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Posted
OK just a medic student here but if it is a "Vagus nerve stimulator" It leads me to think that it is more of a pharm issue for the simple fact of when you stimulate the vagus nerve it should drop your pulse and BP. She was at 140/80 and 112. Now I have no experience with the device but when you perform a vagal manuver isn't that the same as stimulating the vagus nerve?

The VNS is implanted on the left side and connected to the left vagus nerve with the idea that the left vagus does not exert as much control over cardiac function, perhaps someone can elaborate more here. However, there is research on R VNS therapy as well, so right sided-implantation is not contraindicated. I do think though that the way the device is programmed has a lot to do with how much potential there is for side effects, if the pulse is intermittent and at a low voltage setting, it is less likely to exert negative cardiac side effects.

Research that I have seen with R-sided Vagal stim appears to have more cardiac effect, though the evidence base has some that also says no difference.

http://www.blackwell-synergy.com/doi/abs/10.1113/eph8602146

www.blackwell-synergy.com/doi/pdf/10.1111/j.0013-9580.2005.16404.x

Posted

The device was implanted on the left side. Im sure it isnt a simple "hook up electrode here" though i havent read the articles posted about the device yet. The Vagus nerve carries many afferent and efferent signals (the two most noticable are those that innervate cardiac tissue via ACh-R and those that transmit baro/chemo receptor signals from the aortic sinus/bodies to control ventilation). If the device were simply set to depolarize all nerve fibers in the nerve itself, multiple systems would go haywire.

However, in terms of THIS patient, the device WAS NOT ACTIVATED YET. The fact that she needed the device leads me to believe that she had a neurotransmitter deficiency. Extrapyramidal reactions occur most frequently with dopamine antagonists. If she is on schizophrenic meds (probably dopamine antagonist) and has some problems with depression (naturally low levels of dopamine or seratonin) that need to be treated surgically (really low levels of NT) then that might cause the Extrapyramidal reactions.

Posted
The Vagus nerve carries many afferent and efferent signals (the two most noticable are those that innervate cardiac tissue via ACh-R and those that transmit baro/chemo receptor signals from the aortic sinus/bodies to control ventilation). If the device were simply set to depolarize all nerve fibers in the nerve itself, multiple systems would go haywire.

The first company I know of doing VNS was Cyberonics. There is also more recently a company developing a similar neurostimulatioin devie.

Here's some info on VNS:

http://www.vnstherapy.com/depression/hcp/

As for the mechanism of action of vagal stimulation, it's not quite clear how it works, but it is known to alter NT release (nor-epi and dopamine primarily I think). As for selective stimulation of one section of the nerve versus another, I'm not familiar with minute vagus nerve anatomy to say for sure how the electrode is implanted. It is a wrap-around type electrode.

Now, purely from a thinking point of view, I'm not sure it is anatomically possible to have selective depolarization of one region of the nerve and not another. I know in some neural systems the strength of the response is coded by both firing of different types of neurons and intensity of the response is dictated by the number of neurons firing. If you think of a pacemaker analogy, the leads are implanted in different regions depending on the need, so for example a dual chamber device with an A lead and a V lead. Though the leads stimulate that one area that they are implanted, for eg, the V lead in the right ventricular apex gives electrical stim right in that one area, BUT, it spreads right? The electrical impulses generated by a pacemaker do not just selectively affect that one spot, they act to propagate electrical impulses through the conduction system.

So, while I think perhaps there is a particular specific area on the left vagus nerve that the electrode is wrapped, I'm not sure such selective stimulation is possible. I think it has to do more with settings as I mentioned. The pule width, duration of intervention, and voltage setting of the VNS can be altered, and I'm not sure of the physical values, but perhaps they have limited effect on the cardiac system, and they are still able to exert an effect on a neural level in the case of treating refractory depression and refractory epilepsy. If this were a major problem, the device would not have made it through the FDA approval.

Interesting discussion.

Posted

The movement disorder that you are describing sounds more like akisthesia, which is the restless feeling that a patient gets when they feel like they "need to move". It's like restless leg syndrome, but all over the body. This is a common side effect of many antipsychotics, and can happen with one dose or after many. It is temporary and often reversible with benadryl or cogentin (benztropine: think "benadryl" and "atropine". This is essentially it's action).

I agree with ERDoc that with the tachycardia and flushing, this is concerning for serotonin syndrome.

Tardive dyskinesia is a movement disorder characterized by rigidity, difficulty initiating movement, and shuffling gait. It bears some similarity to some aspects of parkinsonism. It is a late effect (the "tardive" part) after years of using the typical antipsychotic drugs. It is permanent and irreversible.

'zilla

Posted

Was she taking any medications like Effexor, Lexapro Paxil, Prozac or Wellbutrin by any chance?

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