Movement disorders in diabetes mellitus: Our observations

We have read with interest the case report by Nahid et al.,¹ regarding diabetic striatopathy (DS) in an adult with ketotic hyperglycaemia. We commend the authors for their contribution and wish to elucidate several vital aspects.

1. Contrary to the authors’ depiction of DS as a rare and ‘life-threatening manifestation’ of diabetes, we contend that the condition’s relative rarity and under-recognition stem from anecdotal evidence such as case reports/series and a handful of retrospective studies.^2–5 Thus, comprehensive analyses on long-term prognosis, recurrence, the emergence of comorbid conditions, and mortality trends are pending.^2,3 From our observations, while DS affects the quality of life if untreated or mismanaged, fatalities specifically attributed to DS have not been reported.

2. In defining DS, the authors align with Chua et al. (2020).⁵ However, a newer and broadly accepted hypothesis by Dubey et al. (2022)⁶ encompasses symptomatic DS, clinically isolated DS, and radiologically isolated DS, challenging the necessity of striatal hyperintensity on T1-weighted magnetic resonance imaging (MRI) and contralateral movement disorder as definitive criteria.⁶ This underscores the prevalence of clinical–radiological discordance and indicates that diagnosis extends beyond mere blood analysis and neuroimaging findings.⁶

3. The report does not address the lack of awareness among neurologists—and by extension, general physicians and endocrinologists—regarding the spectrum of acute onset de novo non-choreoballistic movement disorders associated with DS, which are as prevalent as the classically described hemichorea– hemiballism.^2–10 This oversight by Nahid et al.¹ underscores the need for broader recognition of DS’s neurological manifestations.

4. Although the authors correctly identify poorly controlled chronic glycaemia as a pivotal risk factor for DS and related movement disorders,¹ this does not account for the instances where rapid correction of hyperglycaemia precipitates or exacerbates movement disorders.^2,3 This suggests that both chronic hyperglycaemia and acute glycaemic fluctuations, potentially due to disruption of the basal ganglia circuitry and failure of striatopallidal blood flow autoregulation, contribute to the pathophysiology of DS.⁶

5. We question Nahid et al.’s interpretation¹ of T1 hyperintensity in Figure 2 of their manuscript, proposing instead that the imaging might depict a T2-weighted fluid-attenuated inversion recovery (FLAIR) sequence. The distinction between T2-FLAIR and T1-weighted images, particularly in cerebrospinal fluid darkness and grey–white matter contrast, is critical.¹¹ Furthermore, we challenge the purported clinical–radiological corroborative intensity changes over the right striatum.⁶

Hyperglycaemia-induced movement disorders often demonstrate remarkable reversibility with correction of hyperglycaemia alone.^2–10 We aim to amplify the imperative for clinicians to employ a broader differential diagnosis approach for abnormal limb movements in patients with DS, emphasizing the criticality of precise movement semiology identification, stringent and prompt blood glucose management, and the utilization of appropriate neuroimaging for expedited diagnosis and prevention of complications. Such diligence can facilitate early diagnosis, circumvent severe complications, reduce unnecessary expenditures, and prevent diagnostic and therapeutic errors.