Abstract

Introduction

Diabetic neuropathy is one of the most common long-term complications of type 2 diabetes, Approximately 50% of patients with diabetes mellitus type I or type II will eventually develop neuropathy.^[1–3] The clinical presentation may be polyneuropathy, autonomic neuropathy, polyradiculopathies, or mononeuropathies, although many overlap syndromes occur.

While majority of such patients have distal symmetrical neuropathy, some patients develop focal and multi-focal neuropathies, including cranial nerve palsies.

The most common diabetic cranial mononeuropathies occur in those nerves which supply the extraocular muscles (III , VI  and IV).

The involvement of the third nerve could be congenital or acquired in nature. The main causes of acquired third nerve palsy include: infections (CNS or local), trauma, direct or indirect compression of the nerve anywhere along its path, vascular conditions (ischemic/aneurysms), neoplastic, inflammatory or demyelinating diseases.^[4,5]

 It could be complete or partial, pupil-sparing or involving, isolated or associated with other neurological symptoms.

It is important for the clinician to think about a wide variety of differential diagnoses in patients with diabetes presenting with cranial nerve palsy, as there are significant implications in treatment and prognosis depending on the cause.

Isolated superior division oculomotor nerve palsies are rare and generally result from structural lesions.^[6]

We describe a patient with ptosis as the only manifestation of diabetic superior division oculomotor nerve palsy that recovered partially after the blood sugar was well-controlled.

The neurological examination revealed ptosis of the right upper eyelid. The pupils were equal and normally reactive. The extraocular movement and ocular alignment were normal. Other neurological examination revealed negative findings. During hospitalization, hyperglycemia with the glycated hemoglobin (10.9%).

Brain magnetic resonance imaging showed no significant abnormalities. There was no clinical or laboratory evidence consistent with the diagnosis of myasthenia gravis, Lyme disease, syphilis, temporal arteritis, or other systemic vasculitis.

We controlled her blood sugar aggressively by regular insulin 14 units before each meal  subcutaneous injections and tablet Metformin 500mg before breakfast. With intensive sugar control for 7 days, her blood sugar before discharge was 128mg/dL. After the hyperglycemia improved, the right side ptosis recovered partially within 1 week both subjectively and objectively. The diagnosis of diabetic oculomotor nerve palsy was made. Diabetes induced ischemic injury of nerve fibers innervating levator palpebrae superioris is the most possible cause.