## 4 Discussion  
The findings of IOM can be varied and are not always conclusive. The typical presentation of orbital myositis features the thickening of the affected EOMs, often encompassing the myotendinous junction and the surrounding fat, along with contrast enhancement [19]. We have noted that IOM is frequently associated with hypointense signals in the affected muscle on T1- and T2-weighted MRI sequences. This is particularly evident in chronic lesions that exhibit fibrosis. In contrast, acute lesions are characterized by predominant inflammation and increased intra- and extracellular fluid. These acute lesions typically show hyperintense signals on T2-weighted MRI sequences, as fibrosis has not yet formed. In our case, hyperintense signals were noted in T2-weighted TSE sequences, a typical indicator of inflammation associated with IOM [14]. Additionally, hyperintense muscle signals in fat-suppressed STIR sequences were observed, another marker of inflammation commonly seen in IOM [15]. Furthermore, a gadolinium contrast revealed increased enhancement, which is also characteristic of IOM. However, our case deviates from typical IOM presentations due to the absence of muscle belly enlargement [16]. However, the fact that the thickness of the extraocular muscles is within normal limits does not exclude prior swelling, especially since no previous MRI scans are available for comparison. Another unusual feature in our case is the lack of response to corticosteroid therapy [6]. In our case, the sole effective treatment was strict glycemic control, leading to the patient achieving a compensated diabetic state. Additionally, the situation may have been complicated by corticosteroid therapy, which exacerbated the glycemic imbalance and made it difficult for the patient to maintain stable blood sugar levels [30]. It would be valuable to perform follow-up imaging at one year to assess whether any long-term sequelae have developed, despite the complete resolution of symptoms in this case. Such imaging could provide additional insights into the evolution of the condition over time and help clarify whether any residual effects remain, especially considering the atypical aspects of the case. Long-term follow-up could also help determine if the strict glycemic control remains the only effective intervention or if other therapeutic approaches might be beneficial in the future. In the literature, two cases of IOM associated with diabetes mellitus have been described, both of which regressed promptly with corticosteroid treatment. In the first case, the patient was a 54-year-old woman with well-controlled DM2. In the second case, the patient was a 58-year-old man with poorly controlled DM2. However, in our patient, the only effective intervention was strict glycemic control, and no other causes of orbital myositis were identified [19; 20]. The exact etiopathogenice mechanism linking IOM with glycemic imbalance remains unclear. While there is growing evidence suggesting a potential association, the underlying pathophysiological processes require further investigation. Additional research and studies are needed to better understand the relationship between glycemic dysregulation and IOM, as well as to identify potential biomarkers or therapeutic targets. One condition that MRI can help diagnose, as demonstrated in recent studies, isynonecrosis related to glycemic dysregulation [31]. Fat-suppressed T2-weighted images in such cases have shown nearly 100% sensitivity. MRI can diagnose this condition with high sensitivity and specificity. Typically, T2-weighted images display hyperintensity, while T1-weighted images show isointense to hypointense signals in the affected muscle, accompanied by subcutaneous, perifascal, or peri-muscular edema [32]. Although orbital myonecrosis associated with glycemic dysregulation has not been reported in the literature, it is important to note that this condition predominantly affects the muscles of the lower limbs.