Neural Dysfunction (neural + dysfunction)

Distribution by Scientific Domains

Selected Abstracts

Diet-induced obesity in Sprague,Dawley rats causes microvascular and neural dysfunction

Eric P. Davidson
Abstract Background The objective of this study was to determine the effect of diet-induced obesity (DIO) on microvascular and neural function. Methods Rats were fed a standard or high fat diet for up to 32 weeks. The following measurements were carried out: vasodilation in epineurial arterioles using videomicroscopy, endoneurial blood flow using hydrogen clearance, nerve conduction velocity using electrical stimulation, size,frequency distribution of myelinated fibres of the sciatic nerve, intraepidermal nerve fibre density using confocal microscopy and thermal nociception using the Hargreaves method. Results Rats fed a high fat diet for 32 weeks developed sensory neuropathy, as indicated by slowing of sensory nerve conduction velocity and thermal hypoalgesia. Motor nerve conduction velocity and endoneurial blood flow were not impaired. Mean axonal diameter of myelinated fibres of the sciatic nerve was unchanged in high fat-fed rats compared with that in control. Intraepidermal nerve fibre density was significantly reduced in high fat-fed rats. Vascular relaxation to acetylcholine and calcitonin gene-related peptide was decreased and expression of neutral endopeptidase (NEP) increased in epineurial arterioles of rats fed a high fat diet. In contrast, insulin-mediated vascular relaxation was increased in epineurial arterioles. NEP activity was significantly increased in the skin of the hindpaw. Markers of oxidative stress were increased in the aorta and serum of high fat-fed rats but not in epineurial arterioles. Conclusion Chronic obesity causes microvascular and neural dysfunction. This is associated with increased expression of NEP but not oxidative stress in epineurial arterioles. NEP degrades vasoactive peptides, which may explain the decrease in microvascular function. Copyright © 2010 John Wiley & Sons, Ltd. [source]

Diabetic neuropathy and oxidative stress

Rodica Pop-Busui
Abstract This review will focus on the impact of hyperglycemia-induced oxidative stress in the development of diabetes-related neural dysfunction. Oxidative stress occurs when the balance between the production of reactive oxygen species (ROS) and the ability of cells or tissues to detoxify the free radicals produced during metabolic activity is tilted in the favor of the former. Although hyperglycemia plays a key role in inducing oxidative stress in the diabetic nerve, the contribution of other factors, such as endoneurial hypoxia, transition metal imbalances, and hyperlipidemia have been also suggested. The possible sources for the overproduction of ROS in diabetes are widespread and include enzymatic pathways, auto-oxidation of glucose, and mitochondrial superoxide production. Increase in oxidative stress has clearly been shown to contribute to the pathology of neural and vascular dysfunction in diabetes. Potential therapies for preventing increased oxidative stress in diabetic nerve dysfunction will be discussed. Copyright © 2006 John Wiley & Sons, Ltd. [source]

Self-reported severity of taste disturbances correlates with dysfunctional grade of TMD pain

Summary, Altered central neural processing of sensory information may be associated with temporomandibular disorders (TMD) pain. The objectives of this study were to compare the prevalence of self-reported taste disturbances in TMD pain patients and in a control population, and to determine whether frequency of taste disturbances was correlated with dysfunctional grade of TMD pain. Subjects were 2026 people within a German population sample and 301 consecutive TMD patients diagnosed using the Research Diagnostic Criteria. Taste disturbances were measured using two questions from the Oral Health Impact Profile. Dysfunctional grade of TMD pain was measured with the Graded Chronic Pain Scale. A two-sample test of proportions revealed that TMD patients reported a greater frequency of taste disturbances, 6%, than did the general population subjects, 2% (P < 0·001). Moreover, the frequency of taste disturbances correlated with the dysfunctional grade of TMD pain. For each 1 unit increase in taste disturbance, the odds of observing a higher grade of TMD pain increased by 29% (95% CI: 3,63%, P = 0·03). Analysis by individual taste question and adjustment for age and gender did not substantially affect the results. These findings are consistent with a central neural dysfunction in TMD pain and suggest that a common neural substrate may underlie sensory disturbances of multiple modalities in chronic pain patients. Further research regarding taste disturbances and trigeminally mediated pains such as in TMD is warranted. [source]

Increased glutamate/glutamine compounds in the brains of patients with fibromyalgia: A magnetic resonance spectroscopy study

Manuel Valdés
Objective Fibromyalgia (FM) has been defined as a systemic disorder that is clinically characterized by pain, cognitive deficit, and the presence of associated psychopathology, all of which are suggestive of a primary brain dysfunction. This study was undertaken to identify the nature of this cerebral dysfunction by assessing the brain metabolite patterns in patients with FM through magnetic resonance spectroscopy (MRS) techniques. Methods A cohort of 28 female patients with FM and a control group of 24 healthy women of the same age were studied. MRS techniques were used to study brain metabolites in the amygdala, thalami, and prefrontal cortex of these women. Results In comparison with healthy controls, patients with FM showed higher levels of glutamate/glutamine (Glx) compounds (mean ± SD 11.9 ± 1.6 arbitrary units [AU] versus 13.4 ± 1.7 AU in controls and patients, respectively; t = 2.517, 35 df, corrected P = 0.03) and a higher Glx:creatine ratio (mean ± SD 2.1 ± 0.4 versus 2.4 ± 1.4, respectively; t = 2.373, 35 df, corrected P = 0.04) in the right amygdala. In FM patients with increased levels of pain intensity, greater fatigue, and more symptoms of depression, inositol levels in the right amygdala and right thalamus were significantly higher. Conclusion The distinctive metabolic features found in the right amygdala of patients with FM suggest the possible existence of a neural dysfunction in emotional processing. The results appear to extend previous findings regarding the dysfunction in pain processing observed in patients with FM. [source]