[Neurological manifestations of hypoparathyroidism: diagnostic difficulties. Case report].

Hypoparathyroidism is a rare condition characterized by reduced production of parathyroid hormone or tissue resistance which leads to hypocalcemia and hyperphosphatemia. Neurological manifestations often occur as the first symptoms of hypoparathyroidism and are characterized by a wide variety of symptoms of both the central and peripheral nervous systems dysfunction, which requires a differential diagnosis with a wide range of neurological diseases. Two clinical cases illustrating the features of subacute and chronic hypoparathyroidism are presented. In the case of subacute hypoparathyroidism, a young woman presented with severe tetany involving the oculomotor muscles (paroxysmal strabismus), laryngeal muscles (respiratory stridor), body muscles (opisthotonus, «obstetrician's hand¼) and the development of secondary myopathy. In another case with a long-term chronic course of postoperative hypoparathyroidism, the patient's adaptation to severe hypocalcemia was noted; the clinical features were dominated by cerebral syndromes due to brain structures calcification (Fahr's syndrome). Possible reasons for late diagnosis of hypoparathyroidism, the importance of active detection of symptoms of neuromuscular hyperexcitability and laboratory testing of phosphorus and calcium metabolism are discussed.

[Type 2 diabetes and cognitive functions in patients with chronic cerebrovascular diseases].

BACKGROUND: Type 2 diabetes (Т2DM) both directly and indirectly impacts the development of morphological and functional changes of the central nervous system. AIM: The study was to determine clinical and neurophysiological patterns of cognitive impairment (CI) in patients with chronic cerebrovascular diseases (CCD) and Т2DM. MATERIALS AND METHODS: We examined 132 patients with CCD. First group included 58 patients without Т2DM aged 64.5 [58; 72], second group 74 patients with CCD and Т2DM 63 [57; 70]. Clinical, neurological, neuropsychological, neurophysiological (cognitive evoked potentials (EP) and neurovisualisation (brain MRI) examination was carried out to all patients. RESULTS: Somatic and neurological characteristics of the patients were similar in both groups with the exception of more distinct metabolic changes in Т2DM patients. Neurovisualisation study of the brain MRI in Т2DM patients revealed more distinct changes in the form of white matter hyperintensity and subarachnoidal spaces enlargement. Neuropsychological examination in patients revealed the reduction of intellectual flexibility, constructive praxis disruption, optical spatial dysfunction and deteoration of delayed word recall. Significant disorders in the way of overall cognitive impairment, lobar dysfunction and impaired verbal associative productivity, proved by statistically lower amplitude and higher latency of P300 EP peak were noted in Т2DM patients. Correlation links were detected: for P300 amplitude and direct and inverse number listing test (r=0.366 and r=0.520; p=0.006 and p0.001 respectively); P300 latency and HbA1c (r=0.32; р0.05) in group 2 and glucose levels in both groups (r=0.30; p0.05); inverse relationship of latency with control functions evaluation (r=-0.34; p=0.008). CONCLUSION: CCD especially with Т2DM manifests with neurocognitive imbalance, including control functions disruption and are accompanied by neurophysiological and neurovisualistion changes.

[Painful diabetic polyneuropathy: focus on life quality improvement of patients]. / Bolevaia forma diabeticheskoi polineiropatii: fokus na uluchshenie kachestva zhizni patsienta.

AIM: To evaluate the efficacy and safety of cytoflavin as an additional agent in the treatment of painful diabetic polyneuropathy and to analyze changes in the life quality of the patients studied. MATERIAL AND METHODS: An analysis of treatment data was carried out in 61 patients with verified painful diabetic polyneuropathy, who were divided into 2 groups depending on the therapy regimen. Patients of the main group (n=36) at the start of the therapy with gabapentin additionally received cytoflavin: intravenously, slowly, 10 ml diluted in 0.9% NaCl 200 ml for 10 days, followed by switching to per os 2 tablets 2 times a day for 25 days. Patients of the comparison group used gabapentin in comparable doses as an analgesic symptomatic therapy. Clinical neurological and anamnestic methods were used to monitor and assess the condition of patients. RESULTS AND CONCLUSION: Cytoflavin inclusion in the standard symptomatic treatment of patients with painful diabetic polyneuropathy contributed to a more pronounced decrease in the subjective assessment of pain (VAS scale) by the 10th day (42.8±2.4 mm versus 58.2±2.1 mm in the comparison group) and its maximum level of decline to 21-25 days. The achieved result was maintained by the 35th day (21.4±1.1 mm against 22.4±1.7 mm in the comparison group). At the same time, the quality of life of patients as assessed by SF-36 was significantly increased after treatment. The results obtained, along with the safety of the drug, allow us to recommend its inclusion in the treatment regimens for patients with this pathology.

[Carotid revascularization in type 2 diabetes mellitus. Significance of chronic hyperglycaemia]. / Karotidnaia revaskuliarizatsiia u bol'nykh sakharnym diabetom 2 tipa. Znachenie khronicheskoi giperglikemii.

Patients with type 2 diabetes mellitus (type 2 DM) are typically prone to the development of cerebral atherosclerosis. Presented herein are the results of examination of patients suffering from ischaemic cerebrovascular diseases on the background of type 2 DM subjected to open surgical or endovascular interventions. In patients with cerebrovascular pathology and type 2 DM, atherosclerosis progresses on the background of chronic hyperglycaemia combined with dyslipidaemia, leading to increased incidence of the development of cerebral circulatory impairments and detection of the indications for carrying out angioreconstructive operations on the internal carotid arteries. The presence of type 2 DM is associated with increased risk for the development of ischaemic lesions of the brain matter while performing carotid endarterectomy and endovascular interventions which are associated with higher values of glycaemia (8.0 mmol/l) and glycated haemoglobin (7.8-8 %) prior to the operation.

[Chronic cerebrovascular diseases and metabolic syndrome: approaches to pathogenic therapy of cognitive dysfunction]. / Khronicheskie tserebrovaskuliarnye zabolevaniia i metabolicheskii sindrom: podkhody k patogeneticheskoi terapii kognitivnykh narushenii.

Cognitive decline comprises one of the most important symptoms of chronic cerebral hypoperfusion. It leads not only to social disability of the patients with a subsequent decline in life quality but also to a decrease in adequate control of the course of both vascular pathology and comorbid states. Pathogenetic therapy and prevention of cerebrovascular disease progression, along with general medical measures, should include the drugs normalizing different symptoms of metabolic syndrome (arterial hypertension, diabetes mellitus etc) as well as complex drugs with multiple actions (hemangioma correction, antithrombotic, antioxidant and vasoactive) actions.

[Cerebrovascular diseases: perspectives of pathogenetic metabolic haemangiocorrective treatment].

Metabolic syndrome is a serious risk factor for acute and chronic cerebrovascular disease, which are a leading cause of disabling conditions. The association of proatherogenic effects of the main components of metabolic syndrome--hyperinsulinemia, arterial hypertension, dyslipidemia and obesity--leads to prominent haemorheological and hemostasis changes, which in turn play a pivotal role in the initiation, course and outcome of cerebrovascular pathology. Metabolic syndrome also influences the efficacy of the main pathogenetic therapy of cerebrovascular diseases--antithrombotic therapy. Thus, primary and secondary prevention of cerebrovascular disease in patients with metabolic syndrome should include haemangiocorrective, antithrombotic, antioxidant and endothelium-protective treatment, as well as therapy of the main components of metabolic syndrome.

[Chronic cerebrovascular diseases associated with metabolic syndrome: new treatment approaches].

Metabolic syndrome is a risk factor for acute and chronic cerebrovascular diseases. The development of oxidative stress promotes the progression of cerebral ischemia and treatment of the biochemical disturbances is needed. Use of antioxidants in patients with cerebrovascular diseases and metabolic syndrome reduce such symptoms as insulin resistance, hyperglyceridemia, hyperglycemia. The authors present results of a clinical study of mexidol in 40 patients, aged from 50 to 70 years, with chronic cerebrovascular pathology. Perspectives of using this group of drugs as universal neuroprotectors are discussed.

[Effect of metformin on the magnitude of oxidative stress in patients with type 2 diabetes mellitus].

The final glycated products forming in diabetes contribute to the higher atherogenic oxidative modification of low-density lipoproteins (LDL). The impact of glycemic control on the parameters of free radical oxidation was comparatively studied in patients with type 2 diabetes who received metformin (Glucophage, Nycomed) (Group 1, n = 40) and sulfanylurea preparations (Group 2, n - 30, out of them 15 patients took maninil and 15 had diabeton) good glycemic control caused the magnitude of oxidative stress to reduce, which appeared as the decreased levels of primary (lipid hydroperoxides) and secondary (malonic dialdehyde) products of free radical oxidation in LDL and as the enhanced activity of antioxidative defense enzymes. However, with the identical degree of glycemic control, which was determined by the level concentrations of HbA1c and lipids in both groups, the plasma levels of lipid peroxides decreased by more than 5 times in Group 1 patients receiving metformin than in Group 2 patients and the rate of LDL oxidability reduced by 4.5 times. Such a marked effect of metformin on the attenuated manifestations of oxidative stress is indicative of its antioxidative effect independent of the hypoglycemic effect of the drug.

Interrelation between compensation of carbohydrate metabolism and severity of manifestations of oxidative stress in type II diabetes mellitus.

Glycosylation end-products formed during diabetes mellitus promoted atherogenic oxidative modification of low-density lipoproteins. We evaluated the effects of compensation of carbohydrate metabolism and therapy with antioxidant probucol on parameters of free radical oxidation in patients with type II diabetes mellitus. Compensation of carbohydrate metabolism reduced manifestations of oxidative stress, which was manifested in accelerated enzymatic utilization of reactive oxygen species and lipid peroxides and decreased content of free radical oxidation products in low-density lipoproteins. In patients with type II diabetes mellitus combination therapy with antioxidant probucol decreased the severity of oxidative stress and stabilized carbohydrate metabolism without increasing the dose of hypoglycemic preparations.