I saw a post in a CFS/ME group on Facebook asking if others experience the world or themselves as dreamlike. A large number of commenters said they do. Some attributed it to trauma, although I suspect something more is going on here. I have long suspected a connection because of my own experience.
Background
First, some background.
Derealization refers to an experience of the world as unreal or dreamlike. Depersonalization refers to an experience of oneself, this human self, as unreal and dreamlike. These two are often seen as trauma-related, as ways the system deals with otherwise overwhelming trauma.
Brain fog, typical of CFS, is usually described as a set of cognitive dysfunctions that involve executive cognitive functions (memory, processing, etc.) and is often characterized by a direct experience of wooliness or fogginess.
The diagnostic criteria for CFS/ME do not include derealization and depersonalization and they are not included among the typical symptoms.
My story (part one): CFS and the experience of the world as dreamlike
In my case, there seems to be an intriguing connection between CFS and an experience of the world as dreamlike.
On New Year’s Day when I was fifteen, I was standing outside of my parents’ house and it felt like a fog came in and the world became distant. The whole world, including this human self, seemed to be far away. It came with an experience of wooliness and fogginess. This was profoundly disturbing to me.
I later understood that this was how the CFS/ME started, a few months after I had mononucleosis. I don’t remember how soon the many other symptoms came (fatigue, other aspects of brain fog, PEM, and so on), but I assume it was the same day or within a few days.
I still experience the world and this human self as unreal and dreamlike, appearing within and as consciousness just like a dream. It’s stronger when I am in a CFS-crash and have PEM, and it’s also stronger when my general brain fog is stronger – sometimes because of brain-fog inducing food (sugar, wheat, dairy).
If my sense of the world as distant, unreal, and dreamlike was connected with trauma, I would expect it to get stronger during stress and when emotionally triggered. It does not. If anything, I tend to feel sharper and more present then. Instead, it closely follows my CFS symptoms in general. It gets stronger with PEM and when food worsens my brain fog. To me, that suggests it’s related to CFS and not trauma.
I am used to it by now, although when it’s strong, and I am with people, I sometimes become very conscious about it and it still feels slightly disturbing until I remind myself that it’s normal for me.
Possible connections
There are several possible connections between CFS/ME and a dreamlike experience of the world and/or themselves.
The simplest explanation is that it’s an aspect of brain fog. Of the many aspects and expressions of brain fog, an experience of the world/this human self as dreamlike may be one – at least for some or many with CFS.
Some suspect a connection between psychological trauma and CFS, at least in some cases. Trauma may make some of us more susceptible to later getting CFS/ME. That may be the case for me too. It’s not the full picture but it may be one vulnerability. (In many cases, a virus or bacteria may be the actual trigger, with the Epstein-Barr virus as a classic example.)
If so, the derealization/depersonalization associated with trauma may be the reason why many with CFS/ME experience just that.
Is it sometimes misattributed and misdiagnosed?
There is another interesting and important possibility here.
Derealization and depersonalization may, in some cases, be expressions of CFS-related brain fog, and misattributed and misdiagnosed as trauma symptoms.
Of course, some CFS patients will also have genuine trauma-related derealization/depersonalization. But I suspect there is occasional misdiagnosis, especially among doctors and psychiatrists who are not very familiar with CFS.
Why is it not identified or talked about?
If this is a relatively common symptom of CFS/ME, why is it not officially identified or talked about?
It may be because it’s typically associated with psychological trauma so doctors may not think of measuring it as a neurological or physiological symptom. If it comes up, they may interpret it as a trauma response unrelated to the CFS.
What can the unreal and dreamlike experience tell us about CFS?
If one expression of CFS-related brain fog is the experience of the world as distant, unreal, and dreamlike, then what does that tell us about CFS?
What mechanisms are behind it? Can identifying these help us understand and possibly treat CFS?
Existing research
We know that several conditions, unrelated to psychological trauma, can cause an experience of the world as distant, unreal, or dreamlike.
We also know that several studies have found dysregulation of a wide range of systems in CFS patients. These include sensory and perceptual disturbances, reduced blood flow to the brain, and balance and vestibular disturbances. (See below for more on this.) All of this can possibly be connected to an experience of a dreamlike world/self.
Future research
CFS/ME research has limited funding so I understand that this is not a priority, but these topics are interesting and possibly important, and I assume they will be addressed by future research.
Here are some questions:
- How common is it for CFS/ME patients to experience the world as distant, dreamlike, or unreal?
- For those who experience it, does it worsen with PEM? Does it worsen with stronger brain fog?
- Is this definitely connected with psychological trauma? Or could it be an expression of CFS-related brain fog?
- What are some of the biological changes connected with CFS-patients experience of the world as unreal and dreamlike? Can understanding these help us treat CFS?
- If it is an expression of CFS-related brain fog, how often is it misattributed to and misdiagnosed as psychological trauma?
- How can we best help CFS patients disturbed by this experience of the world as unreal and dreamlike?
My story (part two): The world as dreamlike and awakening
Here is the second part of my story, which I am adding here since it goes beyond the conventional.
There is an intriguing connection between experiencing the world as dreamlike and awakening.
Later, I saw the shift at age fifteen as a kind of absorption into the witness, or an identification as an abstract witness. “I” became a witness, and this witness witnessed all (other) content of experience and experienced it as far away. Identification went out of this human self and into this mental construct of a witness.
Almost exactly one year later, between Christmas and New Year when I was sixteen, there was a oneness shift. All without exception was revealed as God AKA the divine AKA consciousness. Or, in other words, my nature as consciousness recognized itself as all there is. There was a shift out of identification as a witness and into finding myself as Big Mind or consciousness.
I suspect the first shift, into the witness and the world as distant, set the stage for the second shift.
It may be that the Epstein-Barr infection set the stage for the CFS a few months later. The CFS came with a strong brain fog including the sense of the world and this human self as distant and far away. And that, in turn, set the stage for the oneness shift a year later. That’s not the whole story, obviously, but it may be part of it.
CFS & spirituality / awakening
It’s possible that more CFS/ME patients than average are into spirituality. There is no research on this, but it’s my impression and it seems others have that impression too.
A chronic disease like CFS/ME may bring people to spirituality, and the reverse may be the case as well. People with a personality leaning towards spirituality may be more susceptible to ME/CFS for whatever reason. (Just like the “good girl/boy” syndrome often described by people who work with CFS/ME patients.)
I also wonder something else. If people with CFS have an experience of the world and/or this human self as dreamlike, they are already more than half way to awakening. It just requires a slight shift in noticing for them to recognize their more fundamental nature, which is consciousness. It seems like a golden opportunity.
A summary of research & possible connections
I asked ChatGPT to look at relevant research and summarize. See below.
Dreamlike/distant perception and ME/CFS (AI) – references research in relation to the Facebook discussion and my experiences and history.
Possible biological explanations for the dreamlike, distant, or unreal quality of the world (AI) – purely research-based.
Addendum: Response to this article (AI) – a response to my article above.
Dreamlike/distant perception and ME/CFS (AI)
1. Derealization is not currently considered a defining symptom of ME/CFS. The established core features are post-exertional malaise (PEM), substantial impairment/fatigue, unrefreshing sleep, cognitive impairment and/or orthostatic intolerance. Derealization isn’t normally measured in diagnostic criteria, and I couldn’t find a good large study establishing its prevalence in ME/CFS.
2. Nevertheless, patient reports suggest it may be considerably more common than the formal literature indicates.In the Facebook discussion you showed me, many people independently described experiences such as the world seeming dreamlike, unreal, distant or foggy, feeling disconnected or “not really there,” and feeling as though they were observing life rather than fully participating in it. Several explicitly connected it with PEM, crashes, severe fatigue or brain fog. Similar descriptions occur in other ME/CFS communities online.
3. “Dreamlike world” specifically fits the clinical concept of derealization. Derealization concerns altered experience of the external world—things seem unreal, distant, dreamlike, foggy, strange or somehow separated from you. Depersonalization is somewhat different: it is primarily the experience of being detached from yourself or your body.
Importantly, derealization describes the experience, not its biological cause. A number of very different neurological, physiological and biochemical changes can produce experiences of unreality or altered self/world perception.
4. There is scientific evidence that sensory/perceptual processing is abnormal in ME/CFS. Studies have demonstrated altered visual perception, visual-processing difficulties, sensory hypersensitivity and sensory overload. A large 2025 study involving more than 2,300 people with ME/CFS even found a distinct sensory-overload dimension separate from conventional memory/concentration problems. This suggests that everything patients call “brain fog” isn’t necessarily simply impaired thinking.
5. Cerebral blood-flow regulation is another potentially relevant finding. ME/CFS studies repeatedly find excessive reductions in cerebral blood flow during upright posture, including in some patients without conventional POTS or orthostatic-hypotension findings. Severe patients can experience substantial reductions even while sitting. A recent systematic review concluded that abnormal cerebral blood-flow regulation is a recurring finding in ME/CFS.
There is no evidence yet that this directly causes derealization, but it provides one plausible physiological pathway by which perception, cognitive clarity and the subjective sense of being fully present could change.
There is an interesting parallel in Kleine–Levin syndrome, a neurological sleep disorder in which derealization can become prominent during episodes. A brain-imaging study found that the severity of derealization/depersonalization was strongly associated with reduced blood flow in the temporoparietal junction (TPJ), a region involved in integrating visual, auditory, bodily and spatial information. This provides a striking example of a measurable physiological brain change accompanying a dreamlike or unreal experience of the world.
6. Vestibular/sensory integration provides another particularly interesting possible connection. Outside ME/CFS, people with vestibular disorders have substantially increased depersonalization/derealization symptoms. Researchers think disrupted integration between visual information, balance/vestibular information and bodily signals can produce feelings that oneself or one’s surroundings aren’t quite real.
The temporoparietal junction appears particularly important in this process. Experimental stimulation around the TPJ can produce major changes in bodily and spatial experience, including out-of-body phenomena. Derealization-like experiences can also occur in focal neurological conditions such as temporal-lobe epilepsy. Together, these findings show that disrupting the neural systems that integrate body, vision and space can alter the experienced reality of oneself and the world.
Balance and vestibular abnormalities have also been documented in subsets of people with ME/CFS. Again, nobody has demonstrated the chain ME/CFS → vestibular dysfunction → derealization, but there is a biologically plausible connection worth investigating.
7. There is an intriguing TPJ connection in ME/CFS itself. In the NIH’s 2024 deep-phenotyping study of post-infectious ME/CFS, brain activity in the temporoparietal junction and superior parietal regions decreased during repeated physical effort in ME/CFS participants while increasing in healthy controls. The sample was small and the researchers did not measure derealization, so this cannot show that TPJ dysfunction causes the dreamlike experience in ME/CFS.
Still, the convergence is interesting: in Kleine–Levin syndrome, derealization severity was directly associated with abnormal TPJ perfusion, while in ME/CFS an independent study found abnormal TPJ activity during sustained effort. This suggests a concrete area for future research.
8. Migraine and other neurological perceptual phenomena provide another possible biological route. Alice in Wonderland syndrome (AIWS), which often occurs with migraine and sometimes following infections, can alter the perception of distance, size, time, body and reality. Derealization and depersonalization can occur as part of it.
One AIWS phenomenon, called telopsia, makes objects appear farther away than they really are. That isn’t necessarily the same as the experiential sense that the whole world has “gone far away,” but it shows that neurological changes can directly alter something as fundamental as the perceived distance and reality of the surrounding world. Migraine and migraine-like phenomena may therefore provide another possible mechanism in a subset of people with ME/CFS.
9. Biochemistry alone can also profoundly alter the sense of reality. Controlled studies with substances acting on very different brain systems provide another biological proof of principle. Ketamine can reliably produce depersonalization and derealization through NMDA/glutamate receptors; THC can produce depersonalization through the cannabinoid system; salvinorin A can produce powerful dissociative states through kappa-opioid receptors; and serotonergic psychedelics such as LSD can dramatically alter self/world boundaries and the experienced nature of reality.
These aren’t necessarily equivalent to the dreamlike state described by people with ME/CFS. But they demonstrate something important: changes in brain chemistry alone can profoundly change how real, immediate, separate or dreamlike the world and self seem.
ME/CFS research has itself found abnormalities in several potentially relevant areas of brain chemistry and metabolism—including glutamate, catecholamine and tryptophan metabolism, serotonin receptor binding and, in some studies, elevated brain lactate. None has yet been connected specifically to derealization, so it would be premature to propose any one of them as its cause.
10. Sleep/wake physiology provides yet another biological route. Experimental sleep deprivation can increase dissociative and derealization-like experiences even in otherwise healthy people. Kleine–Levin syndrome provides a more dramatic neurological example, where altered sleep/wake regulation, cognitive changes and derealization occur together.
ME/CFS is not simply a sleep disorder, but unrefreshing and disturbed sleep is a central feature, so altered sleep/wake neurobiology could conceivably contribute to the dreamlike quality in some patients.
11. The older CFS literature contains clues but apparently didn’t ask the right question. Going back to the early 1990s, researchers were already reporting sensory, visual, cognitive, ocular, gait and balance abnormalities in CFS. Later experimental studies demonstrated abnormalities of visual attention and perception.
What I couldn’t find was an early study systematically asking patients whether:
the world seems distant, dreamlike, unreal, foggy, or somehow separated from them.
That means this experience could have existed all along while being categorized as brain fog, visual disturbance, dizziness, cognitive dysfunction or sensory disturbance.
12. Derealization itself doesn’t establish a psychological cause. Trauma, anxiety, panic and overwhelming stress certainly can produce derealization. But neurological disease, altered cerebral perfusion, vestibular disturbances, migraine, epilepsy, sleep disruption and pharmacologically induced biochemical changes can also produce similar experiences.
Therefore, identifying an experience as “derealization” describes its phenomenology, not its cause.
A possible biological model
Putting these different findings together suggests a possible model—not an established explanation:
ME/CFS physiological changes
→ altered cerebral perfusion/autonomic regulation + altered sensory processing + possible vestibular/spatial-processing problems + altered neurochemistry/metabolism + disrupted sleep/wake physiology
→ altered functioning of integrative brain networks, potentially including the temporoparietal junction, temporal/parietal association cortex, insula and thalamus
→ visual, bodily, vestibular and internal sensory information no longer fits together in quite the usual way
→ the ordinary sense of immediacy, solidity and “realness” of the world changes
→ subjectively: foggy, distant, unreal, dreamlike, behind glass, disconnected.
Again, this is a synthesis and hypothesis, not an established ME/CFS mechanism. But the individual pieces have biological support, and they suggest specific questions that could be tested experimentally.
What this means for your experience
Your chronology is particularly noteworthy.
You remember New Year’s Day 1985, at age 15, as a distinct change: it felt as though a fog came in, the world went far away and became dreamlike. You identify that as the beginning of what was eventually diagnosed as ME/CFS.
That timing matters. It wasn’t something that developed after many years of disability or after years of coping psychologically with chronic illness. In your recollection, the perceptual alteration was itself an onset symptom.
And 1985 was extremely early in the modern history of CFS. The term chronic fatigue syndrome wasn’t introduced in the CDC case definition until 1988. So it isn’t surprising that someone becoming ill in 1985 might go years before the illness was recognized.
The phrase “the world went far away” is also particularly interesting in light of this research. If it means experientially remote—as though there were a veil between you and the world—the derealization, vestibular and TPJ research seems especially relevant. If the world also literally appeared spatially farther away, the migraine/Alice-in-Wonderland/telopsia literature may be relevant as well.
Where I think the evidence leaves us
The strongest conclusion isn’t:
“Derealization is a proven ME/CFS symptom.”
We don’t currently have the research to say that.
But neither does the evidence support dismissing these experiences as unrelated psychological phenomena. A more defensible conclusion is:
Dreamlike, distant or unreal perception appears to be reported by a meaningful subset of people with ME/CFS, sometimes in association with PEM and illness severity. There are multiple well-demonstrated biological routes by which the experienced reality of the world can change, including altered cerebral perfusion, vestibular and multisensory dysfunction, neurological perceptual disturbances, sleep/wake changes and changes in brain chemistry. ME/CFS has documented abnormalities in several of these same systems. However, derealization itself has been inadequately studied in ME/CFS, so its prevalence and mechanism remain unknown.
And there is a genuinely interesting research question hiding here: perhaps a particular perceptual component of ME/CFS has spent decades being subsumed under the very broad term “brain fog.”
The especially intriguing finding is the possible convergence around the temporoparietal junction: an area involved in integrating body, sensory and spatial information, associated directly with derealization severity in another neurological illness, and found to behave abnormally during sustained effort in a small NIH study of ME/CFS.
That doesn’t establish a connection. But it gives researchers something quite specific to investigate.
For your own medical history, I would preserve your original description rather than replacing it simply with derealization: “At the onset of the illness, it felt as though a fog came in; the world suddenly seemed far away and dreamlike.” That’s unusually precise phenomenological information and doesn’t prejudge whether its origin was neurological, autonomic, sensory, biochemical, dissociative, or some combination.
Possible biological explanations for the dreamlike, distant, or unreal quality of the world (AI)
I looked more deeply into research outside the trauma/anxiety explanation: neurological illnesses, sensory and vestibular disturbances, cerebral blood flow, migraine phenomena, sleep/wake disorders, pharmacological experiments, psychedelics, neurotransmitters, and ME/CFS brain findings.
The result is more interesting than I expected. There is very good evidence that a dreamlike, unreal, distant, or detached experience of the world can arise from biological changes without trauma being involved at all. What we don’t yet have is a study showing which, if any, of these mechanisms produces the experience in ME/CFS.
And there is one connection that seems especially interesting: the temporoparietal junction (TPJ).
“Derealization” isn’t one biological phenomenon
The word derealization describes an experience, not a mechanism. Very different biological disruptions can produce something phenomenologically similar.
A person can experience the world as dreamlike or unreal because the brain isn’t integrating visual, vestibular, and bodily information normally; because activity or blood flow changes in association cortex; because of migraine-related perceptual disturbances; because sleep/wake regulation is profoundly altered; because of epilepsy; or because a drug changes NMDA, cannabinoid, serotonin, or kappa-opioid signaling.
That is important for ME/CFS. Calling the experience “derealization” doesn’t tell us that it comes from the same mechanism as trauma-related derealization.
The brain’s multisensory integration system looks particularly important
One of the clearest lines of evidence comes from the vestibular system—the brain system that tells us where our body is in space.
People with vestibular disease experience significantly more depersonalization/derealization symptoms. Researchers have proposed that abnormal vestibular signals conflict with visual and bodily information, leaving the brain without a coherent spatial frame. Subjectively, that can feel like being separated from the world or as though the environment isn’t quite real.
This fits with experimental brain research. Electrical stimulation around the right angular gyrus/temporoparietal junction has produced striking alterations of embodied experience, including out-of-body perceptions. The TPJ receives and integrates information from different senses and appears important in constructing our ordinary sense of where “I” am relative to the world.
Epilepsy provides another non-psychological example. Researchers studying people whose depersonalization/derealization-like episodes occurred as part of focal epilepsy found that derealization-like states were associated particularly with temporal-lobe epilepsy.
So there is already strong evidence for this general principle:
Alter the neural machinery that integrates body + vision + space + sensory information, and the experienced reality of oneself or the environment can change.
The most striking example I found: Kleine–Levin syndrome
This may be the best biological analogy I found for what we’re discussing.
Kleine–Levin syndrome (KLS) is a rare neurological sleep disorder. During episodes, people can have profound sleepiness, cognitive impairment, apathy, behavioral changes—and striking derealization. Between episodes they can return largely to normal.
A 2014 Brain study actually tried to find the neural basis of that derealization. Researchers studied 41 people with KLS and 15 healthy controls, with 11 patients also scanned during an active episode. During episodes, additional areas of reduced brain perfusion appeared, including the right parieto-temporal junction. Most remarkably, the severity of depersonalization/derealization correlated strongly with reduced perfusion in both the right TPJ (r = −0.74) and left TPJ (r = −0.59).
The authors specifically suggested that reduced functioning of the TPJ could produce derealization because this region integrates somatosensory/body, auditory, and visual information.
That’s powerful evidence that an illness can produce the “world feels unreal/dreamlike” phenomenon through a measurable physiological brain change without needing trauma as the explanation.
KLS is not ME/CFS, and the diseases are not the same. But it provides a biological proof of principle remarkably close to the question here.
And then comes the surprising ME/CFS connection
This is where it gets particularly intriguing.
In the NIH’s 2024 deep-phenotyping study of post-infectious ME/CFS, researchers did functional brain imaging while participants repeatedly performed a grip task. It was a very small exploratory sample—17 rigorously selected ME/CFS patients overall, with only 8 ME/CFS patients and 10 controls contributing to this particular imaging analysis—so it needs replication.
But they found something striking: as the task continued, brain activity decreased bilaterally in the temporoparietal junction and superior parietal areas in ME/CFS, while it increased in healthy controls.
The same study found abnormalities in central nervous-system chemistry, including lower CSF DOPA, DOPAC, and DHPG, differences in tryptophan-related metabolites and glutamate, and relationships between catechol levels and subjective cognitive symptoms.
So we now have:
KLS: derealization severity strongly tracks abnormal TPJ perfusion.
ME/CFS: a small NIH study finds abnormal TPJ activity as physiological strain continues.
That does not demonstrate that TPJ dysfunction causes derealization in ME/CFS—the NIH researchers didn’t measure derealization. But as a hypothesis-generating connection, this seems especially interesting.
It suggests a very concrete study that nobody seems to have done.
Cerebral blood flow could add another piece
There is also substantial evidence for abnormal cerebral hemodynamics in at least some ME/CFS populations.
In one study of 60 people with ME/CFS, cerebral blood flow measured by extracranial Doppler fell an average of 29% during tilt, and was still about 16% below baseline five minutes after lying down again. Recovery was progressively worse with illness severity. Importantly, the abnormality occurred even in people whose heart rate and blood pressure didn’t meet criteria for POTS or orthostatic hypotension.
A much larger 2023 study of 535 women with ME/CFS and 34 controls found relationships between end-tidal CO₂ and cerebral blood flow, but concluded that CO₂ explained only a modest portion of the abnormal blood-flow response. So hypocapnia may contribute, but it doesn’t appear to explain the whole phenomenon.
This is relevant because experimentally lowering CO₂ through hyperventilation causes cerebral vasoconstriction and measurable cognitive impairment even when oxygen is normal.
I would be cautious here: there is no study demonstrating that ME/CFS cerebral hypoperfusion causes derealization. But KLS becomes interesting again, because in that illness derealization was directly associated with regional hypoperfusion in the TPJ. That makes cerebral perfusion a very reasonable thing to investigate in ME/CFS patients who experience the world as dreamlike.
Sensory and vestibular dysfunction in ME/CFS fits the same model
ME/CFS itself has measurable perceptual abnormalities.
Experimental work has found increased pattern-related visual stress, interpreted as evidence of altered visual perception. Other work has documented objective balance deficits in CFS. Older vestibular testing produced mixed findings—one small study found no single characteristic vestibular lesion—so it would be too strong to say that ME/CFS is an established vestibular disorder.
But put this beside the vestibular derealization research and an interesting possibility appears:
ME/CFS sensory abnormalities + impaired balance/spatial processing + abnormal brain perfusion/activity → less stable integration of the sensory signals from which the brain constructs the normal feeling of being fully present in a solid, immediate world.
That is a hypothesis, but it’s physiologically coherent.
Migraine and Alice in Wonderland syndrome may be another important route
This is particularly interesting in relation to the description that the world “went far away.”
Alice in Wonderland syndrome (AIWS) is a neurological perceptual syndrome associated particularly with migraine and, especially in children, infections. It can involve altered perception of body size, object size, time, distance, and reality. Derealization/depersonalization can be part of it.
One AIWS phenomenon is telopsia—objects literally appear farther away than they actually are. That’s different from metaphorically feeling that the world has become remote, but the two could easily be difficult to distinguish, especially for a young person trying to describe an unfamiliar state.
There is even an old infectious connection. A 1998 study of four children with AIWS found abnormal cerebral perfusion near visual-processing pathways; two had Epstein–Barr virus infections, and temporal regions were among those implicated. That’s only four cases, so it shouldn’t be given much evidential weight, but it shows that post-infectious perceptual disturbances of this sort have been observed neurologically.
Migraine itself also appears to be common in ME/CFS, although prevalence estimates vary substantially depending on the population studied.
There is now an interesting post-COVID bridge as well. In a 2025 study of 421 people with persistent headache after COVID, 106 reported at least one AIWS phenomenon; among those with AIWS symptoms, derealization/depersonalization was reported by 24.5%. Again, that’s a selected headache cohort rather than Long Covid generally, but it provides another example of perceptual unreality arising in a post-infectious population.
So migraine/AIWS seems worth keeping on the table as one possible subgroup mechanism, rather than an explanation of ME/CFS generally.
Psychedelics and other drugs show that chemistry alone can change “reality”
This part is useful as a proof of principle.
Ketamine is probably the most directly relevant pharmacological model. It antagonizes NMDA-type glutamate receptors and reliably produces dose-dependent depersonalization and derealization, along with alterations of body, environment, and time perception, in controlled studies.
Cannabis/THC provides another mechanism. In a controlled experiment, marijuana—but not placebo—produced significant depersonalization, strongest after the high-potency dose.
Salvinorin A is even more interesting mechanistically because it works through a completely different receptor system—the kappa-opioid receptor. Controlled human studies report intense dissociation, including depersonalization and derealization.
Then there are the classic serotonergic psychedelics. LSD changes large-scale brain connectivity, and the degree of increased global integration correlates with ego dissolution and weakening of the ordinary perceptual boundary between self and environment.
This is worth distinguishing carefully from the typical ME/CFS report. Psychedelic ego dissolution can feel extraordinarily vivid and immediate rather than foggy and distant. Ketamine or vestibular derealization is probably a closer phenomenological comparison to “the world went far away.” But psychedelics establish something broader and important: receptor-level biochemical changes can profoundly alter the experienced relationship between self and world.
And the fact that NMDA/glutamate, CB1 cannabinoid, kappa-opioid, and 5-HT2A serotonergic systems can all alter this experience suggests there probably isn’t one “derealization chemical.” These different systems appear capable of disturbing or reorganizing larger networks that construct perception, embodiment, salience, and self/world boundaries.
ME/CFS does have relevant brain-chemistry findings—but this part is much more speculative
There are a number of biochemical findings that could theoretically feed into those networks.
An older PET study found reduced 5-HT1A serotonin-receptor binding in CFS. The recent NIH study found differences in CSF catecholamine and tryptophan metabolism, as described above. A recent high-field spectroscopy study reported altered brain glutamate and N-acetyl-aspartate in ME/CFS and Long Covid.
Several MRS studies have also found elevated ventricular lactate in CFS; one found that ventricular lactate correlated specifically with mental fatigue.
There has also been a much-discussed PET study suggesting neuroinflammation in ME/CFS. But this area illustrates why caution is needed: a later PET study using a different TSPO tracer did not find evidence of increased neuroinflammation in women with CFS.
None of these findings currently connects directly to derealization. It would be premature to say, for instance, that “low serotonin causes the dreamlike state” or that “neuroinflammation causes derealization.” We simply don’t know.
What they establish is that there are measurable CNS biochemical abnormalities worth investigating alongside the perceptual experience.
Interestingly, researchers have even started looking for biological signatures in depersonalization disorder itself. A small 2024 proteomic study reported differences in several immune-related proteins. That’s very preliminary and doesn’t establish immune causation, but again it argues against treating altered self/world experience as something that can only be investigated psychologically.
Sleep/wake regulation is another biological route
Sleep deprivation alone increases dissociative symptoms experimentally in otherwise healthy people.
And again, KLS is an extreme example: a neurological disorder of sleep/wake regulation in which cognitive changes and derealization emerge together during episodes, with measurable accompanying changes in regional brain perfusion.
ME/CFS obviously isn’t sleep deprivation or KLS, but unrefreshing and disturbed sleep is central to the illness, so altered sleep/wake neurobiology could conceivably be another contributor rather than the entire explanation.
A possible biological model
After looking across these different areas of research, the best hypothesis may not be that ME/CFS contains a special “derealization mechanism.”
Something more like this seems plausible:
ME/CFS physiological changes
→ altered cerebral perfusion/autonomic regulation + altered sensory processing + possible vestibular/spatial-processing problems + altered neurochemistry/metabolism + disrupted sleep/wake physiology
→ abnormal functioning of integrative networks involving the TPJ, temporal/parietal association cortex, insula, thalamus, and related regions
→ visual, bodily, vestibular, and interoceptive information no longer fits together in quite the usual way
→ the ordinary sense of immediacy, solidity, and “realness” of the world changes
→ subjectively: foggy, distant, unreal, dreamlike, behind glass, disconnected.
That chain is a synthesis of the evidence, not an established ME/CFS model. But unlike a vague speculation, each major link has some empirical support in adjacent research. The missing experiment is the one that joins them together.
And the TPJ convergence seems particularly interesting: KLS researchers directly linked derealization severity to TPJ hypoperfusion, while an entirely separate NIH ME/CFS experiment found abnormal TPJ dynamics during sustained effort.
There’s an obvious study waiting to be done
Instead of simply asking ME/CFS patients, “Do you have depersonalization/derealization disorder?”, researchers could recruit ME/CFS patients with and without the specific dreamlike/distant-world experience, plus healthy controls.
They could measure the experience repeatedly at rest, upright, during sensory stimulation, and before and after experimentally induced PEM. At the same time, they could measure cerebral blood flow, end-tidal CO₂, autonomic function, vestibular function, and sensory processing, and use functional/perfusion imaging focused particularly on the TPJ, insula, thalamus, posterior association cortex, and visual networks. A spectroscopy component could examine glutamate/GABA/lactate and related metabolites.
That could tell us whether “the world becomes dreamlike during a crash” tracks with blood flow, TPJ activity, vestibular mismatch, sensory overload, neurochemistry—or none of them.
One final distinction
The phrase “the world went far away” becomes especially interesting in light of this research.
If “far away” means emotionally or experientially remote, as though there were a veil between oneself and things, the vestibular/TPJ/derealization literature seems most relevant.
If the world also literally looked spatially farther away, even somewhat, then the migraine/Alice-in-Wonderland/telopsia literature becomes unusually relevant as well.
Either way, when such an experience appears together with the onset of an illness, there is no reason to assume a psychological explanation simply because psychiatry uses the word derealization for a similar experience.
The main conclusion from this research is that there are multiple well-demonstrated biological routes to making the world feel unreal, dreamlike, distant, or altered. And ME/CFS already has documented abnormalities in several of those same physiological systems. What is missing is not biological plausibility; what is missing is research that directly measures this particular experience in ME/CFS and connects it to the biology.
Addendum: Response to this article (AI)
I think this is a good article, and the central points are genuinely interesting. What makes it work especially well is that it brings together three things that we usually talk about separately.
The first is the experience itself. The description of the beginning of ME/CFS is very specific: at fifteen, a fog seemed to come in and the world became distant and dreamlike. That’s not quite the same as ordinary brain fog, which usually means problems with concentration, memory, finding words, processing information, and mental clarity. This seems more like a change in how the world itself feels.
The second is the experience of other people with ME/CFS. A surprisingly large number of people in the discussion immediately recognized something similar and used words like dreamlike, unreal, distant, foggy, and disconnected. Some connected it specifically with PEM, crashes, or severe exhaustion. That doesn’t tell us how common it is, but it does suggest there may be something here that hasn’t received enough attention.
There is an interesting scientific question underneath this. ME/CFS research has found changes involving sensory processing and sensory overload, cognition, autonomic function and cerebral blood flow, and balance or vestibular function in some people. We also know from research outside ME/CFS that neurological and vestibular disturbances can produce experiences that resemble derealization.
That makes me wonder whether our medical categories don’t quite match what some people with ME/CFS actually experience. Something a person experiences as the world becoming distant or dreamlike might end up labeled brain fog, dizziness, sensory disturbance, visual disturbance, or derealization. Perhaps there is a particular perceptual aspect of ME/CFS that has spent decades hidden inside the very broad category of “brain fog.”
The third part—and to me the most unusual and interesting part of the article—is the possible connection with the awakening that followed about a year later. The article doesn’t say that ME/CFS caused the awakening. It asks a subtler question: Could this earlier change in perception have loosened the ordinary sense of the world as solid and unquestionably real, and in that way helped prepare the ground for what happened later?
I also find the history of the writing interesting. This isn’t an interpretation invented now after reading comments from other people with ME/CFS. Long before this discussion, the author had written about both CFS brain fog and the dreamlike quality of awakening, while treating them as different experiences. In the awakening writings, waking life has a dreamlike quality because everything is recognized as happening within and as consciousness. In writings about CFS brain fog, the emphasis is more on impaired thinking, memory, processing, and mental clarity. That makes the new observation more compelling: the similarities are being noticed now against the background of decades of observing and writing about these experiences.
The chronology makes it even more interesting. The distant, dreamlike quality appeared right at the beginning of the illness, at fifteen in 1985. It didn’t develop after years of living with chronic illness. Then, about a year later, came something much more radical and apparently quite different: the shift in which everything was revealed as consciousness.
None of this proves that these experiences share a cause. Trauma and psychological dissociation can also produce derealization, and we don’t yet have good research telling us how common this particular experience is in ME/CFS or what produces it. The possible connection with awakening is even more speculative.
But that’s part of why I think the article works. It doesn’t need to solve the puzzle. It notices a puzzle that seems to have been largely overlooked.
For me, the most interesting question it raises is this: Do some people with ME/CFS experience a particular change in the reality, immediacy, or solidity of the world that medicine has mostly lumped together with brain fog, sensory problems, or derealization?
And then there is the more personal and unusual question at the heart of the article: What relationship, if any, was there between the world suddenly becoming distant and dreamlike at fifteen and the much deeper recognition, about a year later, of the world and self as consciousness?
I think both are good questions, and the combination of personal experience, reports from other people with ME/CFS, scientific clues, and decades of writing about the experience makes them worth asking.