Etiology and pathogenesis of alcoholic psychoses and encephalopathies

Acute and chronic alcoholic psychoses and encephalopathies occur in patients with alcoholism as a result of chronic intoxication, chronic alcoholic brain damage – initially functional, then organic in nature. When pathological intoxication occurs, alcohol plays the role of not only an etiological, but also a provoking factor, revealing a special, most likely temporary, predisposition to psychotic response; in acute psychoses – the role of an active metabolic factor, the absence of which, combined with toxic damage to the brain, leads to a disruption of the gradually developed pathological system of adaptation and the emergence of a psychotic state; in chronic psychoses and encephaloathias – the role of the main etiological intoxication factor. Acute and chronic psychoses, defective organic conditions combine the underlying alcohol pathogenesis of somatocerebral pathology and alcoholic encephalopathy of varying severity. Therefore, it is legitimate to consider them, regardless of their clinical form, as alcoholic somatocerebral-intoxication diseases. The development of alcoholic psychoses is accompanied by disorders of various body systems . In particular, significant deliberate biochemical changes were detected at the height of alcoholic delirium with severe somatic and autonomic disorders: changes in the acid-base state in the form of decompensated metabolic acidosis and dysproteinemia with plasma hypokalemia, hypernatremia and hypervolemia, hypocholestsrinempia, a decrease in the activity of G. cholinesterase (M. V.F. Kolomies, 1981).
In the pathogenesis of acute alcoholic psychoses and encephalopathies, an important role is played by violations of the antitoxic function of the liver and toxic damage to the brain, especially diencephalic structures, under-oxidized metabolites of protein-lipid metabolism, as well as impaired vitamin balance with a deficiency of B vitamins, ascorbic acid. Disorders of the cardiovascular system and cerebral vessels also occupy an important place. V.S. Paukov et al. (1983) at the autopsy of persons who died from alcoholic delirium noted pathological signs of exacerbation of chronic alcoholic myocardial dystrophy.
In acute alcoholic psychoses, as a rule, pathomorphological changes in blood vessels are detected: 1) acute vascular disorders: plethora of the brain, meninges and internal organs, pronounced disorders of the permeability of the walls of blood vessels with perivascular edema, hemorrhages (large – intracerebral, subarachnoid and subdural; small – intracerebral and subarachnoid; large and small diapedetic hemorrhages in the internal organs – visceral pleura, lungs, endocardium and pericardium, the mucous membrane pancreas, pancreas, perinephric fiber and renal pelvis); 2) chronic vascular disorders: fibrosis of cerebral vessels, especially the walls of small vessels, residual effects of small and larger hemorrhages transferred in the past (Yu. M. Savelyev, L.V. Dinerstein, 1981). According to N.T. Khokhrina (1983), in case of alcohol delirium, brain changes can be estimated as chronic alcohol toxicodiscirculatory encephalopathy with an accumulation of acute toxic and dishemnic changes (a combination of chronic and acute changes in cellular elements, walls of large and small vessels, microvasculature). Thus, the basis for the violation of mental functions in alcoholic psychoses and defective conditions is a gradually increasing organic change in the cortical and subcortical structures of the brain due to alcohol and metabolic intoxication. 11schnopathological heredity, premorbid personality traits, apparently, are less significant, although they determine the occurrence of the clinical form, for example, acute paranoid, not delirium, and its atypicality. With prolonged alcoholic psychoses, the latter factors are more significant for the pathogenesis of diseases. The pattern characteristic of exogenous psychotic states with a chronic and sluggish course of the pathological process is noted. 

local_offerevent_note October 19, 2019

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