HYPERGLYCORRHACHIA

HYPERGLYCORRHACHIA, HYPOGLYCORRHACHIA, increase and decrease in the amount of sugar in the cerebrospinal fluid (phenomena, at present still being studied); they may have significance in the differential diagnosis of certain nervous diseases; this especially applies to hypoglycorrhachia. In relation to hyperglycorrhachia, it has not yet been established whether it depends on hyperglycemia or arises independently. Sugar in the cerebrospinal fluid is determined by the micromethod of Hagedorn and Jensen; other methods: Folin-Wu and Bang. The figures for normal sugar content in the cerebrospinal fluid are somewhat different among various authors: 45-60 mg% (Eskuchen), 50-70 mg% (Steiner), 55-65 mg% (Mestrezat), 50-75 mg% (Dietel). In the blood, the normal sugar content varies from 100 to 130 mg% (the percentage ratio of cerebrospinal fluid sugar to blood sugar averages 56.2%). Regarding the dependence of sugar changes in the fluid on its content in the blood, as well as as to the degree to which cerebrospinal fluid sugar reflects physiological fluctuations in blood sugar, there is no unity of opinion. It has only been established that the amount of sugar in the fluid is always less than in the blood; these values almost never equalize. The sugar content in the brain ventricles is higher than in the fluid taken from the cisterna magna (according to Ayer-Eskuchen), which in turn contains more sugar than lumbar fluid; thus, in the cerebrospinal fluid on the path from the brain ventricles to the lumbar region, the amount of sugar decreases (to 6.8 mg% according to Dietel); however, this circumstance is not always strictly regular (Dietel). According to Eskuchen, the causes of hyperglycorrhachia may be the following circumstances. I. Primary hyperglycemia (i.e., the passage of sugar from the blood while maintaining the normal ratio of sugar content in blood and fluid = 2:1) - secondary physiological hyperglycorrhachia. II. Violation of the integrity of the filtering apparatus (hemato-encephalic barrier) - secondary pathological hyperglycorrhachia: a) toxic, b) inflammatory, c) congestive, d) functional. III. Destruction of centers regulating carbohydrate metabolism: 1) local - a) toxic, b) inflammatory, c) mechanical (hemorrhage, tumor); 2) general - due to increased pressure both in the blood and in the fluid, with accumulation of cerebrospinal fluid, disturbance of its circulation and increased production, as well as venous hyperemia. - The picture of hyperglycorrhachia in nervous diseases has not yet been fully established. The amount of sugar increases in the cerebrospinal fluid in epidemic encephalitis up to 90 mg%. From other diseases, hyperglycorrhachia was found by Stevenson in syphilis of the brain, progressive paralysis, tabes, tumor and abscess of the brain; by Eskuchen - after an epileptic seizure, in serous meningitis (an observation requiring verification). According to Eskuchen, hyperglycorrhachia is not a specific change for epidemic encephalitis and other diseases and depends on the above factors (high pressure and irritation of sugar-regulating centers). In view of the dependence of hyperglycorrhachia on hyperglycemia, as well as on other factors, its differential diagnostic significance should be limited in this sense. - Hypoglycorrhachia, i.e., sugar content in the cerebrospinal fluid below 50 mg% (sometimes complete absence), is observed in acute inflammations of the meninges (purulent meningitis, epidemic cerebrospinal meningitis, as well as tuberculous meningitis); in serous meningitis, a decrease in sugar is not observed, and sometimes the sugar content is even increased. No direct dependence between the number of cellular elements in the fluid and hypoglycorrhachia has been found, although the role of cellular elements in this sense is not excluded. The presence of bacteria and bacteriogenic substances undoubtedly plays a role in the amount of sugar in the fluid (this can explain the absence of hypoglycorrhachia in aseptic meningitis). No connection has been noted between the classical reactions (globulin, colloidal) and changes in sugar content in the cerebrospinal fluid.