This is an important post for anyone hunting for a test for PSSD. If the CT fibres mentioned here are not fibres that show up distinctly on either skin biopsy or CCM, then these tests may not pick up a very real problem. We need some research on whether CT fibres show around the ankle or in the cornea. The slide above is from a fascinating lecture on Affective Touch by Francis McGlone. Might be worth contacting him to see if he knows.
This post by a regular contributor mentions Dopamine but there are also transmitters like Prokineticin that may be playing a part – see Prokineticin.
One of the most frustrating aspects of post-SSRI sexual dysfunction (PSSD) has been seeing doctors who think that it is indistinguishable from other forms of sexual dysfunction. They ignore that PSSD, along with other post-medication sexual dysfunctions, causes reduced genital sensation- a very unusual symptom. I believe that understanding the cause of this symptom will reveal the etiology of these conditions.
Before I’d heard of PSSD, a psychiatrist diagnosed me with hypoactive sexual desire disorder (HSDD). I was skeptical as in the past I’d had bouts of low libido yet, if I could be bothered to have sex during these periods, my sexual sensation and enjoyment were normal. Now my ‘low libido’ feels different. Sex, even orgasm, isn’t pleasurable at all. Why do these two instances of low libido feel so different?
Given the lack of diagnostic tests, it’s not surprising that clinicians suspect that PSSD is a brain issue. I saw a psychologist who believed that as the same stimulus can feel pleasant or aversive depending on the cause e.g. being stroked by a sexual partner will feel very different from being stroked by a stranger. ‘Erotic touch’ happens in the brain.
Also, women with HSDD have different activity in various areas of the brain compared to normal controls, again affirming her idea that sexual function largely occurs in the brain.
I take issue with this reasoning. Firstly, altered brain activity in an fMRI study does not necessarily mean a problem resides in the brain. (Crudely put, blind people will have altered brain activity compared to sighted people, but nobody thinks that blindness has nothing to do with the eyes.)
Secondly, all sensation occurs in the brain and can be modified according to things like context, mood or experience.
For me, the most telling symptom is that I have altered genital sensation all the time. If this only occurred during sexual activity, one could speculate that I have an arousal disorder. The ongoing nature of this symptom suggests something else. I have long pondered whether PSSD is a sensory issue.
For many years, the physiology of sexual desire and arousal has focused mainly on olfactory and visual stimuli, with very little research on tactile stimulation. In recent years, more research has been conducted on C-tactile afferents (CT afferents). It has been shown that these fibres are responsible for ‘interpersonal’ touch, be it erotic or social.
CT fibres, when stimulated by optimal stroking frequencies, ultimately cause activity in the parts of the brain concerned with social activity and affect. (Discriminative touch is dealt with by completely different areas of the brain and is the remit of Aβ fibres.)
The role of CT afferents in sex is controversial; such fibres are only found in hairy skin and are not found in the clitoris or glans.
It is very difficult to study these fibres in humans as touching the skin will stimulate both CT afferents and Aß fibres. However, their role has been explored in people who have lost their Aß fibres only. Stimulating their CT afferents by stroking their skin evokes faintly perceptible, vaguely pleasurable sensation that is poorly localised.
Studies also show people report pleasant sensations when their skin is stroked at speeds known to cause optimal activity in these CT afferents. Women reporting no preference for the speed at which their skin is stroked also tend to report low sexual desire. However, none of this tells us whether people with various sexual dysfunctions have a problem with their peripheral neurons or whether their brain is not processing the incoming signals properly.
Studying these fibres may now be easier, after a fascinating paper by Elias et al. Here they study a set of sensory neurons which express a G-protein coupled receptor, Mrgprb4. Such neurons have already been shown to respond to gentle stroking- these neurons appear to be analogous to CT afferents in humans.
In this paper, they show that these neurons are important in the sexual receptivity of female mice. Socially isolated female mice adopt sexual postures when these neurons are stimulated, but an absence of these neurons caused female mice to reject males trying to mount them: ‘sexual receptivity is supplanted by aggression’.
This paper should be viewed positively by those suffering from PSSD and related conditions. For the first time we have direct evidence that there are chemically-distinct peripheral neurons that, when stimulated, lead to dopamine release in the brain: a direct skin-to-brain pathway. The stimulation of these neurons is inherently rewarding.
We cannot ignore the possibility of PSSD being a problem of the peripheral neurons. Dysfunction of these specific neurons could explain the sexual anhedonia; the sparing of other neurons could explain why we are diagnostically ‘normal’.
As these neurons are chemically distinct, they could be uniquely sensitive to medications known to cause enduring sexual dysfunction. These markers could cause the neurons to be destroyed by autoimmunity but could also provide tests that could confirm their presence. Understanding the biology of these neurons could lead to the discovery of pathways that could be manipulated by medication.
Research into PSSD is hampered by a lack of awareness and funding; I would be surprised if funding is made available for fMRI studies on PSSD patients any time soon. As nice as it would be to do these expensive studies, they would do nothing to elucidation the biochemical mechanisms of the condition nor point towards treatment.
The paper by Elias et al. shows there is still much to learn about peripheral neurons. It seems far more realistic to me to make sure that these neurons are working properly before we start looking at the brain.
In an era of highly sophisticated brain imaging techniques, it is tempting to assume that brain scans will reveal the workings of the PSSD brain.Yet the brain does not work in isolation and must be viewed as just one part of a very complex system. We ignore the workings of the rest of the nervous system at our peril.
For some of the very latest on CT Fibres – See Larsson and Nagi. The paper seems to open the door to a way in which SSRI withdrawal could both cause PSSD and PGAD.
The material under this heading about ISSM, Dr Clayton and Vortioxetine has been moved to its own post International Society for Sexual Medicine.
Comments about those matters should be directed to the new post and comments on Affective Touch should remain with this post.
Comments on the Anita Clayton Vortioxetine issues have been moved to a new post next door called International Society for Sexual Medicine