[Relation between biochemical indicators of the cerebrospinal fluid and the extent of cerebral infarction]. / Sootnoshenie biokhimicheskikh pokazatelei likvora i velichiny infarkta golovnogo mozga.

The authors assessed liquor biochemical indices, mainly enzymes, on day 1-3 of hemispheric ischemic stroke in correlation with brain infarction size in 90 relevant male patients (mean age 70 +/- 6 years). The brain damage was verified by computed tomography with measuring the infarction lesion. The latter in view, the patients were assigned in three groups: with ischemic lesion less than 5.0 cm3, less than 30 cm3 and greater than 30.0 cm3 or/and multiple lesions. The results were compared with those in patients who had suffered hemispheric ischemic stroke followed by discirculatory encephalopathy.

Postmortem sera and cerebrospinal fluid enzymes.

Antemortem and postmortem sera from 60 dogs were evaluated for lipase, amylase, alkaline phosphatase, gamma-glutamyltransferase, and alanine aminotransferase (AAT); cerebrospinal fluid was examined for AAT and alkaline phosphatase. The postmortem intervals were 3, 6, 12, 24, and 48 h at temperatures of 4, 20, and 37 degrees C. Amylase levels remained stable at 4 and 20 degrees C and may be beneficial for diagnosing pancreatitis. Lipase levels may be useful as an adjunct to amylase values. Serum alkaline phosphatase values increased with postmortem interval; values were higher at 37 degrees C than at 4 degrees C. Other enzymes were of little value for diagnosis.

Cyclic amp concentration and enzyme activities of cerebrospinal fluid in patients with epilepsy or central nervous system damage.

Cyclic adenosine-3',5'-monophosphate (cAMP) concentration in cerebrospinal fluid (CSF) was measured by the protein binding method of Gilman from 62 neurological patients, 46 of them were epileptics and 16 with a central nervous system (CNS) damage. In epileptic patients the CSF concentration of cAMP was significantly elevated (p smaller than 0.02) for 3 days after an attack when compared with those free from attacks for at least 2 weeks. The causality relationship between the rise of cAMP in CSF and an epileptic discharge is discussed. In patient with an active or rapidly progressing CNS damage the cAMP levels in the CSF were significantly higher (p smaller than 0.001) than in those with an old CNS damage. Also some enzyme activities in CSF were measured but no uniform alterations could be found. In damaging processes of the CNS, the cAMP values in the CSF seem to correlate to the activity of the disease.