Pages: 1 2 3 [4]  All   Go Down
Print
Author Topic: VNS a cure-all ???  (Read 92382 times)
0 Members and 2 Guests are viewing this topic.
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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
Logged
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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


Logged
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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
Logged
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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

Logged
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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
Logged
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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
Logged
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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
« Last Edit: January 04, 2015, 02:20:55 PM by dennis100 » Logged
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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/
« Last Edit: November 25, 2013, 08:04:23 AM by dennis100 » Logged
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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
« Last Edit: October 23, 2013, 07:16:09 PM by dennis100 » Logged
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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.
Logged
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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
Logged
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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 


« Last Edit: May 20, 2014, 05:10:00 AM by dennis100 » Logged
Birdbomb
Head Cheese
Administrator
Hero Member
*****

Karma: +9/-1
Offline Offline

Posts: 7791


Head Cheese


WWW
« 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$
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!
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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.
Logged
Birdbomb
Head Cheese
Administrator
Hero Member
*****

Karma: +9/-1
Offline Offline

Posts: 7791


Head Cheese


WWW
« 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!
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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
dennis100
Moderators
Hero Member
*****

Karma: +24/-0
Offline Offline

Posts: 62863


« 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.


« Last Edit: June 06, 2014, 06:00:34 AM by dennis100 » Logged
Pages: 1 2 3 [4]  All   Go Up
Print
Jump to: