Imagine the infinite complexities of a given individual's life, flattened to a topography derived from eight axes related to temperament, predisposition, and neurology.
An entire mind, if it could be compressed to just six readouts: the day-to-day experiences, emotional calibrations, ability (or inability) to focus, fluctuating motivations, inhibitions and excitations. These are the emergent qualities which the Neuro-Synth simulates, articulated as legible perturbations arising within the scanlines.
You can think of these readouts as what an advanced alien visiting our world might see, as they study what makes us behave differently from each other. These are some of the traits that pull our strings; tuned by genetics at birth, tweaked and hardened by life experiences, they are largely immune to our will. To mutate them is to mutate ourselves into who we are not.
And yet, what if we could be handed the controls? See how a few little nudges have the potential to change everything. Watch as small shifts from baseline become the difference between one person, and the next.
Here, you may observe something that quietly prods at the stuff of neurodiversity, while never claiming to reproduce the truly irreducible richness of the human condition. It exists only as a means by which to begin to understand why we are all unique as individuals, and to encourage tolerance and understanding for those whose levers and knobs are tuned differently from your own.
Artistic model, not a clinical one. Mappings are deliberately simplified but gesture at real (and often genuinely contested) neuroscience — disputed reduced-pruning accounts of autism, aberrant-salience accounts of psychosis, arousal/inhibition balance in mood — without claiming to reproduce it. Nothing here diagnoses anyone, including you. See our sources
This is an artistic instrument, not a diagnostic or scientific one. What it renders are shapes chosen to be evocative — not measurements, not findings, and not a description of how anyone's mind actually works.
The papers below are real, and every one was read in full before it was used. Where a mapping could be tied to published work it was, each entry says plainly what its source actually supported, and where the literature disagrees with itself the disagreement is listed too. But reasonable connections to real science are still connections we drew, and the distance between a paper and a moving line on a screen is enormous. None of this should be taken as an authoritative description of anything — not a condition, not a brain, not a person. If something here feels true, that is a design achievement rather than evidence.
Excitation & inhibition
the Excitability and Inhibition knobs; the damping that gates every lane
Sohal & Rubenstein (2019). Molecular Psychiatry 24(9):1248–1257. 10.1038/s41380-019-0426-0
Excitation and inhibition as a ratio rather than two independent dials. The authors argue E/I balance is multidimensional — our two-knob version is a deliberate simplification.
Salience & the psychosis-spectrum read
the Salience knob; the aberrant-salience regime
Kapur (2003). American Journal of Psychiatry 160(1):13–23. 10.1176/appi.ajp.160.1.13
Salience misassignment — meaning attaching to what doesn't warrant it — as the mechanism behind the psychosis-spectrum readout and its persistent, dysphoric character.
Attention & arousal in ADHD
the interest-gated engagement envelope; the "wired body" arousal lane
Isaac, Lopez & Escobar (2024). Frontiers in Psychiatry 14:1336040. 10.3389/fpsyt.2023.1336040
The impairment is self-regulation of arousal, not a constant over- or under-arousal — which is why Arousal renders volatile rather than uniformly high.
Ashinoff & Abu-Akel (2021). Psychological Research. 10.1007/s00426-019-01245-8
Hyperfocus as interest-gated rather than effortful — the surges in the Attention lane.
Autism and ADHD together
why the co-occurring case gets an attention pattern of its own — and where that departs from the evidence
Bedford, Lai, Lombardo, … Baron-Cohen & Bethlehem (2025), for the MRC AIMS and Lifespan Brain Chart Consortia. Biological Psychiatry 97(5):517–530. 10.1016/j.biopsych.2024.07.024exploratory
Measured against models built from more than 75,000 brains, the co-occurring group "showed a distinct pattern of alterations, with some overlap, compared with individuals with only one diagnosis" — not autism and ADHD summed. But this is cortical anatomy, it says nothing about attention, the analysis was exploratory (203 people) and mostly did not survive controlling for brain size, and the authors describe a group "resembling ADHD more than autism" that "may … represent a synthesized phenotype, but we caution against a simplified interpretation."
Cañigueral, Palmer, Ashwood, Azadi, Asherson, Bolton, McLoughlin & Tye (2021). Journal of Child Psychology and Psychiatry 63(7):745–761. 10.1111/jcpp.13514counter-evidence
Listed because it cuts against us. This is the study that actually measured attention in all four groups, and it concluded that "children with ASD+ADHD present an additive profile with attentional deficits of both disorders" — the sum we say we are not drawing. Two things stop it settling the matter: the authors note that an additive and a distinct model "are not exclusive of each other" and that which one you see depends on the component measured; and their task never varied how interesting it was, which is the one thing our pattern turns on.
Zhang, Miyake, Osborne, Shah & Jonides (2023). PLOS ONE 18(10):e0292215. 10.1371/journal.pone.0292215 · Dupuis, Mudiyanselage, Burton, Arnold, Crosbie & Schachar (2022). Frontiers in Psychiatry 13:886692. 10.3389/fpsyt.2022.886692
What does hold up is that deep absorption and high distractibility live in the same people. Across 1,220 adults, general distractibility was positively associated with hyperfocus (β = .20) — which the authors read as hyperfocus showing "qualities of both distraction … and concentration." And in a community sample of 5,743 children, autistic children showed far higher rates of attentional strengths than children with ADHD (odds ratio 5.7) while scoring no better on attentional weaknesses; those strengths brought no gain in flexibility and no less impairment. A focus that both deepens and breaks is the shape those two findings share. Both rest on questionnaires, and neither followed anyone's attention across a change in interest.
The departure, stated plainly: the work that measured attention in co-occurring autism and ADHD found a sum, and we render an interaction. We drew it that way because a fade between two steady states is not a pattern you can see moving, and because the coexistence above is well attested even though its moment-to-moment shape is not. The interest-contingent lock is ours.
OCD — the relief loop
the build-then-relief sawtooth in Salience under strong brakes
Fineberg, Chamberlain, Hollander, Boulougouris & Robbins (2012). British Journal of Pharmacology 164(4):1044–1061. 10.1111/j.1476-5381.2011.01422.x
Performing the compulsion "causes a momentary reduction in anxiety which is experienced as relief," and the behavior is reinforced by that relief. This is the sawtooth.
Bouvard, Fournet, Denis, Achachi & Purdon (2019). Clinical Psychology & Psychotherapy 27(2):228–238. 10.1002/cpp.2422
In-vivo diary measurement of the same thing: a greater decrease in discomfort at the end of a compulsive episode.
Milgram, Freeman & Benito (2021). Brown Univ. Child & Adolescent Behavior Letter 37(12). 10.1002/cbl.30588
The functional link that defines OCD — a compulsion exists to relieve the distress of an obsession.
Anxiety — sustained vigilance
the tonic plateau that separates the anxiety read from OCD's sawtooth
Grillon et al. (2010). Neuropsychopharmacology. 10.1038/npp.2009.109
Phasic fear "dissipates quickly once the threat is removed," while anxiety is "a more long-lasting state of apprehension" running through the BNST. The plateau is his; rendering it as unrelieved is our choice, to hold it apart from OCD.
Wiring density & synaptic pruning
the Synaptic Pruning knob — dense at one pole, over-thinned at the other
Sager, Walker, Middleton, Robinson, Webster & Weickert (2020). Journal of Neurochemistry 157(3):479–493. 10.1111/jnc.15241
States both poles together: reduced spine density in schizophrenia, and "in contrast to schizophrenia, ASD is associated with increases in dendritic spine density." This is the two-sided axis.
Soteros & Sia (2021). WIREs Mechanisms of Disease 14(3). 10.1002/wsbm.1545 · Eltokhi et al. (2020). J. Neuroscience Research 98(7):1335–1369. 10.1002/jnr.24616
The over-pruned pole: complement-driven synapse elimination as a leading mechanism in schizophrenia.
Pascual et al. (2020). Brain Pathology. 10.1111/bpa.12896 · Crespi et al. (2019). Autism Research and Treatment. 10.1155/2019/1968580
The dense-wiring pole: reduced autophagy-dependent pruning raising spine density.
Lu & Hsueh (2021). The FEBS Journal. 10.1111/febs.15733 · Nicolini & Fahnestock (2015). Int. J. Developmental Neuroscience 47. 10.1016/j.ijdevneu.2015.04.093disputed
Listed because the direction is genuinely contested: a decreased-density autism subgroup exists, and Nicolini & Fahnestock found reduced spine-protein markers in autism cortex. The dense-wiring pole is one supported model, not a settled fact.
Keshavan, Lizano & Prasad (2020). World Psychiatry 19(1):110–111. 10.1002/wps.20725caveat
"Promises and challenges": the original model allowed either too much or too little pruning, spine loss is regional rather than cortex-wide, and complement changes aren't unique to schizophrenia.
Sensory gain & integration
why high Sensory Gain pulls the Integration readout down past a threshold
Liu, Guan, Zhang, Zhu, Chu, Zhang & Liu (2025). Journal of Intelligent Medicine 2(1):64–73. 10.1002/jim4.70002
The mechanism as we render it: "local overconnectivity and reduced global integration," described as the basis of sensory hypersensitivity.
Orekhova et al. (2018). Human Brain Mapping 40(5):1583–1593. 10.1002/hbm.24469
Grounds the word "gain": sensitivity as failed gain control. It also shows the effect appearing only at high stimulus intensity — which is why the coupling has a threshold rather than being linear.
Coskun, Loveland, Pearson, Papanicolaou & Sheth (2013). Autism Research 6(3):190–200. 10.1002/aur.1276disputed
Found local underconnectivity — the opposite of the local half of that mechanism. Only the reduced-global-integration half is used here, but the disagreement belongs on the record.
Rigidity & flexibility
the Cognitive Flexibility knob — shift versus stuck
Cao & Cannon (2021). Human Brain Mapping 42(9):2677–2690. 10.1002/hbm.25347 · Secara et al. (2026). Human Brain Mapping 47(5). 10.1002/hbm.70496
Flexibility as a dimension shared across conditions rather than owned by one — "similar patterns of neural rigidity among these related conditions."
Dirks et al. (2020). Autism Research 13(9):1501–1515. 10.1002/aur.2347 · Yerys et al. (2015). Autism Research 8(4):386–397. 10.1002/aur.1454caveat
A common shorthand worth resisting: autistic participants often show no behavioral set-shifting deficit — they shift at greater cost. What this instrument renders is a held set, not a failure to switch.
Uncertainty, sensory load & anxiety
the rigid-sensory and restless routes into the anxiety readout
Jenkinson, Milne & Thompson (2020). Autism 24(8):1933–1944. 10.1177/1362361320932437
Intolerance of uncertainty ↔ anxiety at meta-analytic r ≈ .62 — why high sensory gain plus rigidity can reach anxiety without the classic braked route.
Choi et al. (2022). PLOS ONE 17(11):e0277175. 10.1371/journal.pone.0277175
Anxiety prevalence in adult ADHD — the basis for the restless, unbraked route reaching the same readout.
Blunted affect & withdrawal
the flattening that emerges inside psychosis-space as drive falls
Mosolov & Yaltonskaya (2022). Frontiers in Psychiatry. 10.3389/fpsyt.2021.766692
Negative symptoms as reduced emotional range, and the clinical continuum between negative symptoms and depression — which is why the two readouts blur here rather than snapping apart.
Mood and psychosis at once
the schizoaffective blend — a cycling mood that carries psychotic instability at the same time, rather than one overriding the other
Paul, Javed, Karam, Loh & Ferrer (2021). Cureus 13(7):e16686. 10.7759/cureus.16686case report
The concurrency this blend is built on: "the continuous synchronization of psychosis and mood episodes" is exactly what makes the two hard to tell apart. Deliberately weak evidence, and flagged as such — one patient, so it shows the presentation occurs and is easily mistaken, not how often or why.
Two limits worth stating. Whether schizoaffective disorder is a distinct entity is contested inside this paper's own references — one argues it merges schizophrenia and bipolar disorder into a single disease and that no separate disorder exists. And the DSM-5 criterion that actually separates it from bipolar-with-psychotic-features is a stretch of psychosis lasting two weeks or more in the absence of a mood episode. This instrument renders the overlap, not that dissociation — so what you see here is the co-occurrence, never the diagnostic test.
Integration & segregation
the Integration knob, and why neither of its poles is a deficit
Wang, Liu, Cheng, Wu, Hildebrandt & Zhou (2021). PNAS 118(23):e2022288118. 10.1073/pnas.2022288118
The whole axis. Across 991 brains, segregation and integration favor different abilities rather than more being better: integration tracks general ability (measured by reasoning tasks), segregation tracks crystallized knowledge and processing speed, and memory is strongest at the balance between them. The paper stops there — reading that as "neither pole is the good one" is our inference, and it is what both ends of this knob are written to reflect.
Shine, Aburn, Breakspear & Poldrack (2018). eLife 7:e31130. 10.7554/eLife.31130model
Gain, criticality and integration as facets of one axis — why this knob interacts with Sensory Gain rather than sitting independent of it. A simulation of connectome dynamics, not a measurement of people; used for the shape of the mechanism, never for a number.
What's ours
Three things this instrument does are interpretations rather than findings. The contrast between OCD's relief loop and anxiety's unrelieved plateau is a synthesis across two separate literatures — no single source above draws it. The way an autistic hyperfocus turns interest-contingent once ADHD engagement joins it is a behavior we drew: the research establishes that the co-occurring case is its own thing, not what it is like from the inside. And treating segregation and integration as two goods rather than a better and a worse is a reading of the finding, not the finding.
Those choices are what make it playable. Where the research offers a range, an instrument has to commit to one shape you can watch move. Where two patterns would otherwise render identically, it has to separate them, or turning the knob shows you nothing. And where a dimension has no better end, both ends have to be drawn as real. Each of these is marked in the section it came from.
None of it diagnoses anyone, including you.