Risk Factors Associated With Diabetic Cranial Neuropathy

Objective：The incidence of Cranial nerve lesion (CNL) in diabetic patients is low,but the impact of CNL on patients’ quality of life is considerable. It has notknown the risk factors, prevention and treatments, which are involved in thedevelopment of diabetic cranial neuropathy (DCN). The aim of this study is toinvestigate the incidence of cranial neuropathies, to analyze the associationbetween DCN and various risk factors, such as patients’ natural situations,habits, glucose toxicity, lipotoxicity, and duration of diabetes, diabetestreatment and complications，hence to guide clinical prevention and treatmentof DCN.Methods:We have performed a retrospective study of diabetic patients with cranialnerve lesions who were hospitalized in our hospital from January1st,2004toJanuary1st,2012. The patents have been divided into two groups, namelyDCN group and control group. Through laboratory tests, brain CT and MRI toexclude cerebral infarction, myasthenia gravis, intracranial aneurysms,hyperthyroid ocular disease, intracranial infection, intracranial tumors and otherreasons result in cranial neuropathy. We randomly picked60diabetic patientswithout cranial nerve lesions. And collected each qualified patient’s naturalsituations (age, gender), smoking habit, duration of diabetes,treatments, glucoseindices (fasting plasma glucose (FPG), postprandial glucose (PPG),glycosylated hemoglobin (HbA1C)), lipids metabolic indices (triglyceride (TG),cholesterol (CHOL), high-density lipoprotein cholesterol (HDL-C),low-density lipoprotein cholesterol (LDL-C)), creatinine (CRE), diabeticretinopathy and hypertension history. Analyzed the association between all above factors and diabetic cranial neuropathy。Data were analyzed by SPSSv18statistical software.Results:1、During the period of the survey, a total of863patients with craniallesions and46650diabetic patients were hospitalized. And diabetic cranialneuropathies were identified in92patients, all with type2diabetes. No cranialnerve lesion appeared in patients with type1diabetes. DCN accounted for0.20%of diabetic subjects and10.7%of cranial lesions subjects, includedfacial nerve palsies total of30cases,18cases with oculomotor nerve palsies,41cases with abducens nerve palsies, and3cases with trochlear nerve palsies.We detected that onset of DCN is acute. Majority patients had no obviousincentive before the sudden appearance of the corresponding performance ofthe cranial nerve palsies. Most of patients presented in a single cranial nervelesion, and only on one side of nerves, then multiple cranial neuropathies wererare.2. Compared with the control group, DCP group presented significanthigher FPG and PPG (P <0.05). The difference of treatment was statisticallysignificant (P <0.05), but the impact of oral medication and insulin therapyneed further regression analysis. The DCN cohorts showed a significant higherincidence of retinopathy compared with the control group (P <0.05). There wasan increased tendency toward on HbA1C levels, CHOL levels, LDL levels, ageand duration of diabetes in DCN group, but no statistical difference (P>0.05).No differences on Sex, hypertension and smoking history, TG and CREbetween the two groups.3. Regression analysis showed that the development ofDCN was positively associated with fasting glucose (P <0.05, OR=1.325),postprandial glucose (P <0.05, OR=1.119), and diabetic retinopathy (P <0.05,OR=2.429). Insulin therapy also illustrated a positive correlation with DCN,but no statistical effect (P>0.05, OR=2.063).Conclusion： The present studies demonstrate that fasting plasma glucose andpostprandial plasma glucose are risk factors on developing into diabetic cranialneuropathy. It is meaningful to control FPG levels and PPG levels on theprevention and treatment of diabetic cranial neuropathy. Patients with diabeticretinopathy perhaps indicate who has more possibility to develop into cranialneuropathy. Insulin therapy might be another risk factor can result in diabeticcranial neuropathy.