Neurological Complications Of Diabetes Mellitus Research Articles

Diyabetes Mellitusta Postür, Denge ve Yürüme Bozuklukları

There are several different complications of diabetes mellitus in many body systems. Diabetic neuropathy is one of the most important neurological complication of diabetes mellitus. Neurological complications of diabetes mellitus are predisposing factors for the development of posture, gait and balance disorders and falls. These issues have been briefly reviewed in this article.

Effects of L-glutamine supplementation on the myenteric neurons from the duodenum and cecum of diabetic rats

Peripheral neuropathy is one of the chronic complications of diabetes mellitus and is directly related to gastrointestinal consequences of the disease. Myenteric neurons are affected in some pathological conditions such as diabetic neuropathy. The imbalance between cellular antioxidants and free radicals, leading to an increase in oxidative stress, is considered one of the main factors responsible for neuronal damages in diabetes. Drugs that reduce the oxidative stress may play a significant role in the treatment of neurological complications of diabetes mellitus. To evaluate the effect of L-glutamine supplementation on the myenteric neurons from the cecum and duodenum of Wistar rats with streptozotocin-induced diabetes mellitus. The animals were divided in four groups (n = 5): non-treated normoglycemics, normoglycemics treated with L-glutamine, non-treated diabetics and diabetics treated with L-glutamine from the 4th day of diabetes induction on. The amino acid L-glutamine was added to their diet at 1%. Giemsa's technique was employed to stain the myenteric neurons. We determined the cell body area of 500 neurons in each group studied. The quantitative analysis was performed by sampling in an area of 16.6 mm² in the cecum and 3.6 mm² in the duodenum of each animal. After the supplementation with L-glutamine in the duodenum, we observed a preservation of neuronal density in groups normoglycemic and diabetic (P<0.05). We also observed a preservation of the cell bodies area in diabetic animals (group treated with L-glutamine) (P<0.05). In the cecum, that preservation was not evident. Supplementation with L-glutamine (1%) promoted a neuroprotective effect on the myenteric neurons from the duodenum of rats, both in terms of natural aging and of diabetes mellitus.

METABOLIC CORRECTIONOFNEUROLOGICALCOMPLICATIONS OFDIABETES MELLITUS

The concepts of the metabolic and vascular mechanisms responsible for the occurrence and progression of neurological complications of diabetes mellitus are presented. The results of some investigations demonstrating the efficacy of actovegin in the treatment of diabetic polyneuropathy, encephalopathy, and diabetic foot syndrome are given.

No correlation between impairment of cerebrovascular reserve capacity and electrophysiologically assessed severity of neuropathy in noninsulin-dependent diabetes mellitus

Introduction: Microvascular abnormalities have an important role in the most frequent neurological complications of diabetes mellitus: neuropathy and cerebrovascular disorders. Severity of neuropathy as well as of cerebral microvascular damage can be quantitatively evaluated by instrumental methods like nerve conduction studies and transcranial Doppler. In the present study, we investigated whether a correlation exists between the severity of peripheral neuropathy and the impairment of cerebrovascular reserve capacity (CRC) in 20 patients with Type 2 diabetes mellitus. Methods: CRC was measured by transcranial Doppler and defined as the maximal percentage increase in blood flow velocity in the middle cerebral artery within 20 min after an intravenous dose of 1000 mg of acetazolamide. Nerve conduction studies of the median, ulnar, peroneal, and sural nerves were performed. Severity of neuropathy was scored based on conduction velocities, amplitudes, and distal latencies. Results: There was no correlation between the neuropathic score and CRC ( R=.003, P=.99). Neither CRC nor the neuropathic score correlated significantly with age, duration of diabetes, and serum values of HbA 1c, glucose, insulin, von Willebrand factor, and α 2-macroglobulin. Severity of neuropathy but not CRC correlated with microalbuminuria ( R=.47, P=.038 and R=.14, P=.54). Improper treatment reflected by HbA 1c>10% was associated with significantly more severe albuminuria, higher actual blood glucose level, higher von Willebrand factor activity, and marginally higher neuropathic score (21 vs. 13, P=.096), but was not associated with CRC (44% vs. 42%, P=.81). When duration of diabetes was dichotomized to 15 years and less or over 15 years, CRC was significantly smaller (35% vs. 50%, P=.036) and neuropathy was more severe in the subgroup with longer diabetes duration (19 vs. 11.5 points, P=.07). Conclusions: Although both CRC and peripheral nerve function are affected more severely in patients with long-lasting Type 2 diabetes mellitus, damage in the cerebrovascular system and in the long peripheral nerves occur independently. As in diabetes mellitus pathological changes in autonomic and large peripheral nerves develop simultaneously, decreased CRC in diabetic patients might be predominantly due to structural changes of resistance arteries or to metabolic than to neurogenic factors.

Effect of α-lipoic acid on vascular responses and nociception in diabetic rats

Oxidative stress contributes to the vascular and neurological complications of diabetes mellitus. The aim was to evaluate the effects of treatment with the radical scavenger and transition metal chelator, α-lipoic acid, on endothelium-dependent relaxation of the mesenteric vasculature and on superior cervical ganglion blood flow in 8 week streptozotocin-induced diabetic rats. α-Lipoic acid effects on small nerve fiber-mediated nociception were also monitored. For the in vitro phenylephrine-precontracted mesenteric vascular bed, diabetes caused a 31% deficit in maximum endothelium-dependent relaxation to acetylcholine, and a 4-fold reduction in sensitivity. α-Lipoic acid gave 85% protection against these defects. Acetylcholine responses are mediated by nitric oxide and endothelium-derived hyperpolarizing factor: isolation of the latter by nitric oxide synthase blockade revealed a 74% diabetic deficit that was halved by α-lipoic acid. Superior cervical ganglion blood flow, 52% reduced by diabetes, was dose-dependently restored by α-lipoic acid (ED 50, 44 mg/kg/d). Diabetic rats exhibited mechanical and thermal hyperalgesia, which were abolished by α-lipoic acid treatment. Thus, diabetes impairs nitric oxide and endothelium-derived hyperpolarizing factor-mediated vasodilation. This contributes to reduced neural perfusion, and may be responsible for altered nociceptive function. The effect of α-lipoic acid strongly implicates oxidative stress in these events and suggests a potential therapeutic approach.

Optic disc oedema and diabetes mellitus: a case report with review

Optic disc oedema is a neurological complication of diabetes mellitus. Typically, the patient is a young diabetic with minimal symptomatology but severe bilateral optic disc oedema discovered on routine eye examination. It is a relatively benign condition which on occasion can result in a residual visual deficit, but requires no specific intervention and represents a subgroup of anterior ischaemic optic neuropathy (AION). We present a patient with insulin dependent diabetes and asymptomatic bilateral optic disc oedema, with a brief review of the syndrome and its pathogenesis.