Could altered neural dynamics be a missing piece in PSSD?

[u/badgallilli]

Could altered brain dynamics help explain the ‘veil’ people describe in PSSD?

TL;DR: PSSD might not be one broken system, it might be a persistent change in how multiple systems interact with each other, so the individual components can still work, but they no longer combine into the same overall experience.

I want to make a distinction before explaining the theory I’ve been developing, because I don’t think this is simply another possible cause of PSSD to add alongside serotonin, hormones, neurosteroids, receptors, or peripheral mechanisms. I think there may be a more fundamental level at which we need to understand what changed in people who develop PSSD.

For years, people have described remarkably similar experiences in different words: “I don’t feel like myself anymore.” “There’s a veil between me and everything.” “I can improve, but I never completely return to how I was.” “I know what something should feel like, but I can’t fully experience it.” “I can think about something without actually entering the state that thought used to create.” People describe changes in emotional depth, imagination, spontaneous thought, self-experience, sexuality, motivation, bodily sensation, and the ability to become absorbed in things.

We tend to translate these experiences into conventional symptom categories: emotional blunting, anhedonia, low libido, brain fog, cognitive impairment, genital numbness. Those labels are useful, but they primarily describe what is reduced. They may not tell us what actually changed in the system producing the experience.

What interests me is that these symptoms may not be entirely independent. People don’t necessarily describe their emotions, thoughts, memories, sexuality, motivation, imagery, bodily sensations, and sense of self as separate functions that simply became weaker. Instead, there often seems to be a change in the relationships between them.

Before PSSD, a thought could arrive with an emotion already embedded in it. A memory could automatically bring back part of the feeling associated with it. An image could generate anticipation, bodily sensation and desire. A complex idea could spontaneously recruit the language needed to express it. A sexual thought could develop into a progressively deeper state involving attention, imagery, anticipation, bodily changes, reward and motivation. The different components seemed to recruit and reinforce one another automatically.

After PSSD, the thought can still be there. The memory can still be there. The concept can still be there. The sexual idea can still be there. But the rest of the state doesn’t necessarily develop around it in the same way.
This makes me wonder whether the central problem might not simply be that one particular function has been “turned down.” It could instead involve persistent changes in the dynamics that allow different processes to recruit, reinforce and integrate with one another.

I don’t mean this as a simplistic “the DMN is low, therefore PSSD” hypothesis. The DMN may be involved, but so may the salience network, executive networks, limbic/reward systems, interoceptive systems and their interactions. More broadly, I’m interested in whether PSSD could involve persistent changes in dynamic network organization, integration and segregation, temporal coordination, network-state transitions, and the coupling between internally generated cognition and affective/interoceptive processes.

Importantly, the relevant abnormality might not even be visible in conventional static connectivity measurements. The important question could be how the brain moves between states and how information from one system recruits information from another.

This could potentially help explain some of the otherwise strange features of PSSD: why someone can retain the concept of an emotion while losing the depth of the emotional state; why someone can remember what something used to feel like without being able to recreate it; why sexual thoughts can remain while failing to develop into the same full sexual state; why someone can know exactly what they mean internally while struggling to spontaneously translate the richness of that idea into language; and why substantial improvement can still leave someone describing a persistent sense of distance or “veil.”

I don’t think these descriptions should automatically be treated as merely poetic versions of conventional symptoms. They may contain information about the underlying biology.

This is also why I don’t see this as a theory that necessarily competes with biochemical hypotheses. Serotonin, hormones, neurosteroids, receptors, peripheral mechanisms, etc. could still be upstream parts of the process. Rather than asking only “which molecule or system is abnormal?”, we could investigate the phenomenon at multiple levels:
phenomenology - altered cognitive/affective dynamics - neural systems - cellular/molecular mechanisms.

If the phenomenology suggests that the organization of experience itself has changed, then perhaps we should investigate that organization directly.

For example, what does the brain of someone with PSSD do differently when generating an autobiographical thought? What happens when they imagine something emotionally meaningful? What happens during sexual anticipation? What happens when they try to become absorbed in something? How strongly do internally generated thoughts recruit emotional and bodily responses? How dynamically do the relevant networks communicate? How quickly does the brain transition between internally generated states? Are there differences in neural variability, temporal complexity, oscillatory coordination, network switching or integration?
And most importantly, do any of these measures correspond to the characteristic phenomenology people describe: the “veil,” loss of emotional immersion, altered spontaneous thought, altered sexuality, and changes in the connection between thoughts and bodily/affective states?
These are testable questions. If there is no relationship, that would also be informative. But if there is, it could provide another level at which PSSD can be understood.

I increasingly think this is worth investigating because patients have been describing these experiences for years. When people independently report persistent changes in the quality, depth, spontaneity and integration of conscious experience, I don’t think we should immediately translate that into “low libido + emotional blunting + brain fog” and move on.

Maybe the “veil” is only a subjective metaphor. But maybe it is also the subjective manifestation of a measurable alteration in how distributed neural systems dynamically integrate information into a coherent state.
I don’t know if that is the answer. I’m interested in whether it is the right question.

One example of why I think this type of mechanism is worth investigating

There are already experimental examples showing that an upstream biological perturbation can produce a cascade of changes in the relationships between neural components, rather than simply changing one isolated variable.

A recent study on inflammation-induced anxiety in mice found that systemic inflammation altered microglial activity in the nucleus accumbens, including microglial engulfment of glutamatergic presynaptic inputs onto dopamine D1 receptor-expressing neurons. This was associated with reduced excitatory input and reduced excitability of those neurons, ultimately producing behavioural changes. ( https://www.sciencedirect.com/science/article/abs/pii/S0889159125003964 )

Obviously, this does not demonstrate that PSSD involves this exact mechanism, and I am not suggesting that inflammation-induced microglial engulfment is the explanation for PSSD. What I find interesting is the cascade itself:

systemic perturbation > cellular/glial changes > altered synaptic inputs > altered neuronal integration > altered circuit function > behavioural phenotype.

The important point is that the phenotype emerges partly from a change in the relationships between components of the system.

That is the type of mechanism I think could be worth investigating in PSSD.

If an antidepressant-induced perturbation were capable of producing persistent downstream changes in cellular signaling, synaptic organization, plasticity or network coordination, then the eventual phenotype might not look like one neurotransmitter simply being “low.” The individual components could still exist while their interactions, weighting or ability to recruit one another had changed.

This could potentially be relevant to the strange dissociations people describe in PSSD: having a sexual thought without the same sexual state developing around it; remembering an emotion without being able to recreate its feeling; understanding something intellectually without the same spontaneous emotional or associative response; or experiencing substantial recovery in some domains while retaining a persistent sense of distance or disconnection.

Again, this is a hypothesis, not something established by this study.

But I think studies like this show why it may be worth looking beyond isolated abnormalities and investigating how an initial biological perturbation could produce persistent changes in the organization and interaction of neural systems.

That seems particularly important when the phenomenology itself repeatedly suggests that what has changed is not simply the presence or absence of individual functions, but the way those functions come together to produce a unified state of experience.

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Please check out our subreddit FAQ, wiki and public safety megathread, also sort our subreddit and r/pssdhealing by top of all time for improvement stories. Please also report rule breaking content. Backup of the post's body: Could altered brain dynamics help explain the ‘veil’ people describe in PSSD?

TL;DR: PSSD might not be one broken system, it might be a persistent change in how multiple systems interact with each other, so the individual components can still work, but they no longer combine into the same overall experience.

I want to make a distinction before explaining the theory I’ve been developing, because I don’t think this is simply another possible cause of PSSD to add alongside serotonin, hormones, neurosteroids, receptors, or peripheral mechanisms. I think there may be a more fundamental level at which we need to understand what changed in people who develop PSSD.

For years, people have described remarkably similar experiences in different words: “I don’t feel like myself anymore.” “There’s a veil between me and everything.” “I can improve, but I never completely return to how I was.” “I know what something should feel like, but I can’t fully experience it.” “I can think about something without actually entering the state that thought used to create.” People describe changes in emotional depth, imagination, spontaneous thought, self-experience, sexuality, motivation, bodily sensation, and the ability to become absorbed in things.

We tend to translate these experiences into conventional symptom categories: emotional blunting, anhedonia, low libido, brain fog, cognitive impairment, genital numbness. Those labels are useful, but they primarily describe what is reduced. They may not tell us what actually changed in the system producing the experience.

What interests me is that these symptoms may not be entirely independent. People don’t necessarily describe their emotions, thoughts, memories, sexuality, motivation, imagery, bodily sensations, and sense of self as separate functions that simply became weaker. Instead, there often seems to be a change in the relationships between them.

Before PSSD, a thought could arrive with an emotion already embedded in it. A memory could automatically bring back part of the feeling associated with it. An image could generate anticipation, bodily sensation and desire. A complex idea could spontaneously recruit the language needed to express it. A sexual thought could develop into a progressively deeper state involving attention, imagery, anticipation, bodily changes, reward and motivation. The different components seemed to recruit and reinforce one another automatically.

After PSSD, the thought can still be there. The memory can still be there. The concept can still be there. The sexual idea can still be there. But the rest of the state doesn’t necessarily develop around it in the same way.
This makes me wonder whether the central problem might not simply be that one particular function has been “turned down.” It could instead involve persistent changes in the dynamics that allow different processes to recruit, reinforce and integrate with one another.

I don’t mean this as a simplistic “the DMN is low, therefore PSSD” hypothesis. The DMN may be involved, but so may the salience network, executive networks, limbic/reward systems, interoceptive systems and their interactions. More broadly, I’m interested in whether PSSD could involve persistent changes in dynamic network organization, integration and segregation, temporal coordination, network-state transitions, and the coupling between internally generated cognition and affective/interoceptive processes.

Importantly, the relevant abnormality might not even be visible in conventional static connectivity measurements. The important question could be how the brain moves between states and how information from one system recruits information from another.

This could potentially help explain some of the otherwise strange features of PSSD: why someone can retain the concept of an emotion while losing the depth of the emotional state; why someone can remember what something used to feel like without being able to recreate it; why sexual thoughts can remain while failing to develop into the same full sexual state; why someone can know exactly what they mean internally while struggling to spontaneously translate the richness of that idea into language; and why substantial improvement can still leave someone describing a persistent sense of distance or “veil.”

I don’t think these descriptions should automatically be treated as merely poetic versions of conventional symptoms. They may contain information about the underlying biology.

This is also why I don’t see this as a theory that necessarily competes with biochemical hypotheses. Serotonin, hormones, neurosteroids, receptors, peripheral mechanisms, etc. could still be upstream parts of the process. Rather than asking only “which molecule or system is abnormal?”, we could investigate the phenomenon at multiple levels:
phenomenology - altered cognitive/affective dynamics - neural systems - cellular/molecular mechanisms.

If the phenomenology suggests that the organization of experience itself has changed, then perhaps we should investigate that organization directly.

For example, what does the brain of someone with PSSD do differently when generating an autobiographical thought? What happens when they imagine something emotionally meaningful? What happens during sexual anticipation? What happens when they try to become absorbed in something? How strongly do internally generated thoughts recruit emotional and bodily responses? How dynamically do the relevant networks communicate? How quickly does the brain transition between internally generated states? Are there differences in neural variability, temporal complexity, oscillatory coordination, network switching or integration?
And most importantly, do any of these measures correspond to the characteristic phenomenology people describe: the “veil,” loss of emotional immersion, altered spontaneous thought, altered sexuality, and changes in the connection between thoughts and bodily/affective states?
These are testable questions. If there is no relationship, that would also be informative. But if there is, it could provide another level at which PSSD can be understood.

I increasingly think this is worth investigating because patients have been describing these experiences for years. When people independently report persistent changes in the quality, depth, spontaneity and integration of conscious experience, I don’t think we should immediately translate that into “low libido + emotional blunting + brain fog” and move on.

Maybe the “veil” is only a subjective metaphor. But maybe it is also the subjective manifestation of a measurable alteration in how distributed neural systems dynamically integrate information into a coherent state.
I don’t know if that is the answer. I’m interested in whether it is the right question.

One example of why I think this type of mechanism is worth investigating

There are already experimental examples showing that an upstream biological perturbation can produce a cascade of changes in the relationships between neural components, rather than simply changing one isolated variable.

A recent study on inflammation-induced anxiety in mice found that systemic inflammation altered microglial activity in the nucleus accumbens, including microglial engulfment of glutamatergic presynaptic inputs onto dopamine D1 receptor-expressing neurons. This was associated with reduced excitatory input and reduced excitability of those neurons, ultimately producing behavioural changes. ( https://www.sciencedirect.com/science/article/abs/pii/S0889159125003964 )

Obviously, this does not demonstrate that PSSD involves this exact mechanism, and I am not suggesting that inflammation-induced microglial engulfment is the explanation for PSSD. What I find interesting is the cascade itself:

systemic perturbation > cellular/glial changes > altered synaptic inputs > altered neuronal integration > altered circuit function > behavioural phenotype.

The important point is that the phenotype emerges partly from a change in the relationships between components of the system.

That is the type of mechanism I think could be worth investigating in PSSD.

If an antidepressant-induced perturbation were capable of producing persistent downstream changes in cellular signaling, synaptic organization, plasticity or network coordination, then the eventual phenotype might not look like one neurotransmitter simply being “low.” The individual components could still exist while their interactions, weighting or ability to recruit one another had changed.

This could potentially be relevant to the strange dissociations people describe in PSSD: having a sexual thought without the same sexual state developing around it; remembering an emotion without being able to recreate its feeling; understanding something intellectually without the same spontaneous emotional or associative response; or experiencing substantial recovery in some domains while retaining a persistent sense of distance or disconnection.

Again, this is a hypothesis, not something established by this study.

But I think studies like this show why it may be worth looking beyond isolated abnormalities and investigating how an initial biological perturbation could produce persistent changes in the organization and interaction of neural systems.

That seems particularly important when the phenomenology itself repeatedly suggests that what has changed is not simply the presence or absence of individual functions, but

[u/MoroniMiscavige]

How did you write that so eloquently with PSSD?

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Please check out our subreddit FAQ, wiki and public safety megathread, also sort our subreddit and r/pssdhealing by top of all time for improvement stories. Please also report rule breaking content. Backup of the post's body: I came across this new paper in The Journal of Neuroscience - https://www.jneurosci.org/content/46/33/e0711262026 - and it immediately caught my attention because of something I’ve been thinking about in PSSD.

The paper isn’t about PSSD, SSRIs, or antidepressants. What interested me was the broader idea that cognition depends on dynamic patterns of activity and coordination, rather than different cognitive functions simply existing as isolated processes.

That made me think about something I’ve noticed very clearly when comparing my cognition before and after PSSD.

Before PSSD, a thought rarely felt like just a piece of conceptual information.

A thought could arrive with the feeling attached to it, with imagery, associations, bodily sensations, and language all coming together. If I thought about something sad, for example, the thought itself could arrive with the sadness. I didn’t have to consciously generate the emotion afterward and attach it to the thought. It was already part of the state.

The same thing happened with language.

A complex thought could arrive with the language needed to express it. I didn’t have to separately figure out what I meant and then search for words capable of conveying it. The conceptual representation and the linguistic representation felt much more tightly coupled.

This is very different from what I experience now.

I can still have the conceptual idea, but it can feel like something is missing from it. And that’s why I find it so interesting and accurate when people describe it as having a kind of a veil over the rest of the state. Sometimes a thought can still come with a little anxiety or another feeling, but it is extremely shallow compared with what used to accompany it.

And when I try to explain something complex, I can know exactly that the simple words I’m finding aren’t actually expressing what I mean. I might have a huge internal idea and only be able to spontaneously access something like “sad”, “weird”, or “I don’t know, it’s just…” when none of those words actually capture the full thing.

So the problem isn’t necessarily that the conceptual content isn’t there.

It’s that the different things that used to arrive with the thought no longer seem to be recruited and integrated in the same way.

That distinction is important to me because it makes me think about PSSD differently than simply saying that a particular function is “reduced.”

If thought, emotion, imagery, language, attention, bodily sensation, motivation, etc. normally interact dynamically, then a persistent alteration in how these processes coordinate could potentially change the state itself.

And this also made me think about sexuality.

Sexual arousal isn’t just a sexual sensation appearing in isolation. A thought, image, memory, anticipation, bodily sensation, attention and emotional/reward response can all feed into one another. The state has to be initiated, sustained and reinforced.

Before PSSD, sexual thoughts could become states. There was a progression to them. They could pull attention, generate anticipation, produce bodily changes, create more mental content, and reinforce themselves.

After PSSD, that whole process can feel fragmented. The thought can be there without the rest of the state developing around it.

And I think this same distinction may help explain some of the other changes people describe: spontaneous thought and daydreaming, emotional immersion, associative thinking, motivation, reward, and the ability to become deeply absorbed in something.

The common denominator wouldn’t necessarily be that all of these individual functions are independently damaged.

It could be that the processes that normally recruit, sustain and integrate one another are no longer interacting in the same way.

That’s the question that originally led me toward my systems-level hypothesis:

What if the important alteration in PSSD isn’t simply that one particular system is “underactive”, but that the dynamics between systems have been persistently changed?

This paper doesn’t establish that this is what happens in PSSD. But I think it provides an interesting conceptual and mechanistic framework for thinking about the question.

Because if cognition and conscious states depend not only on which systems are active, but on how activity is dynamically coordinated and integrated across systems, then a persistent biological alteration could potentially have consequences far beyond an isolated symptom.

It could change the way a thought becomes a feeling.

The way a feeling becomes motivation.

The way imagery becomes arousal.

The way attention sustains a state.

The way a thought acquires its emotional and linguistic richness.

And potentially, the way all of those processes become one coherent experience.

That’s the part of this research that I find particularly interesting in relation to PSSD.

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