In their article, Abo AlSamh and colleagues ^{Reference Abo AlSamh, Woo, Bruno, Karnik and Furtado1} provide a timely and valuable characterization of the non-motor and non-ataxia motor features of adult-onset cerebellar ataxia (AOCA) in a cohort of 145 patients recruited from a tertiary Movement Disorders clinic in Alberta, Canada. Their work addresses an important and frequently neglected dimension of these disorders. Clinical attention in ataxia has traditionally centered on the cerebellar motor syndrome, yet non-motor symptoms (NMSs) – including mood disorders, cognitive impairment and pain – are highly prevalent, as shown in this study, and contribute substantially to reduced quality of life. ^{Reference Malek, Makawita, Al-Sami, Aslanyan and de Silva2–Reference Lin, Kuo and Opal4} In fact, in a meaningful proportion of patients, the disability associated with these symptoms equals or even exceeds that caused by the motor syndrome itself. ^{Reference Moro, Moscovich, Farah, Camargo, Teive and Munhoz3,Reference Lin, Kuo and Opal4} Importantly, many NMSs can be managed through lifestyle interventions and pharmacological therapies, making their recognition and treatment central to comprehensive ataxia care. Yet, despite their impact on quality of life, these symptoms remain inconsistently assessed in practice and are too often overshadowed by the traditional focus on gait and coordination.

Despite their importance, NMSs have been systematically and prospectively characterized in only a subset of hereditary ataxias. ^{Reference Hengel, Martus and Faber5} Comparable, structured non-motor data across the broader AOCA spectrum remain scarce, and the Canadian ataxia landscape in particular is poorly explored. The study by Abo AlSamh and colleagues is therefore a welcome contribution: it begins to fill that gap, captures a clinically representative population spanning hereditary and sporadic forms and reinforces the need to embed non-motor assessment within the routine evaluation of these patients.

However, some limitations acknowledged by the authors warrant consideration. NMSs were ascertained from retrospective chart review rather than from validated, prospectively applied instruments, which almost certainly underestimates their true prevalence. The reported frequencies should accordingly be regarded as conservative. In addition, the cohort was assembled before the discovery of two of the most common causes of late-onset ataxia, spinocerebellar ataxia 27B (GAA-FGF14-related ataxia) and RFC1-related CANVAS (cerebellar ataxia, neuropathy and vestibular areflexia syndrome) and disease spectrum, ^{Reference Vegezzi, Ishiura and Bragg6} neither of which was screened. A substantial proportion of patients classified as sporadic adult-onset ataxia of unknown etiology may in fact carry these genotypes, which prevents genotype-specific interpretation within that subgroup.

These caveats notwithstanding, the authors should be commended for conducting this most needed study on the non-motor burden of AOCA. Their findings support routine, structured assessment of NMSs and provide a useful foundation for prospective, instrument-based studies in the Canadian ataxia population and beyond.