Case Presentation: A 32-year-old male patient presented to the emergency department with double vision, preceded by headache, and increased burning in his feet. No other neurologic symptoms were reported. Past medical history was significant for poorly controlled, labile type 1 diabetes mellitus. His home medications included gabapentin for peripheral neuropathy, long-acting and short-acting insulin regimen. Physical examination was unremarkable except for a neurological exam which showed third cranial nerve palsy. The pupils were equal and reactive to light bilaterally. CT angiography of the head and neck revealed no acute ischemia, hemodynamically significant stenosis, aneurysm, or dissection. MRI of the brain also showed no abnormality. A review of his prior HbA1c values showed a decrease of 3.6 % ( 14% to 10.4%) over 3 months. The patient was diagnosed with Treatment Induced Neuropathy of Diabetes (TIND) presenting with simultaneous worsening of peripheral neuropathy and new-onset right oculomotor nerve palsy. The patient was discharged on reduced dose of insulin, targeting a gradual decline in HbA1c after initial stabilization. The patient was also asked to liberalize his diet and was given an eye patch. While his peripheral neuropathy improved, there was not much improvement in his double vision at a two-week follow-up visit.
Discussion: Our patient presented with worsening of peripheral neuropathy and pupil sparing oculomotor palsy. Secondary causes including CVA and aneurysm were excluded from brain imaging. Diabetes-related microvascular disease presenting with pupil sparing oculomotor palsy is commonly seen in patients older than 50 years of age with uncontrolled diabetes and other vascular risk factors like hypertension and dyslipidemia. Absence of hypertension and hyperlipidemia, sudden onset of presentation, and intense control of DM as evidenced by the rapid decline of A1C make TIND the likely cause for his presentation. The paradoxical worsening of his peripheral neuropathy also supports the diagnosis of TIND.
Conclusions: Treatment-induced neuropathy of diabetes (TIND) presenting as a new-onset peripheral neuropathy usually associated with autonomic dysfunction has been documented in the literature. It typically can occur when there is a drop of more than 2% drop in HbA1C in three months. Worsening of existing peripheral neuropathy and retinopathy has also been observed suggesting a common pathophysiological mechanism. However, the onset of a cranial neuropathy temporally linked to intensified glycemic control has not been well reported.Through this case of TIND, we highlight the importance of recognizing this entity as management differs significantly. Quality improvement metrics for practitioners in various institutions often include HbA1c target ranges in diabetic patients. Our case highlights the issues associated with rapid corrections of HbA1c and thus we advocate for a gradual decrease of 2 % every 3 months till target goals are reached.