Are you neurodivergent? Does that include dysautonomia? Do you know viscerally the two are linked - but want to understand exactly how? I am composing a thread for you (yes, you) right this very moment. Stay tuned. #NEISvoid #ADHDtwitter #ActuallyAutistic #POTS #EDS
The manifestations of divergent neurotypes like ADHD are a complex function of dynamic external & internal* stressors. This makes the clinically defined subtypes (predominantly hyperactive/impulsive, predom. inattentive; combined type) largely inaccurate.
*such as dysautonomia
*such as dysautonomia
Two functions of the neurotransmitter norepinephrine or noradrenaline (henceforth NE) are relevant here. As a vasoconstrictor, NE increases blood pressure when the brain needs more oxygenated blood. NE also transports dopamine to the prefrontal cortex. Our adrenals release NE.
Capitalism has hijacked this stress response, burning out our adrenals. This is when we become fatigued, forgetful and unfocused. Reduced dopamine levels in the prefrontal cortex is one possible etiology at play. But there could *also* be globally reduced blood flow to the brain.
Called cerebral hypoperfusion, this is a sign of dysautonomia common in ME/CFS, EDS, POTS and more. NE can ameliorate both these pathophysiologies. Because ND bodyminds under chronic stress rely on it, their adrenal responses become ‘all or nothing’.
A high-stress situation can miraculously clear your head and enable executive function - but only after pushing you beyond the panic threshold. Over time, demands will need to surpass an ever-higher threshold of pressure to activate the release of NE.
When NE is compensating for reduced oxygen and dopamine in the brain, the excess finds a physical outlet in hyperactivity, impulsivity, or self-stimulating behaviours. Suppressing these eventually leads to meltdowns. The NE blocker clonidine can help - but with important caveats.
My chronically elevated NE has become dysautonomia, i.e. hyperadrenergic POTS. When I take clonidine, I feel calm, but I no longer have enough blood flow to my brain upon standing. As I am adapted to POTS, I don't get dizzy, but I experience amnesia and transient derealisation.
Atomoxetine is clonidine’s polar opposite: a NE reuptake inhibitor. It was prescribed to me for ‘predominantly inattentive’ ADHD, but the lethargy was undiagnosed ME/CFS. Even subtherapeutic doses of atomoxetine dangerously worsen hyperPOTS / dysautonomia ahajournals.org/doi/10.1161/hy…
Bupropion is partly comparable to atomoxetine, as it inhibits reuptake of NE in addition to dopamine. It was an effective short-term antidepressant - I had more anxiety, but also the energy to stim! The meds that helped me in the long run directly increase dopamine in the brain.
While methylphenidate greatly helps my prefrontal cortex, L-dopa reaches the whole brain and therefore treats cerebral hypoperfusion more broadly. For me, it treats air hunger, spasticity from (recently de-)tethered cord and dystonia from EDS. That's where I'll wrap up for now.
Credit to @laurenancona for inspiring my thread today. There is definitely more to being neuro- and bio-divergent than the mechanisms I described, but understanding the role of NE is vital and can help inform treatment options.
https://twitter.com/laurenancona/status/1518964120120442880?s=20&t=ht98aKlntqkXcQDid5QbhQ
If even one person can avoid the iatrogenic harm that I suffered from atomoxetine because of me sharing what I learnt, it would bring me profound peace.
• • •
Missing some Tweet in this thread? You can try to
force a refresh
