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العنوان
Clinical and Neurophysiological assessment of Cognitive impairment in Patients with Type 2Diabetes /
المؤلف
Hamza, Manar Hamza Sayed Hamza.
هيئة الاعداد
باحث / منار حمزة سيد
مشرف / حميد مصطفي عزب
hamaid_azab@med.sohag.edu.eg
مشرف / حازم كمال ابراهيم
مناقش / وفاء احمد فرغل
مناقش / طارق علي راجح
الموضوع
Diabetes Complications.
تاريخ النشر
2016.
عدد الصفحات
p 121. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب النفسي والصحة العقلية
تاريخ الإجازة
7/9/2016
مكان الإجازة
جامعة سوهاج - كلية الطب - الامراض العصبية والطب النفسى
الفهرس
Only 14 pages are availabe for public view

from 138

from 138

Abstract

Type 2 diabetes is associated with accelerated cognitive decline and an increased risk of dementia, particularly in older individuals. Previous studies have shown decrements in memory function, executive function, and information-processing speed. These decrements in cognitive functioning are associated with modest brain atrophy and vascular lesions on brain magnetic resonance imaging. Diabetes-related factors, such as insulin resistance, chronic hyperglycemia and lipid disorders probably are relevant determinants. Appropriate management and treatment of type 2 diabetes mellitus could prevent the onset and progression of mild cognitive impairment to dementia. Future treatment protocols should be developed with the cognitive status of patients with type 2 diabetes in mind. Evidence from neurocognitive testing suggests that cognitive dysfunction should be listed as one of the many complications of diabetes, along with retinopathy, neuropathy, nephropathy, and cardiovascular disease.
In our study there were 40 diabetic patients, we assessed there cognitive function using clinical, neurophsiological and radiological methods.
To conclude we found that diabetic patients experience decline in executive functioning. Cognitive impairments in patients with type 2 diabetes are related to structural changes in the brain. These changes are indicative of a vascular etiology, although the increased cortical brain atrophy and the relation with age are also suggestive of other mechanisms such as accelerated brain ageing. Cognitive dysfunction in T2DM appears to be due to permanent brain damage and correlated with the level of glycemic control and duration of diabetes.
We showed prolonged latency of P300 and reduced P300 amplitude at central midline brain area, in T2DM, without any association with disease duration or short-term metabolic control. The observed electrophysiological abnormalities may reflect impairment of attention, short-term memory and speed of information processing, possibly indicating an accelerated ageing process in diabetics. Our findings suggest that surface-recorded ERPs may be useful for detecting and monitoring the changes in brain function associated with diabetes mellitus.
Recommendations.
However, and despite the strength of our findings, this study had some limitations which include a relatively small sample size. Future researches have to include, the following:
-We recommend that more studies with larger numbers must be done to find the exact relation between diabetes and cognitive impairment including large number of patients
-We recommend Longitudinal studies that prospectively assess the relation of the disease process to cognition over time
-We recommend Comprehensive longitudinal evaluation of lab markers of brain damage, cognition, and brain imaging.
-We recommend that further understanding of the relationship between diabetes, cognitive impairment and the use of insulin and oral hypoglycemic.