Diabetic encephalopathy — the diffusion degenerate damage of a brain arising against the background of diabetes. It is characterized by memory violation, decrease in the intellectual sphere, nevrozopodobny changes, an adynamy, vegeto-vascular dysfunction, focal symptomatology. It is diagnosed for diabetics as a result of neurologic survey, the complex analysis of data of EEG, REG, cerebral MRT. Treatment is carried out against the background of antidiabetic therapy, includes vascular, metabolic, vitamin, antioxidant, psychotropic, antisclerous medicines.
The interrelation between cognitive violations and the diabetes (D) was described in 1922. The term "diabetic encephalopathy" (DE) is entered in 1950. Today a number of authors suggests to consider a diabetes complication only the encephalopathy developing owing to dismetabolichesky processes. It is offered to carry the cerebral pathology caused by vascular frustration at SD to distsirkulyatorny encephalopathy (DEP). However in domestic neurology concept DE traditionally includes all pathogenetic forms of encephalopathy: metabolic, vascular, mixed. In such broad understanding diabetic encephalopathy is observed at 60-70% of diabetics.
Reasons of diabetic encephalopathy
Etiologichesky factor of DE — diabetes. Encephalopathy belongs to the late complications developing 10-15 years later from SD debut. The exchange violations, typical for diabetes, leading to defeat of brain fabrics and vessels are its immediate cause. Emergence of DE is promoted:
- Diabetic dislipidemiya. It is characteristic of diabetes of the 2nd type. Dismetabolizm of lipids and cholesterol leads to formation of vascular atherosclerotic plaques. The progressing system and cerebral atherosclerosis is noted at diabetics for 10-15 years earlier, than on average in population.
- Diabetic macrovascular disease. Changes of a vascular wall complicate a blood-groove in cerebral vessels, are the reason of chronic ischemia of a brain, increase risk of a stroke.
- Sharp hypo - hyper glycemic states. The hypoglycemia and ketoacidosis negatively influence a condition of neurons, increase risk of DE and dementia. Researches showed that along with the level of glucose concentration in blood of insulin and S-peptide matters.
- Arterial hypertension. It is observed in 80% of cases of SD. Is a consequence of a diabetic nephropathy or has essentsialny character. Negatively affects brain blood supply, can act as the stroke reason.
Diabetic encephalopathy has the multiple-factor mechanism of development including vascular and metabolic components. Vascular frustration owing to macro - and mikroangiopatiya worsen cerebral haemo dynamics, cause oxygen starvation of brain cages. The patobiokhimichesky reactions which are implemented at a hyperglycemia cause activation of anaerobic glycolysis instead of aerobic, lead to power starvation of neurons. The appearing free radicals have the damaging effect on cerebral fabrics. Formation of glikozilirovanny hemoglobin, is less connecting oxygen, aggravates the hypoxia of neurons resulting from vascular disorders. The hypoxia and a dismetabolizm lead to death of neurons with formation of diffusion or melkoochagovy organic changes of cerebral substance — there is encephalopathy. Destruction of mezhneyronalny communications attracts gradually progressing decrease in cognitive functions.
Symptoms of diabetic encephalopathy
DE arises gradually. At young age of its manifestation accrue after hyper - and hypoglycemic episodes, at elderly — in connection with transferred ONMK. The clinical symptomatology is not specific, includes cognitive frustration, an adynamy, nevrozopodobny symptoms and focal neurologic deficiency. At the beginning of a disease patients complain of weakness, fatigue, disturbing feelings, headaches, problems with concentration of attention.
Nevrozopodobny states are caused somatic (feeling sick) and psychogenic (need of continuous treatment, the fact of development of complications) by factors. Narrowing of interests, concentration on a disease, attacks of spiteful and sad mood are typical. At primary address depressive neurosis is diagnosed for 35% of patients, in process of development of SD the number of patients with depressive violations increases to 64%. Emergence hysterical, disturbing , ipokhondrichesky neurosis is possible. In some cases one look passes into another. Heavy mental deviations are noted seldom.
The asthenic syndrome is characterized by slackness, apathy, combined with vegeto-vascular frustration, sinkopalny states. Violations of the cognitive sphere are shown by the decrease in memory, absent-mindedness which is slowed down by thinking. Among focal symptoms insufficiency of convergence, an anizokoriya (different diameter of pupils), an ataxy (dizziness, unsteadiness of walking), pyramidal insufficiency (weakness of extremities, increase in a tone of muscles) prevail.
Increase of cognitive violations leads to intellectual decrease and dementia (weak-mindedness). The last is the reason of a considerable invalidization of patients, limits their self-service. The situation is aggravated by impossibility of independent implementation by the patient of antidiabetic therapy. Sharp disorders of cerebral haemo dynamics act as complications of DE: the tranzitorny ischemic attacks, ischemic strokes, are more rare — intra cranial hemorrhages. Permanent motive frustration, damage of craniocereberal nerves, violations of the speech, progressing of cognitive dysfunction are a consequence of ONMK.
Diabetic encephalopathy is diagnosed by the neurologist by results of inspection of the neurologic status for patients with SD. Assessment of extent of functional and organic changes of cerebral structures is made by means of tool methods.
- Electroencephalography. Reflects the diffusion nature of changes. Flattening of EEG, an alpha rhythm reduction, emergence pathological a theta - and delta waves is noted.
- Brain MRT. In an initial stage meets standard. In the subsequent reveals nonspecific melkoochagovy diffusion organic changes of degenerate and atrophic character.
- Research of cerebral haemo dynamics. It is carried out by means of a rheoencephalography, duplex scanning, UZDG of vessels of the head, the MR-angiography.
- Laboratory analyses. Allow to estimate metabolic violations. Level of glucose, lipids, cholesterol, S-peptide, insulin is defined.
Differential diagnostics of DE is directed to an exception of infectious defeats and tumors of a brain. It is carried out according to clinical data, is confirmed during a magnetic and resonant tomography.
Treatment of diabetic encephalopathy
Therapy of DE is carried out by the neurologist together with the endocrinologist (diabetology). A necessary condition of treatment — maintenance of adequate concentration of glucose of blood by observance of the corresponding diet, reception of antihyperglycemic medicines, if necessary — insulin therapy. Neurologic treatment is directed to improvement of brain haemo dynamics, maintenance of metabolism of neurons, increase in their resistance to a hypoxia. Regular courses of complex therapy with use of vazoaktivny, antiagregantny, antioxidant, nootropic pharmaceuticals are conducted.
Stimulators of power exchange, group B vitamins, alpha lipoic acid, vitamin E are appointed. In the presence of violations of the motive sphere antikholinesterazny means are recommended (). According to indications therapy is supplemented with hypotensive means (at persistent arterial hypertension) and anti-sclerous medicines from group of statin. The pharmacotherapy of nevrozopodobny states demands adequate selection of medicines as sedatives negatively influence cognitive functions. Mainly atypical tranquilizers are applied (). Consultation of the psychotherapist, sometimes — the psychiatrist is recommended.
Forecast and prevention
Diabetic encephalopathy — the chronic progressing disease. Speed of aggravation of symptomatology directly depends on weight of a current of SD. Systematic observation of the endocrinologist and neurologist, adequate antihyperglycemic treatment, regular courses of neurologic therapy allow to suspend or slow down progressing of cerebral symptomatology, to prevent development of complications. Prevention consists in timely detection and correct treatment of diabetes, correction of hypertensia, therapy of vascular disorders.