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Diabetes is a metabolic disease defined by increased blood glucose level above the references value. Insulin therapy is mandatory for all patients with type 1 diabetes melitus (T1DM). However, the insulin therapy is also the potential factor of hyperglycemia as well as hypoglycemia condition called dysglycemia. Moreover, T1DM leads to late organ changes such as retinopathy and nephropathy primarily due to diabetic angiopathy. Neuropathy is one of diabetic complications which can occur from the beginning of the disease. The pathogenesis of diabetic neuropathy, a structural and morphological abnormality, has been well described. In adults with T1DM diagnosed in childhood more frequent incidence of epilepsy, abnormal EEG and impaired cognitive functions were diagnosed. In children with type I diabetes further in depth studies are needed concerning the structural and functional damage of the central nervous system (cns). Research studies carried out in children have shown that the metabolic and morphological cns changes are the result of both hypo- and hyperglycemia.

Background: Hypoglycemia is an acute disturbance of energy, especially impacting the central nervous system, but direct influence on peripheral nervous function is not detected. The aim of the study was to establish the influence of hypoglycemic moderate and severe episodes on the function of peripheral nerves, hearing and visual pathway., Material and Methods: 97 children with type 1 diabetes (mean age 15.4+/-2.16 years, mean duration of diabetes 8.11+/-2.9 years, mean HbA1c 8,58+/-1.06%), at least 10 years old and with at least 3 years duration of diabetes, were included to study. Nerve conduction studies, visual (VEP) and auditory (ABR) evoked potentials were performed with standard surface stimulating and recording techniques. Moderate hypoglycemic episodes were defined as events of low glycemia requiring help of another person but without loss of consciousness and/or convulsions but recurrent frequently in at least one year. Severe hypoglycemia was defined as events with loss of consciousness and/or convulsions. Univariate ANOVA tests of significance or H Kruskal-Wallis test were used, depending on normality of distribution., Results: The subgroups with a history of hypoglycemic episodes had significant delay in all conduction parameters in the sural nerve (amplitude p<0.05, sensory latency p<0.05, and velocity p<0.005) and in motor potential amplitude of tibial nerve (p<0.005). In ABR wave III latency and interval I-III in subgroups with episodes of hypoglycemia (p<0,05) were significantly prolonged. In analyses of VEP parameters no differences were detected., Conclusions: The study showed influence of hypoglycemic episodes on function of all sural nerve parameters and tibial motor amplitude, and in ABR on wave III and interval I-III. Frequent moderate hypoglycemic episodes were strong risk factors for damage of the peripheral and central nervous systems, comparable with impact of several severe hypoglycemias.

In the presented work, the researches of foreign and Polish authors were reviewed. The aim of this project was to find the answer to the question connected with the character and the cause of diabetes' influence on cognitive functions of patients. Diabetes is a metabolic condition of a various etiologyaetiology. It is distinguished by chronic hiperglycemia with the disorder of metabolism of carbohydrates, fat and proteins as a result of giving off defects and/or working insulin. Cognitive functions are these psychological functions which the human needs in order to be knowledgeable about surroundings, to get the information about oneself and your body, to analyse the situations, to formulate conclusions, to take a right decisions or to function. In the last few years, this typical somatic disease, as the diabetes is, puts pressure on cognitive efficiency of the human body. The vita issue is to get to know this problem not only from medical or psychological point of view but also it has a great influence on patients' better life. The knowledge of this subject should be known among medical surroundings as well as in all the places where the patients live (school, workplace and family).

Fetuin A and matrix GLA protein--MGP are known as extraosseus calcification inhibitors. The aim of the study was to assess the dependence between metabolic status and fetuin A and matrix GLA protein levels in type 1 diabetic patients without ischaemic heart disease. The study was performed in a group consisting of 35 patients with type 1 diabetes mellitus (22 women and 13 men). Mean age of the studied group equaled 38.8 +/- 11.24 years, duration of diabetes mellitus 20.77 +/- 10.11 years. Fetuin A significantly correlated with HDL-cholesterol (r = 0.45; p = 0.007). Total cholesterol, LDL-chol and triglicerides correlated with HbA1c (r = 0.40, p = 0.03; r = 0.41, p = 0.03 and r = 0.37, p = 0.05), HDL-chol significantly correlated with glucose level at the examination day (r = 0.52, p = 0.04). There were also positive correlations of trigliceride with uric acid (r = 0.47, p = 0.09) and cystatin C (r = 0.44, p = 0.02). There were no correlation of MGP with other examined parameters. Initial results of fetuin A and MGP levels in long-term type 1 diabetic patients without ischaemic heart disease draws attention to new parameters in macroangiopathy development.

Unlabelled: Cardiovascular and renal complications among type 1 diabetic patients are predictive factors for sudden cardiac death and stroke. The aim of the study was to assess the prevalence of diabetic nephropathy and autonomic neuropathy in type 1 diabetic patients with and without diastolic dysfunction in echocardiographic examination. The study was performed in a group consisting of 37 patients with type 1 diabetes mellitus. Mean age of the study group equaled 37.24 +/- 10.85 years, duration of diabetes mellitus 21.3 +/- 9.55 years. All patients performed EKG, and cardiovascular autonomic test with ProSciCard according to Ewing battery. The following parameters were assessed: heart rate (HR), standard deviation of HR, RMSDD, VLF, LF, HF, deep breathing test, Ewing supine test and Valsalva maneuver. Systolic and diastolic function was assessed in echocardiography examination at rest. In all patients following laboratory parameters were assessed: HbA1c, total chol, LDL-chol, HDL-chol, triglicerides, uremic acid, glucose, albumin, creatinine, cystatin C, microalbuminuria., Results: mean heart rate in the examined group --78.38 +/- 15.54 /min, VLF--1.59 +/- 1.7; LF--4.22 +/- 1.51, HF--0.82 +/- 0.88, mean heart rate during deep breathing test --79.63 +/- 13.71, Ewing ratio--0.91 +/- 0.11. Cardiovascular autonomic neuropathy and diabetic neuropathy were diagnosed in 3 patients, these patients suffered also from proliferative retinopathy and diabetic nephropathy. The remaining group of 34 patients has normoalbuminuria. Calculated creatinine clearance according to Cockroft-Gault equation was 88.85 +/- 9.60 m/min, cystatin C concentration--0.97 +/- 0.22 ng/ml. In echocardiography exam, there were no abnormalities in systolic function, and diastolic dysfunction was diagnosed in 15 patients. Preliminary results showed that only the cystatin C level significantly differed patients with and without diastolic dysfunction in echocardiographic examination. Cystatin C could be the first sign of renal failure among these patients. Cardiovascular autonomic neuropathy and diabetic nephropathy were diagnosed only in 3 patients with left ventricular diastolic dysfunction in echocardiographic study.

Charcot neuroarthropathy (CN)--chronic and progressive, destructive disease of bones and joints, which develops on the background of neuropathy, is late and uncommon complication of diabetes. It occurs almost exclusively in patients with a mean duration of diabetes at least 10 years. We report the case of woman, who developed an acute phase of CN 11 months after recognition of diabetes. Because of recent recognition of diabetes and good glycaemic control, CN wasn't considered in the differential diagnosis of swelling, pain and warmth of feet. The initial diagnosis was missed, leading in few months, to development of irreversible deformity of both feet.

We report on three patients (two men with recently discovered type 1 diabetes and one woman with type 2 diabetes and secondary failure of oral antidiabetic drugs) who developed acute painful neuropathy after the institution of effective insulintherapy and rapid drop of glycemia. The EMG disclosed in them traits of mixed lesions of motor-sensory neurons at the level of nerve fibres, more evident in sensory nerves of low extremities. In one patient (A) observed for 5 years, in spite of progressive partial remission of clinical symptoms and signs, no improvement in successive EMG was found. The evident therapeutic effect of alpha-lipoic acid in the presented cases needs to be confirmed in appropriate prospective studies.

Unlabelled: The occurrence of autonomic neuropathy in patients with diabetes is associated with increased incidence of cardio-vascular events and increased mortality. The character of such process is not clear yet and the question if the damage to autonomic nerves equally involves particular organs and systems is open. The aim of the study was to assess the concordance of cardio-vascular neuropathy with diabetic gastropathy in type 1 diabetic patients. The study involved 42 subjects with type 1 diabetes mellitus (age 36.7 +/- 8.3 years; duration of the disease 14.8 +/- 33 years). Gastric emptying of solid food was assessed scintigraphically. T1/2 max and residual isotope activity (expressed as the percentage of initial value) at 45th minute of the study were estimated. Autonomic cardio-vascular neuropathy was assessed based on the Ewing battery tests results., Results: 11 of all subjects (group A) showed normal or increased gastric emptying of solid foods (T1/2 max 36.6 +/- 9.3 min, residual activity 39.6 +/- 12.1%) and 31 remaining subjects (group B) demonstrated delayed gastric emptying (T1/2 max 89.2 +/- 11.4 min, residual activity 74.6 +/- 5.2%), which was regarded as diabetic gastropathy symptom. 31 (74%) of all subjects were diagnosed with cardio-vascular neuropathy, 18 of them (43%) showed early autonomic neuropathy and remaining 13 (31%) presented decided cardio-vascular neuropathy. In group A2 (18%) subjects were diagnosed with early and 5 subjects (45%) with decided neuropathy. In group B early and decided autonomic neuropathy was present in 16 (51%) and 8 (26%) subjects. No statistically important difference between both groups was found., Conclusions: The results of the study support the thesis of a disseminated nature of the diabetic autonomic neuropathy and of not concomitant involvement of autonomic nervous system in particular organs and systems of the human body.

Autonomic neuropathy, particularly cardiovascular autonomic neuropathy (CAN) is one of the complications of the diabetes mellitus both types. It leads to life comfort's declination but may also be the direct cause of death in diabetes mellitus patients. It seems that degree of metabolic control and duration of the disease is connected with prevalence and severity of CAN. The aim of our study was to assess cardiac autonomic function in young subjects suffered from insulin-dependent diabetes mellitus (IDDM) with relatively short duration time of the disease. We subdivided 25 (m-12, f-13) IDDM patients aged from 18 to 30 years: mean--26 +/- 38 years, with duration time of the disease up to 10 years, normotensive and without nephropathy and retinopathy. We created 25 healthy volunteers control group with similar age and sex. In all selected subjects full Ewing's battery tests were performed as well as the spectral analysis of power heart rate variability (HRV) was assessed with Finapress device (Ohmeda 2300) and automatically computed with special software. HRV in total spectrum power TP from 0.001-0.5 Hz, high frequency (HF) band from 0.15-0.3 Hz, low frequency (LF) band from 0.03-0.15 Hz and LF/HF ratio were examined both in supine and tilt. All assessed spectral values were significantly lower in IDDM patients then these in controls whereas LF/HF were respectively higher. Valsalva tests and deep breathing HR response tests were significantly differed among groups but within normal limits. We concluded that when spectral analyse was performed, in young IDDM patients with short duration time of the disease, impairment of cardiac autonomic function was observed.

The cause of diabetic neuropathy remains unclear but several mechanisms have been considered. Hyperglycemia with all its metabolic and vascular consequences probably plays the main role. Metabolic consequences of hyperglicemia including increased level of sorbitol and fructose, myoinositol deficiency and Na+/K+ adenosine triphosphate deficiency alter the function of peripheral nerves and lead to an oxidative stress, which changes fatty acid metabolism. Chronic hyperglycemia is also responsible for abnormalities in microcirculation that could lead to local ischemia evoking many endothelial changes. There are also some genetic factors, impaired neurotrophic support and autoimmune damage that influence sensitivity to peripheral nerve damage in diabetes mellitus.

The duration of diabetes, age and genetic predispositions are admitted agents of risk in diabetic neuropathy. The reasons of diabetic neuropathy are suspected in cooperation with various factors among which metabolic disturbances and ischaemia are the most important. The abnormal activation of sorbitol tract is very significant agent of development of diabetic neuropathy. The excess of sorbitol which is accumulating also in nervous tissue causes its damage in osmotic way. At the same time decreasing concentration of myoinositol reduces ATP-ase Na+/K+ activity which is important in impulse conduction. The overproduction of free oxygenic radical (oxidative lesion) and nitrogen oxide (vasodilator) deficiency is inducted by hyperglycaemia and the activation of aldolase reductase. Metabolic disturbances cause the decrease of carnitine concentration what deteriorates nerve sensitivity on growth factor. The activation of sorbitol tract leads to nonenzymatic proteins glycation which causes thickening of basement membrane and proliferation of endothelium cells. In this way increased vascular resistance decreases tissue perfusion and induces nerve hypoxia. The impairment of nerve blood supply depends on altered in diabetes rheological properties. They are inconveniently changed through hyperglycaemia, hyperlypidaemia, dysproteinaemia and excessive aggregation and rigidity of morphotic elements of blood.

Corrected QT interval was determined in diabetic patients and in a group of obese individuals with glucose intolerance. It was shown that the measurements of corrected QT (QTc) interval may be a reliable test in the diagnosis of the autonomic diabetic neuropathy. Its simplicity enables routine measurements in diabetic patients treated in out-patients clinics.

Authors discussed the actual status of information concerning the disturbances in function: 1) of sorbitol biochemical pathway, 2) myoinositol metabolism and 3) activity of Na(+)-K(+)-ATP-ase related to diabetic hyperglycemia. Preliminary data on the possible benefit of aldo-reductase inhibitors therapy are also presented.

The causes of postoperative haematomas after operations for intracranial meningiomas are analysed. The percentage of this complication in this material was 5.2%. The most frequent concomitant disease in this series was arterial hypertension. The majority of postoperative haematomas was observed after longer lasting operations with totally excised large tumour. Perhaps, one of a large number of causes, is slight coagulopathy.

The pathogenesis of neuropathy and other late, degenerative complications of diabetes remains largely unresolved. Metabolic derangements thought to be responsible for their development are induced by chronic hyperglycaemia. The present studies concern as follows: sorbitol accumulation due to increased polyol pathway activity, altered myoinositol metabolism in diabetic nerve, followed by diminished sodium-potassium ATPase activity, nonenzymatic glycosylation of structural proteins and rheologic changes in microcirculation. These processes impair nerve metabolism, function and structure directly or indirectly, due to primary vascular alternations and endoneural hypoxia. Partial elucidation of the mechanism involved in pathogenesis of diabetic neuropathy has provoked emergence of new therapeutic approaches. So far their results are equivocal and require further studies. At present, improved glycaemia control is undoubtedly the most important factor in prevention and treatment of neuropathy and other late complications of diabetes.

Acetylation phenotype was determined in 184 diabetics: 102 patients with Type I (insulin-dependent) and 82 patients with Type II (non-insulin-dependent) diabetes mellitus, who underwent complex investigations to assess the development of sensorimotor and autonomic neuropathy. The control group consisted of 121 healthy subjects of the same age distribution. The results obtained imply that the slow acetylation phenotype may be considered as a significant risk factor of diabetic neuropathy.