This article takes an in depth look at the theoretical reasons to use tVNS for autism disorders.
The recommended frequencies are here
“A recent tVNS study in migraine patients showed that although both 1 and 25 Hz tVNS can improve clinical outcome in patients with chronic migraine, 1 Hz tVNS can produce greater improvement than 25 Hz tVNS (Straube et al., 2015). Studies have suggested that a frequency between 1 and 30 Hz, pulse width of 130–1000 μs and intensity of 4–6 mA is sufficient to elicit a therapeutic effect (Fang et al., 2016; Rong et al., 2016). Therefore, the suggested parameters for tVNS treatment of ASD may set a frequency between 1 and 30 Hz, or altered frequency between 1 and 30 Hz.”
They also discuss the exact area of the ear to stimulate. “In a recent study, investigators compared fMRI signal changes evoked by tVNS at the anterior and posterior sides of the left outer auditory canal. The results showed that fMRI signal changes were in the opposite direction (activation vs. deactivation) in many brain regions with the exception of the insular cortex (positive blood oxygenation level dependent changes in both conditions) (Kraus et al., 2013). Prominent decreases of the blood oxygenation level dependent signals were detected in the parahippocampal gyrus, posterior cingulate cortex and right thalamus (pulvinar) following anterior auditory canal wall stimulation (Kraus et al., 2013). These results suggest that tVNS at different locations of the ear may modulate different brain pathways, more studies are needed to identify the optimal tVNS location for ASD.”
(As an aside, I will only use tVNS in migraine patients if they show a positive HRV profile with its use. Since most migraineurs are quite sensory sensitive, I’m wary in this patient population.)
The effect of tVNS on immune function: “Both VNS and tVNS can modulate immune function by a defense response and the top-down modulation mechanism (Zhao et al., 2011; Bonaz et al., 2013). An animal study showed that electrical stimulation of the efferent vagus nerve inhibits the systemic inflammatory response to endotoxin (lipopolysaccharide) administration through the release of the vagal neurotransmitter acetylcholine (Borovikova et al., 2000). Lerman et al. found that VNS might downregulates inflammatory cytokine release, providing evidence for its anti-inflammatory effect (Lerman et al., 2016). Thus, tVNS might modulate not only the immune function of ASD, but also the interaction between neural plasticity and the immune system (Garay and McAllister, 2010).