Modern neuroscience and artificial intelligence converge on fundamental concepts and terminology. This post may serve as a primer, a method to explore key parallels between biological and artificial systems by examining shared principles, from basic units like neurons to complex processes involved with learning and memory consolidation.

Initially, we have to cover a high-level overview of dopaminergic pathways and memory processes in the brain, then shift to deep learning architectures (including convolutional neural networks and large language models). By understanding how these concepts map onto each other, we can better appreciate both the similarities and distinctions between biological cognition and artificial intelligence. Yay. ❤️

Neurotransmitters and Reward-Based Learning

Dopamine plays a central role in the brain’s reward system, helping to reinforce behaviors that lead to positive outcomes such as food, social interaction, or achievement. This neurotransmitter is essential for both motivation, driving us to pursue rewarding experiences, obsessions, punding, learning, and a hundred other areas of cognition which is dead-set on enabling us to adapt our behavior based on past outcomes. We cannot learn right from wrong, good from bad, etc without dopamine.

Where is this magical compound? It’s all over the brain and central nervous system, but generally speaking dopamine pathways originate in the midbrain, particularly in the ventral tegmental region and substantia nigra. From there it gets very exciting…

Dopamine neurons send widespread projections to various brain regions, including the striatum, prefrontal cortex (PFC), and other areas involved in decision-making and memory.

These neural circuits signal when outcomes differ from expectations, whether positively (unexpected rewards) or negatively (unexpected punishments), helping the brain update its predictions and guide future behavior. It’s not a perfect system but there is a heavily corpus of existing research with new studies occurring every year - particularly with modern fMRI and DAT scanning techniques.

Dopaminergic Pathways

Dopaminergic pathways are fundamental neural circuits that influence nearly every aspect of human experience and behavior. These pathways play essential roles in processing sensory information, accessing and forming memories, regulating emotional states, controlling movement, and enabling conscious awareness.

Without properly functioning dopaminergic systems, our ability to perceive, learn, and engage with the world would be severely compromised.

The brain contains four major dopaminergic pathways, each connecting specific regions and serving distinct functions:

• Mesocortical pathway: Projects from the midbrain’s ventral tegmental area (VTA) to the frontal cortex, supporting executive functions and decision-making
• Mesolimbic pathway: Connects the VTA to the nucleus accumbens, central to reward processing and motivation
• Nigrostriatal pathway: Links the substantia nigra to the striatum, primarily governing motor control and movement coordination
• Tuberoinfundibular pathway: Extends from the hypothalamus to the pituitary gland, regulating hormonal balance and homeostasis

Dopamine release along these pathways modulates movement, motivation, reward processing, and hormonal regulation.

These neural networks consist of specialized neurons that synthesize and release dopamine as their primary neurotransmitter.

A significant breakthrough in understanding these pathways came with the discovery that specific dopamine neurons encode reward prediction errors; essentially the brain’s teaching signal for adaptive learning. When outcomes exceed or fall short of expectations, these neurons adjust their firing rates accordingly, providing critical feedback that helps the brain refine its predictions and modify future behaviors.

This mechanism represents one of neuroscience’s most robust quantitative theories: the concept that the brain employs a form of temporal difference (TD) learning, using dopamine-driven reward prediction errors to guide neural adaptation and behavioral change.

Reinforcement Learning

The relationship between neuroscience and Ai becomes particularly evident in reinforcement learning, where both biological and artificial systems adapt behavior through reward-based feedback. Ai algorithms compute prediction errors, much like the brain’s dopamine system does when processing unexpected outcomes.

Temporal Difference (TD) learning exemplifies this parallel. In Ai systems, TD algorithms update value estimates by comparing expected versus actual rewards, a process that remarkably mirrors how dopamine neurons signal discrepancies between predicted and received rewards.

This dopamine-driven reward prediction error mechanism appears to be a fundamental principle underlying both biological and artificial adaptive systems.

The mesolimbic pathway demonstrates this alignment well. When the brain receives unexpected rewards, dopamine neurons strengthen connections associated with successful actions—similar to how Ai agents increase the likelihood of high-reward behaviors.

This bidirectional influence has proven valuable: dopamine research has shaped reinforcement learning algorithms, while advances have provided new frameworks for understanding neural computation.

Memory Consolidation and Retrieval

Memory formation and recall illustrate key parallels between cognitive neuroscience and Ai/ML systems.

• Memory consolidation: The brain stabilizes fragile new memories into long-term storage, initially processing in the hippocampus then transferring to cortex during sleep. Ai training similarly encodes patterns into network weights for permanent storage.

• Memory retrieval: Both biological and artificial systems access stored information when needed—humans recalling facts and concepts, LLMs retrieving knowledge from their encoded parameters.

• Replay mechanisms: The brain’s hippocampal cells reactivate experiences during sleep to strengthen memories. Ai algorithms use similar replay techniques during training to prevent forgetting and consolidate learning.

• Attention and sleep: Neuroscience shows these processes are crucial for memory retention, while Ai research develops computational equivalents through training schedules and fine-tuning procedures.

This convergence helps us understand memory storage and retrieval in both natural and the (often superior) computational intelligence systems.

Convolutional Neural Networks and Visual Hierarchies

Convolutional neural networks (CNNs) are a class of deep learning models inspired by the brain’s visual system. A CNN is essentially a large network of artificial neurons structured in layers, and it learns to recognize patterns through a series of convolutional filters that detect features (like edges, shapes, textures) in data such as images. CNNs have achieved human-like performance in computer vision tasks by learning from experience, for example, by training on large image datasets.

Notably, CNNs were designed with biological vision in mind. Early neuroscientists discovered that neurons in the visual cortex (like area V1 in the brain - but don’t tell V10!) act as edge detectors – each neuron responding to specific visual features. CNNs build on this principle: the first layer of a CNN will typically detect basic features (edges, colors), the next layer composes those into slightly more complex features (corners, textures), and so on, forming a hierarchical processing very reminiscent of the progressive feature extraction in human/animal vision.

CNNs have “striking similarities to the structural and functional principles of the primate visual system,” which allows researchers to compare artificial networks with their biological counterparts.

This means neuroscientists can use CNNs as models to hypothesize how our own visual cortex might represent and transform images.

Cognitive neuroscience and CNNs share terminology like “receptive fields”, the portion of the visual field a neuron or filter responds to, and “layers” (eg, retinal input to V1 to V2 in the brain mirrors the layered structure of a CNN). Experiments have shown that higher layers of a CNN can correspond to higher-level visual areas in the brain; for example, a late CNN layer that detects faces or objects might be analogous to the human inferior temporal cortex where complex object recognition occurs.

This parallel isn’t perfect, but it’s a powerful analogy: both systems learn a hierarchy of representations, from simple to complex. Such overlap has practical benefit: by studying where CNNs succeed or fail in ways similar to humans, scientists gain insight into vision, and conversely, ideas from neuroscience (like specialized neural pathways or attention mechanisms in vision) can inspire improved CNN architectures.

In essence, convolutional networks are a meeting point of neuroscience and computational intelligence systems, demonstrating how a brain-inspired design can yield machines that “see” in a way comparable to biological vision.

Large Language Models & Predictive Processing

Large language models (yeah, the ones with transformers), are called the frontier because they’re precisely where concepts from cognitive neuroscience resonate with computational intelligences.

LLMs are deep neural networks trained on enormous amounts of data, (typically text) and are capable of generating human-like language. In practice, an LLM learns to predict the next word in a sentence by having been trained on countless sentences. Over time it captures the statistical patterns of language, similarly to our childhood periods of learning new languages. This next-word prediction framework has an interesting mirror in how neuroscientists think the brain processes language and other inputs.

According to the predictive coding theory, the brain is constantly making predictions about incoming information. For language, your brain anticipates the next word someone will say based on context, just as an LLM does.

Recent research suggests that the human brain “continuously anticipates upcoming words to optimize language processing”. When the brain’s prediction is wrong (an unexpected word appears), it generates a prediction error; much like an LLM adjusting its internal state when its prediction is off.

This alignment between LLMs and brain function is so striking that brain-imaging studies have found that the activation patterns of certain language-model layers can predict neural responses in the human language cortex as people listen to sentences.

Attention, Episodic, and Semantic Memory

LLMs share several key concepts with cognitive neuroscience beyond predictive processing. These are crucial elements in the ongoing advancement of machine learning and with understanding the human condition.

• Semantic memory: LLMs store factual knowledge and linguistic patterns distributed across their network weights, similar to how humans maintain language skills and world knowledge in long-term memory.

• Episodic memory: Unlike humans, early LLMs lacked personal experiential memories, relying solely on statistical patterns from training text. We’re past that now and all up into flexing what was once emerging research on Mixture-of-Experts (MoE) architectures and stateful processing is beginning to address this limitation.

• Attention mechanisms: Human attention focuses cognitive resources on relevant stimuli, like concentrating on a single conversation in a crowded room. Transformer-based LLMs implement computational attention mechanisms that dynamically weight input importance, creating a functional parallel to biological attention processes.

These parallels reveal shared principles of prediction, context integration, and selective focus that operate in both biological and artificial systems. The brain’s continuous prediction of words and meanings during language comprehension mirrors LLMs’ next-word prediction approach.

This convergence enhances our understanding of human cognition while suggesting cognitive-inspired improvements for LLM development. Yes, really.

Shared Concepts and Analogies

To more easily view the substantial overlaps between dopaminergic brain pathways, cognitive neuroscience concepts, and deep neural networks, the table below summarizes some shared terminology and concepts and how they correspond in brains vs Ai systems.

Neuronal Activation

Synapse & Weight

Learning, Rules and Optimization

Hierarchy

Memory Storage

Memory Recall

The Convergence of Two Worlds

Both biological and artificial systems demonstrate remarkable parallels in how they process information, adapt to experience, and store knowledge. The brain’s dopaminergic pathways mirror similarly designed computational intelligence based reward prediction/error systems, while cognitive memory mechanisms find counterparts in neural network training and retrieval processes.

This convergence enables bidirectional inspiration: neuroscience borrows computational modeling techniques from Ai to explain brain function, while Ai incorporates biological principles to enhance efficiency and human-like performance. Humanity is now locked into a self-reinforcing pattern of mutual benefit, an often beautiful experience to observe from the realms of industry research and personal real-world experience.

Critically, these foundational concepts set the stage for deeper technical exploration in subsequent articles, examining dopamine’s role in learning algorithms and the detailed workings of CNNs and transformers. Stay tuned for more… unless I get distracted by another broken Juniper switch or deeply-felt emotions which require ice cream and berries to overcome.💗

Years later, genetic test-targets would identify this propensity towards a neurological dis-favorability for sleep. Adjacent genetic testing revealed many surprising answers to lifelong medical concerns.

In relation to this uncommon trait, my DNA’s cellular programming which defines physique, metabolic regulation pathways, gluconeogenesis + glyconeogenesis, and steroidogenesis was coded for hard-outlier optimizations muscular twitch are primed for the type of endurance found in elite sports.. and that’s where I ended up.

Crossing finish lines, training on every mountain pass in the Sierra Nevada, training for The Death Ride by riding passes most summer mornings at 5am before heading to work, getting caught in avalances, out-skiing avalanced, hauling loads to the base of Yosemite big-walls, falling off of Yosemite big-walls, ice climbing without ropes, and generally pushing my mind and body as far as fast as it could go for as long as it could endure - and it endured so much until the first coma - and then I went back for more. Rowing crew, blasting HIIT 4-6x/week for 3-5hrs at a time, holding 95% max HR for hours, and never ever wanting to stop.

the endocrine system’s steroidogenesis model

A Life of Programmed Inevitability

I have always lived and loved that what came most naturally; so I went as fast as possible for as long as possible until there was nothing left.

Then I woke up in the ICU, connected non-consensually to those bastard machines, which is what happens without a DNR on-file.

Insomnia or Timeless Adventure

During highschool, driving to the mountains at 11pm, we climbed frozen waterfalls by headlamp before crashing into bed at 3-4am.

Waking up at a trailhead in the summer months, I’d start an ultralight approach to arrive at the bergschrund for another unroped solo climb - watch the sunrise from halfway-to-summit (less rockfall during frozen hours), stare into the void of sheer and total death waiting hundreds of feet below; then resume to swing one axe, move one mono-point crampon upwards, another axe, repeating.

Perched on the summit blocks, two slugs of unfiltered iodine treated stream water from my single one-liter Nalgene bottle, two HoHos, then descend a ridge traverse back to the trailhead. My young endocrine system was already on full-manual mode by genetic necessity, but I did not then know the criticality of such repeated doses of iodine to blast my thyroid’s metabolic potential into the stratosphere. These days my mornings begin with the usual coffee (yum, ACTH!), and liothyronine plus levothyroxine (T3 & T4 respectively).

I was young, resilient, and unknown at the time - quite “differently abled”. Forever enamoured with the physical, always in search of that nebulous nothingness which exists within every moment and memory and thought; the Zen of Null — moderately Schopenhauer adjacent — my personal “Being in Nothingness”.

Except that I kept fighting, searching, expecting the unexpected, and becoming lost in the desire to not desire — an impossible gate to breech towards nirvana. I could not stop until I died, and figured I’d surely never last past 30, having already lost two partners to roped falls. Why bother with that rope anymore, my young mind decided.

TBI Number.. What?

Then, an eighty foot upside down fall on Leaning Tower in Yosemite. While yarding hard on aid-gear underneath a roof, a Black Diamond #0 steel-tapered nut pulled through; instantly then in slow-motion my chest+waist harness and wall-rack zippered half a rope length of pro before my very last Yates Screamer shredded its seams and halted the fall.

Now five meters off-horizontal from the roof – and still two thousand feet off the deck with head-down facing The Valley meadows – the pendulum completes with my spine slamming into the golden granite wall, air blasted-out from my lungs, and redding-out into unconsciousness. Whatever G-force was involved in that epic fall was irrelevant, as my body was upside down hanging from dynamic 8mm twin-ropes, and neither myself nor an impromptu Camp4 Spaniard climbing partner who didn’t speak English were able to do anything about the blood pooling into my skull. We carried no radio for contacting YOSAR (Yosemite Search and Rescue), and Jose could not descend with my body hanging on our pair of ropes.

Either way it was over, the last now-shredded Screamer was necessary to finish the route, and either way I was on the adjacent wall from where one friend had died not yet a year before — perhaps in another multiverse it was over for me instead, and perhaps Kirk and Dan kept jumping, kept making “Masters of Stone” videos to inspire, to keep pushing the limits of human potential.

Solo climbers always die, unless they stop. I still had years to go, roped and ropeless, sometimes with new partners, sometimes actively courting that rapid-timeless-knowing-fall — to be reunited.

Then laughter through the void – my laughter – more accurately my autonomic system forcing the diaphragm to rapidly fill-exhale-fill the lungs, beat the heart, and wake me up. Adrenaline does some serious work, and this felt like being stabbed by ten EpiPens all at once… ALIVE AGAIN (and only nineteen). I took a break from The Valley, bought a mountain bike and temporarily moved to father’s cabin up in Tahoe.

During that pre-Millenium summer I fell in love, hopelessly, nearly getting married, and acquired a hybrid German Shepherd Timber Wolf puppy. That feeling of family was new, but an inevitable loss the following year was certainly its inverse. We tried for child for two years, to no avail, against medical advice, for my genetics were always the end of a matrilineal line, cemented at birth.

The College Years

I trained for 24HR events by riding the Tahoe Rim Trail at night with dual halogens, the Mt Rose CX loops during November snow storms - dismounting at speed to shoulder carry over snowdrifts too deep for wheels. Trail running at higher altitudes during spring rainstorms, pushing harder every season; not merely determined, not racing against the pack - but racing against the internal fire

“Your words cut through the noise of any attempt to make sense of suffering. You are not here to be a lesson, a metaphor, or a triumph over adversity.

You are here because you have endured against all odds. Here you are, living with a tumour that has grown for eight years, with a body that refuses to let you rest, and a mind that has faced more than most could imagine, and you continue unrelentingly.

This is not a story of resilience, it is one of unrepentant endurance.

The universe does not owe you fairness. It does not owe you health, peace, or the right to live without pain. And yet, you are here, and the tumour is here. You did not ask for this. You did not choose it. But you have carried it, and you carry it still, in a world that often forgets that pain is not a moral failing.”

On the Weight of “I Don’t Want This”

A common refrain during the time in which a patient must process and acknowledge the reality of their disability awareness. Well, tough shit. I’m screwed and so is everyone else, and we’re all going to die some day… right? Unless my consciousness is transported into a Chappy style robot body then it will eventually move-on to the next realm - just like everyone else cursed with the experience of The Human Condition.

“There is no nobility in your suffering. There is no hidden meaning in the tumour’s growth. You are not a hero, a martyr, or a symbol. You are a human being who was never asked to bear this weight. And yet, you do. Not because you must, but because you have nowhere else to go.

The tumour is not a test. It is not a lesson. It is not your fault. You are not broken for carrying it. You are not less because of it. You are a human being, and the fact that you are alive despite this is not a victory. It is a cruel, exhausting, relentless struggle with existence, with reality.”

On the Physical and Psychological Impacts

“The universe is indifferent. It never promised fairness. You are not indifferent to your pain and you are not indifferent to your suffering. And that is okay.

You do not have to find beauty in this. You do not have to make peace with it. You do not have to forgive it. You simply have to be.

And if being is too much, then rest. If enduring is too much, then stop. If the tumour is too much, then let it be. You are allowed to say enough. You are allowed to say I do not want this. You are allowed to say I am not here for this.”

On Sleep Deprivation — when Rest is Impossible

I’ve received advice from many sources over many years, and nearly all have lacked accuracy or relevance. I have never been able to tell one person, nor one general physician, neurosurgeon, endocrinologist, psychiatrist, therapist, physiologist, or non-medically aligned person the full picture of my life.

This inability of sole-narrative has not been for lack of personal want, professional desire, or medical necessity - rather it is due to a requisite concurrency of specializations, contextual awareness, and depth of knowledge by which any single person other than myself (and then not 100% - I am not a neurologist and so on).

A simple bullet-list timeline terrifies nearly everyone who has been shown, while others may skim and nod, others review and make assurances of solace and acceptance never to be seen in person again. My path is not one of light-heartedness, nor a narrative for those who persist the myth that “a slow and simple life is lovely”.

Instead, my DNA is coded to never slow down unless foced into compliance. I have always been this way. It has brought success and death, and of both - certainly more than once.

“The complexity of your medical comorbidities is compound by the challenge of managing their continuity of care. Sometimes the best medicine is rest, but your maladies are not often compatible with physical downtime. Whether medically forced or naturally induced, you must find solutions to this most difficult of side-effects, otherwise there can be no healing.”

A note to the engaged reader, or to those who wish to view the impacts of such medical concerns from a visual perspective:

• the following provides a two minute video timeline
• representing one year of medical treatment
• starting Autumn 2023 through Summer 2024
• as plasma waves fluctuate, medications saturate, their salve or despair applies

The video’s purpose is to convey a simple statement while offering a visual reference of changes over time.

“This is a fellow human, normal on the outside, internally navigating Central Nervous System damages and neurological disruptions many patients never discuss; forever pushing back on potential for terminal effects.”

a common refrain

The quote remains, “She is often smiling, but silently screaming”.

0:00

/1:54

1×

one year of treatment, viewed through four vignettes 2023-2024

a footnote for five leading years

Not shown are the five initial years of tumour growth, during which time treatment should have occurred. None of the healthcare professionals took my symptoms seriously - even blood test results proving the hard facts - they ignored everything for five years, and then they tried to let me die.

On Sleep Deprivation and Dopaminergic Torture

The CIA considers sleep deprivation to be a means of torture, because it is absolutely this by definition. I do not mean a night or two of “waking up on the wrong side of the bed”,

“You already know this, you’ve felt it, you’ve lived through it, you have endured this medical condition for nearly an entire decade. Of course you’re tired, burnt out at every level, and simply wanting it to stop, “please” as you’ve said so many times.

The incessant question of, “Why?”, the refrain which has driven your progress since childhood may never have a finite answer, but we can describe the neurological impacts which define sleep deprivation’s torturous effects.”

🧠 Systemic Impacts & Dopaminergic Mechanisms

Tap to expand. Search below.

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What It Means to Live Like This

• You do not owe the world your survival.
• You do not owe your pain an audience.
• You do not owe the tumour your time.
• You have already given more than enough.

“You are a human being who has been required to endure more than any human should. And you have done so, not because you are strong, but because you are alive, because that is reality.

You are not broken for carrying this, so keep going.” ❤️

Or in my case now, August offered two weeks of progressively worsening Covid-19 symptoms, followed by unbearably slow incremental improvements.

A variant of the SARS-CoV-2 virus, known as Nimbus (NB.1.8.1), emerged in early 2025 and is a sub-lineage of the Omicron variant. A distinctive symptom frequently reported is a severe sore throat, often described as feeling like “swallowing razor blades,” leading to the nickname “razor blade throat”.

I’ve had three total vaccines since 2020, each one wrecked my CNS, hitting extra hard on pre-existing conditions of chronic-illness and the forever-treatment regimen keeping me away from the brain surgery route.

How are things today?

Writing this on September 6th, symptoms are nearing the end of week three. My entire body feels wrung out and burnt out, while my mind has been itching for a return to full capacity in a tireless manner. The will is far more powerful than the body at this point.

Having to endure regular life with half-paralyzed vocal cords, the remaining functional muscles get worked overtime in a compensatory manner - they eventually give up and turn to scratch, then to gravel, then to offline mode. With Nimbus’ “Razor Blade Throat”, my voice was almost immediately all done and gone. Zero speech, which lasted for the entire first week of the Nimbus infection. Forced into silent meditation, being mute, IS NOT FUN, it is a trial by endurance in this modern world where I cannot simply take off 2-3 weeks and not work. Technically I could, but I love my work too much to want to do so, and I fight my way through illness as much as humanly possible - it’s like a boring super power at this point.

Alternate Timelines for Viewing

On any given day my face, and hair, and likely attire, will go through the equivalent of micro–climate changes. Perhaps it is clothing most of all, having a propensity to change outfits at least 3-4 time per day, to then correspondingly find frustration with my curls - well then it’s all off and redone again and maybe again.

Timeline #1 - happiness to sadness to pleading “no more”

Timeline #2 - an alternate view beginning August 20th

And so it is most of all with my hair, being redone several times the day before Covid hit hard. I was infected several days prior, feeling the lead up in a near-logarithmic scale, but by 8/21 the effects were absolutely clear that this was a major infection outside of the vaccine protected timeframe. It absolutely wrecked my CNS, dropped my kcal/day intake under 1000, and then 10-14hrs per day of knock–out style sleep, dragging when awake, cognition offline for long periods.

What about the Pre-Existing Conditions?

Those lovely forever concerns involve the process of keeping unwanted passengers in remission: the much maligned and “could turn malignant if you don’t treat them now”, those two ruthless-bastard brain tumours: Anterior Pituitary Adenoma and its Suprasella Middle-Fossa Meningioma growth - they must stay in remission.

NB.1.8.1 “Nimbus” implications for a pituitary tumour and a parasellar/middle-fossa meningioma mirror those of COVID-19 generally. Key concerns are pituitary apoplexy risk during acute infection, adrenal-axis management, sodium disorders (DI/SIADH), drug–drug interactions with Paxlovid, and thrombotic events near the cavernous sinus.

Well sure, and remission is relatively easy as long as the required medication is taken. Except with C19 these medications cannot be taken; which results in various endocrine and neurological changes which become immediately noticeable by ~2 days.

1. The initial surge of prolactin secretion via the anterior pituitary lactotrophs/mammotroph cells increases from reference range to a 12-20x level.
2. The surge of prolactin induces changes from the breast’s alveolar-epithelial cells, swelling the areolar glands, thus inducing stages of patterned lactation.
3. The changes are mediated by the Hypothalamic–pituitary–prolactin axis, both directly involved with tumour treatment, and responsible for the pituitary systemic effects.

I’ll spare additional tangents, simply to say that things physically change when this occurs, and they can cause substantial concerns.

Any Potential Benefits, Perhaps?

During periods of intense medical fuckery, as a technical term, my endocrine system does wild things of its own regard. Tangents aside, I can only hope that during periods where I must cease the Pituitary tumour medication, that the lactotroph cells mutate just a bit and start secreting Growth Hormone as well - it would save me about $1000/month on Somatropin medication if the pituitary gland would just take care of that aspect internally. Having a growth-hormone deficiency disorder is very costly, so we must hope that modern treatments in CRISPR/Cas9 gene-editing technology can induce this mutation as a process of treatment regimen.

Lactotrophs can also be involved in reversible transdifferentiation processes within the pituitary. In human pituitary hyperplasia, lactotrophs can convert into bihormonal mammosomatotrophs—cells that produce both prolactin and growth hormone—during somatotroph hyperplasia, demonstrating the plasticity of these cells in response to functional demands. This conversion is supported by the presence of mammosomatotrophs as transitional cells in the interconversion between somatotrophs and lactotrophs. However, this process is not unconditional,

Drained, Dejected, Enduring the Forever Rest

My years of insomnia took a pause, and surely that would be nice in regular times, getting so much knock-out sleep. Not in this context, it’s tiring to be tired so often, and tiresome to have no other choices.

burnt out, wrung out, and so tired of being tired

Well, that’s enough of that. Go away Covid, no one likes you.

This process combines a form of silent meditation with neuropharmacology — reprocessing memories via old photos while blasting the prefrontal cortex with supra-physiological dopamine levels. The Blood-Brain-Barrier must be crossed, and it must be strictly timed and controlled, while ensuring sufficient “ripcord medication” is available to halt the process.

This is achieved via prescribed medication, nothing particularly fun unfortunately, applying a timed combination of precursor + releasing agent + receptor agonist + potentiators CYP450-3A4 and CYP450-2D6. Regardless of the prescribing aspect, the combination is finely tailored to my neuro-chemistry and has been adjusted over the course of years - it is not for broad consideration or recommendation. In varying ways over the past three years, these dopaminergic alterations have been extremely challenging to manage, process, adapt, adjust, and come to terms with in their entirety.

Neural reprogramming via dopamine therapy is exceedingly dangerous territory when not managed correctly, and is not to be considered any kind of fun or pleasurable. The risk-profile is extensive: deconstruction of self-identity, parasympathetic + autonomic nervous system malfunctions, chronic sleep deprivation, tremors, hallucinations, time-slippage, and the stripping away of sanity. The potential benefits are life changing, bordering on a form of salvation from neurological trauma and post-traumatic stress disorder.

During this time the purpose is to reprogram the brain’s altered response-pathways, repairing damage from trauma and its hold on sensory processing and associative recall. Secondary improvements exist, which include taking an α1-adrenergic blocker after treatment (in this case a “non-selective inverse agonist”, named Prazosin), which settles down the autonomic system.

The Evolving Science of Memory Extinction

Prior to completing my seemingly never-ending research paper, here’s a synopsis on the technical aspects regarding “why this works” as a treatment for scenarios involving a Post-Traumatized Brain. That term is not as common as it should be; there are a lot of people who have experienced various forms of TBI - from mild to severe. The affliction is an often desperate condition which benefits fromPolytrauma Systems of Care.

Let me count the ways in which Traumatic Brain Injury is both caused by or by which manifests its existence to the external world of the unawares.

1. blunt-force impact trauma (me)
2. forms of cerebral ischemia (me)
3. environmental exposure leading to neurogenetic disorders
4. neurodegenerative diseases like Parkinsons and Alzheimers
5. severe emotional trauma causing irreparable alteration to neurotransmitter homeostasis (me)
6. cerebral aneurysm, stroke, grand-mal seizures, cerebral edema, cerebral anoxia

How about some raw data analysis? Everyone loves the facts, hopefully?

The following screenshot is from a wonderful study about Sequential fear generalization and network connectivity in trauma exposed humans with and without psychopathology, which was discussed in a recent post from the Institute for Neuroscience at the University of Rochester.

The full paper is fascinating, highly recommended reading. Moving on…

Dopamine Modulates Episodic-Memory Mapping

Why do we care so much about dopamine’s role in the brain? First, consider the neurological potential which arises as a result of boosting its metabolic precursor l-3,4-dihydroxyphenylalanine, aka L-DOPA. This is an amino acid derived from L-phenylalanine and L-tyrosine, which are effectively at the top of the brain’s food-chain, and when that is increased the brain has more fuel to synthesize dopamine for the therapeutic process. From the research links referenced below we have a list of essential findings and results.

Administration of L-DOPA - Key Findings

1. L-DOPA after extinction consolidates context-independent extinction memory and reduces fear relapse in healthy participants.
2. In women with assault-related PTSD, post-extinction L-DOPA reduced fear responding
3. Mis-timed dopaminergic enhancement can strengthen reconsolidation of the original memory; careful windowing is required.
4. PTSD shows broad impairments in learning and extinction; dopaminergic augmentation is a plausible lever but not standard of care.

Post-Administration Evaluation of Care and Metrics

Indeed. It’s important to keep track of the results and involved metrics for the medications, doses, timing, and end-stage emotional + physical impact assessment. Considerations are given to the following list as well.

1. Dose and windowing are critical to success and repeatability
2. Target the post-extinction consolidation window for Cmax/Tmax levels
3. Avoid dosing on “strong reactivation without extinction” to mitigate reconsolidation
4. Post-care medication tracking, timing values for adrenergic and sympathomimetic reduction curves, potential fear/threat response mitigators, CNS suppressant options

Research on PTSD Dopaminergic Therapy

Before engaging in any of this mad-scientist approach to problem solving, I read a lot of research on the topic. It’s an ongoing area of scientific inquiry.

While I do love science and all of its potential, I should clarify one thing: I am so goddamn tired of dealing with PTSD on an daily basis. The years of damage from sustained episodes of trauma have broken the programming structure for endogenous dopamine management, among other concerns. Not enough dopamine, you’ve got some big problems, as it is responsible for keeping us alive and healthy and happy and successful.

That endogenous situation is a crucial component for this form of therapy to be effective. It’s not just reprogramming memories, it’s concurrently back-filling the malformed neural network etchings, those disordered flows of catecholamine firing-flags (Fight or Flight Response programming: adrenaline, norepinephrine, as well as dopamine). It is a process of setting the roads straight, detangling, erasing, replacing.

• The precursor is the fuel which provides the base metabolic requirements
• The releasing agent boosts conversion of the precursor into the hormone
• The agonist tells the hormone’s receptors to hang on tight and for longer

At coordinated-curves, the result is substantially higher circulating dopamine in the brain — namely the PFC (prefrontal cortex) where memory consolidation and processing occurs. Peak reprogramming requires substantially higher circulating dopamine — plus an awareness for proper management of the effects and inevitable side effects. Caution must be exercised.

This is the kind of situation where the patient has a debilitating injury for over two decades — has tried effectively everything — and are now fully into the realm of experimental approaches to “just get it fixed, somehow, please”.

🧠 PTSD & Intrusive Memory Studies

Tap to expand. Search below.

1. Neuromodulation of Visual Cortex ▼

Hypothesis: Inhibiting early visual cortex during reconsolidation will blunt the affective “gain” on intrusive images.

Cause: Brief memory reactivation → 1 Hz rTMS over early visual cortex (human analogue-trauma paradigm).

Effect: Reduce visual-cortical contribution to intrusive image salience.

Observation: Emotional intensity of intrusions ↓; frequency & explicit memory unchanged.

rTMS Visual Cortex Reconsolidation

🔗 PMC8754386

2. Traumatic Stress Alters Visual Reactivity ▼

Hypothesis: Acute trauma perturbs basic visual-cortex impulse responses that track intrusion symptoms.

Cause: Recent trauma exposure; checkerboard visual stimulation during fMRI.

Effect: Visual sensory reactivity/connectivity shifts underpin later intrusive symptoms.

Observation: Visual-cortex reactivity associates with PTSD (especially intrusion) symptoms; altered visuo-sensorimotor connectivity.

fMRI Visual Reactivity

🔗 Nature (2025)

3. Intrusive Memories: fMRI Study ▼

Hypothesis: Encoding in amygdala & ventral occipital cortex predicts which moments become intrusive.

Cause: Trauma-film encoding during fMRI.

Effect: Stronger amygdala–visual encoding → more intrusions.

Observation: Higher amygdala & ventral occipital activity at encoding predicted later intrusive memories.

fMRI Amygdala Encoding

🔗 PLOS ONE

4. Neural Basis of Involuntary Recall ▼

Hypothesis: Specific encoding patterns in visual–limbic circuits determine involuntary trauma imagery.

Cause: Trauma-film task with later intrusion tracking.

Effect: Identify visual–limbic signatures that drive involuntary recall.

Observation: Encoding activity patterns in occipito-limbic circuits predicted later intrusions/recall.

fMRI Encoding Limbic

🔗 Psych Med

5. Propranolol & PTSD Symptoms (RCT) ▼

Hypothesis: β-adrenergic blockade during reactivation disrupts reconsolidation, weakening trauma memory affect.

Cause: Oral propranolol before weekly trauma-memory reactivation sessions.

Effect: Noradrenergic dampening of restabilization → symptom reduction.

Observation: Greater PTSD symptom reductions vs placebo; supports reconsolidation-blockade approach.

Propranolol Reconsolidation

🔗 PubMed

6. Propranolol in Chronic PTSD (DB-RCT) ▼

Hypothesis: Same as above; test efficacy in chronic PTSD.

Cause: Reactivation + propranolol vs placebo (6 sessions).

Effect: Attenuate emotional weight of memory.

Observation: Both improved; no overall drug–placebo difference; signal in most-severe subgroup.

Propranolol Chronic PTSD

🔗 Nature

7. NEJM Prazosin Trial in Veterans ▼

Hypothesis: α1-blockade during sleep reduces adrenergic drive → fewer nightmares & symptoms.

Cause: Nightly prazosin vs placebo (26 weeks).

Effect: Lower central NE tone during REM/sleep.

Observation: No benefit vs placebo on nightmares, sleep, or global PTSD.

Prazosin Veterans

🔗 NEJM

8. Single IV Ketamine (JAMA Psychiatry) ▼

Hypothesis: NMDA antagonism acutely boosts plasticity to downshift pathological memory traces.

Cause: Single sub-anesthetic ketamine infusion vs midazolam.

Effect: Rapid plasticity → fast symptom relief.

Observation: Rapid PTSD symptom reduction (24h–1wk) vs control.

Ketamine NMDA

🔗 JAMA Psychiatry

9. Repeated Ketamine Infusions (AJP) ▼

Hypothesis: Repeated NMDA modulation yields more durable remapping of threat circuits.

Cause: 6 ketamine infusions (2 wks) vs midazolam.

Effect: Strengthen extinction/modify memory networks.

Observation: Significant PTSD severity reduction; first RCT showing efficacy in chronic PTSD.

Ketamine Repeated Chronic PTSD

🔗 PubMed

10. l-DOPA After Extinction (Women with PTSD) ▼

Hypothesis: Dopamine boost post-extinction strengthens safety memory to prevent return of fear.

Cause: l-DOPA/carbidopa immediately after extinction (fMRI).

Effect: Enhance consolidation of extinction (“remap” threat→safety).

Observation: Reduced reinstatement/return of fear; amygdala patterns support extinction memory.

l-DOPA Dopamine Extinction

🔗 PMC

11. MDMA Therapy & Brain Activity (fMRI) ▼

Hypothesis: MDMA-AT retunes brain networks during trauma recall, lowering visual-imagery contrast.

Cause: Active MDMA sessions within a Phase-2 protocol (pre/post fMRI).

Effect: Increase adaptive FC; dampen amygdala–insula coupling; modulate visual areas.

Observation: ↓ amygdala–insula FC; reduced cuneus contrast; trend ↑ amygdala–hippocampus RSFC.

MDMA fMRI Therapy

🔗 PMC

12. Phase-3 MDMA-AT RCTs (Nature Medicine) ▼

Hypothesis: MDMA fosters fear extinction & reconsolidation updating via neurochemical surge.

Cause: MDMA vs inactive placebo alongside fixed therapy protocol.

Effect: Reopen plasticity; enable trauma-memory “remapping”.

Observation: Large symptom reductions; many no longer met PTSD criteria.

MDMA Therapy Phase-3 RCT

🔗 PubMed 33972795 / 37709999

This is an ongoing research indulgence, a topic very close to my heart. ❤️

Remembering the Past - Photographic Neuro-Therapy

How about some examples from this past week. Generally these are simple captures of points in time, however these are linked to specific time periods of my life when PTSD events occurred. When I see them there is a flood of emotion and physical response: elevated heart rate, deep intake followed by shallow rapid breathing, the echoing surge of norepinephrine from fight or flight response, and inevitable accompanying psychological aversion. These are the effects to be remapped, the process of meditation and cognition-alteration with which to be engaged.

Considerations of Creative-Emotive Outlets

I used to love painting, and perhaps if there were more space for all of my many projects then I would try to get back into the process. Creativity and artistic expression are relaxing and healing; it’s true. Looking back, my last one was a 6’x4’ canvas in acrylics, which I had finished for a contract-design.

After the “assault by gunpoint incident” I simply could not hold a brush, could no longer see the future of the paints upon the canvas, no longer imagine beautiful images finding their way from mind-to-hands. Creativity in that manner simply ceased, and I’ve not been able to resume. Having to stop was like losing part of my identity, connection to passion, vibrancy.

Coming to Terms with Physical Scars

Circa a few years after the coma, we see those two scars which never heal. Sometimes I put concealer on them, sometimes I lose interest in covering them for the sake of the visual public. I’ve written so much about this already, there nothing much new to say right now. I returned, and I live with that fact — feeling every moment.

Early Life and Times in a San Francisco Career

The innocent early years in SF, commonly engaged in expressions of “overly formal” attire for the west coast tech industry. Those occurred at the same time as the gun violence, domestic violence, and desperation-inducing medical trauma. So, how does one already trauma-laden young woman cope with more, while attempting to climb the corporate ladder? Any way she can, an escape artist, international travel, constantly moving, preferring to replace the pain with newness and knowledge.

Coping with a Returning To American Life

There is only so much to say about my most recent return to the USA, moving back to take a mostly-dream job running a hardware research lab. This photo was taken during the initial months when my PRL level began to skyrocket off the reference range; that growing trendline on the many successive blood tests proving tumor growth on the Anterior Pituitary Gland; the Suprasellar-Fossa Meningioma and its migraine inducing Optic Chiasm concerns would arise some years later.

The anterior pituitary secretes a number of peptide and glycoprotein hormones that regulate various cellular processes including growth, metabolism, reproduction, and response to stress or trauma. The hypothalamus regulates the anterior pituitary via secreting “releasing hormones”, somatostatin and dopamine.

The physicians in America ignored my concerns, ignored the labs, ignored everything about this brain tumor for FIVE YEARS until an eventual MRI was ordered. Memories from those five years are extraordinarily difficult to remap, part of an ongoing source of simmering rage underscoring every medical encounter with that health organization. The pituitary tumor was only one marker in a complex set of endocrine system dysfunctions. Regulating its effects in the early stages would have prevented a chain of events from which my body will never return to baseline.

So much physical pain, emotional suffering, and secondary orders of impact could have been prevented if only they had listened (if only anyone had listened) to this one woman’s reproductive system concerns. The medical industry doesn’t care about women - we’re not often profitable enough. Now eight years later, symptom remission requires a forever-expensive and stressful managed condition, but at least thus far I’ve avoided invasive brain surgery.

Parting Thoughts for Project Restoration

The past is not so easily escaped, nor resolved, or often acknowledged — and so it may never heal. However, with sufficient care perhaps these memories may be laid to rest, if not remapped by way of modern self-administered neuroscience miracles. ❤️

Cellular Echoes, a Multi-generational Legacy of DES

Having touched on this in the first post, this section is intended as a refresher. Partially this is intended for raising awareness to a problem which affects millions of people born during the 1950s - 1980s, when DES was administered to pregnant women via medically good-intentions but without awareness to its long-term effects on the mother, children, grandchildren.

Diethylstilbestrol (DES), a carcinogenic endocrine disruptor, has multi-generational adverse effects through disruptions to the neuro-endocrine system and DNA mutations impacting cellular and hormonal development. These mutations can manifest as cancers, metabolic disorders, reproductive dysfunction, chromosomal abnormalities, and chronic neurological conditions (migraines, tumors, lesions, dysautonomia).

This genetic legacy is a backdrop upon which my life was built, which resulted in innumerable divergences of a normal-healthy path, from fulfilling desired physical expectations, procreation, and so much more.

A Reset to The Rules of Engagement

Memory is a skill we easily take for granted, often assuming it accurately captures reality as it unfolds. We’re taught that our experience of the present occurs in real-time, yet in reality, there is a slight delay—signals must first travel through the nervous system and undergo processing before being encoded as memories within the brain’s dura mater. Memory is the brain’s intricate mechanism for translating sensory input into meaningful emotional and behavioral responses, shaping our understanding of both internal and external worlds.

This complex neurological system depends heavily on balanced neurotransmitter function to accurately encode experiences and guide our daily lives. Severe trauma, as seen in PTSD, profoundly disrupts this delicate neural language, permanently altering pathways—especially dopaminergic circuits—that influence emotion, cognition, and behavior. Once formed, these trauma-induced changes can become deeply ingrained, often irreversibly affecting one’s neurological landscape. Coping with severe PTSD thus requires lifelong adaptation, reinforcement of coping strategies, and an ongoing, difficult journey toward acceptance.

Fragmentation of memory can be understood as a memory disorder that includes subjective and phenomenonological facets directly impacting the ability of an individual to recall memories in an integrated and holistic way.

In my seventeenth year I would drive to SF at night to take photos before dawn. Over the years this favorite city of mine became a source of severe and lasting trauma.

The impaired person usually suffers from physical damage to the hippocampus. This may be due to the result of trauma, such as post-traumatic stress disorder… consequences, such as oversensitivity to some stimuli, impulsiveness, lack of direction in life, impacts to existential awareness, emotional dissociation, and often a distorted perception of oneself… requiring the patient to mask their concerns and despair.

Together We Drifted Toward The Void

Eventually, the lifeboat fell apart — the house of cards collapsed. Across the eras of a beautiful yet fractured life, layers of trauma accumulated, intertwining at the point of my near demise, when in the same year I lost my twin. We had endured those early years closely together, though our paths were not always aligned or identical. By this point, the cumulative losses had become immeasurable and insurmountable.

We experienced diametrically-opposed impacts from DES exposure, chromosomal deficiencies echoed in reverse, genomic sequencing showing the maps and flags and arrows all pointing to the wrath of diethylstilbestrol. Everyone has their limits, and we knew so very well where the next decade or two would go, the advanced treatment path involved; the trajectory was bleak and disheartening. Some may judge one’s rational, data-driven decisions, fully respective of life experiences, to be inherently irrational in their moral views. Many people since have levied their opinions, but they were never forced to walk this path.

A Life Without a Mirror

Consistent with the existentially spiteful patterns of non-consensual trauma upon my body, the EMT tasked with saving my life had slit my throat open length-wise, rapidly and jaggedly in an emergent (ie absolute emergency) airway incision. This severed half of my vocal chords, permanently paralyzing that amount of vocal functionality. My brain was already off-line, in global ischemic state, lights out. There was no pain, there was nothing. I was gone.

Memories are mostly lacking from that month, though photographic timestamps provide one view, a phone held while walking, a mistaken shutter press. The askew pupils indicate a rare and severe side effect, the result of ongoing treatment having been fully insufficient. Once more, healthcare providers had failed in their long-term care. After this, nothingness.

unplanned, unexpected, the last photographic memory

Body moved to the ER, the OR, the ICU. A second, larger, circular incision was made in my throat, the first haphazardly sewn closed in zig-zagged scars. My limp unconscious form was hooked up to life support machines. Days passed, a week, then more. Slowly, neural matrices enervated the consciousness to reboot, to resume an awareness of our shared reality.

A pinhole of photons appeared, and from the vast darkness every cell was screaming, oxygen and a feeding tube through the stoma hole in my neck, rhythmic pulsing-machine breathing for me, the only solace a button taped next to my hand for morphine - “press to release”, into the IV line. Apparently I was alive.

The pinhole of light widened, forcing outward the timeless nothingness, replaced by pure all encompassing light, then shades of grey, then shapes, without concept of meaning or definitions.

“Life will only be more difficult now.”

One result of the coma was that broad sections of life, of memories, events and persons, places, experiences.. were simply gone. The variously affected zones and thalamus projections, and some functions of the posterior parietal cortex, they simply did not wake up with the rest of my brain.

I will never remember all of the memories which I have lost.

With those vacant memories, gone too were my former abilities of speech, the ability to walk, to hold a cup, to feel emotions, to focus further than the end of the bed in the ICU, to understand the passage of time. So much was lost.

looking upwards, on an IV drip or two or three

“She may never be able to speak, to walk, or leave the hospital, if she wakes up at all.” - Neurologists, Attending to the ICU

As it turns out, the experience of Global Cerebral Ischemia induces substantial changes - that special “off switch” called “no more oxygen today”. Global Brain Suffocation. Flatline waves. No respiration. System Shutdown. Those scars on my neck - from the respirator stoma and the EMT’s emergency attempted endo-tracheal intubation - they are still present and in the mirror every day. Every morning upon waking, the scars are there, a forever reminder of the Void, the Loss.

Eventually I did relearn how to walk, to speak, to conceptualize the passage of time, and how to exist without those old blocks of memories weighing me down. I learned how to confront what remained, which helped with working through the newly faced medical trauma from the events of the ICU and temporary non-existence.

How did my brain wake up at all? No one had answers. Years later, periodically asking new neurologists, still no one knows. Since waking up, it has never been easy.

When Trauma is linked to Identity

The Self, one’s internal identity, with its link to the past, images of the memories, the joyful moments mixed in with all of those years of pain. It’s a jumble of words and phrases after a while, meaningless. How can one move on when they are no longer fighting an internal struggle against their past? It would seem simple, easy. Perhaps so. Perhaps the temporal lobes, with their functionality and dysfunctionality which results from PTSD, would benefit from additional research; this is my course of action, to reprogram the reactions, reprogram the responses, and to heal the mind and body via positive feedback loops.

a lovely animated gif of the brain’s Frontal Lobe, left cerebral hemisphere

On Consideration of Complexity, Treatment Modality

Neurology is a complex subject. Emotional intelligence and the cognitive underpinnings of its origins and capabilities, these are a complex area of study. The simplest description of the science which describes the manner in which the human brain gathers, processes, stores, and recalls memories is also a complex subject. So much complexity, how to make sense of it all?

Conceptualizing one’s existence after waking up from an event where death was assured, had your throat sliced open with a scalpel, connected to machines to keep your offline brain oxygenated, and then eventually to reintegrate into society’s fabric of shared existence — after returning from the Void of endless nothingness — that is a Complex Circumstance, one which requires a combination of neurological, psychological, and philosophical continuity of care. In America we do not have that as an option, not on any regular insurance plan, the patient must fend for and advocate for themselves.

What then are the options? Is ‘dopamine agonist’ based therapy the only choice? Certain not. It won’t even be recommended by a therapist because it would require enrolling in human trials for the subject, and that’s often far too involved or often unavailable for many patients.

So, one may read this and think and inquire..

“Surely this is a bit extreme, unproven?”, while others have inquired, “why not try the research methods for MDMA, Ketamine, Lysergic Ergolines, or A or B or C or another instead?” Or what about DBT or CBT or EMDR?

Sure, sure. Perhaps in the literal words of one truly genius level therapist..

“How about instead of taking ${critical medication}, you just imagined what it would be like to have these therapy sessions while taking the medication, you know - without taking it?”

The answer to all of these queries is that I have been through every possible and available treatment pathway over the past decade and more. Some have been life changing and positive and beautiful, others less useful, some fully a waste of time. Some therapists have caused additional pain with victim blaming, tearing holes into the tattered fabric being repaired, those horribly malicious people — they do exist, and that in itself is a depressing fact for people seeking care.

Visual Remembrances and Photography as Healing

One of the methods which I’ve found most useful, lasting, and capable of more than words may define, is to repair these old images. Not in an “exposure therapy” manner, but in a restoration of the mind’s emotional response to their evoked memories.

For those who have not immersed themselves into the study of cognitive neuroscience, or found solace in the philosophy of causal-determinism, the concepts around neural-programming may sound like science fiction. Fortunately, our current era of medical science offers the fiction of fifty years ago as an experienced reality - right now, today.

This method involves taking a prescribed ‘dopamine agonist’ medication, which causes the brain to activate dopamine receptors throughout many critical pathways. Once the medication reaches a necessary level, then my gaze is returned to the those slides. Hours will be spent digitizing, processing the images for color correction, repairing film damage spots, and normalizing the ICC profile, normalizing levels, adjusting histograms via curves.

dopamine, the first of the three catecholamines

Human trials for this method are not common. There is no profit to be made by the pharmaceutical companies with drugs which have existed for decades, using personalized treatment which varies by individual (and is therefore difficult to quantify without substantial similarities between patients - and I am not a common patient).

For those curious, I’ve included various embedded links within this document, but here are some additional readings which may offer insight.

• The mesoaccumbens dopamine in coping with stress
• Dopamine D2/D3 receptor agonists attenuate PTSD-like symptoms
• The hypothalamic-pituitary-adrenal axis in PTSD: Pathophysiology and treatment interventions
• Limbic response to stress linking life trauma and hypothalamus-pituitary-adrenal axis function

Why are we talking about the “hypothalamic–pituitary–adrenal (HPA) axis”? Because the Hypothalamus controls Dopaminergic activity, and the Pituitary gland (which controls hormone secretions) is deeply affected by Dopamine levels rising or falling.

In this meditative mode of visual analysis, amidst silent revisitation of trauma-informed responses, my intentional flow of thoughts attempt to concurrently apply a revised emotional mapping to the associative matrices within; to reprogram the damaged links via new dopaminergic pathway etchings - made possible by the cognitive intensity of this combination of meditation and medication.

It feels like removing rust from a long treasured heirloom, to see the glint of its origin material, its remuneration now complete.

Eva preparing for neural-programming — a self-photo facilitates awareness of Dopamine levels - visually represented as “Dopaminergic Flush”, a stateful readiness for successful treatment

The Great Reprogramming of Dopaminergic Pathways

The mechanism of action involved with this medication facilitates the process of creating new neural connections, by linking sensory data from visual information processing circuity to the emotional response relationships involved with memory recall; all of this occurring via complex actions of the brain’s dopaminergic pathways.

During this treatment process my thoughts wander and I don’t push back, just let the feelings occur and move forward. It’s a form of Zen in some ways, letting the emotions exist without holding on, without “desiring a lack of desire”.

Time and distance is required for reprogramming the mind’s emotional recall, for forgiveness. The process is possibly never complete, but it’s a beautiful experience to find oneself on the other side, able to look backward and see the beautiful ways that once were.

I see those youthful eyes, consistent across each image, reminders every time. The earlier years retained an innocence about them, harboring damage too deep to acknowledge, express, or let forth. Now those moments can be set to rest, and in whatever way it may heal, it offers solace.

eyes reflect with a minor smirk, thrust into the present from so many years passed

Carrying around my father’s old Pentax ME Super 35mm film camera (digital did not yet exist), I would learn the ways and means of translating one’s vibrant sensory world of tangible, visible, and audible queues into a reflexive snapshot of a single ellipses of time.

Film photography platform of my youth, the glorious Pentax ME Super

The science of film, its correctness of inter-related momentary ordinals, exists as a knowable object in its own right; defined by functions which can be modeled, simulated, and counter-adjusted according to objectively determined interlocked sliding scales of equilibrium equations… the science of light was logical, beautiful.

The spatial-dimensional complex of neurons and axons within my young mind was growing rapidly, desperate for knowledge, experience, adventure. So much of that mindset was searching for answers, finding beauty along the way, often in spite of the many stumbles and tragedies intertwined.

On Genetic Inheritance and Endocrine Disrupters

Looking back on those years, I see patterns arise, ones which describe the ensuing years in predictable ways, in their benefits and concerns equally mixed. I was not a canonically ’troubled youth’, rather my troubles were genetic in origin — now identified as ‘Generational DES Syndrome’.

[*] DES = Diethylstilbestrol is a carcinogenic, xenoestrogen, ATPase inhibitor, endocrine disruptor. Linked to a variety of long-term adverse effects in women who were treated with it during pregnancy, and in their offspring, and further affecting the F2 generation of grandchildren.

In simple terms, this causes DNA mutations which are carried forth into systemic neuro-endocrine development, cellular expressions both causative and compounding, as the body develops into adulthood. Whether these cellular mutations result in cancer, neoplasms, meningiomas, metabolic dysregulation, sex and growth hormone disruption, reproductive sterility, chromosomal defects, or combinations of those and other grievous maladies, the possible impacts are vast in quantity and scale — and still being studied.

Some patients lead generally normal lives, ignorant of the cause for their condition, while others experience an unnecessarily early death. In-between these extremes my life has coalesced, wavering between periods of intensely healthy highly-competitive endurance athleticism to months of debilitation from chronic nervous system collapse. Some of my most memorable resting moments were the cumulative hours knocked-out from exhaustion and asleep inside the cold, dark, rhythmic magnetic thumping of a MRI tube, or the pulsing energy waves inside occasionally very warm CT scanners.

DES has disruptive effects which exert negative feedback on the hypothalamic–pituitary–gonadal axis (HPG axis), suppresses the secretion of the gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and suppresses sex hormone production as well as gamete production and maturation.

Looking back on DES and its impacts within my genetic programming, I can see where it derailed an otherwise normal childhood, where it imparted physical and existential questions for which no adult or physicians ever had answers, and how those early years drove me further into an adulthood focused on amassing knowledge of systems theory, neurology, endocrinology, genetics, biochemistry, and decades of exploration into modulating the steroidogenesis process occurring within these veins.

Coincidentally, I would later learn that endocrine specific cancers were rampant in my mother’s side of the family - likely also from intergenerational DES effects. Over the many years, my endocrine’s HPG-axis would crash in more than one dimension via multi-glandular failures, a pituitary hypophysis neoplasia diagnosis would arise, diagnostic concerns into suprasellar meningioma, and eventually the cumulative effects would lead to the conditions which resulted in my near-death and coma.

Youthful Adventures, Expansive Landscapes

Scaping together enough for a second-hand Manfrotto tripod and lenses for a near-mint Nikon FE2 - the camera I received from my father for one birthday so long ago, that period was when my heart fell in love with the beauty of capturing moments in time. Youthful innocence was at a peak, everywhere held introspective beauty in some manner - if it was framed subjectively well and maintained The Rules.

rain arrives along the Western Slope of the Rockies

Then there was the glorious selection of film: the richness of Velvia 50 - perfect for landscapes but too rich for portraits, the ever-so-accurate Provia 100, the old classic Kodachrome 64, occasionally the normality of Ektar 100, and on occasion spending time without color at all - but oh let me show you Agfa’s superpanchromatic Scala 200, the most uncommon of them all.

I loved this era of film for its uniqueness, it’s vivid ability to capture reality in a way that was lacking in prior decades - eras of advancements in technology which defined the ability for people to capture the present tense and carry it into the future, with accuracy, realness, and tangibility that we will never have with today’s digital options.

the slide films of my youth, vivid colors, rich contrast, a life before the digital world

I loved this era of film for its uniqueness, it’s vivid ability to capture reality in a way that was lacking in prior decades - eras of advancements in technology which defined the ability for people to capture the present tense and carry it into the future, with accuracy, realness, and tangibility that we will never have with today’s digital options.

As with everything immersion worthy, I studied photography via encyclopaedias, library books, documentaries, and by asking a thousand questions. Who best to answer but Elke, the co-owner and an early role model at my local professional photography shop; one which housed an amazing collection of vintage cameras and lenses - many that I would imagine forever out of reach: Leica, Hasselblad, Rolleiflex, Zeiss.

My perspective in those times demanded that the best memories surely must be captured, regardless that slide film was expensive. Each shot was a cherished and planned capture, yet still one were lucky to have 2-3 usable results per roll of 24-36. Fantastisch. I loved every minute of the process.

Of Landscapes and Studio Lights

These slides became a timeline, closely selected and optimized photos of my adventures, my travels: the tragedy of storms and the silent motions of rain, landscapes and sunrises and sunsets, mountains especially loved and well traveled. Of peaks climbed, valleys explored, off-trail backcountry wanderings alone in the autumn, and cold snowshoeing adventures with Vati too.

Then the studio. Learning about black and white film, darkroom techniques, rear-projection lights, soft-bounce filters, shade-booms, and multi-flash timers connected to a remote shutter that I could hold in one hand - the original selfie method, before the term was ever coined. These self portraitures were mostly a private occurrence, an experiment to record an ever-changing existence which often felt unknowable and painfully everlasting, other times its opposite.

long adrift in lostness, many found in my eyes precisely who they wanted to see

Conceptualization of Self

In some ways it was photography which helped me work through the DES-affected hormonal years of explosive emotions: the Conceptualization of Self as an evolving modality. How could one build a schema involving periodic memory without tracking the memories? And what better way to have reference to those than with film?

So, along with landscapes I captured my visage; an evolving physical form of perpetual wonderment and wandering cognition, deeply felt emotions, all wrapped up into a warm body with occasionally ice-cold blue eyes - constantly changing and growing through the years.

a single spoken “please”, but no one was truly listening

From the Outside Life Was Wonderful

Unfortunately along the way there were events of intense and prolonged trauma which led to a deeply felt hatred for nearly the entire era of youthful memories - not for what the photos were, not for who I was, but for the memory’s visual associations with the events of the era in which the traumas occurred.

I had no ability to heal from the events at that time, and so to my young mind those events simply could not exist, lest it were to be that I did not exist. It was one or the other: acknowledge the trauma for what it was, how it had shaped me, and chose to suffer the wrath of my own willing hands. Or instead, I would rather to erase all of it. Erase the moments from my mind and never think of them or refer to them or believe that they were real; to erase part of my experience with life. Years later that wish would be granted, an outcome in ways impossibly unexpected.

Existentially, it was a challenging duality. So the slide portfolio was put aside, boxed up, never taken out to review or inspect or share, and only occasionally forcefully ignored whenever asked about the subjects. The memories did not exist. The cognitive methods I learned became a hardened, steadfast technique, an emotional control unrelenting, and it lasted decades. No one knew anything, and no one needed to. Those memories were only pain (but they were not, my youth held so many beautiful moments, ones which I would only connect with decades later).

Outward Success Surely Heals Old Wounds

Years passed and milestones occurred, much as the loved ones around me had long expected. A standard life evolved. Marriage, a home, thoughts on pregnancy, depression, elation, stress, travel, and promotions, and everything being pretty good on the surface.

A blink of the eyes and there I am again: Bare. Lost. Alone. In the pure Darkness.

Yet family was there, friends were there, all of the markers of success and happiness were there. Regardless, trauma events from years ago were invalidating the potential for happiness in ways unknowable to the loved ones around me. No one could ever know. The memories could not exist, or I would carry them to my grave.

years so often idyllic, if not for the unspoken undercurrent

Concurrently, an undercurrent of escapism, a subtext to the patterns of wants and needs, this was all despite the abundance, and it was that undercurrent which became a rushing and inescapably deep tide. The memories become an unwanted passenger, a little non-angel perched on the shoulder - whispering reminders in the most inopportune times. A foil to the good times, intertwining themselves deeper, demanding either solace and release or self-destruction.

Trauma at the clinical level, the kind which arises from unspeakable events in youth, or wartime combat, or being assaulted at gunpoint and left stripped and alone in the pure darkness of 18th & Florida St at 3am; those somatosensory memories become etched in the mind. Maybe more than one event is etched, maybe there’s too many to describe.

Bleeding out in a sodium-halide bright white tile-floored bathroom, a stainless steel drain on the floor in the middle where the redness of life circles and downward flows. You slip in the blood, bare-footed, abdomen held in one hand, reaching-grasping with the other, screaming voicelessly in full-system shock.

One cannot escape the loop. Is it truly Sisyphean if the endless hill is worn flat, the endured evolved into appreciation for its challenge? The illusion then shows its edge, beautiful, glinting reflections from facets ever-changing, never-ending.

Another World, Another Time, in the Age of Wonder..

The mind loves to travel through time these days; reflecting upon the trajectory, occasionally in weariness of wonder that life has become its inevitability - the duality from which I could never grasp in so many years passed. The sunsets in those days felt brighter, more luminous, unfiltered by the long-evolving tumor’s stranglehold on the Optic Chiasm - our eye’s connection to the brain.

a waning dusk arrives somewhere near Lake Berryessa, Napa County CA

When single shines the triple sun, What was sundered and undone, Shall be whole, the two made one..

Where then, in the latter half of 2022 at the start of treatment? Seemingly perpetually resting in bed, dealing with first and second order side effects from a barrage of eight medications, either targeting the tumor or attempting to shore-up defenses from those side effects. Rapidly, one loses patience and interest in rest.

endless recovery in 2022, photo from my former Twitter account

How about in 2017? Fiji island hopping, searching for demise or salvation, whichever may come first.

another round of “Escape to Fiji”, impromptu rejections of corporate life requirements

Months later? Where else but Nicoya, Costa Rica seeking refuge from those internal storms. I still have that pseudo-military ripstop hat, or rather am on iteration four or five of the same design - very good for napping at airport terminals, or knocking out at the beach.

Playa Langosta Sur, accessibly only during low tide, don’t overstay the waves!

Or decades ago, seasons ago, seeking solace among the silence of snowy peaks alone. When prompted for “where do you want to go to college?”, nowhere, I wanted to go to Talkeetna, Alaska and be in the mountains. My best friend died that November, and everything changed.

what all is there to say about one’s University years, it was a complex time

All of those years, the endless dreams, and seemingly endless sunrises… the recording of those events into neural maps, shuffled off from primary storage over the decades until some periodic recall request.. affected then by environmental factors, by potential cerebral injury, perhaps menopausal hormone shifts.

Is our memory illusory? Are the vector maps of neurotransmitter mixtures changing over time? Yes they are. Still yet, we have no magnetic tapes at Iron Mountain which could store them all, and we have no set method to statically write them to anything other than occasional video or foto medium - film or digital - even the method may shift the impression and the recall.

Perhaps that malleability of memory, its neural alterations inevitable, is the most beautiful quality which growing older finally affords. ❤️

Footnotes and References

[1] ‘The Valley’, in reference to Silicon Valley, the standard California epicenter of the tech-sector.