RxISK

Making Medicines Safer for All of Us

Visual, Balance and Erotic Sensory Shocks

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This video reflects a view many doctors have about Visual Snow and in particular a possible link to treatment.

Last week’s Can Antidepressants Cause Visual Snow Syndrome post hinted at what lies beneath the medical surface. The video came our way when Hannaa, one of the papers authors, mentioned VSS to one of her colleagues and was sent the video as his response to patients or anyone who raises VSS and possible links to treatment.

Jonathan Lochhead, another of the authors on the RxISK paper has also mentioned getting a similar response from the editor of a ophthalmology journal and has made it clear that he has found out the hard way how few journals seem to want to publish on the link between medicines and VSS or perhaps any hazard of treatment..

Many people who’ve developed VSS and got in touch with RxISK tell a similar story.  They have often begun to doubt their sanity and doubt it still more when told there is nothing wrong with their eyes and the problem must be ‘mental’.

Neurobabble like thalamo-cortical dysrhythmia may be mentioned but more often they are told they have a Functional Nervous Disorder (FND). This is a real disorder, they are told, by which is meant it’s real for you but in our mind it’s in your mind. If it was still acceptable to use the word hysteria that’s what you’d hear us tell you.

This slide shows you what you might end up facing if you report your visual snow or any SSRI linked visual problems to eye services.

Dismissing people like this may all be facilitated in the case of anyone who is on or has been on an SSRI – it brands them as having ‘functional issues’. Those who develop VSS are often bewildered and, even without this get-out-of-my-office help from their health services, figure they are going mad. While waiting on a psychotherapy referral and assessment for unresolved childhood trauma to materialise, an SSRI will be offered.

VSS, PSSD, PPPD and Akathisia

It must be clear from this that there is a clear overlap between VSS and Post SSRI Sexual Dysfunction (PSSD).

VSS interfaces with PSSD in many ways.

  • Both may start on treatment
  • Both may first appear on stopping treatment
  • Both can appear on treatment and continue on stopping.
  • Both can endure for months or years after stopping.
  • Many folk with PSSD also have VSS
  • Both conditions appear to happen in every country on earth, in both sexes, all ages and in all ethnic groups.
  • Those with either of these conditions risk dismissal by medical services, even though a late onset syndrome continuing after treatment stops – tardive dyskinesia – was first described in 1959. (Tardive refers to the slow or late onset of the problem).

VSS and PSSD likely also interface with Balance problems PPPD – Persisting Perceptual Postural Dizziness – See Balancing our Bodies and Our Selves and Juggling Our Bodies and Our Selves, which can:

  • Start on an SSRI
  • Start on stopping an SSRI
  • Start on treatment and continue on stopping
  • Endure for months or years after treatment stops
  • Many folk with VSS also have PPPD (dizziness).
  • Both conditions appear to happen in every country on earth, in both sexes and in all ages and all ethnic groups.
  • People with PPPD get told an SSRI will help, that they have FND and they are also referred to psychotherapy.

The tightrope walker here is an image from Paul Klee, who as Klee saw it:

‘the tightrope walker is emphatically concerned with his balance‘.

This is not just a matter of physical balance – it affects the balancing of ourselves. Disturbances to any of our senses – vision, hearing, touch, erotic touch and balance – strike at the heart of our selves, as these quotes from Bryn and Roy in a podcast about PSSD bring home.

Bryn:  Getting PSSD undermines your faith in the medical establishment and the whole system of science as we have it – the fact that none of these professionals understand this condition or know anything about it when we know we have it – its not some vague feeling.  Losing you libido is equivalent to going blind or deaf, its that level of sensory impairment

Roy:  The same can be said for losing your emotions – I felt I lost two senses – my sexuality and my emotions

Depending on the situation we’re in when hit by problems linked to our balance, vision or erotic senses, it can be expected that any normal person might start to have panic attacks. Panic attacks are very different to a generalized anxiety state, which is a state of constant but comparatively low grade anxiety. In contrast, it can be difficult to distinguish panic attacks from akathisia.

PPPD offers an interface with akathisia that VSS and PSSD don’t. While there can be brief spells of VSS and PSSD where the problem seems less bad and for some it can clear, for the most part VSS and PSSD are chronic conditions.

PPPD, however, can be episodic and both panic attacks and akathisia are notably episodic. In the case of akathisia while it can continue for weeks or months and perhaps only comes on after treatment stops – tardive akathisia – and lasts for years, it is not there the whole time. There are episodes that may happen 2 or 3 times per day, lasting 30 to 60 minutes, after which the person may end up seeming back to normal.

Treatment

In the case of PPPD, Vestibular Rehabilitation Therapy can help. VRT embodies some of the principles of Interoceptive Exposure Therapy which may be why it helps – see Interoception or Neuroplasticity.

There do not seem to be openings to develop similar approaches for VSS or PSSD.

A 2004 Paper from ‘Eye’ by Clare Fraser from Sydney covers some of the theories behind VSS and the treatment options.

The common factor covering PPPD, VSS, PSSD and Akathisia is that they are bodily not mental states. These problems are linked to our sensory nervous systems, which is where SSRI drugs act. They are not brain based problems – despite the Brain Fog experiences people have in all these states.

These issues will be picked up in DH and RxISK posts over the next two weeks – The Science of Interoception and In Praise of SSRIs.

Research

In the meantime, the VSS paper has been downloaded several hundred times, and is ranking very highly on Google search.

At the heart of PSSD is a very obvious genital numbness that comes on within minutes of a first pill – but it also wears off and disappears completely for over 50% of people when treatment stops.  It happens in maybe 95% of folk, about the same number whose hearts slow in beta-blockers.  But just as the heart rates of some of us speed up on a beta-blocker, so also some folk do not get genitally numb on an SSRI.

If you are one of these folk, can you check if lidocaine/lignocaine ointment makes you genitally numb. Lidocaine numbs about 95% of us, but dentists know roughly 5% don’t get numb gums from it – they have a gene that codes for a variation in sodium channels that means it doesn’t numb.  does this also apply to genitals – we don’t know.

Can people who do not become genitally numb on an SSRI get PSSD? If they can what does their PSSD look like? Most people get chest tuberculosis but some get gut tuberculosis. They are both TB but look very different.

Is there a VSS, PSSD and PPPD equivalent to the tuberculosis gene?

One candidate has to PIEZO2 or PIEZO1 proteins. These proteins are stretch sensors.

People with a PIEZO2 gene variation present with a PSSD-like  Erotic-Sexual profile along with Balance and Vision problems.  See Lam et al.

Here are some names and emails for folk researching PIEZO proteins. Great if some of you could contact them – in any email you can draw their attention to the RxISK Prize.

They don’t have to cure VSS, PSSD or PPPD to get the Prize – a substantial contribution like a genetic test to identify those at risk or to confirm PIEZOs are involved in these conditions so those of us affected can show our doctors and ask innocently whether FND has a gene test like this would be a candidate to win the Prize.

Of course the real incentive should and may well be the Nobel Prize that someone will get for solving these issues.

Reader Interactions

Comments

  1. Interesting blog!
    As you know I have been banging on about FND for some years.
    I think this statement in your blog is maybe misleading.? “they are bodily not mental states. These problems are linked to our sensory nervous systems, which is where SSRI drugs act. They are not brain based problems”
    I would say that they most certainly are brainstem-related problems. Where the brainstem regulates all bodily functions and the autonomic nervous system (and the fight/flight/freeze response) – and of course the brainstem commicates implicitly with the other areas of the brain.
    The work of Mark Solms is interesting – his book “the Hidden Spring”…

    Reply

    • Marion

      We’ll have to agree to disagree. The vigilance system is at the upper end of the spinal cord – the bird brain bit – not anything linked to higher cognitive function or even cognitive processing. It doesn’t contain a mood or anxiety or psychosis centre. I think people get badly misled by figuring this is part of their brain

      David

      Reply

    • Marion

      Let me ask the question i a different way. If the problem is in the eye is that also in the brainstem? Would it also be an FND in your use of that term? Do you view PSSD and PPPD as FNDs? Akathisia?

      Re brainstems, there is a tiny bit of serotonin anywhere near our brains – all in the brainstem where its action essentially is to turn things off.

      D

      D

      Reply

      • Well, I am completely out of my basic common sense depth here!
        But I have come upon this:

        https://www.sciencedirect.com/science/article/pii/S0896627323000806

        In my opinion FND describes a state where the human brain/body system is malfunctioning. The cause of the malfunction(s) may in many cases be due to damage to the functioning of the CNS resulting from eg neurotoxins (which can include psychiatric drugs) &/or other brain damaging injuries – but neurologists prefer to say very firmly that FND is of ‘unknown aetiology’. 🤔

        Reply

        • Marion

          Thanks for this article. On first glance, I think it supports the points I’m making. Gate in this case means closes down input to the brain. If however the input from the eye, from serotonin input to bipolar cells in the retina is reduced or not happening to begin with (which appears to be the case with SSRIs), brain stem gating will also look like it’s affected but the answer is not open the brain stem gate – its fix whatever is happening in retinal bipolar cells (which are not part of the brain).

          We have a serious bias in terms of seeing everything in terms of our brains rather than our bodies. I hope to tackle this in some talks in 10 days time – which will have linked posts.

          Please keep challenging what gets said but also try to keep an eye on the bigger picture which is the way we have been viewing things is killing people and has been a disaster both therapeutically and scientifically.

          David

          Reply

  2. You hold the system to account on so many fronts. But I was just thinking, if you were a brand, which I guess you are – and I was your comms agency which I’m not but could have been– I’d say this revelation (old hat to you) is now probably the most powerful, market disrupting truth:

    ‘The common factor covering PPPD, VSS, PSSD and Akathisia is that they are bodily not mental states. These problems are linked to our sensory nervous systems, which is where SSRI drugs act. They are not brain-based problems – despite the Brain Fog experiences people have in all these states.’

    Why?

    It puts yet another stake through the heart of the wretched serotonin deficit nonsense. I remember you describing it years ago as ‘the paradigm that refuses to shift’. As Jeff Lacasse’s recent research showed, plus ça change for consumer – patients. And even some superannuated biopsychiatrists are reluctant to lose it completely – embroidering the myth with added complexity, other neurotransmitters, a spot of neurogenesis etc.

    The commercially driven brain/mood positioning, the MENTAL health and PSYCHIATRIC drug categorisation plonks SSRIs firmly in the brain department – and even academics who one might hope would know better are still banging on about brains and receptor occupancy as if that were the whole story.?

    What this truth fundamentally disrupts and exposes is the ‘mystery’ of SSRI antidepressants. They are not some intangible medical voodoo – but, as you explain it, chemicals that mute our sensory reactivity – taking the edge off comfortably for some, unbearably for others – and potentially forever for those unfortunate enough to develop tardive syndromes like PSSD , VSS etc.

    This kind of grounded understanding of what they’re actually doing could put consumer- patients far more in control. How much is the sensory muting a trade-off worth making? Is early dizziness, vision abnormalities, sensual numbing, agitated bones tolerable or worth it? It might actually make sense of the PILs – which are full of sensory adverse effects – and teach prescribers how to inform consent (that’ll be the day). It also makes SSRIs un-special, more appropriate for eventual OTC distribution.

    I can’t remember the details – non-scientist – but you did also have a theory about akathisia – how SSRIs – and I guess other drugs – could affect some sort of membrane that covers our bones.

    The bodily-ness of all this makes so much sense – and is, to nick your own concept, the girders on which so many harms can be hung. Suddenly, dysregulating a baby’s sensory development or PSSD or vestibular problems or tinnitus or akathisia all has a coherent framework- exactly the point you’re making. Whereas if the drugs were just fiddling about with fictional serotonin levels in the brain, nothing makes sense.

    I posted your heart of the matter para on X -‘These problems are linked to our sensory nervous systems, which is where SSRI drugs act. They are not brain-based problems’ – where it resonated with a lot of folks. But a few found it was dissonant with their experience or perceptions of how these drugs have harmed them. This was a comment from a very smart member of rxharm – I suggested she ask you direct, but in case she doesn’t:

    ‘Focusing on interoception or PIEZO variants leaves out the neurotoxic and neurocognitive effects. This misses the bigger pathophysiology, risks missing the fact that this harm is iatrogenic.

    But the article does negate toxic injury. It explicitly frames this as “not brain-based,” which removes the neurotoxic and neurocognitive mechanisms entirely. That shifts the interpretation of the harm, even if that isn’t anyone’s intention.’

    I just don’t see it that way – so couldn’t give her a satisfactory response – and it’s yours to explain anyway. But I can’t see how damaging or ,if you’re lucky, dysregulating sensory system reactivity which is then interpreted by the brain, is a a lesser iatrogenic harm or not ‘neurocognitive ‘. Your big point about unbalancing the whole person is fundamental – and much like the atomisation of self felt by those in long term antidepressant withdrawal.

    Over to you to explain.

    Reply

    • Your activities on X may have triggered the next two comments in the sequence. This Visual Shock post is not the paradigm shift I’m aiming at. That comes in a week or two and should give you lots of opportunities to stir the X nest.

      D

      Reply

  3. Dr Healy

    Thank you for this post and for all the work you’ve done making it clear that VSS, PPPD, PSSD and akathisia are real sensory-system injuries rather than psych issues. That clarity has protected a lot of people from being written off with FND or other bogus dx.

    I wanted to respond to one point you made. You wrote that these conditions are “bodily not mental states” and “not brain-based problems.” I understand you’re trying halt the automatic jump to psychogenic, but from a neurophysiology standpoint the divide between “bodily” and “brain-based” doesn’t really exist. Sensory disorders run through both systems at once. They’re central + peripheral networks, not one or the other.

    Vision, balance, interoception and erotic sensation all depend on peripheral receptors as well as brainstem nuclei, thalamic relays and cortical networks that create perception. Even if the initial disturbance starts in the peripheral system, the experiences of snow, numbness, dizziness or akathisia are still processed in the brain. None of these conditions bypass it.

    VSS imaging research studies show visual cortex hyperexcitability, thalamo-cortical dysrhythmia and white-matter changes in the visual pathways. These aren’t psychological findings; they are unmistakably brain findings.

    The same applies to PSSD. Genital numbness is peripheral, but the loss of erotic feeling, desire and emotional reward is cortico-limbic. Sexuality isn’t a localized function; it’s a CNS network.

    PPPD relies on altered vestibular/insular/cortical integration and akathisia is well established as a central drug injury involving basal ganglia and frontal motor circuits. The brain is absolutely involved.

    I fully agree with your effort to push back against the reflexive “FND” label. But saying these conditions are “not brain-based” can invite a different kind of confusion… that if they’re not brain-based, then the brain couldn’t have been harmed. The brain absolutely has been injured.

    I say all of this with deep respect for your work. You’ve been one of the few willing to name these conditions as drug-induced injuries. Thank you for continuing to speak openly when so few others will.

    Reply

    • Grace

      Thanks for this. I’m not trying to write the brain out of the picture – you need to wait for a talk in 10 days time called In Praise of SSRIs, which may help. This Visual Snow post is 2 weeks too early but the VSS post about the paper needed following up in real time.

      Having made this point, if my leg got chopped off, there would be a host of brainstem and cortical changes – perhaps even phantom limb perceptions but the problem would not be brain based or even a combination of brain and body based. It would be missing leg based. Its the same with SSRIs – they act on the 95% of serotonin that is in our bodies.

      We can wipe out the serotonin in the brainstem – Raphe nucleus – and it would make little different to our functioning – certainly not cognitive function.

      On the other hand we’ve known from 1950, we can give LSD, which acts on serotonin, to spiders and their webs become completely disorganized and chlorpromazine reverses this. LSD was first demonstrated to have physiological level (rather than behavioural) effects in the early 1950s on serotonin receptors in the guts of animals leading to I think the earliest hypothesis that serotonin might play a part in nervous disorders..

      My point here is we don’t need to involve higher cognitive functions to explain this – in fact involving them risks making the original problem far worse – as per the James-Lange Theory of the Emotions.

      Consider Jet Lag. This comes about because of the suprachiasmatic nucleus (SCN) which operates outside our brains. It affects every brain circuit – they are all out of whack. It contributes to bad brain fog – which comes about because we are using attention and concentration resources to correct a disruption to embodied knowledge and this is effortful and frustrating because it fails. We figure our brains aren’t working right, when in fact they are working perfectly. Trying to correct this with a pill that works on the brain would be a disaster.

      But the other part of the disaster is that our brain bias means we have failed to look at peripheral systems – ironically because they are too subjective. Parkinsons now looks like it begins in the gut and we have completely missed the effects of dopamine antagonists on peripheral proprioception and other sensory systems.

      In terms of SSRIs, we only recently discovered the existence of mechanosensors – PIEZO proteins – abnormalities of which reproduce the peripheral manifestations of SSRI related toxicity.

      In terms of SSRIs, one of their most salient and immediate effects is a genital numbing that can be reproduced by rubbing lidocaine into the skin of the penis – do brain circuits have anything to do with this. The muting of orgasms that result in addition to more sustained performance in men can be viewed as a direct consequence of reduced sensory input – we don’t need brains to understand it. There would likely be a loss of libido if this was being done every day – as is done with SSRIs – do we need a brain to understand this?

      Let me give you an image that might convey where I think we need to get – we perhaps need to see our selves more like Octopi than we do at the moment. These manage to be highly intelligent, even emotional and humorous it seems without much of a central brain. They appear to have distributed brains – distributed into their tentacles and arms. My focus on sensory receptors is aimed at getting us to recognize that our knowledge centres are a lot more distributed than we usually think and given 70 years of research hasn’t linked any of our major nervous problems, either naturally occurring or drug induced, to Big Brain centres it might be worth consulting our inner Octopus and thinking about our Distributed Knowledge Centres.

      David

      Reply

      • Thank you for expanding on this; it helps clarify the peripheral-first model you’re outlining. My point is that peripheral disruption doesn’t stay peripheral. Looking forward to Part 1 to see where you take this.

        Reply

  4. To suggest SSRI doesn’t cause brain problems, neurotoxicity or some type of brain injury would dismiss many in the SSRI harmed community. There is an abundance of published research and case examples of SSRI’s negatively effecting the brain.

    Reply

    • Kyle

      Good to get this comment. There is no doubt that SSRIs can cause brain damage but this has nothing much to do with what they are doing for or to most people. It can happen as a result of things like carbonic anhydrase activation causing things like hyponatremia (low sodium) which in its own right or through our attempts to correct can lead to osmotic demyelination and very real brain damage.

      Fortunately this is comparatively rare compared to problems like PSSD and VSS and vanishingly rare compared to the normal sensory effects SSRIs have which affect everyone whereas significant hyponatremia etc may affect somewhere in between 1 in 100 or 1 in 1000 and damaging hyponatremia happens in even fewer. SSRIs are not the only drugs that can cause this picture.

      There are things we do with SSRIs that make the risks of brain damage worse – like start people on off in toxic doses. If get people to focus more on what we should be aiming to do with an SSRI my hope is that this will lead to far fewer people being put on toxic doses or having their treatment continued when it shouldn’t be.

      David

      Reply

      • Long term use can cause numerous neurotransmitter changes that can be long term. And despite your theory that serotonin only affects the gut there is a percentage that concentrates on the brain. Which affects cognitive thinking, memory, emotions, pain perception, sleep, etc. dopamine is also affected. And the injury due to SSRI’s also effect other neurochemical systems causing additional symptoms. I respect your research but it’s much more than sensory.

        Reply

        • I didn’t say it just affects the gut. I said it primarily affects the peripheral sensory nervous system. Around 5% of it is in the brainstem in the Raphe nucleus and we can wipe that out without it making much difference to behavior.

          The serotonin actions of SSRIs almost certainly didn’t cause your brain damage. SSRIs and many other drugs do lots of other things that can cause brain damage and this has likely been the cause of yours. The vast majority of people on SSRIs or with withdrawal problems do not have brain damage – any damage they have is in peripheral sensory systems

          D

          Reply

          • A common SSRI induced brain injury can cause Akathisia. Akathisia is primarily related to the brain rather than the peripheral nervous system.
            It’s a movement disorder characterized by a feeling of inner restlessness and a compelling need to be in constant motion. Akathisia is caused by dysfunction in the brain’s dopamine pathways, particularly in areas like the basal ganglia that control movement and motor function.
            The condition is most commonly associated with:
            • Antipsychotic medications (both typical and atypical)
            • Antidepressants (particularly SSRIs)
            • Other medications that affect dopamine signaling in the brain

            SSRI’s effect dopamine. there is significant interaction between serotonin and dopamine systems:
            1. Serotonin-dopamine interaction: Increased serotonin can actually inhibit dopamine release in certain brain regions, particularly in the nigrostriatal and tuberoinfundibular pathways. This is because serotonin and dopamine systems are interconnected.
            2. Regional effects: The effect varies by brain region – serotonin can suppress dopamine activity in areas like the basal ganglia (involved in movement control), which may explain why SSRIs can occasionally cause movement disorders like akathisia.
            3. Clinical manifestations: This serotonin-mediated dopamine suppression can lead to:
            • Akathisia (restlessness)
            • Other extrapyramidal symptoms
            • Sexual dysfunction (dopamine plays a role in sexual function)
            • Emotional blunting in some patients
            So while SSRIs don’t directly block dopamine receptors the way antipsychotics do, they can indirectly reduce dopamine neurotransmission through the complex interplay between serotonergic and dopaminergic systems in the brain..

          • With all due respects. this cut and paste is utter baloney.

            If akathisia was a movement disorder it would be classified as a dyskinesia.

            The words a feeling of inner restlessness tells you its drive by a sensation

            If it had anything to do with dopamine we’d have had a cure decades back given our identification of dopamine receptors and production of agonist. antagonists and partial agonists acting on these receptors

            D

  5. ‘But the other part of the disaster is that our brain bias means we have failed to look at peripheral systems – ironically because they are too subjective. Parkinsons now looks like it begins in the gut and we have completely missed the effects of dopamine antagonists on peripheral proprioception and other sensory systems’.

    I guess this could be seen as relevant to a broader underlying trend or refocus in psychiatry towards the body – having spent years attempting to tinker with the brain, without as far as I can see any improvement in outcomes. Quite the reverse. And it’s significant that, whilst most specialities like Ophthalmology, Cardiology etc. track outcomes over time, psychiatry seems to obfuscate them. Yes – ofc it’s complicated, but I’m sure we could all think of quality of life etc. measures that could apply.

    I was thinking of what seems to be perceived as an epiphany in psychiatry – that what we eat affects how we feel. The ‘Brain Energy’/Keto diet stuff that Chris Palmer has developed – still brain biased conceptually, ‘mental disorders are metabolic disorders of the brain’,

    I’ve not looked into it carefully. But commonsense quite a lot of qual research work on ‘weight management’, and listening to patients diagnosed with all sorts who have recovered by adopting Keto and dumping the pills – leads me to think stable blood sugar levels might be at the root of much of this. I remember that protein and fat are far slower burn that carbs and sugars – which produce quick flares of energy and risk insulin resistance. Any of us know that if we eat ‘badly’ (there is a huge amount of morality around food ofc) and erratically, it radically affects our bodies and how we feel in ourselves – jittery, anxious, miserable etc.

    It’s hard to keep up with your paradigm shifts – but keenly await the next scientific revolution.

    Reply

  6. ‘ It can happen as a result of things like carbonic anhydrase activation causing things like hyponatremia (low sodium)‘

    For me this is really important to think about.

    Reply

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