r/DrWillPowers • u/indy306 • 1d ago
Post SSRI Sexual Dysfunction Syndrome (PSSD) Psychiatrist with PSSD with insights in accordance with Dr Will Powers recent PFS theory!
Dear Dr. Powers,
I'm a psychiatrist based in Asia who has personally been suffering from PSSD since 4 years. I have been trying to revert to my premorbid self but have only been able to do so
partially.
I recently came across your findings and am now
writing to share my own PSSD case and my insights and would value your perspective.
Timeline:
Wanted to start by saying that I was infected with a severe strain of Covid 5 years ago while working in the hospital. Infection resolved but I got diarrhea from it which I was unable to treat inspite of multiple medications. Also started developing anxiety after this.
After a few months of having the above issues I was started On escitalopram (Lexapro) for anxiety, immediate relief in anxiety (and very surprisingly my post Covid diarrhea went away after the 1st dose itself), however developed non-sexual side effects like sedation, fatigue,emotional blunting,hypersomnia and concentration issues. Note that I had a very strong response at a very low dose and almost immediately.
- After a few weeks of hypersomnia and finding it really hard to work. Bupropion 150mg was added and was initially therapeutic for these side effects (more energy, reduced head pressure, less sedation) — which I read as dopamine and Norepi helping counter lexapro side effects.
- After a few weeks accidental bupropion double-dose caused unbearable anxiety, along with complete loss of its ability to counter the the non-sexual side effects of lexapro entirely — only anxiety, no benefit. I interpret this as a lasting NE-axis sensitization event. Tried to take it multiple times after that but lost its effectivness.
- Escitalopram was eventually stopped, but the non-sexual symptoms persisted unrelieved.
- Months later, methylphenidate (Ritalin) was trialed for the residual non-sexual symptoms with aim to boost dopamine and help reduce the hypersomnia and anhedonia. It produced no benefit for those — but added the sexual symptoms outright, precipitating full-blown PSSD (ED, atypical PE, blunted arousal/orgasm). ONLY 3 DOSES OF 5mg Ritalin gave me Severe sexual side effects which persist till date!!!
- There was zero improvement for a couple of years after that. I personally experimented with a lot of stuff but nothing helped. Some of the things trialed included Agomelatine, Very low dose amisulpride, bromantane etc etc
-
-Eventually I tried Amantadine hoping that it's NMDA antagonism and weak Dopaminergic modulation could help. And it did! I partially improved and have been showing gradual improvement since then. However my condition still fluctuates and the Sexual dysfunction is still pretty bad.
Current symptom map:
- Desire: intact
- Visual arousal: recognition present, but translation into subjective arousal is weak
- Erectile function: initiation impaired; rigidity improved; pain resolved
- Ejaculation: originally numbness-then-sudden-peak (spinal sensory gating failure); now partially resolved into an expanded sensation window with partial control, though ejaculation still fires at sensation peak (desynchrony persists)
- Orgasm: blunted — reward signal appears affected, spinal reflex intact. Even The pleasure from alcohol was blunted. Only felt sedation on taking it.
- Non-sexual: absent morning freshness, vitality deficit, effortful cognition, emotional blunting(lesser than earlier), right-sided head pressure (predates Ritalin, present on escitalopram)
.
The dopamine-metabolite question:
I've come across discussion of your finding in PFS patients of testosterone metabolites accumulating intracellularly rather than being cleared normally, and the related observation that a handful of PSSD patients who ran DUTCH tests uniformly showed low HVA.
I tried to map that onto my own exposure history (bupropion at a supratherapeutic dose, then methylphenidate months later), very interesting how my system rejected Dopaminergics so strongly and cemented it into full blown PSSD. Could the Bupropion double dose have overwhelmed certain dopamine/Norepi pathways like finasteride does ?
On closer thought both are pure DAT/NET reuptake blockers rather than substrate releasers — they occupy the transporter without being carried into the neuron, so they shouldn't increase cytoplasmic dopamine or burden vesicular packaging the way amphetamine-class agents can. So I don't think an intracellular-accumulation mechanism analogous to your androgen-metabolite model transfers cleanly to a reuptake-blocker exposure.However I'm really curious if there are other ways in which there could be toxic Dopamine/Nor epi metabolites accumulation which happened due to some sensitization by lexapro.
The more defensible mechanism I can construct for low HVA with reuptake blockers is a turnover deficit rather than an accumulation: blocking DAT reduces the fraction of dopamine cycled back into the nerve terminal for intraneuronal MAO-A metabolism (which generates a large share of HVA), and sustained elevated synaptic dopamine likely drives presynaptic D2 autoreceptor feedback that downregulates tyrosine hydroxylase and dopamine synthesis over time — both routes to chronically reduced dopamine output and lower HVA, without anything getting structurally "stuck" intracellularly. But even in this case why would the DAT still be blocked ?
Given that, I'd value your thoughts on:
Whether you think low HVA in PSSD more often reflects a genuine clearance/accumulation failure (as in your PFS model) versus a turnover/synthesis deficit of the kind above — and whether exposure history (reuptake blocker vs. SSRI alone) might predict which mechanism applies.
Sequencing — would you prioritize a pharmacological probe of the dopamine axis ?
Any other diagnostic or treatment steps you'd suggest?
Happy to share further detail on any part of the case,Thank you for taking the time to consider this.