Hypertensive encephalopathy is a chronic progressive lesion of brain tissues caused by disorders of cerebral hemodynamics in patients with long—term, poorly controlled arterial hypertension. It is clinically manifested by symptoms of dyscirculatory encephalopathy. Hypertensive encephalopathy is diagnosed by comparing the data of a neurological examination, the conclusion of a cardiologist and a psychiatrist, the results of studies of cerebral hemodynamics and brain MRI. Treatment is carried out against the background of taking antihypertensive drugs, includes vascular, nootropic, neuroprotective and symptomatic pharmaceuticals.
ICD 10
I67.4 Hypertensive encephalopathy
General information
Among the causes of dyscirculatory encephalopathy, arterial hypertension ranks second after atherosclerosis. In ICD-10, hypertensive encephalopathy (HE) is distinguished as a separate type of encephalopathy that develops in patients with hypertension or long-term symptomatic hypertension. Unlike atherosclerotic encephalopathy, hypertensive occurs with a predominant lesion of small-caliber cerebral vessels. However, the separation of these encephalopathies is very conditional, since hypertensive encephalopathy is accompanied by the rapid development of atherosclerotic changes in cerebral vessels.
Causes
The main etiological factor of HE is a high level of blood pressure (BP). Arterial hypertension can have a primary character (hypertension) and develop a second time due to kidney damage (chronic pyelonephritis, glomerulonephritis, hydronephrosis), endocrine disorders (pheochromocytomas, hypercorticism, primary hyperaldosteronism), aortic atherosclerosis. The increased risk of developing HE in hypertensive patients is caused by the following factors:
- Uncontrolled high blood pressure figures. Pathological changes in the vessels occur faster in patients who do not receive hypotensive therapy or receive it in insufficient volume. In some cases, it is not possible to completely correct hypertension with the help of drug therapy.
- Hypertensive crises. Each sharp rise in blood pressure negatively affects the condition of the vascular wall, leads to its thinning, increased permeability. Such changes cause subsequent hemorrhagic impregnation of cerebral tissues at the site of thinning.
- Changes in blood pressure. Sharp fluctuations in blood pressure cause hypertrophy of the vascular wall with narrowing of its lumen, increase the wear of vascular tissues. Hypotension, including due to iatrogenic dilation of blood vessels, leads to a slowdown and insufficiency of cerebral blood flow.
- Nocturnal hypertension. Nocturnal rises in blood pressure often have a hidden character. The lack of timely correction of pressure leads to a prolonged spastic state of cerebral vessels with the development of ischemic processes in the tissues supplied by them.
- High pulse pressure. Studies have shown that the difference between systolic and diastolic pressure of 40 mmHg worsens the course of cardiovascular pathology. A constant increase in pulse pressure causes an additional load on the vascular wall and the muscular apparatus.
Pathogenesis
The compensatory reaction to an increase in blood pressure is the narrowing of small arterioles, which prevents their rupture and equalizes pulse pressure. Constant hypertension, frequent pressure rises cause hypertrophy of the muscular layer of the walls of arterioles. As a result, the vascular wall thickens and the lumen narrows. These processes are observed in the vessels of all tissues, but are more pronounced in target organs: the brain, kidneys, and heart. A decrease in the lumen of cerebral arterioles causes a drop in cerebral perfusion, the development of chronic cerebral ischemia. Due to the constant shortage of oxygen and nutrients, degenerative processes occur in the cerebral structures. The addition of atherosclerotic changes exacerbates cerebral circulatory insufficiency and its clinical symptoms.
Morphologically, there is an early lesion of the white medulla, demyelination of nerve fibers, expansion of perivascular spaces. The changes are diffuse, observed symmetrically in both hemispheres, initially localized along the lateral ventricles, spread periventrically. Along with diffuse degenerative processes in the white cerebral substance, there are separate local foci — lacunar infarcts.
Classification
Hypertensive encephalopathy is characterized by a gradual progression of degenerative changes in cerebral tissues and an aggravation of symptoms. Understanding at what stage of the course of the pathological process is necessary for the correct selection of therapy and assessment of the prognosis of the disease. Therefore , specialists in the field of practical neurology distinguish 3 main stages of HE:
- Stage I — subjective complaints of fatigue, inattention, headaches, memory impairment prevail. Objective symptoms are meager, cognitive deviations are detected only with careful special testing.
- Stage II — clear neurological syndromes appear in the clinical picture: vestibular, pyramidal, atactic, dysmnestic, subcortical. In most cases, there is a predominance of one of these syndromes. Cognitive impairment is moderate. Professional activity is difficult, social adaptation is reduced.
- Stage III — there is a combination and simultaneous increase of several neurological syndromes. It is possible to join Parkinsonism, epileptic seizures, pseudobulbar syndrome. There are gross cognitive disorders up to dementia. Work by profession is impossible. Household adaptation is broken.
Symptoms
The disease begins with slowly progressing nonspecific symptoms. Patients complain of difficulty concentrating, memory loss, increased fatigue, frequent cephalgia, sometimes dizziness. As the complaints progress, they become more complicated, the symptoms of individual neurological syndromes are formed. With vestibular ataxia, patients indicate shakiness when walking, impaired coordination. With dysmnestic syndrome, memory disorder dominates, with pyramidal — muscle weakness, more often by the type of mild hemiparesis. Subcortical disorders lead to tremor, hyperkinesis, secondary parkinsonism.
There is a decrease in the speed and productivity of thinking, a narrowing of the circle of interests, the complexity of organizing one’s own activities (apraxia), a violation of motivation. The dysfunction of the cognitive sphere causes the lack of adequate criticism in relation to their condition. There is increased emotional lability, sometimes behavioral and affective disorders. The clinical picture is characterized by “flickering” of symptoms, periodic transient improvement of the condition.
Stage III hypertensive encephalopathy is characterized by gross organic and cognitive symptoms. Apraxia, agnosia, amnesia, disintegration of intellectual abilities, personality change, complete loss of professional skills are noted. Vascular dementia develops, accompanied by inappropriate behavior, mental changes. Neurological symptoms are aggravated, pseudobulbar paralysis is possible: dysarthria, swallowing disorder, violent crying. Due to lacunar infarction, epileptic paroxysms and syncopal states may occur. The increase in pyramidal, atactic, and Parkinsonian syndromes limits the possibility of self-service and independent movement.
Complications
Chronically occurring hypertensive encephalopathy is often accompanied by separate acute episodes that occur against the background of a rapid increase in blood pressure. They are caused by disruption of vascular regulation and hypotonic dilation of intracerebral vessels, the consequence of which is sweating of blood plasma with the formation of perivascular edema. In the absence of timely treatment, acute hypertensive encephalopathy can be complicated by lacunar infarction, ischemic or hemorrhagic stroke. Choking on food due to dysphagia in pseudobulbar syndrome is dangerous with the occurrence of asphyxia, throwing food particles into the respiratory tract with the development of aspiration pneumonia.
Diagnostics
Hypertensive encephalopathy is assumed in every case of the occurrence of characteristic neurological symptoms against the background of chronic arterial hypertension. The diagnostic search is aimed at excluding other cerebral pathology, assessing the degree of existing vascular and cerebral changes. The main stages of diagnosis are:
- Neurologist’s examination. In the initial stage, the neurological status is without features, anisoreflexia is possible. Special cognitive testing determines mild mnestic, praxic and gnostic changes.
- Consultation with a cardiologist. It is necessary to confirm the diagnosis of hypertension. According to the indications, an ECG, EchoCG, and daily blood pressure monitoring are performed
- Examination of the mental sphere. It is performed by a psychiatrist, neuropsychologist if there is a suspicion of mental abnormalities. Mental status is assessed through conversation, observation and testing.
- Laboratory tests. It is important to determine the level of cholesterol, blood lipid spectrum. In a comprehensive examination, a general urine analysis, blood biochemistry, and a Rehberg test are required to assess kidney function.
- Study of cerebral hemodynamics. Duplex scanning of cerebral vessels, transcranial ultrasound, MRI of cerebral vessels is used. Examinations allow to identify narrowing of the lumen of arterioles, to assess its degree, to determine the localization and prevalence of the most pronounced changes.
- Tomography. MRI of the brain is the most informative method in the diagnosis of morphological changes in brain tissues. It allows to identify diffuse degenerative changes, foci of lacunar infarcts in patients with stage II – III HE, to exclude other organic pathology of the brain.
In the presence of paroxysmal activity, electroencephalography, consultation with an epileptologist is indicated. The detection of renal dysfunction based on the results of laboratory tests is an occasion for inclusion in the list of necessary examinations of ultrasound of the kidneys and consultation of a nephrologist. Hypertonic encephalopathy is differentiated from brain tumors, encephalitis, slow CNS infections, Parkinson’s disease, demyelinating diseases, Creutzfeldt-Jakob disease, Alzheimer’s. The vascular nature of the lesion is indicated by the data of cerebrovascular studies, the detection of traces of lacunar infarcts on MRI.
Treatment
The success of HE therapy directly depends on the effectiveness of arterial hypertension correction. Neurological treatment is carried out against the background of hypotensive therapy, treatment of a disease that causes a high level of pressure. The main directions of treatment are: improvement of cerebral perfusion, maintenance of brain tissue metabolism, restoration of central nervous system function. The basic groups of drugs are:
- Vasodilators. They allow to stop the main pathogenetic link of HE — arteriole spasm. Pharmaceutical preparations are used without the side syndrome of “stealing”: calcium channel blockers, a2–adrenergic receptor antagonists, phosphodiesterase inhibitors.
- Drugs that improve microcirculation. Long-term use of anticoagulants is indicated: acetylsalicylic acid, dipyridamole. The use of pentoxifylline contributes to the improvement of blood circulation.
- Neuroprotectors. They are necessary to increase the resistance of nerve cells to chronic hypoxia and reduced intake of nutrients. Antioxidants (ethylmethylhydroxypyridine succinate, lipoic acid), amino acid preparations (gamma-aminobutyric acid, glycine) are used.
- Symptomatic means. They are prescribed depending on the current disorders and symptoms that accompany encephalopathy. With cognitive decline, nootropics are shown, with hyperlipidemia — pharmaceuticals of the statin group, with mental disorders — sedatives, normotimics, tranquilizers, with epileptic paroxysms — anticonvulsants.
Prognosis and prevention
The effectiveness of therapeutic measures depends on the stage of HE, the causal disease, the possibility of a full-fledged correction of blood pressure, the presence of concomitant pathology (atherosclerosis, endocrine disorders). Complex neurological treatment against the background of stabilization of blood pressure in stage I ensures long-term intellectual safety and efficiency of patients. If hypertensive encephalopathy is in stage III, therapy can only alleviate neurological manifestations and somewhat slow down the progression of the disease.
The main preventive measure that can prevent the development of encephalopathy in hypertensive patients is the maintenance of an optimal blood pressure level. Constant dispensary monitoring of the patient by a cardiologist is necessary. An important point of antihypertension therapy is the exclusion of sudden fluctuations and nocturnal rises in blood pressure. Secondary prevention consists in regular observation by a neurologist, repeated courses of vascular and neuroprotective therapy.