No 9 (2017)

Cerebellar infarctions are a relatively rare pathology: 1.5-2.3% of acute cerebrovascular disiorders. Topographical classification of cerebellar infarctions is presented; infarct-induced disorders of its functions are considered. For many years, the cerebellum was considered as the key structure of the brain in the regulation of motor functions. Now it is established that it plays a role in the realization of other functions of the body (psychoemotional, vegetative, etc.). In recent years, experimental studies on the role of the cerebellum in the realization of cognitive functions have been carried out. The spectrum of behavioral and cognitive impairments resulting from cerebellar stroke is defined as a cerebellar cognitive affective syndrome. This syndrome includes a violation of executive functions and is characterized by perseverations, absent-mindedness or inattention, visual-spatial disturbances, difficulties in speech production, and personality changes. At the same time, remote episodic and semantic memory is preserved, and the learning ability is only slightly affected. The etiotropic and pathogenetic therapy of post-stroke CI is primarily aimed at the underlying pathological processes causing cerebrovascular insufficiency such as arterial hypertension, atherosclerosis, heart diseases, etc. For the improvement of cognitive functions, a wide range of nootropic agents are used. They can be divided into the main groups: drugs with neurometabolic action, drugs with neurotrophic action, drugs that affect certain neurotransmitter systems, and vasoactive drugs.

The article presents algorithms for diagnosing the involvement of heart as the target organ in arterial hypertension. The possibilities of different diagnostic methods are shown; diagnostic criteria and their prognostic significance are provided. The article also discusses the choice of antihypertensive drugs in the presence of heart damage as a target organ, and algorithms for the dynamic observation of such patients. The possibilities and advantages of angiotensin-converting enzyme inhibitors in the treatment of patients with arterial hypertension and heart disease are shown. The pathogenetic mechanisms of the involution of left ventricular hypertrophy and improvement of the elasticity of myocardium are discussed in the context of treatment with an angiotensin-converting enzyme inhibitor lisinopril.

The article considers the pathogenetic relationship between the development of neurological complications and most common cardiovascular diseases, and also assesses the possibility of early screening for these conditions. The issues of polypragmasy and the selection of safe therapy for this category of patients are discussed in detail.

Experimental studies have shown that Toll-like receptors-4 (TLR4) play an important role in the pathogenesis of ischemic damage to the myocardium and brain. The blocking of tlr4 genes or the use of antibodies to these receptors can improve the outcome of acute ischemic damage and allow these receptors to be considered as a possible therapeutic target. A comparative evaluation of the activation of TLR4 expression in the pathogenesis of myocardial infarction and ischemic stroke in a clinical study seems relevant. The results of the evaluation of the levels of expression of superficial TLR4 peripheral blood cells (monocytes and granulocytes), their dynamics and clinical significance in patients with ischemic atherothrombotic stroke compared with patients with acute myocardial infarction and control group are presented. Using flow cytofluorimetry method, a significant direct correlation between the expression of TLR4 on blood mononuclear cells and the heart rate, as well as the size of the left heart and the left ventricular end-systolic dimension and left ventricular end-diastolic dimension in patients with myocardial infarction were revealed. In patients with ischemic atherothrombotic stroke, a statistically significant direct correlation of TLR4 expression on mononuclear cells on day 14 and NIHSS scores at the 1, 7 and 14 day of the disease was indentified. The results obtained confirm participation of TLR4 activation in ischemic damage to the myocardium and brain and allow considering them as a possible marker of damage severity.

The study was aimed to the evaluation of the structure of cardiovascular risk factors in elderly and senile patients of the neurological department of the Republican Clinical Hospital of War Veterans. The features of the structure of risk factors in these patients included the presence of comorbid cardiovascular pathology, dyslipidemia, and diabetes mellitus. Arterial hypertension was the leading factor for the progression of chronic cerebral ischemia (CCI) and the stroke risk factor in our study. For the prevention of the progression of clinical manifestations of CCI, primary and secondary prevention of stroke, relevant adequate antihypertensive therapy should be administered taking into account the comorbidity. The long-term use of anticoagulants (dabigatran) by this category of patients with individual choice of doses for atrial fibrillation is justified.

Fabry’s disease is a polysystemic pathology caused by the genetic defect of the α-galactosidase A gene, which has an X-linked inheritance pattern. Clinical manifestations of the disease are associated with the progressive accumulation of glycosphingolipids (globotriosylceramide - Gb3) in cells of renal glomeruli and tubules, cardiomyocytes, cardiac fibroblasts, neurons, vegetative ganglia, endothelium, striated and smooth muscle cells resulting in the development of multisystem organ failure. In Fabry’s disease, heterozygous women may either not have clinical manifestations of the disease, or, on the contrary, suffer as hard as hemizygotic men. Diagnosis of the disease is based on a comprehensive assessment of clinical polymorphism, determination of the activity of the enzyme α-galactosidase A in the blood and carrying out molecular genetic studies. Timely diagnosis and early initiation of substitution therapy allow slowing the progression of multisystem organ failure and significantly improving the quality of life of patients.

Lower back pain (LBP) is an important problem that has a significant impact on the quality of life and adds a large financial burden. Doctors should divide patients with LBP into three categories: nonspecific LBP; LBP associated with radiculopathy or spinal stenosis; LBP associated with other diseases of the spine. The medical history includes psychosocial factors that are associated with a risk of developing chronic pain. Patients with nonspecific LBP usually do not need a imaging study. Physicians should perform imaging and other diagnostic tests in LBP patients with a severe or progressive neurologic deficit and with a suspicion of serious underlying pathology. Magnetic resonance imaging is indicated in patients with constant back pain, symptoms of radiculopathy and spinal stenosis only if they are potential candidates for surgery or epidural steroid injections. Doctors should provide patients with scientifically valid information about back pain in terms of expected treatment; advise patients to stay active; provide information on effective methods of self-treatment. Before the start of therapy, the initial degree of pain, functional deficits, potential benefits and risks of planned treatment should be assessed. For most patients, acetaminophen or non-steroidal anti-inflammatory drugs are first-line drugs. Patients who have not been improved by using self-management methods should receive non-drug therapy with proven benefits. In acute LBP - spinal manipulations; in chronic or subacute LBP - intensive multimodal rehabilitation.

The article systematizes the data describing the mechanisms of the development of the ischemic-hypoxic cascade in stroke, the role of energy deficiency and oxidative stress in this process, the ways of their correction with antioxidant drugs, in particular Mexidol. It is shown that Mexidol has antihypoxic, membranotropic actions, reduces glutamate excitotoxicity, and represents a substrate for increasing energy metabolism in the cell, as a result, Mexidol has a cytoprotective effect, increasing the cell resistance to hypoxia.

There are some literature data on the features of the clinical manifestation and course of the amyotrophic lateral sclerosis (ALS) in patients with different genetic mutations. A recently discovered mutation in the C90RF72 gene in patients with ALS has the characteristic clinical features of the course of the disease - rapid progression (survival less than 3 years) and generalization of the process with the development of severe motor, bulbar symptoms and severe respiratory failure, cognitive impairment and emotional lability. Clinical cases of ALS in two patients with a mutation in the C90RF72 gene are discussed.