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العنوان
Metabolic syndrome and its role in
neuropsychiatric deficit/
المؤلف
AwadAllah,Hossam Sabry Ibrahim
هيئة الاعداد
باحث / حسام صبرى إبراهيم عوض الله
مشرف / أيمن محمد ناصف
مشرف / هالة محمود الخواص
الموضوع
Metabolic syndrome- neuropsychiatric deficit-
تاريخ النشر
2012
عدد الصفحات
155.p:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب النفسي والصحة العقلية
تاريخ الإجازة
1/1/2012
مكان الإجازة
جامعة عين شمس - كلية الطب - Neuropsychiatry
الفهرس
Only 14 pages are availabe for public view

from 119

from 119

Abstract

Metabolic syndrome is a combination of risk factors that increase risk of developing diabetes, cardiovascular and cerebrovsacular diseases. These include abdominal obesity, hypertension, dyslipidemia, impaired glucose tolerance, a prothrombotic state and a proinflammatory state.
The two major underlying risk factors for the metabolic syndrome are abdominal obesity and insulin resistance. The condition is progressive, beginning with borderline risk factors that eventually progress to categorical risk factors. In many patients, the metabolic syndrome culminates in type 2 diabetes, which further increases risk for cardiovascular and cerebrovascular diseases.
The metabolic syndrome is characterized by significant hemorheologic abnormalities known to adversely affect blood flow, particularly in the coronary and cerebral microcirculation ischemia and thus the clinical symptoms of metabolic syndrome.
Stroke is defined as a sudden onset focal neurological deficit of vascular etiology and is a major cause of mortality and morbidity around the world, ranked as the second leading cause of death worldwide, stroke is more often disabling than fatal. The estimated cost of stroke-related healthcare is a staggering 68.9 billion dollars measured in both healthcare dollars and lost productivity.
The nutrient supply to the nucleus cells of the disc can be disturbed at several points. Factors that affect the blood supply to the vertebral body such as vascular risk factors, the metabolic syndrome, all appear to lead to a significant increase in disc degeneration.
Overall obesity does not increase the risk of Parkinson’s disease. Among nonsmokers, abdominal obesity may be a risk factor for Parkinson’s disease, and this association warrants further investigation.
Neuropathies are characterized by a progressive loss of nerve fibers that can be assessed noninvasively by several tests of nerve function, including nerve conduction studies and electromyography, quantitative sensory testing, and autonomic function tests. A widely accepted definition of diabetic peripheral neuropathy is ”the presence of symptoms and/or signs of peripheral nerve dysfunction in people with diabetes after exclusion of other causes. Diabetic neuropathy is classified into several syndromes, each with a distinct pattern of involvement of peripheral nerves. Patients often have multiple or overlapping syndromes.
Peripheral neuropathies have been described in patients with primary (types 1 and 2) and secondary diabetes of diverse causes, suggesting a common etiologic mechanism based on chronic hyperglycemia.
People with the metabolic syndrome have a fivefold increased risk of developing type 2 diabetes if they do not already have it. An association between impaired glucose tolerance and peripheral neuropathy has been construed as further evidence of a dose-dependent effect of hyperglycemia on nerves, though this relationship remains an area of some controversy for type 2 diabetes and prediabetes. Pathologically, numerous changes have been demonstrated in myelinated and unmyelinated fibers.
Over 33% of women and 20% of men aged 65 and older will develop dementia during their lifetime, and many more will develop a milder form of cognitive impairment. Given the anticipated exponential increase in both the incidence and prevalence of cognitive impairment in the next century, it is critical to identify preventative strategies to thwart this critical publich health issue.
Several individual components of the metabolic syndrome have been linked to risk of developing dementia and cognitive impairment. At present, there is very strong evidence suggesting that hypertension, especially that in midlife, is a risk factor for dementia and accelerated cognitive decline.
In addition, multiple studies have shown that diabetes and pre-diabetes increases risk of developing dementia and Mild Cognitive Impairment (MCI). While less studied, dyslipidemia and obesity are increasingly being recognized as possible modifiable risk factors for dementia. However, few studies have looked at the components of the metabolic syndrome as a whole.
A study of middle-aged Japanese-American men, in which a composite score of 7 cardiovascular risk factors was associated with increased risk of developing vascular dementia but not with increased risk of developing AD.
Major depressive disorder is the most prevalent psychiatric illness in the United States, affecting more than 12% of men and more than 21% of women in their lifetime. Previous studies indicate that prevalence of major depression has increased during the past century, although these trends may, in part, be explained by methodological problems.
Depression has been associated with a variety of diseases; specifically it has been implicated in the development of cardiovascular disease/cerebrovascular (CVD) and all-cause mortality. However, little is understood about mechanisms that may account for poor health outcomes associated with depression.
Previous reports have speculated that depression may be linked to adverse health outcomes through an association with the metabolic syndrome. The metabolic syndrome, characterized by elevated abdominal obesity, triglycerides, blood pressure, fasting glucose, and low High-Density Lipoprotein (HDL) cholesterol, has an estimated prevalence of more than 21% in the US population; with obesity and sedentary behavior on the rise, the prevalence of the metabolic syndrome is likely to grow even higher in coming years. The metabolic syndrome is an important risk factor for the development of Cardiovascular Disease (CVD) and all-cause mortality.