Code of the underlying disease according to ICD 167. What is cerebral atherosclerosis and how to treat it. Treatment of the hypertensive form of encephalopathy

RCHD (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical Protocols of the Ministry of Health of the Republic of Kazakhstan - 2014

Other specified lesions of cerebral vessels (I67.8)

Neurology

general information

Short description

Approved

At the Expert Commission on Health Development

Ministry of Health of the Republic of Kazakhstan

Chronic cerebral ischemia (CCI)- slowly progressive brain dysfunction resulting from diffuse and / or small-focal damage to the brain tissue in conditions of a long-term cerebral blood supply insufficiency

The concept of "chronic cerebral ischemia" includes: "dyscirculatory encephalopathy", "chronic ischemic brain disease", "vascular encephalopathy", "cerebrovascular insufficiency", "atherosclerotic encephalopathy". Of the above names, the most common in modern medicine is the term "dyscirculatory encephalopathy"

I. INTRODUCTION

Protocol name: Chronic cerebral ischemia

Protocol code:

ICD-10 code(s):

I 67. Other cerebrovascular diseases

I 67.2 Cerebral atherosclerosis

I 67.3 Progressive vascular leukoencephalopathy (Binswanger's disease)

I 67.5 Moyamoya disease

I 67.8 Cerebral ischemia (chronic)

I 67.9 Cerebrovascular disease, unspecified

Abbreviations used in the protocol:

AG - arterial hypertension

BP - blood pressure

AVA - arteriovenous aneurysm

AVM - arteriovenous malformation

ALAT - alanine aminotransferase

ASAT - aspartate aminotransferase

BA - bronchial asthma

GP - general practitioner

HBO - hyperbaric oxygen therapy

BBB - blood-brain barrier

DS - duplex scanning

GIT - gastrointestinal tract

IHD - ischemic heart disease

CT - computed tomography

LDL - low density lipoproteins

HDL - high density lipoproteins

MDP - manic-depressive psychosis

INR - international normalized ratio

MRI - magnetic resonance imaging

MRA - magnetic resonance angiography

NPCM - initial manifestations of insufficiency of blood supply to the brain

OGE - acute hypertensive encephalopathy

ONMK - acute cerebrovascular accident

TCM - transient cerebrovascular accident

PST - anticonvulsant therapy

PTI - prothrombin index

PET - positron emission tomography

PHC - primary health care

ESR - erythrocyte sedimentation rate

SAH - subarachnoid hemorrhage

SLE - systemic lupus erythematosus

CCC - cardiovascular system

UZDG - ultrasonic dopplerography

Ultrasound - ultrasonography

FEGDS - fibroesophagogastroduodenoscopy

CHEM - chronic cerebral ischemia

CN - cranial nerves

ECG - electrocardiography

EchoCG - echocardiography

EMG - electromyography

EEG - electroencephalography

Protocol development date: year 2014.

Protocol Users: neuropathologist, internist, general practitioner (family doctor), emergency medical doctor, psychotherapist, speech therapist, physiotherapist, physical therapy and sports doctor, psychologist, social worker with higher education, social worker with secondary education, paramedic.

Classification

Clinical classification

CHEM classification(Gusev E.I., Skvortsova V.I. (2012):

According to the main clinical syndrome:

With diffuse cerebrovascular insufficiency;

With a predominant pathology of the vessels of the carotid or vertebrobasilar systems;

With vegetative-vascular paroxysms;

With predominant mental disorders.

By stages:

Initial manifestations;

subcompensation;

Decompensation.

By pathogenesis(V. I. Skvortsova, 2000):

Decreased cerebral blood flow;

Increase in glutamate excitotoxicity;

calcium accumulation and lactate acidosis;

Activation of intracellular enzymes;

Activation of local and systemic proteolysis;

The emergence and progression of antioxidant stress;

Expression of early response genes with the development of plastic protein depression and a decrease in energy processes;

Long-term consequences of ischemia (local inflammatory reaction, microcirculatory disorders, damage to the BBB).

Diagnostics

II. METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

List of basic and additional diagnostic measures

The main (mandatory) diagnostic examinations carried out at the outpatient level:

General blood analysis;

General urine analysis;

Coagulogram (INR, PTI, determination of blood clotting, hematocrit);

Ultrasound of extra/intracranial vessels of the head and neck.

Additional diagnostic measures carried out at the outpatient level:

EEG video monitoring (with paroxysmal disorder of consciousness);

MRI of the brain with perfusion assessment;

MRI tractography.

The minimum list of examinations that must be carried out when referring to planned hospitalization:

General blood analysis;

General urine analysis;

Biochemical analyzes (ALT, AST, urea, creatinine, bilirubin, total protein, cholesterol, LDL, HDL, triglycerides, glucose);

Coagulogram: prothrombin time with subsequent calculation of PTI and INR in blood plasma, determination of blood clotting time, hematocrit;

Determination of glycosylated glucose.

The main (mandatory) diagnostic examinations carried out at the hospital level:

General blood analysis;

General urine analysis;

Wasserman reaction in blood serum;

X-ray of the chest organs (2 projections);

Biochemical analyzes (ALT, AST, urea, creatinine, bilirubin, total protein, cholesterol, LDL, HDL, triglycerides, glucose);

Coagulogram (prothrombin time followed by calculation of PTI and INR in blood plasma, determination of blood clotting time, hematocrit);

Additional diagnostic examinations carried out at the hospital level:

Ultrasound diagnostics is complex (liver, gallbladder, pancreas, spleen, kidneys), exclude somatic and volumetric formations;

X-ray of the chest organs (2 projections);

Ultrasound of the vessels of the brain and brachiocephalic trunk.

Diagnostic measures taken at the stage of emergency care:

Diagnostic criteria:

The clinical picture of CCI is characterized by a combination of disorders:

Cognitive disorders (violation of the ability to memorize, retain new information, decrease in the pace and quality of mental activity, violation of gnosis, speech, praxis);

Emotional disorders: the predominance of depression, loss of interest in what is happening, narrowing the circle of interests;

Vestibular-atactic syndrome;

Akinetic-rigid syndrome;

pseudobulbar syndrome;

pyramidal syndrome;

oculomotor disorders;

Sensory disturbances (visual, auditory, etc.).

Complaints and anamnesis

Complaints: headaches, non-systemic dizziness, noise in the head, memory impairment, decreased mental performance, impaired speech, gait, weakness in the limbs, short-term loss of consciousness (drop attacks), tonic-clonic convulsions, ataxia, dementia.

Anamnesis: myocardial infarction, ischemic heart disease, angina pectoris, hypertension (with damage to the kidneys, heart, retina, brain), atherosclerosis of the peripheral arteries of the extremities, diabetes mellitus, infectious and allergic diseases, intoxication.

Physical examination:

Motor disorders (hemiparesis, monoparesis, tetraparesis, asymmetry of reflexes, the presence of pathological hand and foot reflexes, symptoms of oral automatism, protective symptoms);

cognitive disorders;

Violation of behavior (aggression, delayed reaction, fearfulness, emotional instability, disorganization);

hemianesthesia;

Speech disorder (aphasia, dysarthria);

Visual disorders (hemianopsia, anisocoria, diplopia);

Violations of the cerebellar and vestibular functions (statics, coordination, dizziness, tremor);

Disturbances of bulbar functions (dysphagia, dysphonia, dysarthria);

Damage to the oculomotor cranial nerves;

Paroxysmal disturbance of consciousness (loss of consciousness, bite marks on the tongue);

Violation of urination and defecation;

Paroxysmal conditions (with circulatory failure in the basin of the vertebrobasilar system).

Laboratory research:

Complete blood count: elevated ESR and leukocytosis;

Prothrombin index - an increase in the values ​​of the indicator;

Hematocrit (hematocrit number) - decrease or increase in the values ​​of the indicator;

Determination of blood glucose levels: hypo/hyperglycemia;

Determination of urea, creatinine, electrolytes (sodium, potassium, calcium) - identification of electrolyte imbalance associated with the use of dehydrating therapy.

Instrumental research:

- CT scan of the brain: detection of focal changes in the substance of the brain

- Brain MRI in T1, T2, Flair mode: the presence of "silent" heart attacks, damage to the periventricular and deep white matter (leukoareosis);

- Ultrasound of cerebral vessels and brachiocephalic trunk(extra and intracranial vessels of the head and neck): detection of stenosis of intracranial arteries, spasm of cerebral vessels, SAH;

- EEG: with a first-time epileptic seizure, especially with partial seizures, with suspicion of Todd's syndrome, to identify a non-convulsive epilepticus, which is manifested by sudden confusion;

- Fundus examination: determination of congestive manifestations, or edema of the optic nerve, or changes in the vessels in the fundus;

- Perimetry: detection of hemianopsia;

- ECG: detection of CVS pathology;

- Holter ECG monitoring: detection of embolism, asymptomatic attack of atrial fibrillation;

-Chest X-ray(2 projections): changes in the configuration of the heart in valvular disease, expansion of the boundaries of the heart in the presence of hypertrophic and dilated cardiomyopathy, the presence of pulmonary complications (congestive, aspiration pneumonia, thromboembolism, etc.).

Indications for consultation of narrow specialists:

Consultation of a therapist in the presence of concomitant somatic pathology;

Consultation with an ophthalmologist: in order to identify hemianopsia, amaurosis, strabismus, disturbances of accommodation, pupillary reactions; changes characteristic of a brain tumor, hematoma, chronic venous encephalopathy;

Consultation with a cardiologist: in the presence of hypertension, coronary artery disease (sudden cold clammy sweat, a sharp drop in blood pressure), rhythm disturbances (atrial and paroxysmal and other types of arrhythmias), detection of changes in the ECG or ECG Holter monitoring;

Consultation with an endocrinologist: if there are signs of diabetes and diabetes insipidus, thyroid disease;

Consultation of a speech therapist: the presence of aphasia, dysarthria;

Consultation of a psychotherapist: for the purpose of psychocorrection;

Consultation of a psychiatrist: with severe dementia, manic-depressive psychosis.

Consultation of a neurosurgeon: the presence of a hematoma, stenosis of the vessels of the head and neck, AVA, AVM, tumor or brain metastases;

Consultation of a vascular surgeon: the presence of severe stenosis of the vessels of the brain and neck, the solution of the issue of further surgical treatment;

Cardiac surgeon's consultation: the presence of a cardiac pathology requiring surgical intervention;

Audiologist consultation: in the presence of hearing impairment, noise, whistling in the ears and head.

Differential Diagnosis

Differential Diagnosis:

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Treatment

Treatment goals:

Slow down the progression of the disease;

Improve the quality of life;

In the presence of epileptic seizures, the selection of adequate anticonvulsant therapy (PST).

Treatment tactics:

Normalization of blood pressure, lipids, cholesterol and blood glucose levels;

The use of vasoactive, neuroprotective and neurotrophic drugs.

Non-drug treatment:

Semi-bed (ward).

2) Diet: table number 10 (restriction of salt, liquid).

Medical treatment

Nootropic drugs:

Phenotropil - 100 - 200 mg 1-2 times / day (up to 15 hours of the day);

Piracetam - 20% solution in ampoules in / in or / m, 5 ml per day, followed by transfer to tablet intake of 0.6-0.8 g / day for a long time;

A complex of peptides obtained from the brain in / in 5-10 ml in ampoules.

Antiplatelet agents:

Acetylsalicylic acid (film-coated tablets) - 75-150 mg / day under the control of PTI, coagulogram.

Membrane protectors:

Citicoline: 500 - 2000 mg/day IV or IM; further 1000 mg / day - in sachets (level A);

Neuroprotection:

Magnesium sulfate, 25% solution 30 ml/day (level A);

Glycine, 20 mg/kg body weight (average 1-2 g/day) sublingually for 7-14 days

Inosine + nicotinamide + riboflavin + succinic acid:

20 ml/day intravenously drip slowly (60 drops per minute) for 10 days, then oral tablets of 300 mg - 2 tablets 2 times a day for 25 days (level c);

Ethylmethylhydroxypyridine succinate, infusion at 100 mg/day, followed by transfer to the tablet intake of the drug at a dose of 120-250 mg/day (level B);

Tocopherol acetate (vitamin E): 1-2 ml / m 1 time / day for 7-10 days, then 1 tablet 2 times / day for 2 months.

Vasoactive drugs:

Vinpocetine infusion - 2-4 ml / day in / in - 7-10 days with a transfer to oral administration of 5-10 mg / day for a month;

Nicergoline - 2-4 mg / m or / in 2 times / day, and then tablets of 10 mg 3 times / day for a month;

Benciclane fumarate - at a dose of 100 mg/day IV with the transition to tablet intake at a dose of 100 mg 2 times a day for 2-3 months, the maximum daily dose is 400 mg (level B).

Pentoxifylline at a daily dose of 400-800 mg 2-3 times / day (level B).

Muscle relaxants:

Baklosan, orally 5-20 mg/day for a long time (depending on muscle tone);

Tolperisone hydrochloride, 50-150 mg 2 times a day for a long time (under the control of blood pressure).

For nociceptive pain:

Non-steroidal anti-inflammatory drugs (meloxicam 7.5-15 mg IM or orally, lornoxcam 4-8 mg for pain IM or orally; ketoprofen 100-300 mg IV, IM or orally);

For neuropathic pain:

Pregabalin 150 - 600 mg/day;

Gabapentin 300-900 mg/day.

Lipid-lowering therapy:

Atorvastatin 10-20 mg/day - long-term; the maximum daily dose is 80 mg.

Antihypertensive drugs:

Medical treatment provided on an outpatient basis

1.Basic medicines

Neuroprotective Therapy:

Magnesium sulfate, 25% - 10.0 ml ampoule;

Cortexin -10 mg/day IM for 10 days, vials;

A complex of peptides obtained from the brain of a pig 5-10 ml IV, in ampoules.

Membrane protectors:

Citicolines, 500-2000 mg/day IV or IM; further 1000 mg / day - in sachets;

Choline alfoscerate - 400 mg 2-3 times / day.

Antiplatelet agents:

Acetylsalicylic acid - 75-150 mg / day, film-coated tablets (under the control of PTI, coagulogram);

Nootropic drugs:

Phenotropil - 100 - 200 mg 1-2 times / day (until 15 pm), tablets 100 mg

Piracetam - 10 ml / day - ampoules (5 ml), tablets 0.4 g 3 times a day, ampoules of 5 ml or tablets of 400 mg, 800 mg, 1200 mg.

Antioxidants and antihypoxants:

Inosine + nicotinamide + riboflavin + succinic acid - 1-2 g / day IV - 5.0 ml ampoules; 600 mg / day - tablets. Ampoules of 5.0 ml, tablets of 200 mg;

Ethylmethylhydroxypyridine succinate - 100 mg/day IV, at a dose of 120-250 mg/day - tablets. Ampoules of 100 mg, 2 ml.

Vasoactive agents:

Vinpocetine - 5-10 mg tablets 3 times a day / day; Tablets 5.10 mg, 2 ml ampoules;
- nicergoline - 10 mg tablets 3 times a day, tablets; ampoules 5 mg, tablets 5, 10 mg;
- benziklan fumarate - in / in slowly 50-100 mg / day, ampoules; 100 mg 2 times / day for 2-3 months, tablets. Ampoules of 2 ml, tablets of 100 mg.

Pain relief medications:

Meloxicam - 7.5-15 mg intramuscularly or tablets; tablets of 7.5 and 15 mg, ampoules of 1-2 ml.

Lornoxekam - 4-8 mg - in / m, ampoules; when taken orally - 4 mg 2-3 times / day - tablets; tablets of 4, 8 mg, ampoules of 4 mg.

Ketoprofen 100-300 mg IV, IM or 1 tablet 2 times a day - tablets, capsules. Tablets and ampoules of 100 mg.

Muscle relaxants:

Baclofen - 5 mg tablets - 5-20 mg per day;

Tolperisone - 100 mg / day - ampoules, tablets of 50 mg - 50-150 mg / day.

Oral indirect anticoagulants(antivitamins K):

Warfarin, orally 2.5-5 mg per day under the control of INR. 2.5 mg tablets

Preparations that improve microcirculation:

Pentoxifylline - tablets - 400 mg - 800 mg per day; Tablets 100 mg, 4000 mg, ampoules 100 mg.

Nimodipine - 30 mg tablets 2-3 times a day (level B). Tablets of 30 mg.

Pain relief drugs(neuropathic pain):

Pregabalin - start with a dose of 150 mg to 600 mg / day, capsules; Tablets of 150 mg.

Gabapentin - at a dosage of 300-900 mg per day, capsules of 100, 300, 400 mg. Tablets of 300 mg.

Antioxidants:

Tocopherol acetate (vitamin E) - 1-2 ml / day 5%, 10%, 30% solution in / m - ampoules; 1-2 pills 2-3 times / day for 1-2 months - capsules, pills. Ampoules of 20 ml of 5% and 10% solution in oil.

Lipid-lowering therapy:

Atorvastatin 10-20 mg / day - long-term (2-3 months); the maximum daily dose is 80 mg (tablets). Tablets of 5-10 mg.

Antihypertensive drugs:

Correction of blood pressure is carried out according to the clinical protocol "Arterial hypertension".

Antiepileptic therapy:

The relief of an epileptic seizure or status epilepticus is carried out according to the clinical protocol “Epilepsy. epileptic status.

Medical treatment provided at the inpatient level

1.Basic medicines:

Neuroprotective Therapy:

Magnesium sulfate, solution 25% 10.0 ml; ampoules;

A complex of peptides obtained from the brain of a pig in / in 5-10 ml, ampoules.

Cortexin - in / m 10 mg / day for 10 days, vials.

Membrane protectors:

Citicolines: 500-2000 mg/day IV or IM; further 1000 mg/day in sachets (level A);

Choline alfoscerate - 400 mg 2-3 times / day, tablets.

Nootropic drugs:

Phenotropil - tablets 100 mg.

Piracetam - 5 ml ampoules.

Antioxidants and antihypoxants:

Inosine + nicotinamide + riboflavin + succinic acid - ampoules 5.0-10 ml; 200 mg tablets.

Ethylmethylhydroxypyridine succinate - ampoules of 2 ml, 5 ml, tablets of 125 mg.

Vasoactive agents:

Vinpocetine - 2 ml ampoule;

Nicergoline - 2 ml ampoules;  benziklan fumarate - 2 ml ampoules, 100 mg tablets.

Antihypoxants:

A complex of peptides obtained from the brain of a pig 10-30 mg / day by infusion; ampoules.

Pain relief medications:

In the presence of nociceptive pain: non-steroidal anti-inflammatory drugs:

Meloxicam - 7.5-15 mg per tablet;

Lornoxekam - 4-8 mg tablets; vial 8 mg

Ketoprofen tablets and ampoules 100 mg.

For neuropathic pain:

Pregabalin -150 mg capsules;

Gabapentin - capsules of 100, 300, 400 mg.

Muscle relaxants:

Baclofen - Tablets 10, 25 mg;

Tolperisone - tablets 50 mg.

2. Additional medicines:

Antiplatelet agents:

Acetylsalicylic acid (film-coated tablets) - 75-150 mg;

Antioxidants:

Tocopherol acetate (vitamin E) - Ampoules of 20 ml of 5% and 10% solution in oil.

Lipid-lowering therapy:

Atorvastatin tablets 5-10 mg.

Antihypertensive drugs.

Correction of blood pressure is carried out according to the clinical protocol "Arterial hypertension".

Antiepileptic therapy.

The relief of an epileptic seizure or status epilepticus is carried out according to the clinical protocol “Epilepsy. epileptic status.

Drug treatment provided at the stage of emergency emergency care:

Treatment of arterial hypertension (see the clinical protocol "Arterial hypertension").

Epileptic seizures (see the clinical protocol "Epilepsy", "Epileptic status").

Other treatments

Other types of treatment provided at the outpatient level:

1) Physiotherapy:

electrophoresis;

Electrical muscle stimulation;

Heat treatment (ozokerite treatment; "salt" chamber);

Physiopuncture;

Oxygen cocktail;

Massage;

Ergotherapy;

Hydrokinesitherapy;

Mechanotherapy;

Classes in the Montessori system;

Classes on analytical simulators with the biofeedback program (training on EMG and EEG parameters);

Posturography (robotic);

Proprioceptive correction;

Information

Sources and literature

1. Minutes of the meetings of the Expert Commission on Health Development of the Ministry of Health of the Republic of Kazakhstan, 2014
   1. 1) Schmidt E.V. Classification of vascular lesions of the brain and spinal cord // Zhurn. Neurologist and psychiatrist. 1985. No. 9. pp. 1281-1288. 2) The European Stroke Initiative Executive Committee and the EUSI Writing Committee: European stroke initiative recommendations for stroke management – ​​update 2003. Cerebrovascular Disease 2003;16:311-337. 3) Skvortsova V.I., Chazova I.E., Stakhovskaya L.V., Pryanikova N.A. Primary prevention of stroke. M., 2006. 4) Maiti R, Agrawal N, Dash D, Pandey B. Effect of Pentoxifylline on inflammatory burden, oxidative stress and platelet aggregability in hypertensive type 2 diabetes mellitus patients. Vascul Pharmacol 2007; 47(2-3):118-24. 5) Gusev E.I., Belousov Yu.B., Boyko A.N. General principles of pharmacoeconomic research in neurology: Guidelines. M., 2003. 56 p. 6) A guide to neurology by Adams and Victor. Maurice Victor, Allan H. Ropper - M: 2006. - 680 p. (S. 370-401). 7) Stock V.N. Pharmacotherapy in neurology: A practical guide. – 4th ed., revised. and additional – M.: 2006. – 480 p. 8) Medicines in a neurological clinic: A guide for doctors / E.I. Gusev, A.S. Nikiforov, A.B. Gekht. - M: 2006. - 416 p. Evidence-based medicine. Directory / Edited by S.E. Baschinsky. Moscow, 2003. 9) OS Levin The main medicines used in neurology. Handbook, Moscow, 6th edition. MED press-inform. 2012. 151 p. 10) Schmidt E.V. Vascular diseases of the nervous system. - Moscow. - 2000. - S. 88-190. 11) Adams H., Hachinski V., Norris J. Ischemic Cerebrovascular Disease // Oxford University press. - 2001. - P. 575. 12) Akopov S., Whitman G.T. Hemodynamic Studies in Early Ischemic Stroke Serial Transcranial Doppler and Magnetic Resonance Angiography Evaluation //Stroke. 2002;33:1274–1279. 13) Flemming K.D., Brown R.D. Jr. Cerebral infarction and transient ischemic attacks. Efficient evaluation is essential to beneficial intervention // Postgrad. Med. - 2000. - Vol. 107, no.6. – P. 55–62. 14) Guidelines for the Early Management of Adults with Ischemic Stroke // Stroke. - 2007. - Vol. 38. - P. 1655. 15) Stroke. Principles of treatment, diagnosis and prevention / Ed. Vereshchagina N.V., Piradova M.A., Suslina Z.A. - M.: Intermedica, 2002.- 189 p. 16) P.V. Voloshin, V.I. Taitslin. Treatment of vascular diseases of the brain and spinal cord / 3rd ed., add. - M.: MEDpress_inform, 2005. - 688 p. 17) Stefano Ricci, Maria Grazia Celani, Teresa Anna Cantisani et al. Piracetam for acute ischaemic stroke // Cochrane Database of Systematic Reviews. - 2006. - No. 2. 18) Ziganshina LE, Abakumova T, Kuchaeva A Cerebrolysin for acute ischaemic stroke // Cochrane Database of Systematic Reviews. - 2010. - No. 4 19) Muir KW, Lees KR Excitatory amino acid antagonists for acute stroke // Cochrane Database of Systematic Reviews. - 2003. - No. 3. 20) Gandolfo C, Sandercock PAG, Conti M Lubeluzole for acute ischaemic stroke // Cochrane Database of Systematic Reviews. - 2010. - No. 9. 21) Horn J, Limburg M Calcium antagonists for acute ischemic stroke // Cochrane Database of Systematic Reviews. - 2010. - No. 9. 22) Asplund K Haemodilution for acute ischaemic stroke // Cochrane Database of Systematic Reviews. - 2002. - No. 4. 23) Bath PMW, Bath-Hextall FJ Pentoxifylline, propentofylline and pentifylline for acute ischaemic stroke // Cochrane Database of Systematic Reviews. - 2004. - No. 3. 24) Bennett MH, Wasiak J, Schnabel A et al. Hyperbaric oxygen therapy for acute ischaemic stroke // Cochrane Database of Systematic Reviews. - 2010. - № 9. 25) Diseases of the nervous system. A guide for doctors // Ed. N.N. Yakhno, D.R. Shtulman, M., 2011, T.I, T.2. 26) O.S. Levin The main drugs used in neurology. Handbook, Moscow, 6th edition. MEDpress-inform. 2012. 151 p. 27) "Neurology"

Information

III. ORGANIZATIONAL ASPECTS OF PROTOCOL IMPLEMENTATION

List of protocol developers with qualification data:

1) Nurguzhaev Erkyn Smagulovich - Doctor of Medical Sciences, Professor of the RSE on REM "Kazakh National Medical University named after S.D. Asfendiyarov" Head of the Department of Nervous Diseases

2) Izbasarova Akmaral Shaimerdenovna - RSE on REM "Kazakh National Medical University named after S.D. Asfendiyarov" Associate Professor of the Department of Nervous Diseases

3) Raimkulov Bekmurat Nametovich - Doctor of Medical Sciences, Professor of the RSE on REM "Kazakh National Medical University named after S.D. Asfendiyarov" Professor of the Department of Nervous Diseases

Conflict of interests: In relation to the drug "Actovegin", a justification with an evidence base is given in the Cochrane Community Library, where there are 16 clinical studies on the use of this drug with presented clinical efficacy.

Reviewer:

Tuleusarinov Akhmetbek Musabalanovich - Doctor of Medical Sciences, Professor of the Department of Traditional Medicine of JSC "Kazakh Medical University of Continuing Education"

Conditions for revision of the protocol: revision of the protocol after 3 years and / or when new methods of diagnosis / treatment with a higher level of evidence appear.

Attached files

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People with chronic cardiovascular disease have a history of hypertensive encephalopathy. What it is? This is a violation of the functions of the brain due to a prolonged increase in pressure. Pathology is characterized by impaired vision and hearing, memory problems, short-term loss of consciousness, headache. Hypertensive encephalopathy ICD-10 code: 167.4.

Symptoms of hypertensive encephalopathy

Hypertensive encephalopathy, the symptoms of which are associated with the work of the brain centers responsible for the functions of the sense organs, parts of the body, can manifest themselves in a variety of ways. Basically, hypertensive encephalopathy affects visual function, hearing, and sometimes speech. How this violation manifests itself:

1. Distractedness of the patient.
2. Inconsistency of speech, forgetting certain words.
3. Brief syncope.
4. Visual impairment: blurred vision.
5. Decreased hearing acuity.
6. Psychological depression or irritability, anxiety.
7. Tremor of the limbs and head, movement disorders when walking.
8. Headache.

Encephalopathy in hypertension and symptomatic hypertension is caused by the death of individuals under the influence of ischemia and hypoxia. The lack of oxygen carried by the blood affects all brain functions. Patients suffer transient ischemic attacks, expressed in weakness, dizziness, nausea and darkening in the eyes.

The intellectual function is upset, patients with hypertensive encephalopathy can forget words and their meaning, lose the thread of the conversation. Short-term memory is broken, while these patients perfectly remember long-term events. The emotional sphere is also affected, which manifests itself in the form of depressive states. Anxiety and irritability are caused by a disorder of cerebral circulation.

Coordination of movements is disturbed, as the vessels that feed the cerebellum and subcortical nuclei can be affected. Ischemia of the latter causes extrapyramidal disorders - trembling at rest or during movement. Thus, hypertensive encephalopathy, ICD-10 167.4, has many manifestations.

Causes and pathogenesis

Hypertensive encephalopathy is a pathology that develops with a chronic increase in blood pressure. The cause of absent-mindedness, tinnitus, the appearance of flies in the eyes are vascular changes that have arisen under the influence of persistent arterial hypertension.

High blood pressure causes a violation of blood flow, swelling of the brain tissue. With hypertension, small vessels are also damaged, their walls are impregnated with plasma and become rigid, inelastic. The permeability of capillaries increases under the action of homocysteine, which leads to fluid leakage into the brain tissue, edema.

In elderly patients, the volume of circulating blood decreases, therefore, peripheral vessels, including cerebral ones, narrow under the action of renin, which is a compensatory reaction. The level of aldosterone rises, which exacerbates edema and hypertension of the brain. Increased intracranial pressure leads to severe headaches, as well as nausea and vomiting with irritation of the hypothalamus receptors.

Diagnosis and treatment

Diagnosis includes magnetic resonance imaging, dopplerography of cerebral vessels, electroencephalography, ECHO-EG. Regular measurement of blood pressure is important. They also need to examine the kidneys, which can increase blood pressure. The renin-angiotensin ratio, the content of uric acid in the blood, which increases blood pressure, is important.

Hypertensive encephalopathy, which should be treated by a neurologist or cardiologist, is a dangerous disease. Patients with this disorder are recommended a diet with a restriction of daily salt intake to 3 g. The consumption of fatty foods and starchy foods should be minimized.

Food for hypertensive encephalopathy should be light. Fruit and vegetable juices are rich in potassium, as well as liquid, which will make the blood less viscous and reduce the workload on the heart. Potassium has a diuretic effect that reduces blood pressure and has a beneficial effect on the heart muscle.

You should also reduce the consumption of foods that lead to an increase in uric acid levels. These are rich broths, egg yolks, meat, fish roe. When preparing soups from meat, the first broth merges: it contains a lot of purines, from which uric acid is synthesized in the body. This substance has a toxic effect on the heart, nervous system, increases blood pressure.

To improve the quality of life in patients with hypertensive encephalopathy, antihypertensive drugs, metabolic and vasodilators are used. For the treatment of hypertension use:

• beta blockers;
• calcium antagonists;
• preparations of potassium, magnesium;
• antispasmodics (Drotaverine, Papaverine).

Hearing and vision problems are associated with vascular disorders. Treatment is carried out with vasodilators such as Cavinton, Cinnarizine. To reduce vascular permeability, additives are recommended (Dihydroquercetin, Rutin). They help eliminate swelling.

To increase the resistance of the nervous tissue of the brain to hypoxia, antihypoxic agents are used (Mexidol, Cytoflavin, Glycine). For the treatment of anxiety disorders, sedatives are used (motherwort, valerian, Valocordin). Symptomatic hypertension in kidney disease requires specific treatment.

Hypertensive encephalopathy is a consequence of hypertension and symptomatic hypertension. This disorder progresses in the absence of adequate treatment and leads to dementia of the patient.

Dyscirculatory encephalopathy is a slowly progressive brain dysfunction resulting from diffuse and/or small-focal damage to the brain tissue in conditions of long-term cerebral blood supply insufficiency.

Synonyms: dyscirculatory encephalopathy, chronic cerebral ischemia, slowly progressive cerebrovascular accident, chronic ischemic brain disease, cerebrovascular insufficiency, vascular encephalopathy, atherosclerotic encephalopathy, hypertensive encephalopathy, atherosclerotic angioencephalopathy, vascular (atherosclerotic) parkinsonism, vascular (late) epilepsy.

The most widely of the above synonyms in the domestic neurological practice included the term "dyscirculatory encephalopathy", which retains its meaning to this day.

ICD-10 codes

Cerebrovascular diseases are coded according to ICD-10 in sections 160-169. The concept of "chronic cerebrovascular insufficiency" is absent in the ICD-10. Dyscirculatory encephalopathy (chronic cerebrovascular insufficiency) can be coded in section 167. Other cerebrovascular diseases: 167.3. Progressive vascular leukoencephalopathy (Binswanger's disease) and 167.8. Other specified cerebrovascular diseases, subheading "Cerebral ischemia (chronic)". The rest of the codes from this section reflect either only the presence of vascular pathology without clinical manifestations (vascular aneurysm without rupture, cerebral atherosclerosis, Moyamoya disease, etc.), or the development of acute pathology (hypertensive encephalopathy).

An additional code (F01*) can also be used to indicate the presence of vascular dementia.

Headings 165-166 (according to ICD-10) "Occlusion or stenosis of the precerebral (cerebral) arteries that do not lead to cerebral infarction" are used to code patients with asymptomatic course of this pathology.

ICD-10 code

G93.4 Encephalopathy, unspecified

I67.4 Hypertensive encephalopathy

Epidemiology of dyscirculatory encephalopathy

Due to the noted difficulties and inconsistencies in the definition of dyscirculatory encephalopathy, the ambiguity in the interpretation of complaints, the non-specificity of both clinical manifestations and changes detected by MRI, there are no adequate data on the prevalence of chronic cerebrovascular insufficiency.

To some extent, it is possible to judge the frequency of chronic forms of cerebrovascular diseases based on epidemiological indicators of the prevalence of stroke, since acute cerebrovascular accident, as a rule? develops against a background prepared by chronic ischemia, and this process continues to grow in the post-stroke period.

Causes of dyscirculatory encephalopathy

The causes of both acute and chronic cerebrovascular accidents are the same. Among the main etiological factors, atherosclerosis and arterial hypertension are considered, often a combination of these 2 conditions is detected. Other diseases of the cardiovascular system can also lead to chronic cerebrovascular insufficiency, especially those accompanied by signs of chronic heart failure, cardiac arrhythmias (both permanent and paroxysmal forms of arrhythmia), often leading to a drop in systemic hemodynamics. The anomaly of the vessels of the brain, neck, shoulder girdle, aorta, especially its arch, which may not appear until atherosclerotic development in these vessels, is also important. hypertonic or other acquired process.

Pathogenesis of dyscirculatory encephalopathy

The above diseases and pathological conditions lead to the development of chronic hypoperfusion of the brain, that is, to a long-term shortage of basic metabolic substrates (oxygen and glucose) delivered by the blood flow to the brain. With slow progression of brain dysfunction that develops in patients with chronic cerebrovascular insufficiency, pathological processes unfold primarily at the level of small cerebral arteries (cerebral microangiopathy). Widespread lesion of small arteries causes diffuse bilateral ischemic lesion, mainly white matter, and multiple lacunar infarctions in the deep regions of the brain. This leads to disruption of the normal functioning of the brain and the development of non-specific clinical manifestations - encephalopathy.

Symptoms of dyscirculatory encephalopathy

The main symptoms of dyscirculatory encephalopathy: disturbances in the emotional sphere, polymorphic movement disorders, memory impairment and learning abilities, gradually leading to maladaptation of patients. Clinical features of chronic cerebral ischemia - progressive course, staging, syndromicity.

In domestic neurology, for quite a long time, chronic cerebrovascular insufficiency, along with dyscirculatory encephalopathy, also included the initial manifestations of cerebrovascular insufficiency. At present, it is considered unreasonable to single out such a syndrome as "initial manifestations of insufficient blood supply to the brain", given the non-specificity of asthenic complaints and the frequent overdiagnosis of the vascular genesis of these manifestations. The presence of headache, dizziness (non-systemic), memory loss, sleep disturbance, noise in the head, ringing in the ears, blurred vision, general weakness, increased fatigue, decreased performance and emotional lability, in addition to chronic cerebrovascular insufficiency, may indicate other diseases and conditions .

Screening

To detect dyscirculatory encephalopathy, it is advisable to conduct, if not a mass screening examination, then at least a survey of people with major risk factors (arterial hypertension, atherosclerosis, diabetes mellitus, heart disease and peripheral vascular disease). Screening examination should include auscultation of the carotid arteries, ultrasound examination of the main arteries of the head, neuroimaging (MRI), and neuropsychological testing. It is believed that dyscirculatory encephalopathy is present in 80% of patients with stenosing lesions of the main arteries of the head, and stenoses are often asymptomatic up to a certain point, but they can cause hemodynamic restructuring of the arteries in the area located distal to atherosclerotic stenosis (echeloned atherosclerotic brain damage), leading to to the progression of cerebrovascular disease.

Diagnosis of dyscirculatory encephalopathy

To diagnose chronic cerebrovascular insufficiency, it is necessary to establish a relationship between clinical manifestations and pathology of cerebral vessels. For the correct interpretation of the identified changes, a thorough history taking with an assessment of the previous course of the disease and dynamic monitoring of patients are very important. It should be borne in mind the inverse relationship between the severity of complaints and neurological symptoms and the parallelism of clinical and paraclinical signs with the progression of cerebral vascular insufficiency.

It is advisable to use clinical tests and scales, taking into account the most common clinical manifestations in this pathology (assessment of balance and walking, identification of emotional and personality disorders, neuropsychological testing).

Dyscirculatory encephalopathy is an extremely common disease that occurs in almost every person with arterial hypertension.

Deciphering frightening words is quite simple. The word "dyscirculatory" means disorders of blood circulation through the vessels of the brain, while the word "encephalopathy" literally means the suffering of the head. Thus, dyscirculatory encephalopathy is a term denoting any problems and violations of any functions due to impaired blood circulation through the vessels.

Information for physicians: code dyscirculatory encephalopathy according to ICD 10, code I 67.8 is most often used.

The reasons

There are not so many reasons for the development of dyscirculatory encephalopathy. The main ones are hypertension and atherosclerosis. Less commonly, dyscirculatory encephalopathy is spoken of with an existing tendency to lower pressure.

Constant drops in blood pressure, the presence of a mechanical barrier to blood flow in the form of atherosclerotic plaques create prerequisites for chronic insufficiency of blood flow to various brain structures. Lack of blood flow means malnutrition, untimely elimination of metabolic products of brain cells, which gradually leads to disruption of various functions.

It should be said that frequent pressure drops lead to encephalopathy most quickly, while constantly high or constantly low pressure levels will lead to encephalopathy after a longer time.

A synonym for dyscirculatory encephalopathy is chronic cerebrovascular insufficiency, which, in turn, means the long-term formation of persistent brain disorders. Thus, the presence of the disease should be discussed only with reliably existing vascular diseases for many months and even years. Otherwise, you should look for another reason for the existing violations.

Symptoms

What should be paid attention to in order to suspect the presence of discirculatory encephalopathy? All the symptoms of the disease are rather non-specific and include usually “ordinary” symptoms that can also occur in a healthy person. That is why patients do not seek medical help immediately, only when the severity of symptoms begins to interfere with a normal life.

According to the classification for dyscirculatory encephalopathy, several syndromes should be distinguished that combine the main symptoms. When making a diagnosis, the doctor also takes out the presence of all syndromes, indicating their severity.

• cephalic syndrome. Includes complaints such as headaches (mainly in the occipital and temporal areas), pressure on the eyes, nausea with headache, tinnitus. Also in relation to this syndrome, any discomfort associated with the head should be attributed.
• Vestibulo-coordinating disorders. They include dizziness, throwing when walking, a feeling of instability when changing body position, blurred vision with sudden movements.
• Astheno-neurotic syndrome. Includes mood swings, consistently low mood, tearfulness, feelings of anxiety. With pronounced changes, it should be differentiated from more serious psychiatric diseases.
• Dyssomnic syndrome, which includes any sleep disturbance (including light sleep, "insomnia", etc.).
• Cognitive impairment. They combine memory impairment, decreased concentration, absent-mindedness, etc. With the severity of disorders and the absence of other symptoms, dementia of various etiologies should be excluded (including,).

Discirculatory encephalopathy of 1, 2 and 3 degrees (description)

Also, in addition to the syndromic classification, there is a gradation according to the degree of encephalopathy. So, there are three levels. Dyscirculatory encephalopathy of the 1st degree means the most initial, transient changes in brain functions. Dyscirculatory encephalopathy of the 2nd degree indicates persistent disorders, which, however, only affect the quality of life, usually not leading to a gross decrease in working capacity and self-service. Dyscirculatory encephalopathy of the 3rd degree means persistent gross violations, often leading to disability of a person.

According to statistics, the diagnosis of grade 2 dyscirculatory encephalopathy is one of the most common neurological diagnoses.

Author's video

Diagnostics

Only a neurologist can diagnose the disease. To make a diagnosis, it is required that, when examining the neurological status, there is a revival of reflexes, the presence of pathological reflexes, changes in performance, signs of a violation of the vestibular apparatus. You should also pay attention to the presence of nystagmus, deviation of the tongue away from the midline and some other specific signs that indicate the suffering of the cerebral cortex and a decrease in its inhibitory effect on the spinal cord and reflex sphere.

Only in addition to the neurological examination are additional research methods -, and others. According to rheoencephalography, violations of vascular tone, asymmetry of blood flow can be detected. MR signs of encephalopathy include the presence of calcifications (atherosclerotic plaques), hydrocephalus, and scattered vascular hypodense inclusions. Usually, MR signs are detected in the presence of grade 2 or 3 dyscirculatory encephalopathy.

Treatment

Treatment must be comprehensive. The main factor in successful therapy is the normalization of the causes that caused the development of the disease. It is necessary to normalize blood pressure, stabilize lipid metabolism. Standards for the treatment of dyscirculatory encephalopathy also include the use of drugs that normalize the metabolism of brain cells and vascular tone. The drugs in this group include sermion.

The choice of other drugs depends on the presence and severity of certain syndromes:

• With a pronounced cephalgic syndrome and existing hydrocephalus, they resort to specific diuretics (diacarb, glycerin mixture), venotonics (detralex, phlebodia).
• Vestibulo-coordinating disorders should be eliminated with drugs that normalize blood flow in the vestibular structures (cerebellum, inner ear). The most commonly used betahistine (, vestibo, tagista), vinpocetine ().
• Astheno-neurotic syndrome, as well as sleep disorders, are eliminated by the appointment of light sedatives (glycine, tenoten, etc.). With severe manifestations resort to the appointment of antidepressants. You should also adhere to proper sleep hygiene, normalize the work-rest regime, and limit the psycho-emotional load.
• With cognitive impairment, nootropic drugs are used. The most commonly used drugs are piracetam, including in combination with a vascular component (phezam), as well as more modern drugs such as phenotropil, pantogam. In the presence of severe comorbidities, preference should be given to safe herbal preparations (for example, tanakan).

Treatment with folk remedies for dyscirculatory encephalopathy usually does not justify itself, although it can lead to a subjective improvement in well-being. This is especially true for patients who are distrustful of taking medications. In advanced cases, such patients should be oriented at least to taking constant antihypertensive therapy, and in the treatment, parenteral methods of treatment should be used, which, according to such patients, have a better effect than tablet forms of drugs.

Prevention

There are not so many methods for preventing the disease, but at the same time, standard treatment will not do without prevention. To prevent the development of dyscirculatory encephalopathy, as well as to reduce its manifestations, it is necessary to constantly monitor the level of blood pressure, the content of cholesterol and its fractions. Psycho-emotional overload should also be avoided.

With the existing dyscirculatory encephalopathy, one should also regularly (1-2 times a year) undergo a full course of vasoactive, neuroprotective, nootropic therapy in a day or round-the-clock hospital to prevent the progression of the disease. Be healthy!

Catad_tema Chronic cerebral ischemia - articles

Modern approach to the diagnosis and treatment of chronic cerebral ischemia

MD S.P. Markin
Voronezh State Medical Academy named after V.I. N.N. Burdenko

In recent years, the aging of the population has been observed in the world, primarily due to a decrease in the birth rate. According to the figurative expression of V. Konyakhin, "the young come and go, but the old remain." Thus, in 2000 there were about 400 million people over the age of 65 worldwide. However, this age group is expected to increase to 800 million by 2025.

Changes in the nervous system occupy a leading place among this contingent of people. In this case, the most common lesions of the cerebral vessels, leading to its ischemia, i.e. development of discirculatory encephalopathy (DE).

DE is a syndrome of progressive multifocal or diffuse brain damage, manifested by clinical neurological, neuropsychological and / or mental disorders, caused by chronic cerebrovascular insufficiency and / or repeated episodes of acute cerebrovascular accidents.

In the modern ICD-10 classification, there is no term "dyscirculatory encephalopathy". Instead of the previous diagnosis, it is recommended to use the following disease codes:
167.2 Cerebral atherosclerosis
167.3 Progressive vascular leukoencephalopathy
167.4 Hypertensive encephalopathy
167.8 Other specified cerebrovascular lesions.

However, the term "dyscirculatory encephalopathy" is traditionally used among neurologists in our country. DE is a heterogeneous condition that can have a variety of etiologies. The greatest etiological significance in the development of DE are:
- atherosclerosis (atherosclerotic DE);
- arterial hypertension (hypertonic DE);
- their combination (mixed DE).

In atherosclerotic DE, damage to large main and intracranial vessels (stenosis) predominates. At the same time, in the initial stages of the disease, stenosing changes in one (less often two) main vessels are detected, while in the advanced stages of the process, most (or all) of the main arteries of the head often turn out to be changed. A decrease in blood flow occurs with hemodynamically significant stenosis (narrowing of 70-75% of the area of ​​the lumen of the artery) and then increases in proportion to the degree of narrowing. At the same time, the state of intracranial vessels (development of the collateral circulation network) plays an important role in the mechanisms of cerebral circulation compensation.

In hypertensive DE, the main pathological processes are observed in smaller branches of the vascular system of the brain (perforating arteries) in the form of lipohialinosis and fibrinoid necrosis.

The main pathogenetic mechanisms for the development of DE:
- chronic ischemia;
- "incomplete stroke";
- completed stroke.

The main morphological changes in DE:
- focal changes in the brain (postischemic cysts due to lacunar stroke);
- diffuse changes in white matter (leukoareosis);
- cerebral atrophy (cortex of the cerebral hemispheres and hippocampus).

The defeat of small cerebral arteries (40-80 microns in diameter) is one of the main causes of lacunar stroke (up to 15 mm in diameter). Depending on the localization and size, lacunar infarctions can manifest themselves with characteristic neurological syndromes or be asymptomatic (in functionally “silent” zones - the shell, the white matter of the cerebral hemispheres). With the multiple nature of deep lacunae, a lacunar state is formed (Fig. 1)

Rice. 1. Multiple lacunar foci in the territory of the right middle cerebral artery, according to MRI of the brain

Leukoaraiosis is visualized as bilateral focal or diffuse areas of low density in the white matter on computed tomography and T1-weighted images on magnetic resonance imaging, or as areas of increased density on T2-weighted images on magnetic resonance imaging (Fig. 2).

Rice. 2. Severe leukoaraiosis

Widespread damage to small arteries causes several main types of changes:
- diffuse bilateral lesion of the white matter (leukoencephalopathy) - leukoencephalopathic (Binswanger) variant of DE;
- multiple lacunar infarcts - lacunar variant of DE.

In the clinical picture of DE, a number of main syndromes are distinguished:
- vestibular-atactic (dizziness, staggering, unsteadiness when walking);
- pyramidal (revitalization of tendon reflexes with expansion of reflexogenic zones, anisoreflexia, sometimes foot clonuses);
- amyostatic (trembling of the head, fingers, hypomia, muscle rigidity, slowness of movements);
- pseudobulbar (slurred speech, "violent" laughter and crying, choking when swallowing);
- psychopathological (depression, impaired cognitive functions).

Dizziness - the most frequent complaint of patients with DE (occurs in 30% of cases). Dizziness in the elderly is due to the following causes and their combinations:
- age-related changes in the sensory system;
- a decrease in the compensatory capabilities of the central mechanisms of balance;
- cerebrovascular insufficiency with a predominant lesion of the vertebrobasilar system.

In this case, the leading role is played by the defeat of the vestibular nuclei of the trunk or the vestibulo-cerebellar connections. Of certain importance is the so-called peripheral component, due to atherosclerotic lesions of the vessels of the inner ear.

Movement disorders in old age (up to 40% of cases) are caused by damage to the frontal lobes and their connections with subcortical formations.

The main movement disorders in the elderly:
- “frontal walking disorder” (frontal dysbasia);
- “frontal imbalance” (frontal astasia);
- "subcortical imbalance" (subcortical astasia);
- violation of the initiation of walking;
- "careful" (or uncertain) walking.

Movement disorders are often accompanied by falls. According to a number of researchers, 30% of people aged 65 years and older experience falls at least once a year, while in about half of the cases this happens more than once a year. The likelihood of falls increases in the presence of cognitive impairment, depression, as well as patients taking antidepressants, benzodiazepine tranquilizers, and antihypertensives.

The prevalence of depression among patients with DE (according to the Compass study) is more than 50% (with one third of patients having severe depressive disorders).

Features of the clinical picture of depression in the elderly:
- the predominance of somatic symptoms of depression over mental ones;
- pronounced violation of vital functions, especially sleep;
- a mask of mental symptoms of depression can be anxiety, irritability, "grouchiness", which are often considered by others as features of old age;
- cognitive symptoms of depression are often assessed in terms of senile forgetfulness;
- significant fluctuations in symptoms;
- incomplete compliance with the criteria for a depressive episode (certain symptoms of depression);
- a close relationship between exacerbations of somatic disease and depression;
- the presence of general symptoms of depression and somatic illness.

According to a number of epidemiological studies, from 25 to 48% of people over 65 experience a variety of sleep disorders. At the same time, sleep disorders most often manifest themselves in the form of insomnia: presomnic disorders - 70%, intrasomnic disorders - 60.3% and postsomnic disorders - 32.1% of cases.

The main manifestations of sleep disorders in the elderly:
- persistent complaints of insomnia;
- constant difficulty falling asleep;
- superficial and intermittent sleep;
- the presence of vivid, multiple dreams, often painful content;
- early awakenings;
- a feeling of anxiety when waking up;
- difficulty or inability to fall asleep again;
- lack of feeling of rest from sleep.

Cognitive impairment in depression due to the redistribution of attention, low self-esteem and mediator disorders. Cognitive impairment in depression is characterized by:
- acute / subacute onset of the disease;
- rapid progression of symptoms;
- indications of previous mental pathology;
- persistent complaints about the decrease in intellectual abilities;
- lack of effort when performing tests (“I don’t know”);
- variability of test execution;
attracting attention improves test performance;
- memory for recent and distant events suffers to the same extent.

However, in depression, the subjective assessment of cognitive abilities and the degree of social maladjustment, as a rule, do not correspond to the objective data of testing cognitive functions. A decrease in the severity of emotional disturbances leads to a regression of cognitive disorders associated with depression. Nevertheless, as a result of numerous studies of the hippocampal region in patients with major depressive disorder, evidence has been accumulated that atrophy of the hippocampus occurs during depression. Recently there have even been reports of atrophy of the hippocampus after the first depressive episode [J.P. Olier, France, 2007]. In addition, according to Chicago specialists from the Rush Alzheimers Disease Center, prolonged depression can lead to the development of Alzheimer's disease. So, with each new sign of depression, the likelihood of developing Alzheimer's disease increases by 20%.

Moderate cognitive impairment (UKR) in DE (according to the Prometheus study) occurs in 56% of cases. The relationship of moderate cognitive impairment detected in a patient with DE may be evidenced by:
- the predominance of regulatory cognitive impairments associated with dysfunction of the frontal lobes (violation of planning, organization and control of activities, decreased speech activity, moderate secondary memory impairment with relatively intact recognition);
- a combination of cognitive impairment with affective disorders (apathy, depression, irritability), as well as focal neurological symptoms, including those indicating suffering from the deep parts of the brain (dysarthria, impaired walking and postural stability, extrapyramidal signs, neurogenic urinary disorders).

Table 1 presents a comparative description of the "Alzheimer's type" MCI and DE with MCI.

Table 1. Distinctive characteristics of MCI of Alzheimer's type and DE with MCI

MCI in patients with diffuse white matter lesions appear when their volume exceeds 10% of the volume of the white matter of the hemispheres. However, within 5 years, 70-80% of patients with moderate cognitive impairment "pass" into the group of patients with dementia. At the same time, the presence of "silent" heart attacks, especially multiple ones, is associated with a general deterioration in cognitive activity and increases the risk of developing dementia more than 2 times in the next few years.

DE is the leading cause of vascular dementia. Thus, in the structure of vascular dementia, 67% is dementia due to small vessel disease (subcortical dementia, lacunar status, senile dementia of the Binswanger type). In this variant of dementia, cognitive impairment can progress continuously with episodes of severe deterioration due to strokes. At the stage of dementia, patients are partially or completely dependent on others. The decline in the quality of life of patients with dementia can be most clearly seen by analyzing the works of famous artists who suffered from dementia. Figure 3 shows the early work of the American artist William de Kooning (1904-1997), who was a master of abstract art. In the 80s, he was diagnosed with dementia, which was reflected in the works under the general title "Untitled". Figure 4 shows the paintings painted by the artist at the stage of dementia.

Rice. 3. De Kooning's early work ("Women")

Rice. 4. De Kooning's latest work ("Untitled")

The main clinical manifestations of vascular dementia (according to T. Erkinjuntti (1997) with changes.)

The course of the disease:
- relatively sudden onset (days, weeks) of cognitive impairment;
- frequent stepwise progression (some improvement after an episode of deterioration) and fluctuating course (i.e. differences in the condition of patients on different days) of cognitive impairment;
- in some cases (20-40%) a more inconspicuous and progressive course.

Neurological/psychiatric symptoms
- symptoms detected in the neurological status indicate focal brain damage in the initial stages of the disease (mild motor defect, impaired coordination, etc.);
- bulbar symptoms (including dysarthria and dysphagia);
- walking disorders (hemiparetic, etc.);
- instability and frequent, unprovoked falls;
- frequent urination and urinary incontinence;
- deceleration of psychomotor functions, violation of executive functions;
- emotional lability (violent crying, etc.);
- preservation of personality and intuition in mild and moderately severe cases;
- affective disorders (depression, anxiety, affective lability).

Accompanying illnesses

A history of cardiovascular diseases (not in all cases): arterial hypertension, coronary heart disease.

Depending on the severity of the main symptoms, there are 3 degrees of severity of DE:
1st degree - the presence of focal scattered neurological symptoms, which are insufficient in their severity for the diagnosis of a delineated neurological syndrome (mild cognitive impairments of a neurodynamic nature are detected);
2nd degree - the presence of a sufficiently pronounced neurological syndrome (clinically obvious cognitive impairment, usually of a moderate degree);
3rd degree - a combination of several neurological and neuropsychological syndromes, which indicate a multifocal brain lesion (cognitive impairment reaches the degree of dementia).

As DE progresses, the number of patient complaints decreases significantly, due to a decrease in patients' criticism of their condition. Mainly complaints about instability when walking, noise and heaviness in the head, sleep disturbance remain. At the same time, the severity of social maladjustment increases. Figure 5 shows a fragment of the record of complaints of patient B., 59 years old, suffering from DE of the 3rd degree.

Rice. 5. Complaint of patient B., aged 59, with DE of the 3rd degree

The severity of social maladaptation:
1st stage - the patient is able to serve himself under normal conditions, difficulties arise only with increased stress (emotional or physical);
2nd stage - Requires some help under normal conditions;
3rd stage - due to a neurological and / or cognitive defect, the patient is unable to perform even simple functions, constant assistance is required.

Currently allocate 3 options for the rate of progression of DE:
- fast pace - change of stages faster than in 2 years;
- average pace - change of stages within 2-5 years;
- slow pace - change of stages in more than 5 years

Criteria for diagnosing DE:
- objectively detectable neuropsychological and/or neurological symptoms;
- signs of cerebrovascular disease, including risk factors and / or instrumentally confirmed signs of damage to cerebral vessels (for example, ultrasound data) and / or brain matter (CT / MRI data);
- the presence of a causal relationship between vascular lesions of the brain and the clinical picture;
- the absence of signs of other diseases that can explain the clinical picture.

O.S. Levin (2006) developed diagnostic criteria based on CT and MRI data of various stages of dyscirculatory encephalopathy (Table 2).

Table 2. Neuroimaging changes in DE

Principles of DE treatment:
1) effect on vascular factors (correction of blood pressure, prevention of stroke);
2) restoration of cerebral blood flow, improvement of cerebral metabolism;
3) improvement and stabilization of cognitive functions;
4) correction of other clinical manifestations of the disease.

One of the most promising approaches in the treatment of DE is the appointment of combined drugs with a multimodal effect (antihypoxic, metabolic (nootropic) and vasodilating). Recently, the drug has been widely used for this purpose. Omaron containing 400 mg of piracetam and 25 mg of cinnarizine.

The mechanism of action of piracetam is diverse. One of the theories explaining the many effects of piracetam is the membrane one. According to her, the effects of piracetam may be the result of restoration of membrane fluidity (and it decreases with age):
- specific interaction with the cell membrane;
- restoration of the structure of membranes;
- restoration of liquid properties of cell membranes;
- normalization of cell membrane function.

It is customary to distinguish two main directions of action of piracetam: neuronal and vascular. The neuronal effect is realized due to the improvement of metabolic processes due to the optimization of oxygen consumption and glucose utilization. It has been proven that piracetam interacts with the transmitter system, providing a modulating effect. Improving the neuronal effect facilitates cognitive processes. In a number of studies with double-blind control, it was found that the use of piracetam significantly increases higher mental functions not only in the conditions of the so-called physiological aging, but also in patients with psycho-organic syndrome during senile involution. In addition, in recent years, studies have appeared confirming the effectiveness of piracetam in the early stages of Alzheimer's disease.

The vascular effect of piracetam is manifested due to its effect on microcirculation and blood cells: a decrease in platelet aggregation, an increase in the deformability of erythrocytes. As a result, piracetam exhibits an antithrombotic effect and significantly improves the rheological properties of blood, which, in turn, is the basis for the normalization of impaired cerebral circulation.

However, cerebrovascular pathology is accompanied not only by metabolic disorders, but also by disorders of cerebral hemodynamics, as a result, another group of drugs is widely used in neurological practice - vasoactive agents, in particular cinnarizine. Cinnarizine - a selective blocker of slow calcium channels, inhibits the entry of calcium ions into cells and reduces their content in the plasma membrane depot, reduces the tone of the smooth muscles of arterioles, reduces their response to biogenic vasoconstrictor substances, increases the elasticity of erythrocyte membranes, their ability to deform, reduces blood viscosity.

When piracetam is combined with cinnarizine, the action of both drugs is potentiated. Thus, the time to reach the maximum concentration of cinnarizine in the blood plasma is 1-4 hours, while piracetam is 2-6 hours. As a result, the vascular effect precedes the nootropic one, which improves the delivery of piracetam to the area of ​​cerebral ischemia. In addition, the use of omarone neutralizes the side effects of each of the components: piracetam (irritability, internal tension, sleep disturbances, irritability) and cinnarizine (weakness, depression, drowsiness). Omaron is prescribed 1 tablet 3 times a day for 2-3 months.

In a multicenter (5 clinical centers of the Russian Federation) open randomized study, which included 90 patients who had a stroke (prescription from 1 month to 1 year), compared the efficacy and tolerability of omarone (1 tablet 3 times a day) in combination with basic therapy (hypotensive drugs, antiplatelet agents and statins) when used for 2 months. compared to basic therapy.

The results of the study showed that in the omaron therapy group, a significant improvement in all cognitive functions was noted after a month of treatment. The improvement was most significant after two months of treatment. In the control group, the dynamics was much less pronounced. So, as an example, below are the results of performing tests for memorizing 5 words and drawing a clock (Fig. 6, 7).

Rice. 6. Dynamics of indicators of the memorization test of 5 words

Rice. 7. Dynamics of indicators of the clock drawing test (points)

In addition, a significant decrease in the severity of depressive and anxiety disorders was noted in the omarone treatment group (Fig. 8).

Rice. 8. Dynamics of depression and anxiety scale indicators

The study established good tolerability of omarone, no side effects when combined with other drugs used to prevent recurrent stroke, and no effect of omarone on systemic hemodynamics.

Literature

1. Damulin I.V. Dyscirculatory encephalopathy: pathogenesis, clinic, treatment. Guidelines - Moscow - 2005 - 43 p.

2. Damulin I.V. Actual aspects of neurogeriatrics in the practice of a therapist. Guidelines for general practitioners - Moscow - 2004 - 23 p.

3. Kamchatnov P.R. Chronic disorders of cerebral circulation - Moscow - 2008 -39 p.

4. Levin O.S. Pathogenetic therapy of cognitive impairment - Moscow - 2008 - 12 p.

5. Levin O.S. Dyscirculatory encephalopathy: modern ideas about the mechanisms of development and treatment - Moscow - 2006 - 24 p.

6. Markin S.P. Violation of cognitive functions in medical practice. Methodological guide - Moscow - 2007 - 42 p.

7. Parfenov V.A. et al. Open randomized multicenter study of the efficacy and safety of omaron in patients with stroke and mild cognitive impairment - Moscow - 2008 - 15 p.