Âîïðîñû êëèíè÷åñêîé îôòàëüìîëîãèè 48 Îôòàëüìîëîãè÷åñêèé aeóðíàë ¹ 4, 2012 Dysfunction of the ocular motor nerves in patients with microvascular disease is a common cause of acquired diplopia [1] . Most of these cases were attributable to underlying systemic vascular diseases such as diabetes mellitus or hypertension [2] . One report calculated that the incidence of cranial nerve palsy in diabetics was 5 to 10 times higher than in nondiabetics [3] . Because both diabetic ophthalmoplegia and

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... tic retinopathy resulted from disturbances of normal microvascular function, it was suggested that the prevalence of each should be directly proportional [2] . A variety of neuro-ophthalmic manifestations have been associated with diabetes. Focal demyelinization of the cranial nerves with subsequent recovery appears to be the mechanism for development of cranial nerve palsies [4] . Diabetes mellitus was considered to be responsible for cranial nerve palsies more than arterial hypertension. The Purpose of this study is to detect the incidence of extraocular muscle palsy among diabetic patients and also to study the risk factors that may be associated. MATERIALS AND METHODS. The study included 932 diabetic patients, whether type 1 (108 patients; 11.59 %) or type 2 (824 patients; 88.41 %) diabete mellitus, who attended the diabetes outpatient clinic in Mansoura University, Egypt over two months from 12 January 2012 to 11 March 2012. They were 253 males (27.15 %) and 679 females (72.85 %) and their age ranged from 17 to 85 years with a mean age of (53.35±10.26) years. A detailed history and blood laboratory profile were obtained for each patient. Information was collected concerning age, sex, time of onset of diabetes, type of treatment for diabetes (oral hypoglycemic agents or insulin), presence of chronic complications of diabetes, history of other underlying medical conditions especially arterial hypertension and medical history. Ophthalmoscopic examination was done for all patients as well as eyelid movement, ocular motility in all directions of gaze, presence and type of any diplopia and if present, a diplopia chart was mapped and if diabetic retinopathy was diagnosed, it was recorded as non-proliferative or proliferative. Fasting and 2-hour postprandial blood sugar were tested for all patients. Data were expressed as mean ± standard deviation (SD) and/ or as percentage. Student's t-test was used for statistical evaluation of the data. Statistical significance was posted at level p<0.05. RESULTS During the period of the survey a total of 932 diabetic subjects were examined. The mean known duration of diabetes was (9.61±7.37) years with a range from one month to 40 years. Of these, 348 patients (37.34 %) were receiving oral hypoglycemic drugs while 584 pa-tients (62.66 %) were on insulin therapy. Antihypertensive drugs were prescribed for 695 patients (74.57 %) and the other 237 (25.43 %) were not hypertensive. Fundus examination revealed non-proliferative diabetic retinopathy in 77 patients (8.26 %) and 55 patients (5.90 %) had proliferative changes while the other 800 (85.84 %) had no clinically detectable diabetic retinopathy. Mean fasting blood glucose was (162.80±64.01) mg/ dl with a range from 46 to 452 mg/dl while mean 2-hour postprandial blood sugar was (241.18±103.23) mg/dl with a range from 59 to 780 mg/dl. Facial and ocular muscle palsy was identified in five patients (0.54 %). Of these five diabetic patients, one (20 %) was man and four (80 %) were women; the mean age was (54.00±5.43) years with a range from 49 to 62 years and the known duration of diabetes was (10.60±8.08) years with a range from one to 22 years. All these five patients were of type 2 diabetes mellitus (three of them (60 %) were on oral antidiabetic treatment and two (40 %) on insulin therapy). Four of them (80 %) were receiving treatment for arterial hypertension and were controlled while one (20 %) was not hypertensive. Three patients (60 %) had non-proliferative diabetic retinopathy while the fundi of the other two (40 %) had no visible diabetic changes. Mean fasting blood glucose was (214.67±43.88) mg/dl with a range from 164 to 240 mg/dl while mean 2-hour postprandial blood sugar was (330.67±200.05) mg/dl with a range from 192 to 560 mg/dl. The five cases of cranial nerve palsy included two cases (40 %) of facial nerve palsy ( fig.1 ), two cases (40 %) of abducent (VI) nerve palsy ( fig.2A&B ) and one case (20 %) of isolated inferior rectus (partial III nerve) palsy ( fig.3A&B ). No fourth nerve palsy was identified in the considered period. The onset of palsy was abrupt in all the cases and all the patients presented with clinical signs of the affected cranial ocular nerves (double vision, loss of or impaired motility of the eyeball, deviation of the eyeball, or inadequate closure of the eyelids). While these patients were found to have a more poorly controlled diabetes than other none-paretic patients, the differences in the fasting and 2-hour postprandial blood sugar were statistically non-significant. The differences in other risk factors including age, duration of diabetes, type of treatment, associated uncontrolled hypertension and presence and stage of diabetic retinopathy were also not statistically significant.