Radiologic Location of Ventricular Tip and the Patency of Ventriculoperitoneal Shunt

Proximal cerebrospinal fluid shuntmalfunction due to ventricular catheter occlusion remains the most common sourceof the shunt problem. The position of the hole-bearing segment of the catheter affects the long term patency of the ventricular catheter of a cerebrospinalfluid shunt.Placementof thissegmentnear thechoroidplexus or injured ependyma increases the probability of obstruction. Accurate locationof ventriculoperitoneal(V-P)shunt tip inrelation to foramen Monro canbe well establishedby plain radiographyregardless of agesor sizes and shapes of head dueto the fact that foramen Monro tothe spatial matrix of the skull is constant. Of 147patients who underwentV-P shunt operations, 49(33.3%)patients had more thanone operations. Radiologicgradingof theventricularcatheterposition is compared betweensingle operatedgroup andreoperated group.Single operated group showed excellentin 33.6%, good41.8%, poor 24.4%of accuracy rateof catheter tip position. Incases ofreoperation, placement ofcatheter tipresulted in excellent 12.5%, good21.8%, and poor 65.6%.These results indicatethat accurate location of ventricular catheter tip affects favorably to the patency of V-P shunt.

Experimential Brain Stem Compression

Patterns of brain-stem compression and secondary brain-stem evoked postentials were investigated to correlate with expanding mass volume and location in mass-induced supratentorial brain compression in cats in which the subjects were divided into four experimental group i.e., frontal, temporal, parietal, and occipital brain-compressed groups. Postmortem insepection of the brain-stem showed either unilateral or bilateral dorsal herniation of the brain in frontal and temporal brain-compressed groups and dorsolateral herniation in parietal and occipital brain-compressed groups, respectively. Microscopic examination revealed that the secondary brain-stem hemorrhages were mostly caused by venous bleeding secondary to venous congestion, the bleeding being more severe in occipital brain-compressed group. As the intracranial pressure was raised by expansion of a supratentorial balloon, the late components of the BSEP were suppressed first, followed by the suppression of the early components. In BSEP recording a significant change was observed in Vth wave with prolongation of latency and decrease in amplitude. This finding suggests that the midbrain is the most vulnerable to compression ischemia. In parietal group, the Vth wave started to be prolonged at 0.4ml of balloon expansion and totally disappeared at 1.8ml of expansion.

A Study of the Effect of Naloxone on the Lipid Peroxidation and the Fine Structure of the Myelin Sheath in the Injured Spinal Cord

Spinal Cord contusions in cats were produced experimentally by impact injuries to the surgically exposed cord at the second lumbar vertebral level. As a step in the investigation of the possible effect of spinal cord trauma on biochemical and ultrastructural changes in the injured cord, activities of lipid peroxidation were measured in the frozen-dried sample of the spinal cord and the fine structure of the myelinated nerve fiber in the white matter were observed before and after the cord injury. An increase of lipid peroxidation level was found as early as 30 minutes after the injury and the highest concentration was reached at 4 hours of injury. Fine structures of the myelinated nerve fibers were changed progressively with the lapse of time after the injury. By 1 hour after the contusion the myelinated nerve fibers showed moderately enlarged periaxonal space, attenuation and disarray of the myelin sheaths. By 4 hour after the contusion, there appeared disarray of the myelin sheaths, greatly enlarged periaxonal space and irregulary contoured axons. The effect of naloxone of the lipid peroxidation and fine ultrastructure of the myelinated nerve fibers were studied, and the results of this study suggested that naloxone have a beneficial effect on the change in lipid peroxidation and the preservation of the myelinated nerve fibers after injury.