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Swedish study finds ~30% reduction in overall ME symptom scores from intranasal mechanical stimulation of the vagus nerve

Hipsman

Senior Member
Messages
542
Location
Ukraine
Where did u buy the device please?
I bought everything from www.tenspros.com
Specifically these Items:
1583606059187.png
Most importantly you need ear clips for this, 9V batter charger is nice too.
1-2 pairs of ear clips should be enough, I just bough more b/c of expensive international shipping, so I don't have to buy more in future.
 

junkcrap50

Senior Member
Messages
1,330
Not new info. Just some additional information regarding Intranasal Kinetic Oscillation Stimulation. fMRI confirmed that it works to normalize the autonomic nervous system by normalizing aberrant intrinsic functional activity in the limbic and primary sensory systems. 1 treatment cured migraine patients for 3-6 months.

https://pubmed.ncbi.nlm.nih.gov/27622142/
Resting-state fMRI study of acute migraine treatment with kinetic oscillation stimulation in nasal cavity
Abstract
Kinetic oscillatory stimulation (KOS) in the nasal cavity is a non-invasive cranial nerve stimulation method with promising efficacy for acute migraine and other inflammatory disorders. For a better understanding of the underlying neurophysiological mechanisms of KOS treatment, we conducted a resting-state functional magnetic resonance imaging (fMRI) study of 10 acute migraine patients and 10 normal control subjects during KOS treatment in a 3 T clinical MRI scanner. The fMRI data were first processed using a group independent component analysis (ICA) method and then further analyzed with a voxel-wise 3-way ANOVA modeling and region of interest (ROI) of functional connectivity metrics. All migraine participants were relieved from their acute migraine symptoms after 10-20 min KOS treatment and remained migraine free for 3-6 months. The resting-state fMRI result indicates that migraine patients have altered intrinsic functional activity in the anterior cingulate, inferior frontal gyrus and middle/superior temporal gyrus. KOS treatment gave rise to up-regulated intrinsic functional activity for migraine patients in a number of brain regions involving the limbic and primary sensory systems, while down regulating temporally the activity for normal controls in a few brain areas, such as the right dorsal posterior insula and inferior frontal gyrus. The result of this study confirms the efficacy of KOS treatment for relieving acute migraine symptoms and reducing attack frequency. Resting-state fMRI measurements demonstrate that migraine is associated with aberrant intrinsic functional activity in the limbic and primary sensory systems. KOS in the nasal cavity gives rise to the adjustment of the intrinsic functional activity in the limbic and primary sensory networks and restores the physiological homeostasis in the autonomic nervous system.

They seem to have confirmed it with a more powerful MRI, judging by these conference presentations:
https://www.ismrm.org/18/program_files/EP16.htm
1609275146930.png


http://archive.ismrm.org/2018/4537.html
1609275124085.png
 

Tella

Senior Member
Messages
397
I'm looking at possible building a small nasal vibrator for a friend who has chronic non-allergic rhinitis. The nasal stimulation is being researched help that too. Will post details if I end up building it.
Are u an engineer? Why not buy the correctly made stuff?
if people wanna try stuff they should buy safe stuff and not put earbuds up their nose.....
 

junkcrap50

Senior Member
Messages
1,330
Are u an engineer? Why not buy the correctly made stuff?
if people wanna try stuff they should buy safe stuff and not put earbuds up their nose.....
No. Not an engineer. But it's simple electronics and wiring. It'd be a fun little project for me. You can't buy this. And even if you could it'd be office medical equipment for 1,000s of dollars. My device would be easy and simple: encapsulated 7mmx20mm vibration motor, PWM speed controller, mini lcd voltage display, and battery. Seal all connections. Dial it in to get the frequency as mentioned in the papers.
 
Messages
600
From the Discussion section of the paper:

Our findings paint a picture of ME as a truly multifaceted disorder involving inflammation with a possible origin at the immune-microbe interface in the gut. Chronic immune stimulation is likely given the symptomatology, but also elevated cytokine levels are found that correlate with symptom severity (5) and immune cell deficiencies (6). The deficiencies in cellular metabolism are not typically seen in other inflammatory diseases, although transient metabolic adaptations are common during immune responses (44).

It is important to note that ME is a heterogeneous disease and the likelihood of finding one pathogenic mechanism shared by all patients is low. We believe that one unifying concept could be the failure in upregulating disease tolerance mechanisms in the event of an infection or virus reactivation and this is what we propose herein. Such disease tolerance mechanisms are important in limiting the reduction in host fitness as a consequence of the infection directly or as a consequence of the elicited immune defenses (41). Our data of upregulated disease tolerance pathways upon INMEST treatment support the hypothesis that ME is a result of a failure to upregulate disease tolerance mechanism when faced with infection and thereby leading to a deterioration of physiological functions (Fig. 6D), although the precise mechanisms of this remains to be unraveled. The reasons why ME patients differ so much in their symptomatology could be explained by differences in the underlying infectious disease or immune activation, and the relevant disease tolerance pathway failing to be induced. The reasons for why ME patients would fail to upregulate disease tolerance pathways remains to be determined, although one interesting lead comes from an observation made of mutations in the enzyme IDO2 seen in 20/20 patients with severe ME (https://www.omf.ngo/2018/10/19/heal...on-the-molecular-basis-of-me-cfs-at-stanford/) and has led to the formulation of the metabolic trap hypothesis of ME (45). However, the IDO-enzymes are also involved in disease tolerance, specifically upon exposure to Endotoxin, a component of Gram-negative bacteria in the gut (46, 47).
[...]

So after having endured endotoxin exposure due to gut leakage the body fails to upregulate disease tolerance because of a dysfunctional enzyme. I would say this can make alot of sense, ties a few things together...
 

Rufous McKinney

Senior Member
Messages
13,249
Just thinking about how my first negative reaction was the food allergies at one year of age. Which seemed to manifest as rashes if I recall my childhood correctly.

so the food enters the mouth goes down the throat reaches teh stomach and arrives at the gut. The gut microglial get triggered first.

Off we go?
 
Messages
600
Just thinking about how my first negative reaction was the food allergies at one year of age. Which seemed to manifest as rashes if I recall my childhood correctly.

so the food enters the mouth goes down the throat reaches teh stomach and arrives at the gut. The gut microglial get triggered first.

Off we go?
Hmm correct me if im wrong but i dont think there is microglia in the gut, only the brain. But if the food triggered some immune reaction in the gut then it might cause inflammation in the brain via something called afferent neuroimmune signalling.

So what do you think about the disease tolerance upregulation failure theory?

Also did anyone try the intranasal vagus nerve stimulation?
 

Husband of

Senior Member
Messages
313
I recall some researcher speculating that the reason why women get cfs more than men is that women’s immune systems need to be able to adjust to some parasites (babies) and therefore are more likely to get confused. In other words they have to tolerate some pathogens rather than resist. So the process of balancing tolerance with resistance is more likely to get out of whack.