Diabetic encephalopathy is a diffuse degenerative brain lesion that occurs against the background of diabetes mellitus. It is characterized by memory impairment, a decrease in the intellectual sphere, neurosis-like changes, asthenia, vegetative-vascular dysfunction, focal symptoms. It is diagnosed in diabetics as a result of neurological examination, complex analysis of EEG, REG, and cerebral MRI data. Treatment is carried out against the background of antidiabetic therapy, includes vascular, metabolic, vitamin, antioxidant, psychotropic, anti-sclerotic medications.
G93.4 Unspecified encephalopathy
The relationship between cognitive impairment and diabetes mellitus (DM) was described in 1922. The term “diabetic encephalopathy” (DE) was introduced in 1950. Today, a number of authors suggest that only encephalopathy developing as a result of dysmetabolic processes is considered a complication of diabetes. Cerebral pathology caused by vascular disorders in DM is proposed to be attributed to dyscirculatory encephalopathy (DEP). However, in Russian neurology, the concept of DE traditionally includes all pathogenetic forms of encephalopathy: metabolic, vascular, mixed. In such a broad sense, diabetic encephalopathy is observed in 60-70% of diabetics.
The etiological factor of DE is diabetes mellitus. Encephalopathy refers to late complications that develop 10-15 years after the onset of diabetes. Its direct cause is metabolic disorders typical of diabetes, leading to damage to brain tissues and blood vessels. The emergence of DE is promoted by:
- Diabetic dyslipidemia. It is characteristic of type 2 diabetes. Dysmetabolism of lipids and cholesterol leads to the formation of vascular atherosclerotic plaques. Progressive systemic and cerebral atherosclerosis is observed in diabetics 10-15 years earlier than the average in the population.
- Diabetic macroangiopathy. Changes in the vascular wall complicate blood flow in the cerebral vessels, cause chronic cerebral ischemia, and increase the risk of stroke.
- Acute hypo-, hyperglycemic conditions. Hypoglycemia and ketoacidosis negatively affect the state of neurons, increase the risk of DE and dementia. Studies have shown that along with glucose levels, the concentration of insulin and C-peptide in the blood is important.
- Arterial hypertension. It is observed in 80% of cases of DM. It is a consequence of diabetic nephropathy or has an essential character. Negatively affects the cerebral blood supply, can cause a stroke.
Diabetic encephalopathy has a multifactorial mechanism of development, including vascular and metabolic components. Vascular disorders due to macro- and microangiopathy worsen cerebral hemodynamics, cause oxygen starvation of brain cells. The pathobiochemical reactions realized in hyperglycemia cause activation of anaerobic glycolysis instead of aerobic, lead to energy starvation of neurons. Emerging free radicals have a damaging effect on cerebral tissues. The formation of glycosylated hemoglobin, which binds less oxygen, exacerbates hypoxia of neurons resulting from vascular disorders. Hypoxia and dysmetabolism lead to the death of neurons with the formation of diffuse or small—focal organic changes in the cerebral substance – encephalopathy occurs. The destruction of interneuronal connections entails a gradually progressive decrease in cognitive functions.
DE arises gradually. At a young age, its manifestations increase after hyper- and hypoglycemic episodes, in the elderly — in connection with the transferred ACVA. Clinical symptoms are nonspecific, including cognitive disorders, asthenia, neurosis-like symptoms and focal neurological deficit. At the beginning of the disease, patients complain of weakness, fatigue, anxiety, headache, problems with concentration.
Neurosis-like conditions are caused by somatic (poor health) and psychogenic (the need for constant treatment, the fact of complications) factors. Typical are narrowing of interests, concentration on the disease, attacks of an angry and dreary mood. At the initial treatment, depressive neurosis is diagnosed in 35% of patients, with the development of DM, the number of patients with depressive disorders increases to 64%. Hysterical, anxiety-phobic, hypochondriac neurosis may occur. In some cases, one type passes into another. Severe mental abnormalities are rarely noted.
Asthenic syndrome is characterized by lethargy, apathy, combined with vegetative-vascular disorders, syncopal states. Cognitive disorders are manifested by a decrease in memory, absent-mindedness, slow thinking. Among the focal symptoms, convergence insufficiency, anisocoria (different pupil diameters), ataxia (dizziness, unsteadiness of walking), pyramidal insufficiency (weakness of limbs, increased muscle tone) prevail.
The increase in cognitive impairment leads to intellectual decline and dementia. The latter is the cause of significant disability of patients, limits their self-care. The situation is aggravated by the inability of the patient to independently carry out antidiabetic therapy. Complications of DE are acute disorders of cerebral hemodynamics: transient ischemic attacks, ischemic strokes, less often intracranial hemorrhages. The consequences of ACVA are persistent motor disorders, damage to the cranial nerves, speech disorders, and the progression of cognitive dysfunction.
Diabetic encephalopathy is diagnosed by a neurologist based on the results of a neurological status examination in patients with DM. Assessment of the degree of functional and organic changes in cerebral structures is carried out using instrumental methods.
- Electroencephalography. Reflects the diffuse nature of the changes. There is flattening of the EEG, reduction of the alpha rhythm, the appearance of pathological theta and delta waves.
- MRI of the brain. In the initial stage, it corresponds to the norm. Subsequently, it reveals nonspecific small-focal diffuse organic changes of a degenerative-atrophic nature.
- Study of cerebral hemodynamics. It is carried out using rheoencephalography, duplex scanning, ultrasound of the vessels of the head, MR angiography.
- Laboratory tests. Allow to evaluate metabolic disorders. The level of glucose, lipids, cholesterol, C-peptide, and insulin is determined.
Differential diagnosis of DE is aimed at excluding infectious lesions and brain tumors. It is carried out according to clinical data, confirmed during magnetic resonance imaging.
DE therapy is performed by a neurologist together with an endocrinologist (diabetologist). A necessary condition for treatment is to maintain an adequate concentration of blood glucose by following an appropriate diet, taking hypoglycemic drugs, and, if necessary, insulin therapy. Neurological treatment is aimed at improving cerebral hemodynamics, maintaining the metabolism of neurons, increasing their resistance to hypoxia. Regular courses of complex therapy with the use of vasoactive, antiplatelet, antioxidant, nootropic pharmaceuticals are conducted.
Energy metabolism stimulants, B vitamins, alpha-lipoic acid, vitamin E are prescribed. In the presence of motor disorders, anticholinesterase agents (neostigmine) are recommended. According to indications, therapy is supplemented with antihypertensive agents (with persistent hypertension) and antisclerotic drugs from the statin group. Pharmacotherapy of neurosis-like conditions requires an adequate selection of drugs, since sedatives negatively affect cognitive functions. Mainly atypical tranquilizers (mebikar) are used. It is recommended to consult a psychotherapist, sometimes a psychiatrist.
Prognosis and prevention
Diabetic encephalopathy is a chronic progressive disease. The rate of exacerbation of symptoms directly depends on the severity of the course of DM. Systematic observation of an endocrinologist and neurologist, adequate hypoglycemic treatment, regular courses of neurological therapy can suspend or slow down the progression of cerebral symptoms, prevent the development of complications. Prevention consists in timely detection and correct treatment of diabetes, correction of hypertension, therapy of vascular disorders.