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Author Topic: VNS a cure-all ???  (Read 92381 times)
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dennis100
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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


« Last Edit: October 23, 2012, 02:16:37 AM by dennis100 » Logged
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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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