A clinically critical but conceptually ignored step in clinical diagnosis is response to treatment. It is a given that most psychiatric diagnoses are to some degree provisional, differential and evolving, and it is normative for diagnosis to shift contingent on evolving clinical patterns. If a diagnosis linearly suggests a treatment, and the patient and clinician perceive a beneficial response, this is generally confirmatory of diagnosis. Response to treatment is of course not part of conventional diagnostic guidelines, but this unquestionably influences both patient and clinician thinking and prescribing patterns. In this context, attention-deficit hyperactivity disorder (ADHD) is a salutary example. It is possibly the case that patients are more likely than clinicians to be reinforced in their own conceptualisations of illness by treatment response.

Clinical medical decision-making, while utilising criteria- and trial-based and related evidence, has been argued to extend beyond science, being essentially an interpretive practice contingent on clinical deduction. A physician explores the person’s history together with the presenting signs and symptoms, and pattern fits these with empirical data and their clinical experience to construct a provisional and evolving model of the illness. Doctors begin with the individual story, pattern fit this to their own clinical experience, trial data, diagnostic frameworks and guidelines and apply this to the individual patient using clinical judgement in an iterative and evolving manner. In this context, response or lack thereof to treatment predicated on an initial assessment is a critical element in the evolving assessment process. ^{Reference Montgomery1}

ADHD is arguably unique in medicine. Because most people prescribed a stimulant will perceive effects that are widely regarded as beneficial in domains including sustained attention, alertness, mood, energy and focus – notwithstanding that some people do have adverse events from such treatment – the pharmacological effects of stimulant treatments overlap with, but are independent of, diagnosis and are evident across the spectrum, from overtly clinically unwell through to unarguably normal people. In other words, the act of treatment can reinforce the diagnosis by dint of improving the domains with which the person identifies and presents. It may therefore also reinforce clinician and patient confidence in the diagnosis and hence prescribing habits. The critical point is that this perceived treatment response may be independent of the presence or absence of a threshold diagnosis of ADHD. Response to treatment therefore risks being a false diagnostic reinforcer, confirming the presence of this diagnosis independent of whether this is present. The reinforcing effect of stimulant response probably applies mainly in diagnostically ambiguous cases. The nature and degree of benefit is probably greater in individuals with transdiagnostic attentional instability, who may experience more perceived gains than those without such vulnerabilities. It needs to be acknowledged that there are some neuroimaging data demonstrating that frontal–striatal function is differentially affected by methylphenidate in ADHD compared with healthy children, with the caveat that neuroimaging has not had the sensitivity or specificity to be clinically predictive across psychiatric disorders. ^{Reference Vaidya, Austin, Kirkorian, Ridlehuber, Desmond and Glover2}

In counterpoint, if for example a clinician diagnoses a disorder like bipolar disorder that linearly suggests initiation of first-line lithium treatment, clear and dramatic response to lithium will support the diagnosis. However, if the patient is incorrectly diagnosed or non-responsive, they and the treating clinician will perceive no benefit and adverse events may emerge. This will probably prompt reconsideration of the treatment, as well as other differential diagnoses. Lithium has no meaningful effects on mood in otherwise healthy people. Similarly, antidepressants do little for mood in people who are not clinically depressed, and antipsychotics do not make thinking more rational in people who are non-psychotic. Therefore, in the normative situations where there is a degree of diagnostic uncertainty or where comorbidity with other potential explanatory conditions is present, the clinician may consider treatment response in an evolving diagnostic formulation.

Conceptually the effects of a treatments such as lithium, antidepressants and antipsychotics could be regarded as targeting pathology, as they have no meaningful psychotropic effects in otherwise healthy people – we could call them pathomodal, from the Latin modus, ‘modal’ meaning pertaining to a mode, measure or manner. This seems to be a class effect of most conventional psychotropics, albeit with some fuzziness in boundaries. In counterpoint, the effects of stimulants in ADHD can be conceptualised as targeting physiology because the effects of the drugs are independent of diagnosis and are evident across the spectrum, from clearly unwell to clearly normal people. We could call them physiomodal. Stimulants have a long history of recreational use, precisely because they cause subjectively beneficial effects in all people in domains that happen to overlap with the symptoms of ADHD. This seems to be a class effect of recreational and abusable drugs, as well as benzodiazepines. ^{Reference Dodd, Berk and Stahl3}

The backdrop to this observation is a substantial rise in the diagnosis and treatment of ADHD in many countries, ^{Reference Khadka, Peltier, Fassett, Mensah, Yeh and Chiu4} and in the degree of controversy around these rates of diagnosis and treatment. Contention exists around whether this increased level of diagnosis reflects previous diagnostic or therapeutic neglect or contemporary diagnostic exuberance. In terms of nosology, there is a longstanding debate between categorical and spectral conceptualisations of mental illness. ^{Reference Arildskov, Thomsen, Sonuga-Barke, Lambek, Østergaard and Virring5} ADHD would be an exemplar of a phenotype that exists on the continuum without any clear bimodal pattern or break point. In such situations, treatment response risks becoming a self-reinforcing diagnostic indicator. The issue is that there is clinically a blind spot that this phenomenon is indeed the case.

So, what are clinicians to make of this? The first and obvious issue is to be aware of the unique conceptual bias and blind spot that stimulants will reduce the symptoms conceptualised as part of ADHD independent of whether a clinical diagnosis is present or warranted, or if other conditions or explanations better explain those symptoms. This supports tighter conceptualisation of diagnosis and greater rigour in diagnosis. Notwithstanding the controversies in the field, there is clearly a group of people who struggle with clear ADHD and benefit greatly from treatment. ^{Reference Li, Coghill, Sjölander, Yao, Zhang and Kuja-Halkola6} This is true not only of symptoms and functioning, but there is also recent evidence of real-world benefits including reductions in self-harm, unintentional injury, traffic crashes and crime, mindful of methodological challenges. Nevertheless, awareness of this blind spot may help to continue to support those who need, and benefit, from treatment. but also reduce the risks of over-diagnosis and over-treatment. Empirical research strategies to disentangle genuine treatment effects from diagnostic inflation – e.g. longitudinal studies comparing outcomes in patients with subthreshold versus full-syndrome ADHD, or trials examining response sustainability across severity levels – could address the wider issue.