Navigating the Glucose Surge: Painful Trigeminal Neuropathy and Transient Speech Disturbance in a Patient With Severe Hyperglycemia and Rapid Glycemic Correction

Background: Uncontrolled diabetes mellitus can lead to neurological complications such as seizures, altered mental status, and chorea, most commonly in the context of diabetic ketoacidosis (DKA) or hyperglycemic hyperosmolar state (HHS).Treatment-induced neuropathy of diabetes (TIND) is a rare and underrecognized complication associated with rapid improvement in glycemic control.It typically presents with acute-onset neuropathic pain, weakness, or autonomic dysfunction within eight weeks of glycemic improvement, and less frequently with focal or cranial neurological deficits.Case presentation: We report a 72-year-old man with poorly controlled type 2 diabetes mellitus (T2DM) and hypertension who presented with transient expressive aphasia evolving to persistent dysarthria during severe hyperglycemia with hyperosmolality, in the absence of DKA or HHS.After rapid correction of glycemia over several days, he developed continuous left facial pain in the trigeminal distribution with focal tenderness, a presentation consistent with painful trigeminal neuropathy rather than classic trigeminal neuralgia, accompanied by transient confusion.Computed tomography (CT), magnetic resonance imaging (MRI), vascular imaging, and an extensive diagnostic workup were unremarkable, excluding cerebrovascular and structural causes.The temporal association between the facial pain and rapid glycemic correction raised TIND as a possible, atypical, cranial nerve-predominant explanation; however, this diagnosis remained presumptive, as no baseline HbA1c was available to document the glycemic trajectory required by accepted diagnostic criteria.The facial pain resolved promptly with gabapentin.Conclusions: This case illustrates two temporally distinct neurological processes: severe hyperglycemiaassociated neurological dysfunction preceding treatment and facial neuropathic pain following rapid glycemic correction, rather than a single unifying syndrome, with TIND as a possible, but not confirmed, explanation for the latter.It highlights the differential diagnosis of acute neurological events in patients with diabetes, in whom evaluation for cerebrovascular disease remains essential even when initial imaging is unremarkable, and underscores the potential importance of cautious glycemic correction and neuropathic pain-directed symptomatic management.