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dennis100
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« on: January 23, 2011, 07:25:59 AM »

Alcohol addiction /Alzheimer's Disease /Anxiety /Arrhythmias /Atrial fibrillation /Autism /Bronchoconstriction /Bulimia Nervosa /Burn-induced organ dysfunction /Comorbid Personality Disorders /Coronary Artery Disease /Chronic heart failure /Chronic Heart Failure in Rats /Cognition /Dramatic first words spoken in 2 children after vagus nerve stimulation /Dravet syndrome /Drop-attacks /Eating disorders /Fibromyalgia /Gut injury and lung permeability in trauma-hemorrhagic shock /Heatstroke /Heroin-Seeking Behavior in Rats /Infarct size /Intestinal epithelial barrier breakdown /Lennox-Gastaut syndrome /Medication-refractory mental illness /Memory /Migraine and Cluster Headaches /Obesity /Mood disorders in elderly population /Mood in patients with refractory epilepsy (positive effect) /Multiple sclerosis /Myocarditis /Obsessive Compulsive Disorder /Peripheral arterial occlusion disease /Persistent hiccups /Postoperative cognitive dysfunction in elderly patients /Post-traumatic epilepsy /Rasmussen's encephalitis /Rheumatoid Arthritis /Ringing in the ears /Sepsis /Spinal trigeminal neuronal /Status epilepticus /SUDEP in children and adolescents /Tinnitus /Tourette's Syndrome /Transient focal cerebral ischemia /Trauma-hemorrhagic shock /Traumatic brain injury /Treatment resistant depression /Treatment resistant epilepsy /Tuberous Sclerosis /Visceral pain-related affective memory.

Alcohol addiction
http://freshpatents.com/Cranial-nerve-stimulation-for-treatment-of-substance-addiction-dt20060907ptan20060200208.php
http://www.ncbi.nlm.nih.gov/pubmed/22945180

Alzheimer's Disease
http://www.ncbi.nlm.nih.gov/pubmed/12444809

Anxiety
http://www.ncbi.nlm.nih.gov/pubmed/20633378

Arrhythmias
http://academic.research.microsoft.com/Publication/28966906/arrhythmias-and-vagus-nerve-stimulation

Atrial fibrillation
http://www.ncbi.nlm.nih.gov/pubmed/21555706
http://www.ncbi.nlm.nih.gov/pubmed/21489033
http://www.ncbi.nlm.nih.gov/pubmed/23179922

Autism
http://www.ncbi.nlm.nih.gov/pubmed/20515333

Bronchoconstriction
http://www.ncbi.nlm.nih.gov/pubmed/22551486

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

Burn-induced organ dysfunction
http://www.ncbi.nlm.nih.gov/pubmed/19482432

Chronic heart failure
http://www.ncbi.nlm.nih.gov/pubmed/23229137

Chronic Heart Failure in Rats
http://academic.research.microsoft.com/Publication/6455772/vagal-nerve-stimulation-markedly-improves-long-term-survival-after-chronic-heart-failure-in-rats

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

Comorbid Personality Disorders
http://clinicaltrialsfeeds.org/clinical-trials/show/NCT01119053

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

Dramatic first words spoken in 2 children after vagus nerve stimulation
http://www.ncbi.nlm.nih.gov/pubmed/20434697

Dravet syndrome
http://www.ncbi.nlm.nih.gov/pubmed/23207687

Drop-attacks
http://www.ncbi.nlm.nih.gov/pubmed/21396833

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

Fibromyalgia
http://www.ncbi.nlm.nih.gov/pubmed/21812908

Gut injury and lung permeability in trauma-hemorrhagic shock
http://www.ncbi.nlm.nih.gov/pubmed/22846937

Heatstroke
http://www.ncbi.nlm.nih.gov/pubmed/23424673

Heroin Seeking Behavior in Rats
http://www.ncbi.nlm.nih.gov/pubmed/21362452

Hiccups
http://www.ncbi.nlm.nih.gov/pubmed/15926725

Intestinal epithelial barrier breakdown
http://www.ncbi.nlm.nih.gov/pubmed/21610431

Lennox-Gastaut syndrome
http://livingwithlgs.com/vagus-nerve-stimulation.aspx
http://www.ncbi.nlm.nih.gov/pubmed/23471536

Medication-refractory mental illness
http://www.ncbi.nlm.nih.gov/pubmed/12059125

Memory
http://www.ncbi.nlm.nih.gov/pubmed/16957488

Migraine and Cluster Headaches
http://www.ncbi.nlm.nih.gov/pubmed/21812772

Mood disorders in elderly population
http://www.ncbi.nlm.nih.gov/pubmed/19519563

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

Myocarditis
http://www.ncbi.nlm.nih.gov/pubmed/19481875

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

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

Positive effect on mood in patients with refractory epilepsy
http://www.ncbi.nlm.nih.gov/pubmed/22130047

Peripheral arterial occlusion disease
http://www.ncbi.nlm.nih.gov/pubmed/22009541

Postoperative cognitive dysfunction in elderly patients
http://www.ncbi.nlm.nih.gov/pubmed/19631475

Posttraumatic epilepsy
http://www.ncbi.nlm.nih.gov/pubmed/22978542

Rasmussen's encephalitis
http://dx.doi.org/10.1016/j.yebeh.2010.10.024

Reduces infarct size
http://www.ncbi.nlm.nih.gov/pubmed/19446004

Rheumatoid Arthritis
http://www.medgadget.com/2012/11/vagus-nerve-stimulation-for-rheumatoid-arthritis-interview-with-anthony-arnold-ceo-of-setpoint-medical.html

Ringing in the ears
http://www.ncbi.nlm.nih.gov/pubmed/21627982

Sepsis
http://www.ncbi.nlm.nih.gov/pubmed/19840870

Severe anxiety disorders
http://www.ncbi.nlm.nih.gov/pubmed/23245749

Severe mental diseases
http://www.ncbi.nlm.nih.gov/pubmed/23266132

Spinal trigeminal neuronal
http://www.ncbi.nlm.nih.gov/pubmed/22800563

Status epilepticus
http://www.ncbi.nlm.nih.gov/pubmed/11359111

SUDEP in children and adolescents
http://www.ncbi.nlm.nih.gov/pubmed/23295425

Tinnitus
http://www.ncbi.nlm.nih.gov/pubmed/23245749

Tourette's Syndrome
http://www.ncbi.nlm.nih.gov/pubmed/16703589

Transient focal cerebral ischemia
http://www.ncbi.nlm.nih.gov/pubmed/22420043

Trauma-hemorrhagic shock
http://www.ncbi.nlm.nih.gov/pubmed/23247120

Traumatic brain injury
http://www.ncbi.nlm.nih.gov/pubmed/22695423
http://www.ncbi.nlm.nih.gov/pubmed/22404761
http://www.ncbi.nlm.nih.gov/pubmed/23485054

Tuberous Sclerosis
http://www.nhs.uk/Conditions/Tuberous-sclerosis/Pages/Treatment.aspx

Visceral pain-related affective memory
http://www.ncbi.nlm.nih.gov/pubmed/22940455





Device treatment may silence ringing in the ears

http://www.msnbc.msn.com/id/41044597/ns/health-health_care/

http://www.ncbi.nlm.nih.gov/pubmed/21627982

_____________________________________________________________________________

Event Date 09/01/2002
Event Type Injury Patient Outcome Life Threatening; Hospitalization
Event Description
During the process of a post-implant follow up call with the pt, the mfr's representative learned that the pt is experiencing the following problems: edema in their throat, enlarged veins in their chest area, discomfort in their arm including numbness and tingling, tightness in their chest, and device migration. Further info revealed that during the pt's follow-up visit with their physician, they complained of breakthrough seizures, bowel incontinence, trouble breathing and rash. The pt reported that they were coughing up "yellowish/blood tinged matter. " during subsequent follow-up visits, the pt complained of headaches, ringing in their ears and chronic pain. On the office visit in 2002, the pt indicated that the vns is working well.

http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfmaude/detail.cfm?mdrfoi__id=443116

Event Date 09/17/2002
Event Type Injury Patient Outcome Required Intervention;
Event Description
Patient reported that they were experiencing painful stimulation. The device was programmed to off in 07/2002 and turned back on in 2002. Ever since the device was turned back on, the patient has been experiencing the following symptoms and attributes these symptoms to vns: dizziness, inability to sleep (insomnia), increase cough, weight loss (25 lbs), ringing in the ears (tinnitus), heart rate and rhythm changes, only with stimulation (arrhythmia). The patient was not experiencing the painful stimulation anymore as reported initially. The patient used their magnet to turn off their device and all of the above symptoms were gone except the ringing in ears. The physician programmed the patient's output current and magnet output current to 0ma (off) again. The physician checked the patient's blood levels for any chemical imbalance. If the blood level results are normal, then the physician will recommend explant.


http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfmaude/detail.cfm?mdrfoi__id=426466

Event Date 08/01/2001
Event Type Injury Patient Outcome Disability;
Event Description
Reporter indicated that patient began to have ringing in left ear (mid to 08/2001). When patient presses on ear, the pt has pain. The next month the patient began to have shaking in left hand. Patient has been on dilantin and clonazapam up until the end of 08/2001. Patient is currently on neurotonin (200mg 3 times/day). Patient explains that the neurotonin gives the pt a tingling feeling.

http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfmaude/detail.cfm?mdrfoi__id=352302



« Last Edit: September 12, 2016, 10:00:19 PM by dennis100 » Logged
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« Reply #1 on: January 23, 2011, 09:27:58 AM »

Don't forget folks, the COMMENT section is OPEN, Let's give them the facts of life.
« Last Edit: January 24, 2011, 12:40:02 AM by dennis100 » Logged

"If you are going through hell, keep going." (Sir Winston Churchill, 1874-1965)
VNS implanted Sept 02, turned off Dec 04, Generator ex-planted Nov 07
Electrodes are in me for LIFE!
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« Reply #2 on: January 23, 2011, 10:13:19 PM »

How to Get Rid of Persistent Hiccups

www.livestrong.com/article/112086-rid-persistent-hiccups

http://www.ncbi.nlm.nih.gov/pubmed/15926725

______________________________________________________________________

Event Date 01/01/2001
Event Type  Injury   Patient Outcome  Hospitalization; Required Intervention
Manufacturer Narrative

 
Event Description

It was initially reported in a peer-review journal that the patient had a continuous 3-month episode of severe hiccups refractory to either; home remedies or chlorpromazine, baclofen, or methocarbamol. At the onset of symptoms, the generator settings were output current - 2. 75ma pulse width - 500 usec frequency - 30hz. Due to the hiccups the patient became significantly sleep deprived and developed complex partial status requiring hospitalization. During hospitalization, the generator was turned off, and the hiccups ceased within 30 min. Trials of reprogramming the generator over the next 2 weeks resulted in tolerance without hiccups being achieved at an output current of output current 1. 0 ma pulse width 250 usec frequency - 30 hz.
 

http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfMAUDE/detail.cfm?mdrfoi__id=2478702



« Last Edit: May 16, 2014, 08:01:41 AM by dennis100 » Logged
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« Reply #3 on: January 23, 2011, 10:14:02 PM »

Vagus Nerve Stimulation May Help Prevent Obesity

www.musc.edu/pr/vns.htm

http://www.ncbi.nlm.nih.gov/pubmed/20600417
« Last Edit: October 06, 2012, 04:42:47 PM by dennis100 » Logged
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« Reply #4 on: January 23, 2011, 10:50:27 PM »

VNS Therapy May Improve Cognition in Alzheimer's Disease Patients.
 
http://www.prohealth.com/library/showarticle.cfm?libid=5052

http://www.ncbi.nlm.nih.gov/pubmed/12444809
« Last Edit: October 06, 2012, 04:42:00 PM by dennis100 » Logged
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« Reply #5 on: January 23, 2011, 11:23:49 PM »

VNS alleviates chronic anxiety in pilot study

www.musc.edu/catalyst/archive/2008/co6-27vns

http://www.ncbi.nlm.nih.gov/pubmed/20633378

____________________________________________________________________

Panic/anxiety
http://www.vnsmessageboard.com/index.php/topic,4042.0.html
« Last Edit: October 22, 2012, 03:47:26 PM by dennis100 » Logged
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« Reply #6 on: January 23, 2011, 11:27:43 PM »

Vagus Nerve Stimulation for the Treatment of Fibromyalgia

www.faqs.org/patents/app/20090264959

http://www.ncbi.nlm.nih.gov/pubmed/21812908
« Last Edit: October 06, 2012, 04:46:39 PM by dennis100 » Logged
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« Reply #7 on: January 23, 2011, 11:37:47 PM »

Vagus Nerve Stimulation Relieves Chronic Refractory Migraine and Cluster Headaches
 
www.headachedrugs.com/archives2/vagus.html

http://www.ncbi.nlm.nih.gov/pubmed/21812772

http://www.ncbi.nlm.nih.gov/pubmed/19415436

_________________________________________________________________
HEADACHES
http://www.vnsmessageboard.com/index.php/topic,3997.0.html
« Last Edit: October 22, 2012, 03:02:02 PM by dennis100 » Logged
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« Reply #8 on: January 24, 2011, 07:19:30 AM »

How frightening to think VNS may be used for these problems when CYBX and the FDA can't acknowledge the damage done to so many with epilepsy and depression.

Serious side effects, deaths and the inability to obtain certain testing for other health issues has caused chaos for many.  I pray the work that Dennis, Dispatch and others have done to enlighten the general public will prevent further heartache!
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« Reply #9 on: January 24, 2011, 11:14:40 PM »

 Grin Geez, THANKS Oreo!!!  I hope I've enlightened some!!!

Scarey reading there because VNS causes headaces, ringing in the ears, and so many other yuck side effects.  Treatment for obesity--only because it makes a person vomit AND vagus nerve damage will cause weight loss due to gastroperesis. 

Makes me wonder about VNS for treatment in brain injury and stroke.  It is so on right now with the FDA and Cybersucks, so let's just add more VNS can supposedly fix.  PLEASE, are these people serious?  I don't believe it can fix a brain injury when all it did for me is cause a greater one.

Frustrating because it's all about money, and the safety of it is tossed out.
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VNS for TRD implant November, 2006.  Complete device removal including coils April, 2008.

"I reckon it's again my turn to win some or learn some..." Jason Mraz

ALL MY POSTINGS ON THE VNS MESSAGE BOARD ARE NON-TRANSFERABLE
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« Reply #10 on: September 29, 2012, 04:39:44 AM »

Vagal Nerve Stimulation Markedly Improves Long-Term Survival After Chronic Heart Failure in Rats


http://academic.research.microsoft.com/Publication/6455772/vagal-nerve-stimulation-markedly-improves-long-term-survival-after-chronic-heart-failure-in-rats



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« Reply #11 on: September 29, 2012, 04:45:17 AM »

Vagal neurostimulation in patients with coronary artery disease   


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

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« Reply #12 on: September 29, 2012, 04:45:57 AM »

Arrhythmias and vagus nerve stimulation  

http://academic.research.microsoft.com/Publication/28966906/arrhythmias-and-vagus-nerve-stimulation


_________________________________________________________________________

Chest pain/Shortnrss of breath
http://www.vnsmessageboard.com/index.php/topic,3911.0.html

Misc Cardiac
http://www.vnsmessageboard.com/index.php/topic,4008.0.html

Cardiac Arrest
http://www.vnsmessageboard.com/index.php/topic,3832.0.html

Tachycardia
http://www.vnsmessageboard.com/index.php/topic,3862.0.html

Bradycarda
http://www.vnsmessageboard.com/index.php/topic,3850.0.html

Pacemaker/ICD
http://www.vnsmessageboard.com/index.php/topic,4011.0.html

Intraoperative bradycardia/asystole
http://www.vnsmessageboard.com/index.php/topic,3842.0.html

Left arm
http://www.vnsmessageboard.com/index.php/topic,3861.0.html

JAW
http://www.vnsmessageboard.com/index.php/topic,4034.0.html

Fainting/dizziness
http://www.vnsmessageboard.com/index.php/topic,3849.0.html

Drop attacks
http://www.vnsmessageboard.com/index.php/topic,3847.0.html
 
Cardiac Deaths
http://www.vnsmessageboard.com/index.php/topic,3868.0.html

Sudden death/dead in bed
http://www.vnsmessageboard.com/index.php/topic,4203.0.html

Unexplained deaths
http://www.vnsmessageboard.com/index.php/topic,3840.0.html
« Last Edit: October 22, 2012, 04:16:30 PM by dennis100 » Logged
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« Reply #13 on: October 05, 2012, 10:34:48 PM »

None of this makes any sense folks. I'm beginning to fear the worst.
« Last Edit: October 05, 2012, 11:05:55 PM by dennis100 » Logged
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« Reply #14 on: October 06, 2012, 01:20:57 PM »

The VNS would be a nice effecient way to help the overpopulation problem. Approve the device for every treatment resistant malady. Rid the country of all the undesirables.

It would go a long way in balancing the budget.

Ever wonder why the FDA has not taken any action in removing this deadly device from the market?
« Last Edit: September 16, 2013, 03:20:34 AM by dennis100 » Logged
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« Reply #15 on: October 06, 2012, 01:23:21 PM »

Overpopulation
From Wikipedia, the free encyclopedia

http://en.wikipedia.org/wiki/Overpopulation
« Last Edit: October 29, 2012, 07:38:33 AM by dennis100 » Logged
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« Reply #16 on: October 06, 2012, 03:08:59 PM »

Lennox-Gastaut syndrome

http://livingwithlgs.com/vagus-nerve-stimulation.aspx
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« Reply #17 on: October 06, 2012, 03:11:32 PM »

Obsessive Compulsive Disorder

http://www.ocdcentral.info/tag/vagus-nerve-stimulation
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« Reply #18 on: October 06, 2012, 03:12:30 PM »

Treatment-resistant anxiety disorders

http://www.ncbi.nlm.nih.gov/pubmed/20633378

__________________________________________________________________

Panic/anxiety
http://www.vnsmessageboard.com/index.php/topic,4042.0.html

« Last Edit: October 22, 2012, 03:56:42 PM by dennis100 » Logged
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« Reply #19 on: October 06, 2012, 03:13:16 PM »

Autism

http://www.ncbi.nlm.nih.gov/pubmed/20515333
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« Reply #20 on: October 06, 2012, 03:30:55 PM »

Tuberous Sclerosis

http://www.nhs.uk/Conditions/Tuberous-sclerosis/Pages/Treatment.aspx
« Last Edit: October 07, 2012, 02:50:18 PM by dennis100 » Logged
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« Reply #21 on: October 06, 2012, 03:31:35 PM »

Comorbid Personality Disorders

http://clinicaltrialsfeeds.org/clinical-trials/show/NCT01119053

_____________________________________________________________________

mental Health
http://www.vnsmessageboard.com/index.php/topic,3837.0.html

Worsening depression
http://www.vnsmessageboard.com/index.php/topic,4001.0.html
« Last Edit: October 22, 2012, 04:42:00 PM by dennis100 » Logged
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« Reply #22 on: October 06, 2012, 04:18:32 PM »

Vagus nerve stimulation has a positive effect on mood in patients with refractory epilepsy

http://www.ncbi.nlm.nih.gov/pubmed/22130047

______________________________________________________________________

Murder & Violence
http://www.vnsmessageboard.com/index.php/topic,4228.0.html
« Last Edit: October 22, 2012, 03:55:03 PM by dennis100 » Logged
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« Reply #23 on: October 06, 2012, 04:19:36 PM »

Peripheral arterial occlusion disease

http://www.ncbi.nlm.nih.gov/pubmed/22009541
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« Reply #24 on: October 06, 2012, 04:21:14 PM »

Transient focal cerebral ischemia

http://www.ncbi.nlm.nih.gov/pubmed/22420043
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« Reply #25 on: October 06, 2012, 04:22:21 PM »

Bronchoconstriction

http://www.ncbi.nlm.nih.gov/pubmed/22551486

_____________________________________________________________________

Respitory
http://www.vnsmessageboard.com/index.php/topic,3961.0.html

« Last Edit: October 22, 2012, 04:25:27 PM by dennis100 » Logged
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« Reply #26 on: October 06, 2012, 04:24:31 PM »

Spinal trigeminal neuronal

http://www.ncbi.nlm.nih.gov/pubmed/22800563
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« Reply #27 on: October 06, 2012, 04:25:30 PM »

Gut injury and lung permeability in trauma-hemorrhagic shock

http://www.ncbi.nlm.nih.gov/pubmed/22846937
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« Reply #28 on: October 06, 2012, 04:26:32 PM »

Visceral pain-related affective memory

http://www.ncbi.nlm.nih.gov/pubmed/22940455
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« Reply #29 on: October 06, 2012, 04:27:45 PM »

Posttraumatic epilepsy

http://www.ncbi.nlm.nih.gov/pubmed/22978542
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« Reply #30 on: October 06, 2012, 04:29:06 PM »

Traumatic brain injury

http://www.ncbi.nlm.nih.gov/pubmed/22695423

http://www.ncbi.nlm.nih.gov/pubmed/22404761

______________________________________________________________________________

Compare Dr. Naritoku's patent file date to the neurological devices panel date.

Dr. Naritoku committed perjury (A felony) by failing to disclose he had applied for a patent that involved vagus nerve stimulation less than a month before the CDRH Neurological Devices Panel met.

Dr. Naritoku's U.S. PATENT
 
Methods of treating traumatic brain injury by vagus nerve stimulation
Filed May 30, 1997 - Issued Aug 15, 2000

http://www.google.com/patents?id=nXoEAAAAEBAJ&printsec=frontcover&dq=Dean+Naritoku&hl=en&sa=X&ei=uh8VT4PBHKrO2wWwtr2ECg&ved=0CD0Q6AEwAw


1997 CDRH Neurological Devices Panel
Friday, June 27, 1997
 
DR. NARITOKU: Mr. Chairman and panel, thank you for inviting me to speak. My name is Dean Naritoku. I am an associate professor of neurology and pharmacology at the Southern Illinois University School of Medicine in Springfield, Illinois. I have been an investigator in both the E03 and E05 studies and have been a consultant for Cyberonics. Otherwise, I do not have a financial interest in the company, and my travel was also covered by Cyberonics.

pg. 72

http://www.fda.gov/ohrms/dockets/AC/97/transcpt/3299t1.pdf



Dean Naritoku, M.D.

GRANTS
Laboratory Research Funding - Principal Investigator
 
Prior to 1997
 
Cyberonics, Inc: Vagus Nerve Stimulation for Intractable Partial Epilepsy. $84,586; 11/90-1992.
 
Cyberonics, Inc: Functional Anatomy of Vagus Nerve Stimulation. $25,000. 7/1/93 - 6/30/94.
 
Cyberonics, Inc.: E05: Assessment of vagus nerve stimulation (VNS) for adjunctive treatment of epilepsy patients who have refractory partial onset seizures with alteration of consciousness. $189,875; 4/95-3/97.
 
Cyberonics, Inc.: XE5: Open-Label Treatment of Refractory Partial Onset Seizures Using Vagus Nerve Stimulation. Principal Investigator - Dean K. Naritoku, M.D. ;30,000 11/95 - 8/97
 
Cyberonics, Inc: "Studies on the role of brain monoamines in the anticonvulsant effect of vagus nerve stimulation (VNS)." (co-principle investigator with R. Browning) $9094; 7/1/95-6/30/97.
 
Funding as co-investigator
 
Cyberonics: "Studies on the enhancement of memory storage processed by vagus nerve stimulation (VNS)." Principle investigators: R. Jensen; $16,659; 7/1/95-6/30/95.
 
Grand total of $355,214 for Dr. Naritoku prior to his testimony before the Neurological Devices Panel.
 
after 97'

Cyberonics, Inc. "An investigation of the capacity of vagus nerve stimulation to alter the course of recovery of function from brain damage in laboratory rats." (Douglas Smith and Robert A. Jenson, co-principal investigators) $40,000. 7/14/98-7/13/00.
 
http://www.minifellow.net/Naritoku.html




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« Reply #31 on: October 06, 2012, 05:09:03 PM »

Others from the patent office with Dr. Naritoku's name.


An apparatus and method for adjunct (add-on) therapy of partial complex epilepsy, generalized epilepsy and involuntary movement disorders

Filed Oct 26, 1998 - Issued Mar 20, 2001

Overview

An apparatus and method for adjunct (add-on) therapy of partial complex epilepsy, generalized epilepsy and involuntary movement disorders comprises an implantable lead-receiver, an external stimulator having controlling circuitry and a power source, and an electrode to inductively couple the stimulator to the lead-receiver. The external stimulator emits electrical pulses to stimulate a cranial nerve such as the left vagus nerve according to a predetermined program. In a second mode of operation, an operator may manually override the predetermined sequence of stimulation.

http://www.google.com/patents?id=EkAGAAAAEBAJ&pg=PA2&dq=Dean+Naritoku&hl=en&sa=X&ei=KCEVT4WPH-HK2AXcxcyDCg&ved=0CDEQ6AEwADgK


An apparatus and method for adjunct (add-on) therapy of dementia and Alzheimer's disease

Filed Oct 26, 1998 - Issued Jul 31, 2001

Overview

An apparatus and method for adjunct (add-on) therapy of dementia and Alzheimer's disease comprises an implantable lead-receiver, an external stimulator having controlling circuitry and a power source, and an electrode to inductively couple the stimulator to the lead-receiver. The external stimulator emits electrical pulses to stimulate a cranial nerve such as the left vagus nerve according to a predetermined program selected from at least two predetermined programs.

http://www.google.com/patents?id=jXIIAAAAEBAJ&pg=PA2&dq=Dean+Naritoku&hl=en&sa=X&ei=KCEVT4WPH-HK2AXcxcyDCg&ved=0CDQQ6AEwATgK

An apparatus and method for adjunct (add-on) therapy of painful syndromes

Filed Oct 26, 1998 - Issued Mar 27, 2001

Overview

An apparatus and method for adjunct (add-on) therapy of painful syndromes comprises an implantable lead-receiver, an external stimulator having controlling circuitry and a power source, and an coil to inductively couple the stimulator to the lead-receiver. The external patch contains means for compensating for the change in axis of external transmitting and internal receiving coils. The external stimulator emits electrical pulses to stimulate a cranial nerve such as the left vagus nerve according to a predetermined program. The pre-determined programs include both short term and long term stimulation.

http://www.google.com/patents?id=JqoGAAAAEBAJ&pg=PA2&dq=Dean+Naritoku&hl=en&sa=X&ei=KCEVT4WPH-HK2AXcxcyDCg&ved=0CDcQ6AEwAjgK


Methods of modulating brain neural plasticity, improving memory and learning, improving recovery from traumatic brain injury, preventing epilepsy, treating memory disorders and chronic memory impairment, and treating persistent impairment of consciousness in humans and animals by vagus nerve stimulation

Filed Jul 10, 2000 - Issued Jan 15, 2002


Overview

Methods of modulating brain neural plasticity, improving memory and learning, improving recovery from traumatic brain injury, preventing epilepsy, treating memory disorders and chronic memory impairment, and treating persistent impairment of consciousness in humans and animals by vagus nerve stimulation are provided. These methods comprise selecting an appropriate human or animal subject and applying to the subject's vagus nerve an electrical stimulation signal having parameter values effective in modulating the electrical activity of the vagus nerve in a manner so as to modulate the activity of preselected portions of the brain.


http://www.google.com/patents?id=__MKAAAAEBAJ&printsec=frontcover&dq=Dean+Naritoku&hl=en&sa=X&ei=giEVT5e8DcjK2AWWvrWECg&ved=0CDUQ6AEwAQ



Method and system for spinal cord stimulation

Filed Sep 26, 2000 - Issued Nov 26, 2002

Overview

A method of performing a medical procedure, such as surgery, is provided. The spinal cord is stimulated in order to control at least one physiological function. The medical procedure is performed and stimulation of the spinal cord is stopped.

http://www.google.com/patents?id=N6ALAAAAEBAJ&pg=PA2&dq=Dean+Naritoku&hl=en&sa=X&ei=giEVT5e8DcjK2AWWvrWECg&ved=0CEEQ6AEwBQ

A method of performing a medical procedure, such as surgery, is provided. A nerve is stimulated to adjust the beating of the heart to a first condition, such as a stopped or slowed condition

Filed Sep 26, 2000 - Issued Mar 11, 2003

Overview

A method of performing a medical procedure, such as surgery, is provided. A nerve is stimulated to adjust the beating of the heart to a first condition, such as a stopped or slowed condition. The medical procedure is performed on the heart or another organ. The stimulation of the nerve is stopped to adjust the beating of the heart to a second condition, such as a beating condition. The heart itself may also be stimulated to a beating condition, such as by pacing. The stimulation of the nerve may be continued to allow the medical procedure to be continued. Systems and devices for performing the medical procedure are also provided.

http://www.google.com/patents?id=fMoOAAAAEBAJ&pg=PA2&dq=Dean+Naritoku&hl=en&sa=X&ei=giEVT5e8DcjK2AWWvrWECg&ved=0CEcQ6AEwBw

Methods of improving memory and learning in humans and animals by vagus nerve stimulation

Filed Jan 14, 2002

Overview

are provided. These methods comprise selecting an appropriate human or animal subject and applying to the subject's vagus nerve an electrical stimulation signal having parameter values effective in modulating the electrical activity of the vagus nerve in a manner so as to modulate the activity of preselected portions of the brain.

http://www.google.com/patents?id=DC2RAAAAEBAJ&printsec=frontcover&dq=Dean+Naritoku&hl=en&sa=X&ei=giEVT5e8DcjK2AWWvrWECg&ved=0CDIQ6AEwAA

Methods of treating persistent impairment of consciousness by  in humans and animals by vagus nerve stimulation are provided.

Filed Jan 14, 2002

Overview

Methods of treating persistent impairment of consciousness in humans and animals by vagus nerve stimulation are provided. These methods comprise selecting an appropriate human or animal subject and applying to the subject's vagus nerve an electrical stimulation signal having parameter values effective in modulating the electrical activity of the vagus nerve in a manner so as to modulate the activity of preselected portions of the brain.

http://www.google.com/patents?id=Cy2RAAAAEBAJ&printsec=frontcover&dq=Dean+Naritoku&hl=en&sa=X&ei=giEVT5e8DcjK2AWWvrWECg&ved=0CDgQ6AEwAg

The medical procedure includes stimulation of a patient's heart while stimulating a nerve of the patient in order to modulate the patient's inflammatory process.

Filed Dec 1, 2003 - Issued May 29, 2007

Overview

A method of performing a medical procedure is provided. The medical procedure includes stimulation of a patient's heart while stimulating a nerve of the patient in order to modulate the patient's inflammatory process. More particularly, the medical procedure includes pacing the ventricles of the patient's heart while stimulating the vagal nerve of the patient. Systems and devices for performing the medical procedure are also provided.


http://www.google.com/patents?id=OR6AAAAAEBAJ&pg=PA3&dq=Dean+Naritoku&hl=en&sa=X&ei=giEVT5e8DcjK2AWWvrWECg&ved=0CEoQ6AEwCA



ELECTRICAL AND MAGNETIC STIMULATORS USED TO TREAT MIGRAINE and other primary headaches such as cluster headaches, including sinus symptoms that resemble an immune-mediated response (“sinus” headaches),

Filed May 17, 2011

Overview

Non-invasive electrical nerve stimulation devices and magnetic stimulation devices are disclosed, along with methods of treating medical disorders using energy that is delivered noninvasively by such devices. The disorders comprise migraine and other primary headaches such as cluster headaches, including sinus symptoms that resemble an immune-mediated response (“sinus” headaches), irrespective of whether those symptoms arise from an allergy that is co-morbid with the headache. The disclosed methods may also be used to treat other disorders that may be co-morbid with migraine headaches, such as anxiety disorders. In preferred embodiments of the disclosed methods, one or both of the patient's vagus nerves are stimulated non-invasively. In other embodiments, parts of the sympathetic nervous system and/or the adrenal glands are stimulated.

http://www.google.com/patents?id=8hHxAQAAEBAJ&pg=PA34&dq=Dean+Naritoku&hl=en&sa=X&ei=fyIVT7OVJ8ng2QXmsYiDCg&ved=0CDoQ6AEwAzgK


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« Reply #32 on: October 06, 2012, 05:09:47 PM »

Drop-attacks

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

_______________________________________________________

Drop Attacks
http://www.vnsmessageboard.com/index.php/topic,3847.0.html
 
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« Reply #33 on: October 06, 2012, 05:10:37 PM »

Chronic heart failure

http://www.ncbi.nlm.nih.gov/pubmed/21972326
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« Reply #34 on: October 06, 2012, 05:11:44 PM »

Dramatic first words spoken in 2 children after vagus nerve stimulation

http://www.ncbi.nlm.nih.gov/pubmed/20434697

___________________________________________________________________

Vocal cord paralysis
http://www.vnsmessageboard.com/index.php/topic,3863.0.html

Voice/larynx
http://www.vnsmessageboard.com/index.php/topic,3992.0.html
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« Reply #35 on: October 07, 2012, 02:39:37 PM »

Sepsis

http://www.ncbi.nlm.nih.gov/pubmed/19840870

_________________________________________________________________

Sepsis
http://www.vnsmessageboard.com/index.php/topic,3892.0.html
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« Reply #36 on: October 07, 2012, 02:41:57 PM »

Congestive Heart Failure

http://www.ncbi.nlm.nih.gov/pubmed/19964772
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« Reply #37 on: October 07, 2012, 02:43:03 PM »

Atrial fibrillation

http://www.ncbi.nlm.nih.gov/pubmed/21555706

http://www.ncbi.nlm.nih.gov/pubmed/21489033
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« Reply #38 on: October 07, 2012, 02:45:10 PM »

Myocarditis

http://www.ncbi.nlm.nih.gov/pubmed/19481875
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« Reply #39 on: October 07, 2012, 02:48:17 PM »

Transcutaneous vagus nerve stimulation may attenuate postoperative cognitive dysfunction in elderly patients

http://www.ncbi.nlm.nih.gov/pubmed/19631475
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« Reply #40 on: October 07, 2012, 02:52:47 PM »

Bulimia Nervosa

http://www.ncbi.nlm.nih.gov/pubmed/16516303
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« Reply #41 on: October 07, 2012, 02:53:32 PM »

Mood disorders in elderly population

http://www.ncbi.nlm.nih.gov/pubmed/19519563
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« Reply #42 on: October 07, 2012, 02:54:16 PM »

Burn-induced organ dysfunction

http://www.ncbi.nlm.nih.gov/pubmed/19482432
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« Reply #43 on: October 07, 2012, 02:56:49 PM »

Tourette's Syndrome

http://www.ncbi.nlm.nih.gov/pubmed/16703589
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« Reply #44 on: October 07, 2012, 02:57:37 PM »

Reduces infarct size

http://www.ncbi.nlm.nih.gov/pubmed/19446004
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« Reply #45 on: October 07, 2012, 02:58:51 PM »

Memory

http://www.ncbi.nlm.nih.gov/pubmed/16957488
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« Reply #46 on: October 07, 2012, 02:59:37 PM »

Cognition

http://www.ncbi.nlm.nih.gov/pubmed/16651013
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« Reply #47 on: October 07, 2012, 03:00:28 PM »

Medication-refractory mental illness

http://www.ncbi.nlm.nih.gov/pubmed/12059125

______________________________________________________________________

mental Health
http://www.vnsmessageboard.com/index.php/topic,3837.0.html
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« Reply #48 on: October 07, 2012, 03:32:05 PM »

Event
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« Reply #49 on: October 07, 2012, 03:33:04 PM »

Inhibits heroin-seeking behavior


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 #50 on: October 10, 2012, 12:21:36 AM »

Intestinal epithelial barrier breakdown

http://www.ncbi.nlm.nih.gov/pubmed/21610431
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« Reply #51 on: October 16, 2012, 01:38:37 AM »

Rasmussen's encephalitis

http://dx.doi.org/10.1016/j.yebeh.2010.10.024
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« Reply #52 on: May 18, 2013, 01:21:16 AM »

 Vagus Nerve Simulator's usages.

1)Alcohol addiction 2)Alzheimer's Disease 3)Anxiety 4)Arrhythmias 5)Atrial fibrillation 6)Autism 7)Bronchoconstriction 8)Bulimia Nervosa 9)Burn-induced organ dysfunction 10)Comorbid Personality Disorders 11)Coronary Artery Disease 12)Chronic heart failure 13)Chronic Heart Failure in Rats 14)Cognition 15)Dramatic first words spoken in 2 children after vagus nerve stimulation 16)Dravet syndrome 17)Drop-attacks 18)Fibromyalgia 19)Gut injury and lung permeability in trauma-hemorrhagic shock 20)Heatstroke 21)Heroin-seeking behavior 22)Infarct size 23)Intestinal epithelial barrier breakdown 24)Lennox-Gastaut syndrome 25)Medication-refractory mental illness 26)Memory 27)Migraine and Cluster Headaches 28)Obesity 29)Mood disorders in elderly population 30)Mood in patients with refractory epilepsy (positive effect) 31)Multiple sclerosis 32)Myocarditis 33)Obsessive Compulsive Disorder 34)Peripheral arterial occlusion disease 35)Persistent hiccups 36)Postoperative cognitive dysfunction in elderly patients 37)Post-traumatic epilepsy 38)Rasmussen's encephalitis 39)Ringing in the ears 40)Sepsis 41)Spinal trigeminal neuronal 42)SUDEP in children and adolescents 43)Tinnitus 44)Tourette's Syndrome 45)Transient focal cerebral ischemia 46)Trauma-hemorrhagic shock 47)Traumatic brain injury 48)Treatment resistant depression 49)Treatment resistant epilepsy 50)Tuberous Sclerosis 51)Vaginal-Cervical self-stimulation in women with complete spinal cord injury 52)Visceral pain-related affective memory.


Vagal nerve stimulation...... A good way to thin out the population. You know,.........."in order to build a more perfect union"



Alcohol addiction
http://freshpatents.com/Cranial-nerve-stimulation-for-treatment-of-substance-addiction-dt20060907ptan20060200208.php
http://www.ncbi.nlm.nih.gov/pubmed/22945180

Alzheimer's Disease
http://www.ncbi.nlm.nih.gov/pubmed/12444809

Anxiety
http://www.ncbi.nlm.nih.gov/pubmed/20633378

Arrhythmias
http://academic.research.microsoft.com/Publication/28966906/arrhythmias-and-vagus-nerve-stimulation

Atrial fibrillation
http://www.ncbi.nlm.nih.gov/pubmed/21555706
http://www.ncbi.nlm.nih.gov/pubmed/21489033
http://www.ncbi.nlm.nih.gov/pubmed/23179922

Autism
http://www.ncbi.nlm.nih.gov/pubmed/20515333

Bronchoconstriction
http://www.ncbi.nlm.nih.gov/pubmed/22551486

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

Burn-induced organ dysfunction
http://www.ncbi.nlm.nih.gov/pubmed/19482432

Chronic heart failure
http://www.ncbi.nlm.nih.gov/pubmed/23229137

Chronic Heart Failure in Rats
http://academic.research.microsoft.com/Publication/6455772/vagal-nerve-stimulation-markedly-improves-long-term-survival-after-chronic-heart-failure-in-rats

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

Comorbid Personality Disorders
http://clinicaltrialsfeeds.org/clinical-trials/show/NCT01119053

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

Dramatic first words spoken in 2 children after vagus nerve stimulation
http://www.ncbi.nlm.nih.gov/pubmed/20434697

Dravet syndrome
http://www.ncbi.nlm.nih.gov/pubmed/23207687

Drop-attacks
http://www.ncbi.nlm.nih.gov/pubmed/21396833

Fibromyalgia
http://www.ncbi.nlm.nih.gov/pubmed/21812908

Gut injury and lung permeability in trauma-hemorrhagic shock
http://www.ncbi.nlm.nih.gov/pubmed/22846937

Heatstroke
http://www.ncbi.nlm.nih.gov/pubmed/23424673

Hiccups
http://www.ncbi.nlm.nih.gov/pubmed/15926725

Inhibits heroin-seeking behavior
http://www.ncbi.nlm.nih.gov/pubmed/21362452

Intestinal epithelial barrier breakdown
http://www.ncbi.nlm.nih.gov/pubmed/21610431

Lennox-Gastaut syndrome
http://livingwithlgs.com/vagus-nerve-stimulation.aspx
http://www.ncbi.nlm.nih.gov/pubmed/23471536

Medication-refractory mental illness
http://www.ncbi.nlm.nih.gov/pubmed/12059125

Memory
http://www.ncbi.nlm.nih.gov/pubmed/16957488

Migraine and Cluster Headaches
http://www.ncbi.nlm.nih.gov/pubmed/21812772

Mood disorders in elderly population
http://www.ncbi.nlm.nih.gov/pubmed/19519563

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

Myocarditis
http://www.ncbi.nlm.nih.gov/pubmed/19481875

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

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

Positive effect on mood in patients with refractory epilepsy
http://www.ncbi.nlm.nih.gov/pubmed/22130047

Peripheral arterial occlusion disease
http://www.ncbi.nlm.nih.gov/pubmed/22009541

Postoperative cognitive dysfunction in elderly patients
http://www.ncbi.nlm.nih.gov/pubmed/19631475

Posttraumatic epilepsy
http://www.ncbi.nlm.nih.gov/pubmed/22978542

Rasmussen's encephalitis
http://dx.doi.org/10.1016/j.yebeh.2010.10.024

Reduces infarct size
http://www.ncbi.nlm.nih.gov/pubmed/19446004

Ringing in the ears
http://www.ncbi.nlm.nih.gov/pubmed/21627982

Sepsis
http://www.ncbi.nlm.nih.gov/pubmed/19840870

Severe anxiety disorders
http://www.ncbi.nlm.nih.gov/pubmed/23245749

Severe mental diseases
http://www.ncbi.nlm.nih.gov/pubmed/23266132

Spinal trigeminal neuronal
http://www.ncbi.nlm.nih.gov/pubmed/22800563

SUDEP in children and adolescents
http://www.ncbi.nlm.nih.gov/pubmed/23295425

Tinnitus
http://www.ncbi.nlm.nih.gov/pubmed/23245749

Tourette's Syndrome
http://www.ncbi.nlm.nih.gov/pubmed/16703589

Transient focal cerebral ischemia
http://www.ncbi.nlm.nih.gov/pubmed/22420043

Trauma-hemorrhagic shock
http://www.ncbi.nlm.nih.gov/pubmed/23247120

Traumatic brain injury
http://www.ncbi.nlm.nih.gov/pubmed/22695423
http://www.ncbi.nlm.nih.gov/pubmed/22404761
http://www.ncbi.nlm.nih.gov/pubmed/23485054

Tuberous Sclerosis
http://www.nhs.uk/Conditions/Tuberous-sclerosis/Pages/Treatment.aspx

Vaginal-Cervical self-stimulation in women with complete spinal cord injury
http://www.ncbi.nlm.nih.gov/pubmed/15451368
http://www.ncbi.nlm.nih.gov/pubmed/11928182

Visceral pain-related affective memory
http://www.ncbi.nlm.nih.gov/pubmed/22940455


Vagal inhibition

May 31, 2012 | Filed under: Forensic Medicine,General Health | Posted by: admin

Vagal inhibition is condition that causes sudden death to occur within seconds or a minute or two due to minor trauma or relatively simple and harmless peripheral stimulation.

Pressure on the baroreceptors situated in the carotid sinuses, carotid sheaths, and the carotid body (located in the internal carotid artery just above the bifurcation of common carotid artery, and situated about the level of angle of mandible) causes an increase in blood pressure in these sinuses with resultant slowing of the heart rate, dilatation of blood vessels and a fall in blood pressure. The vagal inhibition leaves the person dead instantly.

In normal persons, pressure on the carotid sinus causes minimal effects with a decrease in heart rate of less than six beats per minute, and only a slight reduction (less than 10 mm. Hg) in blood pressure. Some individuals show marked hypersensitivity to stimulation of the carotid sinuses, characterized by bradycardia and cardiac arrhythmia ranging from ventricular arrhythmias to cardiac arrest.

http://healthdrip.com/wp-content/uploads/2012/05/vagal-inhibition-300x172.jpg



Vagal Inhibition

Stimulation of the corotid sinus baroreceptors causes impulses to pass via Herring nerve to the afferent fibers of the glossopharyngeal nerve (9th cranial nerve) ; these in turn link in the brain stem to the nucleus of the vagus nerve (10th cranial nerve) causing the vagal inhibition.

Parasympathetic efferent impulses then pass to the heart via the cardiac branches of the vagus nerve. Stimulation of these fibers causes a profound bradycardia. This reflex arc is independent of the main motor and sensory nerve pathways. There is wide network of sensory nerves in the skin, pharynx, glottis, pleura, pentoneum covering viscerr or extending into the spermatic cord, cervix, urethra, perineum and coeliac plexus.

Afferent fibers from these tissues pass into the lateral tracts of the spinal cord, effect local reflex connections over several segments and also pass to the brain. The vagal nucleus is controlled by the synaptic connections in the spinal cord, which may be facilitated from both the sensory central cortex and from the thalamic centres. The latter may be responsible for emotional tone noted in the vagal reflex.

Parasympathetic stimulation of the heart can be initiated by high neck compression, pressure on carotid sinus or sometimes by direct pressure over the trunk of the vagus nerve.

Causes of vagal inhibition

(1) The commonest cause of such vagal inhibition is pressure on the neck particularly on the carotid sinuses as in hanging or strangulation.

(2) Unexpected blows to the larynx, chest, abdomen and genital organs.

(3) Extensive injuries to the spine or other parts of the body.

(4) Impaction of food in larynx or unexpected inhalation of fluid into the upper respiratory tract.

(5) Sudden immersion of body in cold water.

(6) The insertion of an instrument into the bronchus, uterus, bladder or rectum.

(7) Puncture of a pleural cavity usually for producing a pneumothorax.

(8 ) Sudden evacuation of pathological fluids, e.g., ascitic or pleural.

(9) Sudden distension of hollow muscular organs, e.g., during attempts at criminal abortion, when instruments are passed through the cervix or fluids are injected into the uterus.

(10) In degenerative diseases of the heart, e.g., sinus bradycardia and partial or complete A-V block; parasympathetic stimulation further depress the heart rate and may induce a Stokes-Adams attack which may be fatal. There is great variation in individual susceptibility.

Death from vagal inhibition is accidental and caused by microtrauma. The stimulus should be sudden and abnormal for the reflex to occur. The reflex is exaggerated by a high state of emotional tension, and also any condition which lowers voluntary cerebral control of reflex responses, such as a mild alcoholic intoxication, a degree of hypoxia or partial narcosis due to incomplete anesthesia.

Autopsy

When death results from vagal inhibition, there are no characteristic postmortem appearances. The cause of death can be inferred only by exclusion of other pathological conditions, and from the accurate observations by reliable witnesses, concerning the circumstance of death.

A soldier was dancing with his girl friend in the presence of many others in a hall. While dancing, he playfully ‘tweaked” (pinched) her neck. She dropped down dead on the spot. There were no injuries or signs of asphyxia. Death was as a result of vagal inhibition.


Related Posts:
•Sudden death
•Modes of death – Asphyxia, Coma and Syncope
•Syncope (fainting) – causes, symptoms and treatment
•Anticholinergic syndrome
•Brain stem death

http://healthdrip.com/vagal-inhibition/


« Last Edit: June 22, 2013, 01:58:44 AM by dennis100 » Logged
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« Reply #53 on: May 18, 2013, 03:33:08 AM »

Zapping the vagus nerve 24/7 will eventually lead to vagal inhibition. The FDA adverse event report below is a good example. This poor person's vagal nerve was fried.

Event Date 05/29/2001
Event Type Injury Patient Outcome Other; Required Intervention
Event Description
An article about the histological appearance of a chronically stimulated vagus nerve in a pediatric reporter indicated vns therapy moderated a patient's atonic episodes, but the patient experienced "occasional hospitalizations for status epilepticus. " the patient passed away due to asphyxiation (reported on medwatch 1644487-2008-02703). The vns therapy system was explanted with "1. 5 cm of unstimulated nerve superiorly and inferiorly. " the electrodes were dissected from the nerve "revealing grossly normal nerve above and below the stimulator. " "abundant inflammatory cells were present around the stimulated nerve section. " "severe myelin loss and occasional myelin digestion chambers were seen in the nerve fibers. With modified trichrome and luxo fast blue stains, this loss was estimated to be nearly 90%. " good faith attempts to obtain additional information have been unsuccessful to date.

http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfMAUDE/Detail.CFM?MDRFOI__ID=1241164
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« Reply #54 on: July 29, 2013, 08:23:23 AM »

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.

http://www.ncbi.nlm.nih.gov/portal/utils/pageresolver.fcgi?recordid=1375125005981721

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« Reply #55 on: August 13, 2013, 05:58:39 AM »

Eur Heart J. 2011 Apr;32(7):847-55. doi: 10.1093/eurheartj/ehq391. Epub 2010 Oct 28.
Chronic vagus nerve stimulation: a new and promising therapeutic approach for chronic heart failure.
De Ferrari GM, Crijns HJ, Borggrefe M, Milasinovic G, Smid J, Zabel M, Gavazzi A, Sanzo A, Dennert R, Kuschyk J, Raspopovic S, Klein H, Swedberg K, Schwartz PJ; CardioFit Multicenter Trial Investigators.
Collaborators (16)
Source
Department of Cardiology, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy. g.deferrari@smatteo.pv.it
Abstract

AIMS: In chronic heart failure (CHF), reduced vagal activity correlates with increased mortality and acute decompensation. Experimentally, chronic vagus nerve stimulation (VNS) improved left ventricular (LV) function and survival; clinically, it is used for the treatment of drug-refractory epilepsy. We assessed safety and tolerability of chronic VNS in symptomatic CHF patients, using a novel implantable nerve stimulation system. The secondary goal was to obtain preliminary data on clinical efficacy.

METHODS AND RESULTS: This multi-centre, open-label phase II, two-staged study (8-patient feasibility phase plus 24-patient safety and tolerability phase) enrolled 32 New York Heart Association (NYHA) class II-IV patients [age 56 ± 11 years, LV ejection fraction (LVEF) 23 ± 8%]. Right cervical VNS with CardioFit (BioControl Medical) implantable system started 2-4 weeks after implant, slowly raising intensity; patients were followed 3 and 6 months thereafter with optional 1-year follow-up. Overall, 26 serious adverse events (SAEs) occurred in 13 of 32 patients (40.6%), including three deaths and two clearly device-related AEs (post-operative pulmonary oedema, need of surgical revision). Expected non-serious device-related AEs (cough, dysphonia, and stimulation-related pain) occurred early but were reduced and disappeared after stimulation intensity adjustment. There were significant improvements (P < 0.001) in NYHA class quality of life, 6-minute walk test (from 411 ± 76 to 471 ± 111 m), LVEF (from 22 ± 7 to 29 ± 8%), and LV systolic volumes (P = 0.02). These improvements were maintained at 1 year.

CONCLUSIONS: This open-label study shows that chronic VNS in CHF patients with severe systolic dysfunction may be safe and tolerable and may improve quality of life and LV function. A controlled clinical trial appears warranted.

Comment in
Chronic vagal nerve stimulation for the treatment of human heart failure: progress in translating a vision into reality. [Eur Heart J. 2011]

PMID:21030409[PubMed - indexed for MEDLINE]  Free full text

http://www.ncbi.nlm.nih.gov/pubmed/21030409

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« Reply #56 on: August 13, 2013, 06:01:35 AM »

Psychiatr Danub. 2012 Sep;24 Suppl 1:S14-20.
The current perspective of neuromodulation techniques in the treatment of alcohol addiction: a systematic review.
Herremans SC, Baeken C.
Source
Department of Psychiatry University Hospital, Brussels, Belgium. sarah.herremans@uzbrussel.be

Abstract
BACKGROUND: Alcohol dependency can be considered as a chronic mental disorder characterized by frequent relapses even when treated with appropriate medical or psychotherapeutic interventions. Here, the efficacy of different neuromodulation techniques in alcohol addiction, such as transcranial direct current stimulation (tDCS), repetitive transcranial magnetic stimulation (rTMS), deep brain stimulation (DBS), vagal nerve stimulation (VNS) and electroconvulsive therapy (ECT) is critically evaluated.

METHODS: A broad literature search on electronic databases such as NCBI PubMed, the Web of Knowledge, the Cochrane Library was conducted. Additionally, we searched recent handbooks on neuromodulation and/or addiction.

RESULTS: Studies investigating these neuromodulation techniques in alcohol addiction remain to date rather limited and especially tDCS and rTMS applications have been investigated. Overall, the clinical effects seem modest. The use of VNS and ECT has yet to be investigated in alcohol dependent patients.

CONCLUSIONS: Neuromodulation techniques have only recently been subject to investigation in alcohol addiction and methodological differences between the few studies restrict clear-cut conclusions. Nevertheless, the scarce results encourage further investigation in alcohol addiction.

PMID: 22945180 [PubMed - indexed for MEDLINE] Free full text

http://www.ncbi.nlm.nih.gov/pubmed/22945180
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« Reply #57 on: August 13, 2013, 06:03:48 AM »

J Clin Psychiatry. 2002 Nov;63(11):972-80.
Cognition-enhancing effect of vagus nerve stimulation in patients with Alzheimer's disease: a pilot study.
Sjögren MJ, Hellström PT, Jonsson MA, Runnerstam M, Silander HC, Ben-Menachem E.
Source
Institute of Clinical Neuroscience, Göteborg University, Mölndal, Sweden. magnus.sjogren@medfak.gu.se

Abstract
BACKGROUND: Vagus nerve stimulation (VNS) is an established treatment method for therapy-refractory epilepsy and, in Europe, for treatment-resistant depression also. Clinical and experimental investigations have also shown positive effects of VNS on cognition in epilepsy and depression. The purpose of the present pilot study was to investigate the effect of VNS on cognition in patients with Alzheimer's disease.

METHOD: All the included patients (N = 10) met the National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association criteria for the diagnosis of Alzheimer's disease. Before the implantation of the vagus stimulator (NeuroCybernetic Prosthesis), the patients underwent neuropsychological tests (e.g., Alzheimer's Disease Assessment Scale-cognitive subscale [ADAS-cog] and Mini-Mental State Examination [MMSE]), computerized tomography of the brain, medical/neurologic and psychological examinations (status evaluation), and lumbar puncture with investigation of the cerebrospinal fluid. The presence of depressive symptoms was rated using the Montgomery-Asberg Depression Rating Scale. The VNS was initiated 2 weeks after the implantation, and the patients were followed up with regular investigations and tests over 6 months. Response was defined as improvement or absence of impairment in ADAS-cog and MMSE scores after 3 and 6 months.

RESULTS: After 3 months of treatment, 7 of 10 patients were responders according to the ADAS-cog (median improvement of 3.0 points), and 9 of 10 patients were responders according to the MMSE (median improvement of 1.5 points). After 6 months of treatment, 7 patients were responders on the ADAS-cog (median improvement of 2.5 points), and 7 patients were responders on the MMSE (median improvement of 2.5 points). VNS was well tolerated, and its side effects were mild and transient.

CONCLUSION: The results of this open-label pilot study suggest a positive effect of VNS on cognition in patients with Alzheimer's disease. Further studies are warranted.

PMID:12444809[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/12444809

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« Reply #58 on: August 13, 2013, 06:06:38 AM »

Brain Stimul. 2008 Apr;1(2):112-21. doi: 10.1016/j.brs.2008.02.001. Epub 2008 Mar 28.
A pilot study of vagus nerve stimulation (VNS) for treatment-resistant anxiety disorders.
George MS, Ward HE Jr, Ninan PT, Pollack M, Nahas Z, Anderson B, Kose S, Howland RH, Goodman WK, Ballenger JC.
Source
Department of Psychiatry, Medical University of South Carolina, Charleston, South Carolina 29425, USA. georgem@musc.edu

Abstract
BACKGROUND: Vagus nerve stimulation (VNS) is an effective anticonvulsant device and has shown antidepressant effects in chronic treatment resistant depression. Because the vagus nerve sends information to brain regions important in anxiety regulation (locus coeruleus, orbitofrontal cortex, insula, hippocampus and amygdala), this pathway might be involved in perceiving or manifesting various somatic and cognitive symptoms that characterize anxiety disorders. On the basis of this reasoning and reports of anxiolytic effects of VNS in patients treated for epilepsy and depression, we organized an open-label pilot acute trial of adjunctive VNS on top of stable medications, followed by long-term follow-up, to assess the safety and potential efficacy of VNS for patients with treatment resistant anxiety disorders.

METHODS: Eleven adult outpatients with treatment resistant obsessive-compulsive disorder (OCD), panic disorder (PD), or posttraumatic stress disorder (PTSD) were recruited. Patients had failed several medication trials as well as cognitive behavioral therapy (CBT). All patients were rated with the Hamilton Anxiety Scale (HAM-A) and the clinical global impressions improvement scale (CGI-I). Patients with OCD were also rated with the Yale-Brown Obsessive Compulsive Scale (Y-BOCS). Patients were maintained on their current psychotropic medications at fixed doses during the acute 12-week phase. Changes in medications and VNS stimulus parameters were allowed during the long-term follow-up. Response was defined as a 50% or greater improvement on the HAM-A for all patients and a 25% or greater improvement on the Y-BOCS for patients with OCD.

RESULTS: Eleven patients were recruited. Seven patients had a primary diagnosis of OCD, two had PTSD, and one had PD. One OCD patient changed their mind and was never implanted. One patient with OCD withdrew consent before the end of the acute phase, so long-term results were available for nine patients. Three patients were acute responders, based on the HAM-A, and there was some improvement in anxiety ratings over time (with statistically significant improvements at 14 of 18 quarters during long-term follow-up). Of the seven patients with OCD who received stimulation, three were acute responders, based on the Y-BOCS, and there was some improvement in Y-BOCS scores over time (with statistically significant improvements at 7 of 18 quarters during long-term follow-up). VNS was relatively well tolerated. Four years after implantation, four patients (diagnoses two OCD, one PD, one PTSD) were still receiving VNS with continued and sustained improvement in anxiety scores compared with their baseline scores.

CONCLUSIONS: These patients with treatment-resistant anxiety disorders generally tolerated VNS treatment, and there was evidence of acute and long-term improvement in some patients. These open data suggest that further double-blind studies assessing the VNS role in treating anxiety disorders, particularly OCD, may be warranted.

PMID:20633378[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/20633378

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« Reply #59 on: August 13, 2013, 06:15:38 AM »

Circulation. 2011 May 24;123(20):2204-12. doi: 10.1161/CIRCULATIONAHA.111.018028. Epub 2011 May 9.
Continuous low-level vagus nerve stimulation reduces stellate ganglion nerve activity and paroxysmal atrial tachyarrhythmias in ambulatory canines.
Shen MJ, Shinohara T, Park HW, Frick K, Ice DS, Choi EK, Han S, Maruyama M, Sharma R, Shen C, Fishbein MC, Chen LS, Lopshire JC, Zipes DP, Lin SF, Chen PS.
Source
Krannert Institute of Cardiology, Division of Cardiology, Indiana University School of Medicine, Indianapolis, IN, USA.

Abstract
BACKGROUND: We hypothesize that left-sided low-level vagus nerve stimulation (LL-VNS) can suppress sympathetic outflow and reduce atrial tachyarrhythmias in ambulatory dogs.

METHODS AND RESULTS: We implanted a neurostimulator in 12 dogs to stimulate the left cervical vagus nerve and a radiotransmitter for continuous recording of left stellate ganglion nerve activity, vagal nerve activities, and ECGs. Group 1 dogs (N=6) underwent 1 week of continuous LL-VNS. Group 2 dogs (N=6) underwent intermittent rapid atrial pacing followed by active or sham LL-VNS on alternate weeks. Integrated stellate ganglion nerve activity was significantly reduced during LL-VNS (7.8 mV/s; 95% confidence interval [CI] 6.94 to 8.66 versus 9.4 mV/s [95% CI, 8.5 to 10.3] at baseline; P=0.033) in group 1. The reduction was most apparent at 8 am, along with a significantly reduced heart rate (P=0.008). Left-sided low-level vagus nerve stimulation did not change vagal nerve activity. The density of tyrosine hydroxylase-positive nerves in the left stellate ganglion 1 week after cessation of LL-VNS were 99 684 μm(2)/mm(2) (95% CI, 28 850 to 170 517) in LL-VNS dogs and 186 561 μm(2)/mm(2) (95% CI, 154 956 to 218 166; P=0.008) in normal dogs. In group 2, the frequencies of paroxysmal atrial fibrillation and tachycardia during active LL-VNS were 1.4/d (95% CI, 0.5 to 5.1) and 8.0/d (95% CI, 5.3 to 12.0), respectively, significantly lower than during sham stimulation (9.2/d [95% CI, 5.3 to 13.1]; P=0.001 and 22.0/d [95% CI, 19.1 to 25.5], P<0.001, respectively).

CONCLUSIONS: Left-sided low-level vagus nerve stimulation suppresses stellate ganglion nerve activities and reduces the incidences of paroxysmal atrial tachyarrhythmias in ambulatory dogs. Significant neural remodeling of the left stellate ganglion is evident 1 week after cessation of continuous LL-VNS.

PMID:21555706 [PubMed - indexed for MEDLINE] PMCID: PMC3101282 Free PMC Article

http://www.ncbi.nlm.nih.gov/pubmed/21555706
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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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« Reply #90 on: August 13, 2013, 07:48:04 AM »

Neurosci Lett. 2009 Aug 14;459(3):147-51. doi: 10.1016/j.neulet.2009.05.018. Epub 2009 May 13.
Vagus nerve stimulation reduces infarct size in rat focal cerebral ischemia.
Ay I, Lu J, Ay H, Gregory Sorensen A.
Source
MGH/MIT/HMS A.A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital-East, 149 13th Street, Charlestown, MA O2129, USA. iay@partners.org

Abstract
Background and purpose: We sought to determine the effect of vagus nerve stimulation (VNS) on infarct size after transient focal cerebral ischemia in rats. Methods: Ischemia was produced by transient filament occlusion of the right middle cerebral artery. Stimulating electrodes were implanted on the cervical part of the right vagus nerve. Electrical stimulation was initiated 30 min after the induction of ischemia, and delivered for 30s at every 30 min for 3h in experimental group 1 and at every 5 min for 1h in experimental group 2. All the procedures were duplicated but no stimulus was delivered in the control group. Functional deficit was evaluated and animals were killed to determine the infarct size 24h after ischemia. Results: Ischemic lesion volume was smaller in VNS-treated animals as compared with control animals; the relative percentage of contralateral hemispheric volume that underwent infarction was 16.2+/-3.2% in the VNS and 33.0+/-5.0% in the control arms in experimental group 1 (p<0.05). The respective values for experimental group 2 were 19.8+/-0.5% and 37.9+/-2.6% (p<0.05). VNS-treated animals were significantly more likely to have better functional scores at 24h as compared with control animals. The functional score improved by 50% in experimental group 1 and 44% in experimental group 2 (p<0.05 for both groups). Conclusion: VNS appears to offer protection against acute ischemic brain injury.

PMID:19446004[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/19446004
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« Reply #91 on: August 13, 2013, 07:49:47 AM »

Vagus Nerve Stimulation for Rheumatoid Arthritis: Interview with Anthony Arnold, CEO of SetPoint Medical
by Janelle Chang on Nov 16, 2012 • 11:14 am

SetPoint Medical based out of Valencia, CA presented at the ACR annual meeting this past weekend and highlighted positive first-in-human results from an open label pilot study focused on RA. The study results suggested that by stimulating the vagus nerve using a commercially available neuromodulation device, the inflammatory reflex can be regulated to improve “clinical manifestations of rheumatoid arthritis (RA)”.  Although the study used a commercially available device, SetPoint is developing a proprietary neuromodulation device which is smaller and more compact, allowing it to be implanted directly on the vagus nerve. The device is also designed to be programmed using an iPad, eliminating the need for a custom programmer like other neuromodulators on the market. It is also projected to be more cost-effective over currently approved drugs to treat RA. Medgadget interviewed Anthony Arnold, CEO of SetPoint Medical (via phone) to discuss this new product, treatment, and the company’s focus for 2013.

Janelle Chang, Medgadget: Can you provide a brief explanation of the clinical procedure and how the device works?

Anthony Arnold Vagus Nerve Stimulation for Rheumatoid Arthritis: Interview with Anthony Arnold, CEO of SetPoint Medical

Anthony Arnold, SetPoint Medical: The procedure is traditional where [a physician] performs surgery in the cervical neck area, right below your chin and implants the device on the vagus nerve. There are a few other companies that have been doing this for other indications now for more than 15 years. Tens of thousands of patients have had their vagus nerve stimulated for epilepsy, or heart failure. This is the first time the vagus nerve has been stimulated in humans for an inflammatory disease such as RA. SetPoint’s device is 95% smaller than the devices in use today. The entire device is implanted right on the vagus nerve…. About an inch long segment of a number 2 pencil [size-wise].

 

Janelle Chang: What is the current gold standard for this type of condition and how is this device a possible improvement?

Anthony Arnold: Current drugs on the market such as Enbrel and Remicade sell billions of dollars per year and the market is growing more than 10% each year because the drugs do work for many people…. But not all patients want to be on these types of potent drugs due to the concern over serious side effects. We help the physicians by giving them another tool or alternative to these potent drugs and help reduce the healthcare cost for these patients by up to 75%. The device, procedure, plus management of the device will cost approximately as much as 18 months of today’s drug therapy. Since the device will last about 10 years, patients will get 10 years of device therapy for the cost of only 12 to 18 months of drug therapy.

 

SetPoint Medical Vagus Nerve Stimulation for Rheumatoid Arthritis: Interview with Anthony Arnold, CEO of SetPoint Medical

Janelle Chang: How does this differ from other vagus nerve stimulators on the market?

Anthony Arnold: Difference is with the frequency and duration of the pulses we deliver (compared to commercially available neuromodulation devices) – we administer few pulses at a lower power. Because we deliver fewer pulses over a shorter duration of time with a different pattern, our device can be much, much smaller. The device is so small it can be directly attached to the nerve itself and since it can be programmed with an iPad, making it user friendly.

 

Janelle Chang: Is there any risk to overstimulating the vagus nerve?

Anthony Arnold: Haven’t found any risk to overstimulating it. Biggest concern around overstimulation would be the nerve getting too used to it. Studies and experience with tens of thousands of patients implanted for other diseases have shown that’s not a significant concern. If you over stimulate with too much power, the patient can feel it and tell you it’s really uncomfortable and the degree of stimulation can be adjusted.

 

Janelle Chang: Why did the company choose to focus on RA versus other inflammatory diseases for the first generation product?

Anthony Arnold: We selected RA to start because it is a disease that responds rapidly to both drug and device therapy. When you start treating a patient and you don’t see a result within 2 weeks it’s unlikely it’s going to work. If you don’t see a result within a month it’s not going to work. The objective markers in the disease and the visible signs and symptoms are easy to measure and observe and there are standards already agreed upon. Compared to Crohn’s disease for example, some of the markers are good but the end points are much harder to discern and responses can require a longer time to observe.

 

Janelle Chang: What were the patient inclusion/exclusion criteria and study end points?

Anthony Arnold (supplemented by ACR poster presentation): The open label pilot study was patterned after a Phase 1 study for drugs e.g. Embrel so that the results could be reasonably compared. We recruited similar patient populations (male/female, 18-75 years of age) and sickness levels (at least 6 months onset RA as defined by 2010 ACR/EULAR criteria). Patients were “drug naïve” patients, largely disabled by the disease and with poor quality of life. The study end points included analysis of biomarkers (e.g. FACS, serum cytokines, LPS-induced TNF release assay), synovial biopsy, and various ACR and EULAR response rates. Six of the eight enrolled showed significant and meaningful improvement by EULAR and ACR standards.

 

Janelle Chang: Are larger clinical trials planned and will they focus exclusively on RA or other inflammatory diseases?

Anthony Arnold: In 2013, we will continue to develop the device but will put significant focus towards a randomized trail modeled much like a Phase 2 drug trial to prove in a blinded study the same results we saw in our pilot. We plan to include around 100-150 patients across multiple centers around the world. We also plan to do a similar pilot study specifically targeted at Crohn’s disease across Europe because for a Crohn’s patient there are very few therapies available unlike RA.

Company website: SetPoint Medical…

http://www.medgadget.com/2012/11/vagus-nerve-stimulation-for-rheumatoid-arthritis-interview-with-anthony-arnold-ceo-of-setpoint-medical.html


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« Reply #92 on: August 13, 2013, 07:52:56 AM »

Neuroscience. 2011 Aug 25;189:207-14. doi: 10.1016/j.neuroscience.2011.05.024. Epub 2011 May 26.
Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors.
Nichols JA, Nichols AR, Smirnakis SM, Engineer ND, Kilgard MP, Atzori M.
Source
School of Behavioral and Brain Sciences, University of Texas at Dallas, Richardson, TX, USA; Department of Neuroscience, Baylor College of Medicine, Houston, TX, USA. jnichols@cns.bcm.edu

Abstract
Vagus nerve stimulation (VNS) is an FDA approved treatment for drug-resistant epilepsy and depression. Recently, we demonstrated the capacity for repeatedly pairing sensory input with brief pulses of VNS to induce input specific reorganization in rat auditory cortex. This was subsequently used to reverse the pathological neural and perceptual correlates of hearing loss induced tinnitus. Despite its therapeutic potential, VNS mechanisms of action remain speculative. In this study, we report the acute effects of VNS on intra-cortical synchrony, excitability, and sensory processing in anesthetized rat auditory cortex. VNS significantly increased and decorrelated spontaneous multi-unit activity, and suppressed entrainment to repetitive noise burst stimulation at 6-8 Hz but not after application of the muscarinic antagonist scopolamine. Collectively, these experiments demonstrate the capacity for VNS to acutely influence cortical synchrony and excitability and strengthen the hypothesis that acetylcholine and muscarinic receptors are involved in VNS mechanisms of action. These results are discussed with respect to their possible implications for sensory processing, neural plasticity, and epilepsy.

Copyright © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.
PMID:21627982[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/21627982
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« Reply #93 on: August 13, 2013, 07:54:52 AM »

Int Immunopharmacol. 2010 Jan;10(1):9-17. doi: 10.1016/j.intimp.2009.10.003. Epub 2009 Oct 17.
Is neuroimmunomodulation a future therapeutic approach for sepsis?
Kumar V, Sharma A.
Source
Department of Microbiology, Panjab University, Chandigarh, India. vij_tox@yahoo.com

Abstract
Sepsis is considered as a disease of profoundly and uncontrollably activated innate immune response against bacterial infection or their products. Thus, regulation of innate immune response plays a critical role in controlling exaggerated systemic inflammation responsible for sepsis development. However, treatment of patients suffering from sepsis or its more severe form (i.e. severe sepsis or septic shock) with available antibiotics or immunomodulatory agents did not prove effective in controlling multi organ damage and mortality. Therefore it is important to explore cascades of mechanisms associated with pathogenesis of sepsis causing high mortality. The nervous system via peripheral nervous system (PNS) or sympathetic nervous system (SNS) along with hypothalamic pituitary axis (HPA) regulates the innate immune response. Thus the nervous system may play an important role in fine tuning and precise regulation of exaggerated innate immune response via different pathways (i.e. cholinergic pathway activated by vagus nerve stimulation, alpha- or beta-adrenergic receptor activation etc.) in sepsis. Hence neuroimmunomodulation can be a future approach to treat sepsis.

PMID:19840870[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/19840870

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« Reply #94 on: August 13, 2013, 07:56:53 AM »

Biol Psychiatry. 2013 Jun 1;73(11):1071-7. doi: 10.1016/j.biopsych.2012.10.021. Epub 2012 Dec 13.
Rapid remission of conditioned fear expression with extinction training paired with vagus nerve stimulation.
Peña DF, Engineer ND, McIntyre CK.
Source
Cognition and Neuroscience Program, School of Behavioral and Brain Sciences, The University of Texas at Dallas, Dallas, Texas, USA.

Abstract
BACKGROUND: Fearful experiences can produce long-lasting and debilitating memories. Extinction of conditioned fear requires consolidation of new memories that compete with fearful associations. In human subjects, as well as rats, posttraining stimulation of the vagus nerve enhances memory consolidation. Subjects with posttraumatic stress disorder show impaired extinction of conditioned fear. The objective of this study was to determine whether vagus nerve stimulation (VNS) can enhance the consolidation of extinction of conditioned fear.

METHODS: Male Sprague-Dawley rats were trained on an auditory fear conditioning task followed by 1 to 10 days of extinction training. Treatment with vagus nerve or sham stimulation was administered concurrently with exposure to the fear conditioned stimulus. Another group was given VNS and extinction training but the VNS was not paired with exposure to conditioned cues. Retention of fear conditioning was tested 24 hours after each treatment.

RESULTS: Vagus nerve stimulation paired with exposure to conditioned cues enhanced the extinction of conditioned fear. After a single extinction trial, rats given VNS stimulation demonstrated a significantly lower level of freezing, compared with that of sham control rats. When extinction trials were extended to 10 days, paired VNS accelerated extinction of the conditioned response.

CONCLUSIONS: Extinction paired with VNS is more rapid than extinction paired with sham stimulation. As it is currently approved by the Federal Food and Drug Administration for depression and seizure prevention, VNS is a readily available and promising adjunct to exposure therapy for the treatment of severe anxiety disorders.

Published by Elsevier Inc.
Comment in

    Fear and anxiety take a double hit from vagal nerve stimulation. [Biol Psychiatry. 2013]

PMID:23245749[PubMed - in process]
PMCID:PMC3604026[Available on 2014/6/1]

http://www.ncbi.nlm.nih.gov/pubmed/23245749
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« Reply #95 on: October 01, 2013, 11:47:51 PM »

Vagus Nerve Stimulation to Augment Recovery From Minimally Conscious or Persistently Vegetative States After Traumatic Brain Injury

http://clinicaltrialsfeeds.org/clinical-trials/show/NCT01260090
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« Reply #96 on: October 02, 2013, 12:03:23 AM »

Damage to the vagus nerve brings on death via vagal inhibition.


Just like what almost happened to me.

Reader's Digest
http://www.vnsmessageboard.com/index.php/topic,4490.0.html
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« Reply #97 on: October 03, 2013, 10:16:17 AM »

Vagal inhibition
May 31, 2012 | Filed under: Forensic Medicine,General Health | Posted by: admin

Vagal inhibition is condition that causes sudden death to occur within seconds or a minute or two due to minor trauma or relatively simple and harmless peripheral stimulation.

Pressure on the baroreceptors situated in the carotid sinuses, carotid sheaths, and the carotid body (located in the internal carotid artery just above the bifurcation of common carotid artery, and situated about the level of angle of mandible) causes an increase in blood pressure in these sinuses with resultant slowing of the heart rate, dilatation of blood vessels and a fall in blood pressure. The vagal inhibition leaves the person dead instantly.

In normal persons, pressure on the carotid sinus causes minimal effects with a decrease in heart rate of less than six beats per minute, and only a slight reduction (less than 10 mm. Hg) in blood pressure. Some individuals show marked hypersensitivity to stimulation of the carotid sinuses, characterized by bradycardia and cardiac arrhythmia ranging from ventricular arrhythmias to cardiac arrest.
vagal inhibition

vagal inhibition

Stimulation of the corotid sinus baroreceptors causes impulses to pass via Herring nerve to the afferent fibers of the glossopharyngeal nerve (9th cranial nerve) ; these in turn link in the brain stem to the nucleus of the vagus nerve (10th cranial nerve) causing the vagal inhibition.

Parasympathetic efferent impulses then pass to the heart via the cardiac branches of the vagus nerve. Stimulation of these fibers causes a profound bradycardia. This reflex arc is independent of the main motor and sensory nerve pathways. There is wide network of sensory nerves in the skin, pharynx, glottis, pleura, pentoneum covering viscerr or extending into the spermatic cord, cervix, urethra, perineum and coeliac plexus.

Afferent fibers from these tissues pass into the lateral tracts of the spinal cord, effect local reflex connections over several segments and also pass to the brain. The vagal nucleus is controlled by the synaptic connections in the spinal cord, which may be facilitated from both the sensory central cortex and from the thalamic centres. The latter may be responsible for emotional tone noted in the vagal reflex.

Parasympathetic stimulation of the heart can be initiated by high neck compression, pressure on carotid sinus or sometimes by direct pressure over the trunk of the vagus nerve.

Causes of vagal inhibition

(1) The commonest cause of such vagal inhibition is pressure on the neck particularly on the carotid sinuses as in hanging or strangulation.

(2) Unexpected blows to the larynx, chest, abdomen and genital organs.

(3) Extensive injuries to the spine or other parts of the body.

(4) Impaction of food in larynx or unexpected inhalation of fluid into the upper respiratory tract.

(5) Sudden immersion of body in cold water.

(6) The insertion of an instrument into the bronchus, uterus, bladder or rectum.

(7) Puncture of a pleural cavity usually for producing a pneumothorax.

(8 ) Sudden evacuation of pathological fluids, e.g., ascitic or pleural.

(9) Sudden distension of hollow muscular organs, e.g., during attempts at criminal abortion, when instruments are passed through the cervix or fluids are injected into the uterus.

(10) In degenerative diseases of the heart, e.g., sinus bradycardia and partial or complete A-V block; parasympathetic stimulation further depress the heart rate and may induce a Stokes-Adams attack which may be fatal. There is great variation in individual susceptibility.

Death from vagal inhibition is accidental and caused by microtrauma. The stimulus should be sudden and abnormal for the reflex to occur. The reflex is exaggerated by a high state of emotional tension, and also any condition which lowers voluntary cerebral control of reflex responses, such as a mild alcoholic intoxication, a degree of hypoxia or partial narcosis due to incomplete anesthesia.

Autopsy

When death results from vagal inhibition, there are no characteristic postmortem appearances. The cause of death can be inferred only by exclusion of other pathological conditions, and from the accurate observations by reliable witnesses, concerning the circumstance of death.

A soldier was dancing with his girl friend in the presence of many others in a hall. While dancing, he playfully ‘tweaked” (pinched) her neck. She dropped down dead on the spot. There were no injuries or signs of asphyxia. Death was as a result of vagal inhibition.

http://healthdrip.com/vagal-inhibition/
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« Reply #98 on: October 03, 2013, 10:37:04 AM »

Report casts doubt on VNS approval

A Senate committee report showing that a vagus nerve stimulation device was approved for treatment-resistant depression over the objections of "more than 20 [Food and Drug Administration] scientists, medical officers, and management staff" could add to the difficulties patients and psychiatrists have reportedly had in securing insurance coverage for the device.

The report, the culmination of a yearlong investigation by the Senate Finance Committee, said that given the findings, "it is questionable whether or not the VNS Therapy System for TRD met the agency's standard for safety and effectiveness."

The committee said it began investigating the treatment-resistant depression approval after allegations about potential improprieties were brought to its attention. The committee has oversight of the FDA, and also of the Centers for Medicare and Medicaid Services. The Senate panel said in its report that it was seeking to ensure that federal health dollars are being properly spent.

The VNS device was approved in July 2005 for treatment-resistant depression. It has been available for treatment-resistant epilepsy since 1997, and is covered by Medicare and Medicaid for that indication.

Medicare has paid for VNS for treatment-resistant depression in some individual cases but has not yet made a national coverage decision, according to Skip Cummins, chief executive officer of Cyberonics Inc., the company that makes the VNS device.

Mr. Cummins said he thought that the approval was proper and added that a senior FDA official with a lot of device experience had overruled reviewers who had less familiarity with treatment-resistant depression and implantable devices. "The report itself is full of half-truths and distortions, and reflects the perspectives of fewer than eight FDA staffers who disagreed with the ultimate decision," he said in an interview.

The committee investigation found that Dr. Daniel Schultz, director of the FDA's Center for Devices and Radiologic Health, decided to approve the device despite objections from other FDA staffers. The Neurological Devices Panel of the Medical Devices Advisory Committee voted 5-2 in June 2004 to approve VNS for treatment-resistant depression, with the conditions that the company conduct a postmarketing dosing study and compile an outcomes registry.

In August 2004, the FDA issued a nonapprovable letter, going against the panel's recommendation. Cyberonics submitted additional data and responded to a warning letter, citing manufacturing deficiencies. Eventually, with Dr. Schultz's guidance, the company won approval, according to the Senate Committee report, which questioned the propriety of his assistance.

"Instead of relying on the comprehensive scientific evaluation of its scientists and medical officers, it appears that the FDA lowered its threshold for evidence of effectiveness," the report said.

Mr. Cummins disagreed. In two studies, after 2 years of VNS adjunctive therapy, 56% of the patients had a meaningful clinical benefit, more than one-third had at least a 50% improvement in symptoms, and 20% were free from symptoms, he said (J. Clin. Psychiatry 2005;66:1097-104 and Biol. Psychiatry 2005;58:364-73).

Reimbursement for treatment-resistant depression has been spotty. Mr. Cummins said 115 different insurers have approved 1-35 individual implants each. In August 2005, the Blue Cross Blue Shield Association's Technology Evaluation Center said that given the available evidence, it could not make a coverage recommendation. Cyberonics helps patients and physicians get prior authorization. So far, it has received 7,000 such requests, but only 550 patients have been granted approval, Mr. Cummins said.

The company estimates that 15%-20% of the 4 million Americans with depression have a treatment-resistant form of the illness.

BY ALICIA AULT


http://www.thefreelibrary.com/Report+casts+doubt+on+VNS+approval.-a0149222466
« Last Edit: October 03, 2013, 10:40:11 AM by dennis100 » Logged
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« Reply #99 on: October 03, 2013, 10:54:23 AM »

Take another look at the possible off-label usages of the device.

1)Alcohol addiction 2)Alzheimer's Disease 3)Anxiety 4)Arrhythmias 5)Atrial fibrillation 6)Autism 7)Bronchoconstriction 8 )Bulimia Nervosa 9)Burn-induced organ dysfunction 10)Comorbid Personality Disorders 11)Coronary Artery Disease 12)Chronic heart failure 13)Chronic Heart Failure in Rats 14)Cognition 15)Dramatic first words spoken in 2 children after vagus nerve stimulation 16)Dravet syndrome 17)Drop-attacks 18)Eating disorders 19)Fibromyalgia 20)Gut injury and lung permeability in trauma-hemorrhagic shock 21)Heatstroke 22)Heroin-Seeking Behavior in Rats 23)Infarct size 24)Intestinal epithelial barrier breakdown 25)Lennox-Gastaut syndrome 26)Medication-refractory mental illness 27)Memory 28)Migraine and Cluster Headaches 29)Minimally Conscious or Persistently Vegetative States After Traumatic Brain Injury 30)Obesity 31)Mood disorders in elderly population 32)Mood in patients with refractory epilepsy (positive effect) 33)Multiple sclerosis 34)Myocarditis 35)Obsessive Compulsive Disorder 36)Peripheral arterial occlusion disease 37)Persistent hiccups 38)Postoperative cognitive dysfunction in elderly patients 39)Post-traumatic epilepsy 40)Rasmussen's encephalitis 41)Rheumatoid Arthritis 42)Ringing in the ears 43)Sepsis 44)Spinal trigeminal neuronal 45)Status epilepticus 46)SUDEP in children and adolescents 47)Tinnitus 48)Tourette's Syndrome 49)Transient focal cerebral ischemia 50)Trauma-hemorrhagic shock 51)Traumatic brain injury 52)Tuberous Sclerosis 53)Vaginal-Cervical self-stimulation in women with complete spinal cord injury 54)Visceral pain-related affective memory.

Vagal nerve stimulation is also suppose to be good for treatment resistant epilepsy & treatment resistant depression

It makes absolutely no sense folks!

My personal favorite is # 22. Heroin-Seeking Behavior in Rats.

Why the inaction on the part of the FDA?

It's not like the FDA is unaware. I spoke with the #2 man of the FDA's device division a couple of years ago voicing my concerns and was assured he would conduct a full investigation of Cyberonics and their device.

Genocide?

That's what I'm beginning to think!  
« Last Edit: November 18, 2013, 01:54:39 AM by dennis100 » Logged
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« Reply #100 on: October 23, 2013, 07:10:56 PM »

J Psychiatr Res. 2004 May-Jun;38(3):237-40.
Vagus nerve stimulation (VNS) is effective in a rat model of antidepressant action.
Krahl SE, Senanayake SS, Pekary AE, Sattin A.
Source

Neurology Service, VA Greater Los Angeles Healthcare System, Bldg. 114, Suite 217, 11301 Wilshire Blvd., Los Angeles, CA 90073, USA. scott.krahl@med.va.gov
Abstract

Depression is a common but debilitating illness that afflicts a large population and costs the US economy a staggering $40 billion dollars per year.. Clinical studies have demonstrated that vagus nerve stimulation (VNS) is an effective treatment for medication-resistant depression. Understanding VNS's antidepressant mechanisms is key to improving the therapy and selecting the best surgical candidates, and demonstration that VNS is effective in a validated test of antidepressant activity allows us to elucidate these mechanisms in a cost-effective manner. In the present study, Wistar Kyoto rats were implanted with a cuff electrode on the left cervical vagus nerve. The next day, they were placed into a water-filled Plexiglas cylinder for 15 min. After this forced-swim session, one of three treatment conditions were administered over 4 consecutive days: 30 min per day of continuous VNS, 10 mg/kg of desipramine twice per day, or three daily electroconvulsive shocks (ECS). Yoked controls underwent sham procedures, but received no treatment. On the fourth day, the rats were given a 5-min, videotaped swim test. A blinded observer used the videotape to calculate the percentage of time that the rats were immobile (an index of depression) during the swim test. VNS significantly reduced immobility time as compared to unstimulated controls, indicating good antidepressant efficacy. This reduction did not differ statistically from that obtained from rats treated with either desipramine or ECS, two standard antidepressant treatments. These results indicate that VNS is an effective antidepressant in the forced-swim test, allowing us to now investigate possible therapeutic mechanisms.

http://www.ncbi.nlm.nih.gov/pubmed/15003428



OK here is how it works. Depression is a debilitating illness that afflicts a large population and costs the US economy a staggering $40 billion dollars per year. FDA's Dr. Daniel G. Schultz approved the VNS for depression against the unanimous opinion of his scientific staff in February 2006. Why does he do it? He does it to save the economy a staggering $40 billion dollars a year.

It will kill them sooner or later via vagal inhibition and no one would be any the wiser.

Genocide?

That's what I'm really beginning to think! 



Top FDA Official Approves Medical Device Despite Lack of Efficacy
Union of Concerned Scientists

In an extraordinary move, a top Food and Drug Administration (FDA) official approved a medical device against the unanimous opinion of his scientific staff in February 2006. Dr. Daniel G. Schultz, FDA's Director of the Center for Devices and Radiology and Health, approved a surgically implanted vagus nerve stimulator for treatment of cases of severe depression even though, as reported in the New York Times, the device "had not proved effective against depression in its only clinical trial for treatment of that illness."¹

FDA scientists "repeatedly and unanimously" recommended rejecting approval of the device, manufactured by Cyberonics, as a depression treatment, though at one point an advisory panel did provisionally recommend approving the device. An investigation by the Senate Finance Committee found that Dr. Schultz had overruled more than twenty FDA officials who recommended against approval.² According to the New York Times, the decision represented the first time in the agency's history that a director "approved a device in the face of unanimous opposition from staff scientists and administrators beneath him."³

The vagus nerve stimulator is surgically implanted into the base of the neck and sends electrical signals to the heart, brain and other parts of the body.4 The device was approved as a treatment for epilepsy in 1997. The company requested FDA approval for treating cases of severe depression after some device recipients reported improved moods. Anecdotal evidence suggesting that the nerve stimulator could help seriously depressed patients did not hold in clinical research. The one comprehensive study of the device in clinically depressed patients failed to show convincingly that the device had any positive effect on the patients.5 Critics have detailed how, following the initial failed trial, Cyberonics has "relied upon a series of non-randomized, unblinded studies with questionable control groups to make its claim for the effectiveness of the device."6 In short, Cyberonics never proved its device to be safe and effective, as is required by the FDA.

By overruling his scientific advisors, Dr. Schultz set in motion a potential windfall for Cyberonics. Public Citizen reported that the market for patients with epilepsy using the device was approximately 30,000, but the potential market for sufferers of treatment-resistant depression was over 4,000,000. The FDA defended the apparatus' approval as a means for helping those with severe depression who "are otherwise on their way to institutionalization, because of the seriousness of their illness."7

The New York Times, however, reported that FDA reviewers were "bewildered" by the decision. As one agency scientist said, "in my opinion, they do not have adequate data, and I don't understand how this can move forward." Another scientist argued that approval of the device was "akin to approving an experimental product."8

Dr. Peter Lurie, deputy director of Public Citizen's Health Research Group, argues that the FDA needs to relearn a simple principle: "If it doesn't work, it shouldn't be approved."9


1. Gardiner Harris, "Device Won Approval Though FDA Staff Objected," New York Times, 17 February 2006, accessed 22 September 2006.
2. Committee on Finance, United States Senate. Review of the FDA’s approval process for the vagus nerve stimulation therapy system for treatment-resistant depression. February 2006, accessed December 8, 2006.
3. Ibid.
4. Ibid
5. Rush AJ, Marangell LB, Sackeim HA, George MS, Brannan SK, Davis SM et al. Vagus nerve stimulation for treatment-resistant depression: a randomized, controlled acute phase trial. Biological Psychiatry 2005;58:347-354.
6. “Electronic Device Should Not Be Approved for Treatment of Depression, Public Citizen Tells FDA,” Public Citizen, 11 May 2005, accessed 22 September 2006.
7. Harris.
8. Ibid.
9. Public Citizen.

http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&ved=0CGEQFjAA&url=http%3A%2F%2Fwww.ucsusa.org%2Fscientific_integrity%2Fabuses_of_science%2Fnerve-stimulator.html&ei=CCCrT66kAcno2AXBvOzABg&usg=AFQjCNGCok493kDnSuGouYVkH1_Ke3PWFA
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« Reply #101 on: October 23, 2013, 08:10:24 PM »

Vagal inhibition. Yeah, that's the way to do it. Kill them by slowing destroying that vital nerve. Nobody could possibly be smart enough to ever figure that one out.
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« Reply #102 on: October 23, 2013, 09:09:48 PM »

Event Date 05/29/2001
Event Type Injury Patient Outcome Other; Required Intervention
Event Description
An article about the histological appearance of a chronically stimulated vagus nerve in a pediatric reporter indicated vns therapy moderated a patient's atonic episodes, but the patient experienced "occasional hospitalizations for status epilepticus. " the patient passed away due to asphyxiation (reported on medwatch 1644487-2008-02703). The vns therapy system was explanted with "1. 5 cm of unstimulated nerve superiorly and inferiorly. " the electrodes were dissected from the nerve "revealing grossly normal nerve above and below the stimulator. " "abundant inflammatory cells were present around the stimulated nerve section. " "severe myelin loss and occasional myelin digestion chambers were seen in the nerve fibers. With modified trichrome and luxo fast blue stains, this loss was estimated to be nearly 90%. " good faith attempts to obtain additional information have been unsuccessful to date.

http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfMAUDE/Detail.CFM?MDRFOI__ID=1241164
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« Reply #103 on: October 23, 2013, 10:53:50 PM »

The VNS is nothing but a deadly placebo.

That's all it is folks! A deadly placebo!
_________________________________

There is absolutely nothing therapeutic about zapping our most vital nerve 24/7. The FDA knows that. The vagus nerve can handle only so much abuse until it gives out and you die by vagal inhibition.

When death results from vagal inhibition, there are no characteristic postmortem appearances. The cause of death can be inferred only by exclusion of other pathological conditions, and from the accurate observations by reliable witnesses, concerning the circumstance of death.

Vagal inhibition
http://www.vnsmessageboard.com/index.php/topic,4227.0.html 


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« Reply #104 on: December 26, 2013, 08:55:34 AM »

Dennis, please don't ignore the few that really have had help.  Although not one person I know personally has kept their vns active or in their body.  Once the vagus nerve has been fried, or scar tissue built up so removal of the electrodes is impossible, and the vns has become useless, THEN those who it might have helped at one point, begin to complain about the permanent damage it has done.  Hmmm.....vn$
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"If you are going through hell, keep going." (Sir Winston Churchill, 1874-1965)
VNS implanted Sept 02, turned off Dec 04, Generator ex-planted Nov 07
Electrodes are in me for LIFE!
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« Reply #105 on: December 31, 2013, 09:04:52 AM »

Dennis, please don't ignore the few that really have had help. 

Yeah, I know what you are getting at BB. Placebos can be a useful tool in medicine.
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« Reply #106 on: January 02, 2014, 09:18:22 AM »

Yesterday, I read an article on how a young man's life was totally changed when he had a DBS implanted to treat his Tourette Syndrome. His situation was so bad he had no quality of life.  It was so bad they had to put him to sleep for the surgery, which makes me wonder how they managed to map his brain in the first place, something the article failed to mention.

Irreversible damage is done to the body with every surgery, no matter the benefits.  The trade is for the quality of life.

There will always be a better mouse trap, humane or not, it's still a trap.  Pharmaceuticals, or medical devices are NOT a cure, they only make the symptoms more manageable. Eventually, they all will fail to work at some point in time.

We don't need more drugs or devices, we need CURES!
« Last Edit: January 02, 2014, 09:20:02 AM by Birdbomb » Logged

"If you are going through hell, keep going." (Sir Winston Churchill, 1874-1965)
VNS implanted Sept 02, turned off Dec 04, Generator ex-planted Nov 07
Electrodes are in me for LIFE!
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« Reply #107 on: June 02, 2014, 05:43:24 AM »

Let's just look at the facts. About the only thing the VNS has been proven to do is stop someone's heart from beating. In theory it is suppose to help in epilepsy and depression (treatment resistant kinds). Who's theory? The FDA? Now take a look at the possible future indications for the device and think about it for awhile.

Alcohol addiction /Alzheimer's Disease /Anxiety /Arrhythmias /Atrial fibrillation /Autism /Bronchoconstriction /Bulimia Nervosa /Burn-induced organ dysfunction /Comorbid Personality Disorders /Coronary Artery Disease /Chronic heart failure /Chronic Heart Failure in Rats /Cognition /Dramatic first words spoken in 2 children after vagus nerve stimulation /Dravet syndrome /Drop-attacks /Eating disorders /Fibromyalgia /Gut injury and lung permeability in trauma-hemorrhagic shock /Heatstroke /Inhibits heroin-Seeking Behavior in Rats /Infarct size /Intestinal epithelial barrier breakdown /Lennox-Gastaut syndrome /Medication-refractory mental illness /Memory /Migraine and Cluster Headaches /Obesity /Mood disorders in elderly population /Mood in patients with refractory epilepsy (positive effect) /Multiple sclerosis /Myocarditis /Obsessive Compulsive Disorder /Peripheral arterial occlusion disease /Persistent hiccups /Postoperative cognitive dysfunction in elderly patients /Post-traumatic epilepsy /Rasmussen's encephalitis /Rheumatoid Arthritis /Ringing in the ears /Sepsis /Spinal trigeminal neuronal /Status epilepticus /SUDEP in children and adolescents /Tinnitus /Tourette's Syndrome /Transient focal cerebral ischemia /Trauma-hemorrhagic shock /Traumatic brain injury /Treatment resistant depression /Treatment resistant epilepsy /Tuberous Sclerosis /Vaginal-Cervical self-stimulation in women with complete spinal cord injury /Visceral pain-related affective memory.


VNS in Reader's Digest
http://www.newamerica.net/node/35911

« Last Edit: June 02, 2014, 08:48:35 AM by dennis100 » Logged
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« Reply #108 on: June 02, 2014, 11:46:15 AM »

In theory it is suppose to help in epilepsy and depression (treatment resistant kinds).
Why treatment resistant? Could it be we are nuisance medical cases so they use a VNS to get rid of us?


While the VNS stimulates, slowly but surely the vagus nerve is being destroyed. You die via vagal inhibition. The VNS was designed to ruin the nerve. The placebo effects are the selling point. Doctors are aware of that fact. They know what's going on. The VNS is a placebo, a very deadly one. That's all it is folks.


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