Mouse Anti-Human CKBB monoclonal antibody, clone CD117

A biochemical marker of brain cell damage, the BB-isozyme of the intracellular enzyme Creatine Kinase (CK), was used to evaluate any possible injury to the brain, caused by an operation for a ruptured intracranial aneurysm (SAH). CSF-CK BB was assessed before and at intervals after operation in a series of 60 patients, aged 29-71 (mean 51 years) operated on for intracranial aneurysms, all but one after SAH. The m/f ratio was 18/42. 35 of the 60 patients were operated on acutely, i.e. within 72 hours after the SAH. CK BB was determined as CKB-activity after immunological inactivation of CKM. Normally there should be almost no detectable enzyme activity in the CSF. The pre-operative CK BB-activity was 0.01 + - 0.01 mikrokatal in the patients in Hunt and Hess grade I who were operated on > 7 days after their SAH, and 0.05 + - 0.04 in those operated on acutely, probably still reflecting the effects of the SAH on the brain. The mean per-operative CK BB increase was 0.11 + - 0.17 for patients who had an uneventful postoperative course, compared to 0.39 + - 0.49 for those showing some degree of immediate post operative deterioration. This difference is significant at the 1% level. 52 of the 60 patients showed a rise of CK BB after operation. The mean increase for those patients operated upon in a good state and without any complication or postoperative deterioration was 0.02 + - 0.03 mikrokatal, which could therefore be considered as a ''normal'' or acceptable elevation. The per-operative increase for the whole group was 0.14 + - 0.19 and 0.28 + - 0.38 after late and early operation respectively. A temporary arterial clip was applied for 1 to 27 (totally) minutes in 18 patients. The mean increase for that group did not differ significantly from the rest. The study shows that an operation for intracranial aneurysm causes at least some brain cell damage even in the absence of any clinical signs of deterioration, and more so with early than with late operation. The use of a temporary clip, at least for less than 7 minutes, does not per se cause any further brain cell damage, as mirrored by the CK BB.

The aim of this study was to examine whether an increase in the serum concentrations of the two brain enzymes creatine kinase BB (CK-BB) and neuron specific enolase (NSE) can be demonstrated in patients with acute head injury and whether such an increase reflects release from damaged brain tissue. In 60 patients who had suffered minor to sever head injury, serial blood samples were drawn during the first hours after impact, and CK-BB and NSE were measured by radio-immuno-assay. Computed tomography (CT) was also performed shortly after admission to hospital, and was repeated 1-3 days later in selected patients. Increased serum concentrations of both CK-BB and NSE were found in 88% of the patients with moderate to severe head injury (group 1, n = 18) and in 23% of the patients with minor head injury (group 2, n = 42), whereas CT showed contusion in only 41% and 2% of the group 1 and 2 patients, respectively. The following findings suggest that the enzymes had been released from brain tissue: 1) The maximum concentrations of CK-BB and NSE correlated with the severity of injury as assessed clinically and with the volume of contusion as estimated from CT(r = 0.79 with CK-BB, r = 0.72 with NSE). 2) The maximum concentrations of CK-BB and NSE were closely correlated (r = 0.87). 3) The ratio between CK-BB and NSE was approximately the same in a subgroup of 10 patients with multiple trauma as in the group as a whole (median 2.2 versus 2.0). Measurements of the serum concentrations of CK-BB and NSE in patients with acute head trauma, therefore, appears to provide information about the presence and, to some degree, extent or the resulting brain injury. Further studies are required to reveal the value of such measurements in the management of patients with acute head trauma.