Amimia
Historical document, translated for reference. It reflects medical knowledge of the 1920s–30s and is not medical advice.
Summary
Amimia refers to the absence or reduction of expressiveness in facial musculature, which can result from paralysis, paresis, or ataxia of facial muscles. It can also occur as an isolated disorder affecting expressive movements, associated with conditions affecting the thalamus and extrapyramidal system, or as a feature of various psychiatric disorders.
Encyclopedia article (1928–1936)
AMIMIA, absence or reduction of expressiveness in facial musculature, may be a consequence of pareses, paralyses, or ataxias of the said musculature, and in such cases, this A. lacks independent significance. A. may also be observed as an isolated disorder while the elementary functions of facial musculature remain intact, and is then one type of disorder of associated or expressive movements. Such disorders occur in diseases of the thalami optici (see) and the extrapyramidal system (see); the most characteristic example is A. in parkinsonism (see) as a consequence of past lethargic encephalitis. Additionally, A. may be characteristic of various mental diseases, in which two types are distinguished: asthenic A. and hypersthenic A. Asthenic A. is observed in dementia, stupor, and certain forms of progressive paralysis; hypersthenic A. occurs in catatonia, religious delusions, and during hallucinations. AMINOAZOT, nitrogen of the NH2 group, which is attached to a carbon atom that is bonded either to hydrogen atoms or to another carbon atom. In the animal organism, A. is found, mainly, in the form of amino acids and amines. In proteins and peptides, A. serves to link amino acids together; this bond is broken during acid and alkaline hydrolysis and under the influence of proteases (see). A. of protein digestion products enters the blood from the small intestines in the form of amino acids, and from the large intestines in the form of amines, which are formed here from amino acids under the influence of microbes. The entry of amino acids into the bloodstream occurs very slowly, so that the amount of A. in the blood never reaches significant levels. According to many authors, the amount of A. in the blood decreases as it passes through the liver, which apparently depends on the deaminating activity of the latter, converting A. into urea nitrogen. Principles for determining A.: 1. According to Sørensen—free alkaline-reacting amino groups are bound by formaldehyde, after which an equivalent amount of acidic (carboxyl) groups can be titrated with alkali. 2. According to van Slyke—decomposition of amino groups by nitrous acid with liberation of free nitrogen and gasometric determination of the latter. 3. According to Folin—colorimetrically, by the colored reaction with β-sulfo-naphthoquinone. These methods give relative figures suitable for comparative determinations, but the absolute value of the results obtained is not very reliable. According to Folin, 100 cubic cm of blood contains 4-8 mg of A. Studies by Bang give values of the same order, who investigated the changes in the amino nitrogen fraction of blood under various physiological and pathological conditions and arrived at the following results: 1. A. is distributed between plasma and erythrocytes in favor of the latter [due to adsorption of amino nitrogen-containing products by blood corpuscles (Zbarsky)]. 2. The amount of A. does not change during fasting and during enhanced feeding. This, however, is doubtful, as indicated by the work of London and others. 3. When amino acids are introduced into the intestine or bloodstream, an increase in blood A. is observed; correspondingly, significant amounts of A. are excreted in the urine. Simultaneously, the content of A. in tissues increases, where it is deposited from the blood. In cases where A. was not excreted in the urine, the animal died (apparently due to acid poisoning). 4. In experimental nephritis (mercuric chloride, chromium salts), the amount of A. in the blood remains constant. 5. In experimental phosphorus poisoning, a sharp increase in blood A. occurs, which can be explained either as a result of impaired deaminating activity of the liver, or as a result of autolysis of the latter. An increase in A. was also observed by other authors in some cases of liver disease. Bang's data can only be considered preliminary due to the inaccuracy of the methodology used. A. is also found under normal conditions in lymph and other tissues; it is constantly present in urine, where it can be determined by one of the above-mentioned methods.
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“Amimia.” Soviet Medical Encyclopedia. English translation of Bolshaya Meditsinskaya Entsiklopediya, 1st ed. (Moscow, 1928–1936), ed. N. A. Semashko. https://sovietmedicalencyclopedia.pages.dev/article/amimia/