but what's actually going on
in my brain?
Behind an adult ADHD diagnosis lie different mechanisms: a shifted circadian rhythm, a nervous system stuck in overdrive, mitochondrial exhaustion after years of compensating. The programme targets the mechanisms, not the label. Four coordinated lines of intervention, from cellular energy support to brain-network resynchronisation. Not against methylphenidate; not reduced to it either.
passion and
procrastination
When people talk about adult attention deficit, the picture that comes to mind is still the daydreamer at the back of the classroom. The clinical reality is somewhere else. These patients can pour twelve hours of unbroken focus into a project they care about, never glance at a clock. That's the opposite of inattention. And yet, faced with three minutes of admin paperwork, getting started becomes impossible.
This isn't about willpower. The neurochemical system that motivates, directs and gets things moving works in bursts: intense when the topic engages, stalled when it bores. Add chronic procrastination, a poor grip on time, blurted-out remarks, relationships that wear thin, and a sleep debt no good night's rest ever quite settles.
The diagnosis usually comes late, often through burnout, depression, or a cognitive fog that won't lift. Fifteen or twenty years of compensating, and the system finally gives out: that's when people stop, seek help, and someone finally puts a name to what they've been carrying all along. Adult ADHD affects 2.5 to 4 % of the population. Most don't know it. Women in particular slip past the radar — their picture leans toward inattention rather than restlessness, and no one thinks to look.
three functions,
the same circuits
The dopamine system doesn't only steer attention. It also governs fine motor control and circadian timing — the inner clock that decides when you feel sleepy, when you're alert, when you wake up. The same circuits are involved. That convergence has a precise clinical consequence, well documented but widely overlooked in practice: delayed sleep phase syndrome shows up in 70 to 80 % of adults with ADHD, depending on the cohort.
The clock doesn't explain everything. After years of compensating, the nervous system runs down: cortisol flattens, mitochondria can't keep up, the prefrontal cortex operates in low gear. Whether it's long-standing ADHD, burnout, persistent cognitive fog or chronic sensory overload, the downstream result is the same: a brain that no longer has the energy to do what's asked of it.
Attention, rhythm and cellular energy share the same substrates: intervening on all of them amplifies the effects.
In practical terms, these patients would naturally fall asleep between 1 and 4 AM if left alone, and their cognitive peak comes in late afternoon or evening. Pushed into ordinary social hours, they live with permanent desynchronisation. Mornings are a fog, midday a fight; the afternoon finally clicks. That misalignment is what amplifies the attention symptoms — and explains why so many adults with ADHD seem to "catch up" on productivity once the rest of the world goes quiet.
adult ADHD in everyday life
The adult picture shows up as a set of patterns most patients describe as "just how I am," without realising they all stem from the same underlying neurobiology.
Chronic procrastination
Hard to start anything whose payoff is far off. The work eventually gets done — but at the last possible minute, under the pressure of a deadline.
Hyperfocus
Total absorption in something engaging, twelve hours without glancing at a clock. And yet, three minutes of admin paperwork can be enough to bring everything to a halt.
Poor sense of time
Time runs on a different scale. Systematically underestimating how long things take, running late, forgetting. Not carelessness — wiring.
Chronic sleep debt
Late sleep onset (1 to 4 AM if left alone), forced wake-ups the next morning. No weekend ever quite catches up on it.
Burnout as the entry point
Fifteen or twenty years of compensating, until something gives. The diagnosis very often arrives at that moment. Sometimes it's a "cognitive" depression: no sadness up front, just an executive fog that won't lift.
Verbal impulsivity
Cutting in, answering before the question lands. Over time, friction at home and at work builds up.
four levers, one logic
The programme rests on a four-layer architecture. Each layer targets a distinct mechanistic level, from cellular energy through to arousal regulation. The order matters: we restore the system's energy capacity first, before asking it to resynchronise.
Energy restoration
After months or years of compensating, the nervous system runs on low power: prefrontal mitochondria no longer produce enough energy to sustain attention, planning or executive control. Blood photobiomodulation (intravenous LLLT) acts directly on complex IV of the mitochondrial respiratory chain (cytochrome c oxidase): it restarts ATP production and reduces inhibitory nitric oxide. GlyNAC (glycine + N-acetylcysteine) restores intracellular glutathione reserves in parallel.
- Restarted cerebral cellular energy production
- Reduced mitochondrial oxidative stress
- Restored glutathione reserves
- Particularly marked support in cases of burnout or chronic cognitive fatigue
Temporal and sensory recalibration
The Giger MD coordinates rhythmic movements of arms, legs and trunk in lying position, accurate to the millisecond. The MOTOmed coupled with neuro-auditory stimulation layers auditory input onto controlled cycling. The cerebellum is the brain's metronome: when it's out of tune, attention slips, auditory filtering collapses, and cognitive fatigue spikes by end of day. Neuro-auditory stimulation has a dual mechanism: auditory filtering and indirect vagus nerve activation through the auricular branch (Arnold's branch).
- Auditory filtering in noisy settings
- Steadier arousal, less residual restlessness
- More tolerance for monotonous tasks
- Lower cognitive load by end of day
- Resynchronisation of cerebral timing networks
Noradrenergic activation
The locus coeruleus (LC) is the centre of noradrenergic arousal. Two distinct afferent pathways can reactivate it. Morning: 10,000 lux on waking activates specific retinal ganglion cells (ipRGC) that project directly to the LC. Night: transcutaneous trigeminal nerve stimulation (vTNS) activates the LC via the supraorbital branch. Both pathways converge on the same target through independent routes. If a patient has residual photosensitivity (common after burnout), vTNS offers a workaround.
- Easier mornings
- Sharper focus early in the day
- Less procrastination
- Gradual realignment of late chronotype
- Nocturnal noradrenergic regulation
Metabolic support
No multivitamin complex. Two molecules whose mechanism makes sense in this context. MagTein (magnesium L-threonate): the only form documented to cross the blood-brain barrier in significant quantities, supporting synaptic plasticity and deep sleep. Meriva (phytosome curcumin): enhanced-bioavailability form targeting the low-grade neuroinflammation that accompanies chronic exhaustion states. Each supplement is introduced one at a time, with ten to fifteen days of observation between additions.
- Synaptic plasticity and deep sleep quality
- Reduced low-grade inflammation
- Complementary support for brain recovery
three months in three stages
The initial assessment
We start by listening. The history-taking covers the questions no one usually asks: when do you fall asleep on a free Saturday with no work pressure, when does your cognitive peak hit, how does Monday morning compare to Saturday morning, was there a burnout, the cognitive fog that lingers, the fatigue that rest doesn't fix. Targeted blood work alongside (ferritin, vitamin D, thyroid panel, inflammation markers, membrane fatty acid profile).
The intensive phase (6 to 8 weeks)
Two to three neurorehabilitation sessions a week at the centre (Giger MD, MOTOmed/neuro-auditory stimulation). Blood LLLT on a personalised schedule. Daily bright-light therapy from the moment you wake up. Nocturnal vTNS if prescribed. Supplements introduced gradually after the blood work. A follow-up consultation every two to three weeks to adjust whatever needs adjusting.
The consolidation phase
Sessions at the centre space out. Morning light, vTNS and supplements continue, woven into the daily routine. At three months, we reassess on concrete indicators: sleep quality, morning start-up speed, tolerance for monotonous tasks, end-of-day cognitive load, residual cognitive fog.
what people ask us
who pays for what
Giger MD, MOTOmed, neuro-auditory stimulation — covered by basic insurance on prescription where there's a recognised physiotherapy comorbidity. Otherwise supplementary insurance depending on contract, or the patient
Complementary medicine: supplementary insurance depending on contract, or the patient
Complementary medicine: supplementary insurance depending on contract, or the patient. Device on rental
Prescribed by a doctor, reimbursed by LAMal
Lamp at your expense (~50 CHF), personal equipment used at home
At your expense. Products and doses validated in consultation
limitations of
our programme
ADHD isn't cured. The substrate is constitutional. The programme optimises network regulation and restores the nervous system's energy capacity, so that daily life becomes markedly more manageable and reliance on medication lighter, when that's clinically possible.
Methylphenidate remains essential in certain situations. Other levers exist, complementary or alternative depending on the profile, with documented mechanisms.
The "adult ADHD" label covers different profiles: long-standing ADHD that decompensates, burnout with cognitive sequelae, a nervous system in overdrive since childhood. The upstream mechanisms differ, but they converge downstream: prefrontal energy deficit, circadian desynchronisation, insufficient noradrenergic tone. The programme acts on that common ground.
Results vary depending on severity, how long the picture has been there, comorbidities, and how consistently the protocol is followed. The method stays constant: patients measure for themselves, on concrete indicators, what's happening before and after. Sleep quality. Morning start-up speed. Cognitive load by end of day. If nothing shifts, you see it. If something shifts, you see that too.
this programme is
a fit for you if
- You have an adult ADHD diagnosis or a clinical picture that points that way (chronic procrastination, hyperfocus, poor time management, sleep debt)
- You're coming out of a burnout and the cognitive fog persists despite rest
- You live with chronic executive fatigue that nothing resolves
- You're looking for an approach that complements or replaces methylphenidate, grounded in neuroplasticity and biological-rhythm regulation
- You know you're a late chronotype, badly aligned with ordinary social hours
- You're ready to commit to a structured 6 to 8-week protocol with regular follow-up — consistency matters more than intensity here
- Van Veen MM, Kooij JJ, Boonstra AM, et al. Delayed circadian rhythm in adults with attention-deficit/hyperactivity disorder and chronic sleep-onset insomnia. Biol Psychiatry. 2010;67(11):1091-6. DOI
- Bijlenga D, Vollebregt MA, Kooij JJS, Arns M. The role of the circadian system in the etiology and pathophysiology of ADHD: time to redefine ADHD? Atten Defic Hyperact Disord. 2019;11(1):5-19. DOI
- Slutsky I, Abumaria N, Wu LJ, et al. Enhancement of learning and memory by elevating brain magnesium. Neuron. 2010;65(2):165-77. DOI
- Kumar P, Liu C, Hsu JW, et al. Glycine and N-acetylcysteine (GlyNAC) supplementation in older adults improves glutathione deficiency, oxidative stress, mitochondrial dysfunction, inflammation. Clin Transl Med. 2021;11(3):e372. DOI
- McGough JJ, Sturm A, Cowen J, et al. Double-blind, sham-controlled, pilot study of trigeminal nerve stimulation for attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2019;58(4):403-411. DOI
- Arnsten AFT. Toward a new understanding of attention-deficit hyperactivity disorder pathophysiology: an important role for prefrontal cortex dysfunction. CNS Drugs. 2009;23(Suppl 1):33-41. DOI
- Chang JPK, Mondelli V, Satyanarayanan SK, et al. Cortisol and inflammatory biomarker levels in youths with ADHD: evidence from a systematic review with meta-analysis. Transl Psychiatry. 2021;11:430. DOI
- Hamblin MR. Mechanisms and mitochondrial redox signaling in photobiomodulation. Photochem Photobiol. 2018;94(2):199-212. DOI
does any of this
fit your everyday?
A 30-minute info session lets us ask the right questions, gauge whether the programme makes sense in your case, and decide together whether it's worth taking further.
1204 Genève