| OCR Text |
Show ORIGINAL CONTRIBUTION A Case of Bilateral Simultaneous Sixth Cranial Nerve Palsies Secondary to Diabetes Mellitus Ay § e Oytun Bayrak, MD, Hacer Erdem Tilki, MD, and Dilek Kasim, MD Abstract: Ocular motor cranial nerve palsy secondary to diabetes mellitus usually affects one cranial nerve at a time. We report a patient with simultaneous bilateral sixth nerve palsies attributed to diabetes. Although an extremely rare cause of this phenomenon, diabetes may be the explanation after other causes have been excluded. (/ Neuro- Ophthalmol 2006; 26: 177- 179) Ocular motor ( third, fourth, or sixth) cranial nerve palsy is common in diabetic patients but is usually limited to a single cranial nerve ( 1,2). Bilateral cranial nerve palsies secondary to diabetes have rarely been reported ( 3- 7). We describe a patient with simultaneous bilateral sixth nerve palsies attributed to diabetes mellitus. CASE REPORT A 71- year- old man was admitted to the hospital because of a 1- month history of painless acute horizontal diplopia. Neuro- ophthalmologic examination was normal except for bilateral impairment of abduction more pronounced on the left ( Fig. 1), hypoactive deep tendon reflexes, and distal gradient hypesthesia. He had a history of surgery for laryngeal cancer 13 years earlier and had been diagnosed with diabetes mellitus 1 month earlier. There was no history of neurologic or cardiac disease, hypertension, cigarette smoking, or alcohol consumption. He had been taking an oral hypoglycemic agent for approximately 1 month. Laboratory examinations included a normal blood count, erythrocyte sedimentation rate, renal and liver function tests, thyroid function tests, and cerebrospinal fluid formula, including cytocentrifuge examination for neoplastic cells. There was an elevated Department of Neurology, Ondokuz Mayis University, Samsun, Turkey. Address correspondence to Ayse Oytun Bayrak, MD, Ondokuz Mayis University, Department of Neurology, 55139 Samsun, Turkey; E- mail: oytun. bayrak@ gmail. com plasma glucose level of 145 mg/ dL ( normal, 70- 110 mg/ dL) and HgAlC of 8.5% ( normal, 4- 6%). A pyridostigmine test for myasthenia gravis was negative. Repetitive nerve stimulation test of the trapezius and orbicularis oculi muscles was normal. Skull x- rays and MRI/ magnetic resonance angiography including the neck and head were normal. Given the normal examinations, we tentatively attributed the ocular motor findings to diabetes mellitus. The patient was prescribed an oral hypoglycemic agent, a controlled diet, and aspirin. Five months later, the ocular motor findings had disappeared ( Fig. 2). DISCUSSION Ocular motor cranial nerve palsies are common in diabetes, but our case represents an uncommon event in diabetes: bilateral simultaneous nerve palsies. In 1958 ( 8) and 1966 ( 9), Rucker reported the distribution and causes of paralysis of the ocular motor nerves in 2,000 patients but did not analyze cases of bilateral involvement. In 1976, Keane ( 10) analyzed 125 cases of bilateral sixth cranial nerve palsies; none was classified as diabetic. In 1981, Rush and Younge ( 11) analyzed 1,000 patients with ocular motor cranial nerve palsies and found bilateral involvement of the sixth cranial nerve in 33. None was caused by vascular disorders. In more than half of the cases, the bilateral sixth cranial nerve involvement was associated with head trauma, pontine neoplasm, or aneurysm of the posterior circulation. In that series, 8 patients had bilateral third cranial nerve palsies, 2 of which remained idiopathic. Thirteen patients had bilateral fourth nerve palsies, none from diabetes. In another large study of patients with ocular motor cranial nerve palsies ( 3), there were 53 cases of bilateral sixth nerve palsies; none was attributed to diabetes. Nine patients had bilateral third nerve palsies, 3 of undetermined cause and none from diabetes. Of the 21 bilateral fourth nerve palsies, none was attributed to diabetes. Considering both studies together ( 3,11), there were 15 ( 1.5%) cases with multiple cranial nerve palsies that were attributed to a vascular cause, 3 of them ( 0.3%) with diabetes. Two of these diabetic cases had asymmetric third and fourth cranial nerve palsies; J Neuro- Ophthalmol, Vol. 26, No. 3, 2006 177 J Neuro- Ophthalmol, Vol. 26, No. 3, 2006 Bayrak et al I * ^^ r ^ m FIG. 1. At presentation, the patient has reduced abduction bilaterally. the other was not further described. Sergott et al ( 4) reported two cases of bilateral third and fourth cranial nerve palsies associated with diabetes. In both cases, the ophthalmoplegia resolved completely within a few months. Jay and Nazarian ( 5) described a patient with bilateral sixth nerve palsy associated with temporal arteritis and diabetes. The cranial neuropathy was attributed to diabetes. In a 2003 study of 2,229 patients with ocular motor palsy, Trigler et al ( 6) reported 8 ( 0.1%) cases with multiple simultaneous palsies attributable to diabetes; 5 were unilateral and 3 were bilateral. The unilateral cases involved third and sixth cranial nerves in all but one case, which had combined third and fourth cranial nerve palsies. The bilateral cases consisted of a right third and left sixth nerve palsy, a right fourth and left sixth nerve palsy, and a right sixth and left fourth cranial nerve palsy. There were no cases of bilateral sixth nerve palsy associated with diabetes. In a study of 137 patients with sixth cranial nerve palsy over 178 © 2006 Lippincott Williams & Wilkins Simultaneous Bilateral Sixth Cranial Nerve Palsies J Neuro- Ophthalmol, Vol. 26, No. 3, 2006 FIG. 2. Five months after presentation, bilateral abduction deficit has resolved. a period of 15 years, Patel et al ( 12) found 4 cases of bilateral sixth nerve palsy but none was associated with diabetes. One of the cases was, however, classified in the undetermined group. The etiology of the other 3 cases was not mentioned. In 2005, Keane ( 7) analyzed 979 cases with multiple optical motor cranial nerve palsies in which 25 cases were attributed to diabetes mellitus but an undocumented number had other potential causes. The essence of this review is that multiple simultaneous ocular motor cranial palsies are not safely attributed to diabetes. Most cases will eventually be connected to neoplastic or inflammatory disease of the cranial base meninges. A proper workup with high- definition imaging and spinal fluid examination is indicated. REFERENCES 1. Ross AT. Recurrent cranial nerve palsies in diabetes mellitus. Neurology 1962; 12: 180- 5. 2. Zorilla E, Kozak GR Ophthalmoplegia in diabetes mellitus. Ann Intern Med 1967; 67: 968- 76. 3. Richards BW, Jones FR Jr, Younge BR. Causes and prognosis in 4,278 cases of paralysis of the oculomotor, trochlear and abdusens cranial nerves. Am J Ophthalmol 1992; 113: 489- 96. 4. Sergott RC, Glaser JS, Berger LI Simultaneous, bilateral diabetic ophthalmoplegia. Report of two cases and discussion of differential diagnosis. Ophthalmology 1984; 91: 18- 22. 5. Jay WM, Nazarian SM. Bilateral sixth nerve pareses with temporal arteritis and diabetes. Journal of Clinical Neuro- Ophthalmology 1986; 6: 91- 5. 6. Trigler L, Siatkowski RM, Oster AS, et al. Retinopathy in patients with diabetic ophthalmoplegia. Ophthalmology 2003; 110: 1545- 50. 7. Keane JR. Multiple cranial nerve palsies: analysis of 979 cases. Arch Neurol 2005; 62: 1714- 7. 8. Rucker CW. Paralysis of the third, fourth and sixth cranial nerves. Am J Ophthalmol 1958; 46: 787- 94. 9. Rucker CW. The causes of paralysis of the third, fourth and sixth cranial nerves. Am J Ophthalmol 1966; 61: 1293- 8. 10. Keane JR. Bilateral sixth nerve palsy: analysis of 125 cases. Arch Neurol 1976; 33: 681- 3. 11. Rush JA, Younge BR. Paralysis of cranial nerves III, IV and VI. Cause and prognosis in 1,000 cases. Arch Ophthalmol 1981; 99: 76- 9. 12. Patel SV Mutyala S, Leske DA, et al. Incidence, associations, and evaluation of sixth nerve palsy using a population- based method. Ophthalmology 2004; 111: 369- 75. 179 |
