Cerebral ischemia could be observed as acute metabolic crisis, when
oxygen and
glucose supply is compromised and synthesis of energy is insufficient. Apart from the excitotoxicity, increased production of
reactive oxygen species with consequent lipid peroxidation is also included in neuronal cell damage. Furthermore, these toxic compounds could also be produced during the process of secondary
inflammation of ischemic tissue. In the early stage of
ischemia, as a systemic response to acute stress, there is an increase in
glucose level in cerebrospinal fluid (CSF) and peripheral blood. According to the metabolic crisis and
acidosis in ischemic brain tissue we investigated index of lipid peroxidation (ILP) and
glucose utilization (
IGU) in CSF of 53 patients of both sexes, aged 55-70 years with
cerebral infarction. Control group comprised 15 patients with sudden onset of motor deficit subjected to diagnostic lumbar radiculography and suspected on discal genesis. ILP in CSF, as the
indicator and sequela of neuronal cell membranes damage, was two fold increased in the acute period of
cerebral infarction and maximal values (3.5 times) were noticed 24 hours after the ischemic episode compared to controls. Besides the increase in
glucose concentration in peripheral blood and CSF of patients with
cerebral infarction,
IGU was decreased (37%) with minimal values (32%) 24 hours after the
ischemia. These changes indicate that
glucose is available but cells are incapable to metabolize it. We concluded that ILP and
IGU in CSF of patients with
cerebral infarction could be indicators of metabolic dysfunction and neuronal cell damage. Also, these results suggest the significance of polyvalent
therapy including antioxidative and
antiinflammatory agents in acute phase of
cerebral ischemia.