Is ADHD an expression of an autistic-catatonic continuum?

Attention-Deficit/Hyperactivity Disorder (ADHD) is a neurodevelopmental disorder characterised by persistent patterns of inattention, hyperactivity, and impulsivity, which may be expressed in three recognised clinical presentations: predominantly inattentive, predominantly hyperactive-impulsive, and combined ¹.

A comparable articulation emerges on the side of catatonia. Recent factor-analytic evidence has resolved its phenomenology into a three-factor structure: hypokinetic, hyperkinetic, and parakinetic – with the parakinetic factor, referring to bizarre, iterative, or stereotyped motor manifestations such as mannerisms, specifically associated with neurodevelopmental disorders ². That catatonia admits of such sub-typing is already an implicit dimensional reading of a construct long treated as categorical, and the notion of a catatonic spectrum is the natural integration of this internal articulation. Catatonia, in turn, has undergone a long nosological trajectory since its original description by Kahlbaum, who characterised it as a distinct clinical entity defined by motor, behavioural, and affective features including stupor, mutism, posturing, negativism, and excitement ³. Incorporated by Kraepelin into the framework of dementia praecox and for several decades relegated to a subtype of schizophrenia, its scope was extended in DSM-IV to encompass mood disorders ³ and it is currently recognised in DSM-5 as a transdiagnostic psychomotor syndrome occurring across a wide range of psychiatric, neurological, and medical conditions⁴^,⁵. The DSM-5 category of “catatonia without specification” further acknowledges the existence of subthreshold conditions and thereby providing the formal nosological ground for a catatonic spectrum that extends between the highest degrees of stupor or excitement and subthreshold attitudes, such as staring into space or acting out of control. In this context, a self-assessment questionnaire named Catatonia Spectrum (CS) was developed to explore the symptomatology of the catatonic spectrum during the lifespan ⁶. The CS would therefore represent a complementary tool, and not a substitute for the diagnosis of catatonia made according to DSM, investigating, alongside nuclear symptoms, all those subthreshold, atypical and partial manifestations that often precede the diagnosis of the disorder by years. This spectrum approach has previously been applied successfully to other mental disorders ⁷^⁻¹¹. Within populations with neurodevelopmental disorders, the conceptualisation of catatonia has continued to evolve along similar lines: epidemiological evidence indicates that catatonia occurs in up to 10-17% of adolescents and young adults with ASD,¹²,¹³ and some scholars have proposed that, in this population, ASD and catatonia share a common psychopathological continuum, in which both represent expressions of a common vulnerability¹², possibly underpinned by shared neurobiological mechanisms ¹⁴^,¹⁵. The autistic-catatonic continuum model further proposes that catatonia is best understood as a late-onset manifestation of underlying neurodevelopmental vulnerability rather than as a discrete ASD comorbid category, sustained by overlapping alterations in motor regulation, behavioural reactivity, and volitional processes ⁶^,¹⁴.

Within this framework, ADHD-related psychomotor dysregulation could be conceptualised, at least in a subset of individuals, as a parallel manifestation– either subthreshold or full-blown – of an autistic-catatonic continuum, an interpretation which allows apparently opposite motor phenomena to be read as expressions of a common dysregulation of motor intentionality and arousal, and which invites a reconsideration of the phenomenology of ADHD itself: the inattentive presentation, often characterised by difficulties in initiation, reduced goal-directed behaviour, and subjective experiences of mental “blocking”, bears a clinical resemblance to sub-stuporous states marked by reduced psychomotor initiative, slowed responsiveness, and diminished volitional engagement, as described in ASD individuals with catatonia ¹⁶^⁻¹⁸, while the hyperactive-impulsive and the combined presentations may reflect a state of psychomotor overactivation resembling the hyperactive dimension of catatonia. Without implying that ADHD constitutes a prodrome of catatonia, this interpretation supports the hypothesis that all three ADHD presentations may express, under different motor phenotypes, a shared position within a broader psychomotor regulation spectrum whose apparently opposite poles could correspond to distinct motor translations of a common underlying activation. This view is consistent with dimensional models of arousal regulation and with evidence of shared neurobiological substrates, including fronto-striatal circuit dysfunction and alterations in GABAergic and glutamatergic systems ¹⁹^⁻²¹. Moreover, the state-regulation model of ADHD posits dysregulated arousal, rather than executive dysfunction alone, as a core mechanism, a conceptualisation compatible with the arousal dysregulation underlying catatonic phenomena – a convergence further suggested by case reports and a systematic review describing the resolution of catatonic states following stimulant administration in patients refractory to first-line treatments ²²^⁻²⁷.

If empirically supported, this perspective may offer a more integrated framework for understanding ASD-ADHD co-occurrence without resorting to the now outdated concept of comorbidity, facilitate the recognition of subclinical catatonia, and inform transdiagnostic treatment strategies targeting arousal and psychomotor regulation. Important limitations should nonetheless be acknowledged: phenomenological similarities do not necessarily imply shared pathophysiology, direct evidence linking ADHD to catatonic dimensions remains scarce, and there is a substantial risk of overextending a unifying model in the absence of robust empirical validation. Further research is therefore needed to test this hypothesis through integrative approaches combining clinical assessment, dimensional assessment instruments, neurocognitive profiling, and neurobiological measures, with particular attention to the systematic mapping of a psychomotor continuum possibly spanning apparent hypoactivation and hyperactivation across ADHD and ASD populations, which may help to clarify whether these conditions share a common regulatory core.

In conclusion, conceptualising ADHD within an autistic–catatonic continuum represents a promising though still preliminary framework which, while it may enrich our understanding of psychomotor dysregulation across neurodevelopmental conditions, demands careful empirical validation before its clinical and nosological implications can be translated into diagnostic or therapeutic models.