Hypertonic encephalopathy

One of the complications of hypertension and symptomatic arterial hypertension is hypertensive encephalopathy. According to ICD-10, it is called hypertensive. This is an ischemic brain injury that occurs due to a shortage of blood supply to altered cerebral arteries of predominantly small caliber. In this case, a polymorphic symptom complex appears, the manifestations of which depend on the size and localization of lesions of the nervous tissue.

Content

  • 1Changes in the brain in hypertension
  • 2How this can manifest itself
    • 2.1Acute hypertensive encephalopathy
    • 2.2Clinic of chronic hypertensive encephalopathy
  • 3Examination
  • 4Principles of treatment
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Changes in the brain in hypertension

Even a single increase in blood pressure adversely affects the state of the nervous tissue, because in this case there is a sharp breakdown in the self-regulation of the tone of the arterioles and venules. The pathological reaction involves small vessels in all tissues, but the so-called target organs suffer the most. They include the brain, kidneys and heart.

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During a moderate increase in arterial pressure, the protective mechanism of constriction of small vessels is activated, which prevents their rupture and stabilizes the pulse pressure in different parts of the arteries. With frequent or persistent arterial hypertension, the muscular layer of the arteries of the small and medium-sized arteries gradually thickens, hypertrophy. This leads to a narrowing of the lumen of blood vessels with a decrease in blood perfusion, as a result of which the brain and internal organs begin to experience chronic hypoxia (or ischemia) - a constant deficit of oxygen and nutrients substances. A hypertensive variant of chronic ischemic brain disease develops, which in our country is often also called discirculatory encephalopathy.

The appearance of signs of encephalopathy is one of the criteria for the second stage of hypertension. And at stage 3, brain tissue damage is found in almost all patients suffering from uncontrolled arterial hypertension. Especially insidious are the so-called headless hypertension (with a predominant increase in diastolic pressure) and low-symptom hypertensive crises. After all, a person at the same time feels tolerable and therefore usually does not receive systematic therapy. And the accumulating changes in the brain gradually lead to the formation of an irreversible neurological deficit and an intellectual-mnestic decrease.

A rapid and pronounced increase in blood pressure sometimes causes damage to the inner shell (endothelium) of small vessels and the disruption of compensatory mechanisms. Excessive spasm of arterioles soon gives way to paralysis, there is a pronounced passive stretching of the walls of small vessels with blood, with a significant increase in the permeability of capillaries. This condition is called acute hypertensive encephalopathy.

In case of a crisis as a result of rapidly increasing vascular changes, plasma and even uniform elements of blood rush into surrounding tissues, which manifests itself plasmorrhagia, diapedesis impregnation and hemorrhages of different sizes along the walls vessels. Develops a filtration cerebral edema with multiple different-caliber foci of ischemic softening of the nervous tissue. The condition of the venules also changes, which affects the absorption of cerebrospinal fluid and leads to an increase in intracranial pressure.

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How this can manifest itself

The brain performs many functions. It has areas responsible for tone and reduction of different muscle groups, sensory organs, balance, vasomotor and respiratory centers. Understanding and production of speech (written and oral), all kinds of memory, emotions, control of basic needs, alternation of sleep-wake cycles - all this is also a consequence of the brain. Therefore, the consequences of nerve cell damage or their hypoxia in hypertensive encephalopathy may be different. Symptoms and their degree of severity will depend on which parts of the brain are involved in the pathological process and how extensive the emerging pockets of ischemia.

In acute hypertensive encephalopathy, many manifestations are reversible, they pass as the edema of the tissues is reduced and normal blood flow is restored by the capillary bed. The death of nerve cells at first may not affect the functioning of the brain if the ischemic foci are small, small and not located in strategically important areas. But as the number of dead neurons increases, symptoms will appear that persist even after the hypertensive crisis is relieved. At the initial stages of chronic encephalopathy, they are meager and are detected only when the neurologist performs special tests. In the future, a polymorphic clinical picture is formed, which will include motor, sensory and cognitive disorders of varying severity.

Acute hypertensive encephalopathy

Acute encephalopathy develops during the current hypertensive crisis, and the level of blood pressure may vary. In hypertensive patients with "experience an increase in systolic pressure above 180-190 mm Hg is usually critical. Art. And in individuals prone to hypotension, the breakdown of cerebral vascular autoregulation can develop already at rates of 140/90 mm Hg. Art.

The main signs of acute hypertensive encephalopathy:

  • a strong growing headache, usually of a pressing and bursting nature, initially localized in the occipital region and then extending to the entire head;
  • nausea, sometimes vomiting with little or no relief;
  • sudden vision impairment due to edema of the optic disc and small-to-small bleeding in the retina of the eye;
  • severe nonsystemic dizziness;
  • deterioration in coughing, straining, sneezing, neck tension;
  • epileptiform convulsive seizures;
  • narrowing of consciousness, state of stunning;
  • meningism (the detection of individual meningeal signs in the absence of inflammation of the meninges);
  • possible transient mildly expressed peripheral paresis and disturbance of surface sensitivity.

Most often, many of these symptoms are attributed to the "normal" hypertensive crisis. But in fact, they testify to involvement in the pathological process of the brain and the development of uneven edema of the nervous tissue. In the absence of adequate therapy, the condition is aggravated by the appearance of ischemic foci, in which the activity of neurons decreases and even their death. Acute hypertensive encephalopathy can become a harbinger of an onset stroke.

Clinic of chronic hypertensive encephalopathy

In the course of chronic encephalopathy, 3 stages are isolated. At first, subjective complaints of attention distraction, fatigue, slight deterioration predominate short-term memory, transient dizziness, frequent headaches of varying intensity and localization. Neurological examination of sensitivity disorders, paresis and vestibulo-atactic syndrome is not revealed. Possible anisoreflexia, symptoms of oral automatism, easy changes in gnosis, praxis and memory during in-depth special tests.

The second stage of hypertensive encephalopathy is the period of the emergence of distinct neurological syndromes and local symptoms. Complaints are complicated, but sometimes a decrease in cognitive functions can lead to a lack of critical assessment of their condition. In this case, a person with hypertension usually refuses the recommended treatment, that has a negative effect on the course of hypertensive disease and leads to rapid progression encephalopathy.

When examined at stage 2 of hypertensive encephalopathy, a neurologist can identify one or more syndromes: pyramidal, dyspnestic, amyostatic, and discoordinate. At the same time, the clinical picture flickers. Along with focal neurological disorders in a person, initiative and motivation may be impaired, ability to predict and organize their own activities, which significantly reduces ability to work. The defeat of the frontal lobes leads to the formation of pseudobulbar syndrome and sometimes to the disinhibition of behavior. Often there are emotional lability, increased sensitivity, tearfulness, sensitivity to criticism.

Sometimes accompanying behavioral and affective disorders already at this stage of hypertensive encephalopathy serve as an excuse for turning to a psychiatrist, which can establish a diagnosis of organic brain disease (OCGM) of vascular genesis or other nosological forms with a lesion of the nervous tissue.

At the third stage, all existing disorders are deepened, and other neurological syndromes join them. A lacunar infarction may develop. With focal lesions of the brain, recurrent epileptiform seizures sometimes develop. Cognitive decline can reach the degree of dementia. In elderly people, arterial hypertension can provoke the development of Parkinsonian syndrome. At this stage, the manifestations of hypertensive encephalopathy are the cause of a person's disability, and in some cases a solution to the issue of his incapacity is required.

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Examination

Diagnosis of hypertensive encephalopathy includes several stages:

  • verification of hypertension (or symptomatic arterial hypertension) as the most likely cause of brain damage, clarification of the type of course of the disease and its causes;
  • a neurologic examination to identify all available symptoms, including cognitive disorders;
  • if necessary, counseling the psychiatrist to eliminate diseases that may lead to similar complaints;
  • general clinical examination, especially the conduct of a general and biochemical blood test, which would exclude as a cause cerebral symptoms marked anemia, diabetes mellitus, toxic brain damage in renal or hepatic insufficiency;
  • Exclusion of syphilitic damage of the central nervous system;
  • exclusion of severe generalized atherosclerosis (using blood test and ultrasound of cervical arteries);
  • visualization of the brain with MRI or CT;
  • if there are indications, an EEG to evaluate the bioelectic activity of the brain.

In some cases, a spinal tap is used to determine the pressure of the CSF and then analyze the resulting fluid. MRI (or CT) of the brain at the first stage of hypertensive encephalopathy usually does not reveal any changes, only sometimes the expansion of Virchow spaces is noted. But starting from stage 2 periventricular and subcortical is determined ischemic foci with cavities in the center, called lacunas. And often they are "dumb that is, their appearance was not accompanied by a stroke clinic. Also, diffuse leuko-arazis and increasing cerebral atrophy with expansion of the ventricles and subarachnoid spaces are revealed. A characteristic feature of hypertensive encephalopathy is the predominant lesion of white matter and subcortical structures, which distinguishes this disease from atherosclerotic vascular disease of the head the brain.

In the development of acute hypertensive encephalopathy, it is necessary to exclude subarachnoid hemorrhage, hemorrhagic stroke, acute toxic encephalopathy and other conditions.

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Principles of treatment

When identifying signs of hypertensive encephalopathy, the primary task is to select adequate antihypertensive therapy. In this case, drugs are prescribed that allow you to monitor the baseline blood pressure level and gently gradually reduce it to the target figures. The opinion is erroneous that at the age of 65-70 years the normal pressure is 150/90 mm Hg. This level can be customary and comfortable for the patient, but at the same time it is the cause of the growing irreversible changes in the brain.

Hypotensive therapy is selected individually. Preference is given to long-acting drugs, which allows maintaining a stable level of pressure during the day. It is often necessary to use combined agents that contain ACE inhibitors, diuretics, beta-blockers and calcium antagonists in various combinations.

In acute encephalopathy, diuretic drugs with anti-edematous action are necessarily prescribed, and the balance of electrolytes in the blood is monitored. And the level of blood pressure is reduced gradually to prevent total brain ischemia.

Simultaneously with antihypertensive therapy for chronic hypertensive encephalopathy, drugs for improvement of blood circulation (disaggregants and, if necessary, thrombolytics), metabolic agents, vitamins. And with increasing cognitive impairment, nootropics are added. The drugs affecting the state of the vascular wall and possessing a neuroprotective effect are shown.

Most often appoint trental (pentoksifillin), mexidol, cerebrolysin, aspirin preparations (preferably in a protective intestine-soluble shell), clopidogrel, dipyridamole (quarantil). With cognitive impairments, nootropics and antidemia drugs of different groups are shown, and for gross behavioral and affective disorders disorders (anxiety, depression) by appointment of a psychiatrist can be used sedative, antidepressant and normotimicheskie preparations.

Hypertensive encephalopathy requires complex treatment, so patients with this disease are usually observed by doctors of different specialties. Competent therapy can reduce the rate of progression of the disease, and in the early stages even achieve reverse development of the existing symptoms.

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