performed within 90 minutes of burn, whereas expression was significantly altered in burn.

CONCLUSION: Postinjury VNS prevents gut epithelial breakdown when performed within 90 minutes of thermal injury. This could represent a therapeutic window and clinically relevant strategy to prevent systemic inflammatory response distant organ injury after trauma.

PMID:21610431[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/21610431
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« Reply #76 on: August 13, 2013, 07:06:30 AM »

LIVIVG with LGS
Vagus Nerve Stimulation

Although antiseizure medications are the mainstay of treatment for LGS, there are non-pharmacologic adjunctive therapy options that are also available.1 One of them is called vagus nerve stimulation (VNS). In this therapy, an implant sends small electrical impulses to the brain to help control seizures. This therapy option is not approved for the treatment of LGS in the United States.

The vagus nerve is a large nerve in the neck. In VNS, short bursts of electrical energy are directed into the brain through the vagus nerve. The energy comes from a battery that is surgically implanted under the skin—usually in the chest. The procedure takes 50-90 minutes with the patient under general anesthesia.2

The battery is programmed to deliver small stimulations to the vagus nerve every few minutes,2 like a pacemaker for the brain. Holding a special magnet over the device can allow users to stimulate the vagus nerve as needed, such as when an “aura” occurs before a seizure.2

In VNS, short bursts of electrical energy are directed into the brain to treat seizures.


VNS is used in addition to medicines

In 3 small, published studies, selected patients were given VNS therapy as adjunctive therapy in addition to antiepileptic medication. Approximately three-fourths of patients with LGS experienced more than a 50% reduction in seizure frequency with a follow-up period as long as 5 years.3

Side effects of VNS

VNS therapy may not be for everyone. It can often cause hoarseness during stimulation. Other common side effects include tingling in the throat, shortness of breath with exertion, cough, and occasional stomach problems.4

Talk to your doctor to see what options are available for your loved one.

Learn more: Corpus callosotomy »


References:
1.     Hosain S, Nikalov B, Harden C, Li M, Fraser R, Labar D. Vagus nerve stimulation treatment for Lennox-Gastaut syndrome, J Child Neurol. 2000;15:509-512.
2.     Vagus nerve stimulation. Epilepsy.com. http://www.epilepsy.com/epilepsy/vns. December 15, 2006. Accessed August 20, 2012.
3.     Glauser TA, Morita DA, Stannard KM. Lennox-Gastaut syndrome. eMedicine Web site. http://emedicine.medscape.com/article/1176735-treatment. Updated April 26, 2010. Accessed August 20, 2012.
4.     About Epilepsy Overview. Epilepsy Foundation Web site. http://www.epilepsyfoundation.org/aboutepilepsy/treatment/VNS/overview.cfm. Accessed August 20, 2012.

http://livingwithlgs.com/vagus-nerve-stimulation.aspx
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« Reply #77 on: August 13, 2013, 07:08:42 AM »

Mayo Clin Proc. 2002 Jun;77(6):552-6.
Electroconvulsive therapy and newer modalities for the treatment of medication-refractory mental illness.
Rasmussen KG, Sampson SM, Rummans TA.
Source
Department of Psychiatry and Psychology, Mayo Clinic, Rochester, Minn 55905, USA. rasmussen.keith@mayo.edu

Abstract
Severe mental illnesses often remain chronic and refractory to medication, leading to substantial morbidity and mortality. For more than 60 years, electroconvulsive therapy has been the only nonpharmacological psychiatric procedure available to treat severe or medication-refractory major depressive disorder and other psychiatric conditions. Memory dysfunction remains the most serious adverse effect, and current research focuses on attempts to ameliorate this complication. Transcranial magnetic stimulation and vagus nerve stimulation, 2 new neuropsychiatric technologies, are emerging as possible additions to our therapeutic armamentarium. Besides providing therapeutic benefits, these 3 methods may help elucidate the pathophysiology of psychiatric illness.

PMID:12059125[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/12059125
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« Reply #78 on: August 13, 2013, 07:10:39 AM »

Cogn Behav Neurol. 2006 Sep;19(3):119-22.
The influence of vagus nerve stimulation on memory.
Ghacibeh GA, Shenker JI, Shenal B, Uthman BM, Heilman KM.
Source
Department of Neurology, University of Florida, Gainesville, FL 32610-0236, USA. ghacig@neurology.ufl.edu

Abstract
BACKGROUND: Vagus nerve stimulation (VNS) has been shown to improve memory.

OBJECTIVE: The purpose of this study was to learn at which stage of memory formation this influence occurs.

METHODS: Ten subjects who had been implanted with vagus nerve stimulators for the treatment of intractable seizures performed tasks that assessed learning and retention (Hopkins Verbal Learning Test) during actual and sham VNS.

RESULTS: We found that VNS had no effect on learning but enhanced consolidation, which led to improved retention.

CONCLUSIONS: The means by which VNS improves retention is probably related to the increased activity in the nucleus of the tractus solitarius and the locus coeruleus-central adrenergic system that activates the amygdala and increases long-term potentiation in the hippocampus.

PMID:16957488[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/16957488
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« Reply #79 on: August 13, 2013, 07:12:30 AM »

Headache. 2011 Oct;51(9):1408-18. doi: 10.1111/j.1526-4610.2011.01967.x. Epub 2011 Aug 3.
Neurostimulation for primary headache disorders: Part 2, review of central neurostimulators for primary headache, overall therapeutic efficacy, safety, cost, patient selection, and future research in headache neuromodulation.
Jenkins B, Tepper SJ.
Source
Neurological Center for Headache and Pain, Cleveland Clinic, Cleveland, OH 44195, USA.

Abstract
This article is the second of 2 articles reviewing neurostimulation for primary headaches. In Part 1, we described methods, pathophysiology and anatomy, and history of neuromodulation in the treatment of headache, as well as reviewing the literature on peripheral neuromodulation for primary headaches. Peripheral targets for stimulation include percutaneous nerves, transcranial holocephalic, occipital nerves, auriculotemporal nerves, supraorbital nerves, cervical epidural, and sphenopalatine ganglia. In Part 2, we describe available literature on central neuromodulation in primary headaches. Central stimulation targets include vagus nerve and deep brain structures. Part 2 also analyzes overall therapeutic efficacy, safety, cost, patient selection, and recommendations for further research of neurostimulation modalities based on available data.

© 2011 American Headache Society.
PMID:21812772 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/21812772
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« Reply #80 on: August 13, 2013, 07:14:18 AM »

Recent Pat CNS Drug Discov. 2009 Jun;4(2):149-59.
Mood disorders in elderly population: neurostimulative treatment possibilities.
Rosenberg O, Shoenfeld N, Kotler M, Dannon PN.
Source
Brain Stimulation Unit, Beer Ya'acov Mental Health Center, Israel.

Abstract
Treatment of mood disorders is one of the most challenging territories in elderly. Effectiveness of different treatment strategies could be related to age, sex and physical conditions. The side effect profile in this population also affects pharmacological interventions. Our review includes the neurostimulative treatment strategies in elderly. However, possible treatment strategies such as electroconvulsive therapy (ECT), transcranial magnetic stimulation (TMS), vagus nerve stimulation (VNS) and deep brain stimulation (DBS) were less studied in elderly. ECT was found to be an effective treatment procedure in mood disorders. Few double-blind sham controlled studies were conducted and demonstrated effectiveness of TMS. DBS has lack of double-blind studies. ECT seems to be the golden standard for the treatment resistant elderly patients, yet side effect profile of ECT in elderly will be discussed. Double -blind sham controlled studies with larger samples are necessary to confirm preliminary results with transcranial direct current stimulation (tDCS), magnetic seizure therapy (MST) and VNS, DBS.

PMID:19519563 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/19519563
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« Reply #81 on: August 13, 2013, 07:23:39 AM »

Neuroreport. 2013 Mar 27;24(5):251-3. doi: 10.1097/WNR.0b013e32835f00a3.
Vagus somatosensory-evoked potentials are prolonged in patients with multiple sclerosis with brainstem involvement.
Polak T, Zeller D, Fallgatter AJ, Metzger FG.
Source
Department of Psychiatry, Psychosomatics and Psychotherapy, Laboratory for Psychophysiology and Functional Imaging, University Clinic Wuerzburg, Wuerzburg, Germany. polak_t@klinik.uni-wuerzburg.de

Abstract
Vagus somatosensory-evoked potentials (VSEP) were proposed as a neurophysiological indicator of brainstem dysfunction based on prolonged latencies found in Alzheimer's dementia and Parkinson's disease. We now aimed at a further confirmation of this view independent from neurodegenerative diseases and hypothesized that VSEP in multiple sclerosis with brainstem affection show prolonged latencies, too. In 15 patients with multiple sclerosis according to McDonald and 15 healthy controls after stimulation of the auricular branch of the vagus nerve at the tragus (electrical square impulses, impulse width 0.1 ms, interstimulus interval 2 s, intensity 8 mA), evoked potentials were recorded from electrode positions C3-F3, C4-F4, Fz-F3 and Fz-F4. Analysis of variance showed a significant main effect of the factor diagnosis on latency P1 (F(1,24)=7.067, P=0.001), no significant effect for latencies N1 and P2 nor for the amplitudes. A subgroup of patients with signs of brainstem affection showed a trend for longer P1 latencies (F(1,11)=5916, P=0.033) as compared with the group without. We take this result as further hint for VSEP to be generated at brainstem level which needs confirmation in larger-scale studies and other brainstem-affecting diseases. The method could be suitable for the demonstration of the involvement of differential brainstem nuclei in various neurodegenerative diseases.

PMID:23407276[PubMed - in process]

http://www.ncbi.nlm.nih.gov/pubmed/23407276

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« Reply #82 on: August 13, 2013, 07:25:03 AM »

Med Hypotheses. 2009 Nov;73(5):725-7. doi: 10.1016/j.mehy.2009.04.036. Epub 2009 May 29.
Vagus nerve stimulation may be used in the therapy of myocarditis.
Li H, Yang TD.
Source
Department of Anesthesiology, Xinqiao Hospital, The Third Military Medical University, Chongqing, China.

Abstract
Although a large number of different causes have been identified as leading to myocarditis, inflammation plays a pivotal role in its pathological process. No specific methods are available in the therapy of myocarditis except symptomatic treatment. Vagus nerve stimulation has been found to lower the heart rate and recover the normal heart rhythm which may relieve the cardiac symptoms in myocarditis. Furthermore, the acetylcholine that secreted by vagus nerve stimulation was found to inhibit the production of such inflammatory cytokines as tumor necrosis factor-alpha (TNF-alpha), interleukin 1beta (IL-1beta). Based on the above, we hypothesized that vagus nerve stimulation can be used in the therapy of myocarditis and lead to relief of symptoms and inhibition of inflammatory process which may kill two birds with one stone.

PMID:19481875[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/19481875
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« Reply #83 on: August 13, 2013, 07:26:32 AM »

Appetite. 2010 Oct;55(2):245-52. doi: 10.1016/j.appet.2010.06.008. Epub 2010 Jun 19.
Chronic vagus nerve stimulation decreased weight gain, food consumption and sweet craving in adult obese minipigs.
Val-Laillet D, Biraben A, Randuineau G, Malbert CH.
Source
INRA, UMR1079 SENAH, Domaine de la Prise, Saint Gilles, France. david.val-laillet@rennes.inra.fr

Abstract
Chronic vagus nerve stimulation (VNS) is known to influence food intake and body weight in animals and humans. The aim of our work was to evaluate the effects of long-term VNS in adult obese minipigs. Eight minipigs were fed ad libitum a Western diet to cause obesity, after which half of the animals were implanted with bilateral vagal electrodes connected to constant current stimulators (2mA, 30Hz, 500-μs pulse, ON 30s, OFF 5min). The other animals were implanted with sham devices. Animals were weighed weekly and their daily consumption was measured. Still 14 weeks after surgery, VNS animals (70.3±3.3kg, P>0.10) did not significantly gain weight compared to sham animals (80.6±8.0kg, P<0.05). Furthermore, food consumption decreased in VNS animals (-18%, P<0.02) compared to sham animals (+1%, P>0.10). When subjected to a three-choice meal test (high-fat vs. high-carbohydrates vs. balanced diet), VNS animals decreased their sweet-food consumption compared to sham animals (P<0.05), and increased their balanced diet consumption in comparison to pre-surgery levels. Our results showed that chronic VNS decreased weight gain, food consumption and sweet craving in adult obese minipigs, which indicates that this therapy might be used to decrease appetite in the context of morbid obesity.

Comment in
Neurogastroenterology: modification of basal brain metabolism and neuronal activity is an acquired feature of obesity. [Nat Rev Gastroenterol Hepatol. 2011]

PMID:20600417[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/20600417

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« Reply #84 on: August 13, 2013, 07:28:54 AM »

OCD Central | Obsessive Compulsive Disorder Central
A guide containing and detailing the ins and outs of obsessive compulsive disorder including symptoms, causes, types, treatment and more.

Treat Chronic Depression
www.fisherwallace.com
The Fisher Wallace Stimulator®. FDA-Cleared for Depression.

OCD Treatment: Other Methods

Other methods of trying to cure obsessive compulsive disorder are mostly used when methods based on therapy, drugs and alternative drugs have failed. This normally happens with more severe forms of obsessive compulsive disorder.

One such treatment is by using tranquilizers. These, as stated above, are prescribed to people exhibiting severe OCD. It is considered that tranquilizers help diminish compulsions by relaxing the muscles of the body. However, tranquilizers must be used cautiously since they are habit-forming if overused.

Electroconvulsive therapy (ECT) has also been found useful in treating refractory and severe cases of obsessive compulsive disorder. Don’t know what that means? It’s just a fancy name for electroshocks. It is a very controversial treatment method and it is based on administering anesthetized patients electrically induced seizures. It is important to know that a large scale study on ECT concluded that such therapy has adverse side-effects on the patients such as memory loss or learning impairment and these side-effects persist at least six months after treatment and even in perpetuity.

Another method known as a treatment for OCD is psychosurgery. This is also a “last resort” method. In this case, a surgical lesion is made on the cingulate cortex. According to a study, 30% of patients showed marked improvement after such a procedure. Psychosurgery replaced lobotomy which had severe side effects like unexpected brain damage and strange memory loss. In psychosurgery, magnetic resonance imaging is used to select the proper place in the brain in which to perform surgery.

Two other surgical options are deep-brain stimulation and vagus nerve stimulation. Deep-brain stimulation is a surgical treatment whereby a device called a brain pacemaker is implanted. This device sends electrical impulses to parts of the brain. One big plus for this method is that its effects are reversible. On the other hand, vagus nerve stimulation is using an implanted stimulator that is sending impulses to the left vagus nerve located in the neck through a lead wire that is implanted under the skin. Both methods have shown promising results in treating obsessive compulsive disorder but no clear clinical study has been made in order to draw a clear conclusion so one should take this with a grain of salt and one should ask for advice from an expert.

This concludes our article on the treatment of OCD through other methods. If you want to add on top of what we wrote here or if you’d like to share your experience regarding treating obsessive compulsive disorder through other methods then don’t hesitate to post a comment.

http://www.ocdcentral.info/tag/vagus-nerve-stimulation

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« Reply #85 on: August 13, 2013, 07:34:38 AM »

Clin Neurol Neurosurg. 2012 May;114(4):336-40. doi: 10.1016/j.clineuro.2011.11.016. Epub 2011 Nov 30.
Vagus nerve stimulation has a positive effect on mood in patients with refractory epilepsy.
Klinkenberg S, Majoie HJ, van der Heijden MM, Rijkers K, Leenen L, Aldenkamp AP.
Source
Department of Neurology, Maastricht University Medical Centre, Maastricht, The Netherlands. S.Klinkenberg@mumc.nl

Abstract
BACKGROUND: Preliminary research on the efficacy of vagus nerve stimulation (VNS) indicated additional effects on neuropsychological variables like mood and quality of life (QOL).

OBJECTIVES: The objectives of this prospective longitudinal observational cohort study were to assess the effects of VNS on mood, QOL and cognition in patients with refractory epilepsy and to determine whether these effects occur dependent of seizure control.

METHODS: We included 41 patients with refractory epilepsy; treated with VNS as part of usual patient care. A neuropsychological battery was performed during baseline and repeated after 6 months of VNS in order to compare neuropsychological variables before and after VNS. All patients completed seizure diaries.

RESULTS: Significant improvements were observed for both mood and QOL after 6 months of VNS; based on the results in the POMS and QOLIE-89 questionnaires (p<0.05). There was no significant change in cognition. Mean percentage change in seizure frequency was -9.0%, while 20% of the patients achieved a seizure frequency reduction of 50% or more. No significant correlation was found between changes in seizure frequency and improvements in mood or QOL.

CONCLUSIONS: VNS is associated with improvements in both mood and QOL in patients with refractory epilepsy. Since these improvements appeared to be independent of seizure control, the results of this study indicate an additional antidepressant effect of VNS, which can be of extra value in view of the high co-morbidity of mood disturbances in patients with epilepsy.

Copyright © 2011 Elsevier B.V. All rights reserved.
PMID:22130047[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/22130047
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« Reply #86 on: August 13, 2013, 07:37:26 AM »

Zentralbl Chir. 2011 Oct;136(5):431-5. doi: 10.1055/s-0031-1283739. Epub 2011 Oct 18.
[Vagal stimulation - a new possibility for conservative treatment of peripheral arterial occlusion disease].
[Article in German]
Payrits T, Ernst A, Ladits E, Pokorny H, Viragos I, Längle F.
Source
LK Wiener Neustadt, Chirurgie, Wiener Neustadt, Österreich. thomas.payrits@air-line.at

Abstract
BACKGROUND: The options for the conservative therapy of PAD, and also the achievable benefits are well documented in the S3-guidelines and the TASC-II guidelines. Upon vagal stimulation with a P-STIM device a significant extension of the pain-free and maximum walking distance could be noticed. As this fact continued beyond the end of the therapy, we may have found a new, conservative therapy option to manage PAD.

PATIENTS AND METHODS: In a prospective single centre study we reviewed 31  patients with PAD (Fontaine stages  II and III) who were treated by vagal stimulation with a P-STIM device. The following parameters were analysed: indication, duration of therapy, improvement of pain-free walking distance after therapy and complications.

RESULTS: 31  patients received a vagal stimulation therapy for intermittent claudication in Fontaine stages  II (97 %) and III (3 %). The duration of treatment averaged 6  weeks (minimum 2 weeks, maximum 9  weeks). 27 out of 30  patients were able to increase their pain-free walking distance up to a hundred-fold of the initial values. 3  patients could not give any information about increasing their walking distance in meters, but they reported about an obvious amelioration. All patients reported a continuing improvement after 4  weeks and after further 12  weeks, partly even about additional enhancement. Just 1  patient could not improve his walking-distance -after 3  periods of therapy. This was the only -patient with an isolated diabetic microangiopathy without stenosis or occlusions in the large vessels.

CONCLUSION: The considerable increase in pain-free walking distance after vagal stimulation therapy by P-STIM is appreciably better than those which were described for supervised exercise therapy or pharmacotherapy with Naftidrofuryl or Cilostazol. On the basis of these results we think that vagal stimulation by P-STIM might be a new option for treating intermittent claudication.

© Georg Thieme Verlag KG Stuttgart ˙ New York.
PMID:22009541[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/22009541
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« Reply #87 on: August 13, 2013, 07:38:54 AM »

Med Hypotheses. 2009 Dec;73(6):938-41. doi: 10.1016/j.mehy.2009.06.033. Epub 2009 Jul 23.
Transcutaneous vagus nerve stimulation may attenuate postoperative cognitive dysfunction in elderly patients.
Xiong J, Xue FS, Liu JH, Xu YC, Liao X, Zhang YM, Wang WL, Li S.
Source
Department of Anaesthesiology, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100144, China.

Abstract
Postoperative cognitive dysfunction (POCD) is a decline in cognitive function for weeks or months after surgery. It may affect the patients' length of hospital stay, quality of life, the rehabilitation process, and work performance. Prolonged POCD occurs frequently after cardiac surgery, and the risk of POCD increases with age. The pathophysiology of POCD has not been well understood. However, emerging evidences indicate that various inflammatory mediators are involved in the pathophysiology of POCD and inflammatory response may a potential pathogenic factor. The vagus nerve stimulation has been shown to decrease production and release of pro-inflammatory cytokines through the cholinergic anti-inflammatory pathway (CAP) in both animal model and human. Considering that the inflammation plays a definite role in the pathogenesis of POCD and the vagus nerve can mediate inflammation via CAP, we hypothesize that the transcutaneous vagus nerve stimulation may attenuate POCD by decreasing inflammatory response in elderly patients.

PMID:19631475[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/19631475

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« Reply #88 on: August 13, 2013, 07:41:11 AM »

J Neurosurg. 2012 Nov;117(5):970-7. doi: 10.3171/2012.8.JNS122. Epub 2012 Sep 14.
Efficacy of vagus nerve stimulation in posttraumatic versus nontraumatic epilepsy.
Englot DJ, Rolston JD, Wang DD, Hassnain KH, Gordon CM, Chang EF.
Source
Comprehensive Epilepsy Center, University of California, San Francisco, California 94143-0112, USA. EnglotDJ@neurosurg.ucsf.edu

Abstract
OBJECT: In the US, approximately 500,000 individuals are hospitalized yearly for traumatic brain injury (TBI), and posttraumatic epilepsy (PTE) is a common sequela of TBI. Improved treatment strategies for PTE are critically needed, as patients with the disorder are often resistant to antiepileptic medications and are poor candidates for definitive resection. Vagus nerve stimulation (VNS) is an adjunctive treatment for medically refractory epilepsy that results in a ≥ 50% reduction in seizure frequency in approximately 50% of patients after 1 year of therapy. The role of VNS in PTE has been poorly studied. The aim of this study was to determine whether patients with PTE attain more favorable seizure outcomes than individuals with nontraumatic epilepsy etiologies.

METHODS:Using a case-control study design, the authors retrospectively compared seizure outcomes after VNS therapy in patients with PTE versus those with nontraumatic epilepsy (non-PTE) who were part of a large prospectively collected patient registry.

RESULTS: After VNS therapy, patients with PTE demonstrated a greater reduction in seizure frequency (50% fewer seizures at the 3-month follow-up; 73% fewer seizures at 24 months) than patients with non-PTE (46% fewer seizures at 3 months; 57% fewer seizures at 24 months). Overall, patients with PTE had a 78% rate of clinical response to VNS therapy at 24 months (that is, ≥ 50% reduction in seizure frequency) as compared with a 61% response rate among patients with non-PTE (OR 1.32, 95% CI 1.07-1.61), leading to improved outcomes according to the Engel classification (p < 0.0001, Cochran-Mantel-Haenszel statistic).

CONCLUSIONS:Vagus nerve stimulation should be considered in patients with medically refractory PTE who are not good candidates for resection. A controlled prospective trial is necessary to further examine seizure outcomes as well as neuropsychological outcomes after VNS therapy in patients with intractable PTE.

PMID:22978542[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/22978542
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« Reply #89 on: August 13, 2013, 07:46:27 AM »

Case Report
Vagus nerve stimulator treatment in adult-onset Rasmussen's encephalitis

    Jelena Grujica,
    Christian G. Bienb,
    Claudio Polloc,
    Andrea O. Rossettia, Corresponding author contact information, E-mail the corresponding author

    a Service de Neurologie, Département de Neurosciences Cliniques, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Switzerland
    b Department of Epileptology, University of Bonn Medical Centre, Bonn, Germany
    c Service de Neurochirurgie, Département de Neurosciences Cliniques, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Switzerland

    http://dx.doi.org/10.1016/j.yebeh.2010.10.024, How to Cite or Link Using DOI

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Abstract

We describe a patient with adult-onset Rasmussen's encephalitis (RE) responsive to vagus nerve stimulation. This previously healthy woman developed RE in the right hemisphere at the age of 27. Despite antiepileptic drug polytherapy, she continued to experience subcontinuous, simple-partial left-sided motor seizures and slowly progressive cognitive impairment. Resective surgery was not considered owing to the preservation of left motor skills. She was implanted with a vagus nerve stimulator at the age of 41; after 6 months she experienced a greater than 50% reduction in seizure frequency, which persisted over 2 years together with improvement of her neurological and cognitive status.

http://dx.doi.org/10.1016/j.yebeh.2010.10.024
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