MJB ADHD · Static reading view · Interactive version
Status: drafted · Content checked 2026-10-06
Five live questions arising from one person's observations — each with competing explanations and the observations that would tell them apart. Questions, not conclusions, and never a reason to self-experiment.
Good questions are the end point of an evidence trail. Each one below starts from an observation, lists several explanations, and names what would distinguish them. None is established; none should change anyone's treatment on its own.
Matthew reports that walking, posture and spasm were markedly better on dexamfetamine and worsened when it stopped; genetic testing for a hereditary spastic paraplegia has been discussed.
AUTHOR-ACCOUNTReviews describe juvenile or early-onset parkinsonism with variable levodopa response mainly in SPG7 and SPG11, alongside dystonia and ataxia in several types.
R13Single case reports describe SPG7 with levodopa-responsive parkinsonism and with loss of dopamine-transporter signal on imaging.
R12R14| Competing explanation | What would point towards it |
|---|---|
| A genetic movement disorder with a dopamine component | A pathogenic variant confirmed by a specialist; dopamine-transporter imaging findings |
| Two unrelated conditions | Movement findings independent of medication timing |
| Indirect benefit (energy, effort, organisation) | Improvement in effort-dependent tasks but not in tone or reflexes |
| Musculoskeletal or functional contributors | Specific examination findings |
Observable test: structured, clinician-observed movement measures at matched times, with a specialist interpreting any genetic result.
Individual differences in VMAT2 storage capacity or leakage might change how much an amphetamine can release, and so how strongly someone responds. This is not an established ADHD mechanism.
Amphetamines act partly by disturbing vesicle storage, so storage is mechanistically relevant to their effect.
R8Competing explanations: absorption and conversion differences; dose; adaptation after long treatment. Observable test: research imaging of vesicle transporters exists but is not a clinical tool; in practice, carefully recorded dose–response at a stable time of day is the usable proxy.
Matthew reports a consistent difference between generic dexamfetamine 5 mg and Amfexa 10/20 mg.
AUTHOR-ACCOUNTAmfexa 10 and 20 mg tablets contain no povidone or crospovidone; Amfexa 5 mg contains crospovidone.
W4Competing explanations: different total dose; different timing; expectation; manufacturer differences other than excipients. The Amfexa 5 mg tablet is a natural test case for the povidone idea, because it is the same brand with a crospovidone ingredient. Observable test: pharmacist-confirmed products, same strength and timing, consistent records over repeated normal use.
Physical strain may compete for the same limited regulatory capacity, so cognitive symptoms worsen on high-pain days.
Competing explanations: poor sleep from pain; low mood; sedating pain medicines. Observable test: daily ratings of pain, sleep and specific cognitive slips over several weeks, analysed together.
Vesicle loading depends on an ATP-driven proton gradient; if cellular energy supply were limited, storage might falter under sustained demand, producing worse function late in the day or after exertion.
Competing explanations: ordinary fatigue, deconditioning, sleep debt, medicine wearing off. Observable test: whether worsening tracks exertion and time-since-dose separately, recorded consistently.
Every research claim here comes from case reports, reviews or mechanism studies. Case reports show something can happen; they cannot show how often, or whether it explains one person.
All five are open. Some may be wrong. They are included because a well-framed question is more useful to a clinician than a confident guess.
Genetic test results, specialist neurology assessment and dispensing history are needed before Q1 and Q3 can be advanced in this case.