Objective:

N/A

Background:

This case report describes a rare occurrence of isolated cranial nerve III palsy in a 26-year-old male with B12 deficiency, emerging after a dental procedure. Vitamin B12 plays a crucial role in maintaining myelin, and its deficiency can impair nerve function, causing demyelination. However, isolated cranial nerve involvement is uncommon. 
Cranial nerve palsies following dental anesthesia have been documented, with mechanisms such as vascular trauma, intravascular injection, or orbital spread contributing to nerve dysfunction. This case highlights how B12 deficiency may increase susceptibility to such events, with the dental procedure potentially acting as a trigger. 

Design/Methods:

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Results:

A 26-year-old male with no significant medical history presented to the ophthalmology clinic with double vision, a day after molar extraction. On examination, the left eye had a dilated pupil, ptosis, and limited adduction and supraduction, consistent with cranial nerve III palsy and hyperreflexia in his lower extremities. Serum and cerebrospinal fluid studies for metabolic, infectious, and autoimmune etiologies were unremarkable, except for decreased B12 (110) and vitamin D (17). Computed tomography angiography (CTA) was negative for vascular malformations. Brain MRI revealed a high T2 signal and contrast enhancement near the brainstem at the cranial nerve III exit, consistent with his clinical presentation. His symptoms resolved completely with three days of intravenous steroids and B12 supplementation, with no recurrence. 

Conclusions:

B12 deficiency is a known cause of nerve demyelination, but isolated cranial nerve III involvement is unusual without other neurological signs. In this case, local anesthesia might have exacerbated the underlying B12 deficiency, leading to the nerve palsy. While cranial nerve dysfunction after dental anesthesia is documented, the exact mechanism in this scenario remains unclear.