• Korean Journal of Veterinary Research
• /
• v.41 no.4
• /
• pp.467-475
• /
• 2001

Cardiac arrest, hypoxia, shock or seizure has been known to induce cerebral ischemia. This study was designed to investigate the effect of ischemia on hippocampal pyramidal layer induced by transient bilateral occlusion of the common carotid arteries. Mature Mongolian gerbils were sacrificed at days 2, 4, and 7 after carotid occlusion for 10 minutes. Sham-operated gerbils of control group were subjected to the same protocol except for carotid occlusion. During operation for ischemia, body temperature was maintained $37{\pm}0.5^{\circ}C$ in all gerbils. Paraffin-embedded brain tissue blocks were cut into coronal slices and stained with H-E stain or immunostain by TUNEL method. Neurons with the oval and prominent nucleus and without the eosinophilic cytoplasm in the subfield of hippocamapal pyramidal layer were calculated as to be viable neurons. Their chromatins were condensed or clumped. Their nuclei appeared multiangular or irregularly shrinked. The width of the pyramidal layer was reduced due to the loss of nuclei. At day 2 after reperfusion, some neurons in the CA1 subfield were slightly eosinophilic. But most neurons in the CA2 subfield were strongly eosinophilic. At day 4 day, most neurons in the CA1 subfield were severely damaged and at day 7 day, only a few survived neurons were observed. Survived neurons per longitudinal 1mm sector in the CA1, CA2, CA3, and CA4 subfields of pyramidal layer were investigated. At day 2, the mean numbers of pyramidal neurons in CA1, CA2, CA3, and CA4 subfiedls were 104.5/mm (54.3%), 51.0/mm (33.8%), 105.5/mm (85.6%), and 124.3/mm (93.5%) compared to the nonischemic control group, respectively. At day 4, the mean numbers of pyramidal neurons in CA1, CA2, CA3, and CA4 subfields were 3.2/mm (1.7%), 51.5/mm(34.2%), 95.3/mm (77.4%), and 112.5/mm (84.6%), respectively. At day 7, the mean numbers of pyramidal neurons in CA1, CA2, CA3, and CA4 subfiedls were 0.8/mm (0.4%), 5.7/mm(3.8%), 9.8/mm (8.0%), and 5.0/mm (3.7%), respectively. The mean numbers of apoptotic positive neurons in the CA1 subfield at day 2, 4, and 7 after reperfusion were 67.8/mm, 153.2/mm and 123.7/mm, respectively. These results suggest that the transient cerebral ischemia cause severe damages in most neurons at day 7 and that the prosminent apoptotic positive neurons in hippocampal pyramidal layer are the delayed neuronal death induced by ischemia.

• Journal of Korean Neurosurgical Society
• /
• v.61 no.3
• /
• pp.363-375
• /
• 2018

Intraoperative monitoring (IOM) utilizes electrophysiological techniques as a surrogate test and evaluation of nervous function while a patient is under general anesthesia. They are increasingly used for procedures, both surgical and endovascular, to avoid injury during an operation, examine neurological tissue to guide the surgery, or to test electrophysiological function to allow for more complete resection or corrections. The application of IOM during pediatric brain tumor resections encompasses a unique set of technical issues. First, obtaining stable and reliable responses in children of different ages requires detailed understanding of normal age-adjusted brain-spine development. Neurophysiology, anatomy, and anthropometry of children are different from those of adults. Second, monitoring of the brain may include risk to eloquent functions and cranial nerve functions that are difficult with the usual neurophysiological techniques. Third, interpretation of signal change requires unique sets of normative values specific for children of that age. Fourth, tumor resection involves multiple considerations including defining tumor type, size, location, pathophysiology that might require maximal removal of lesion or minimal intervention. IOM techniques can be divided into monitoring and mapping. Mapping involves identification of specific neural structures to avoid or minimize injury. Monitoring is continuous acquisition of neural signals to determine the integrity of the full longitudinal path of the neural system of interest. Motor evoked potentials and somatosensory evoked potentials are representative methodologies for monitoring. Free-running electromyography is also used to monitor irritation or damage to the motor nerves in the lower motor neuron level : cranial nerves, roots, and peripheral nerves. For the surgery of infratentorial tumors, in addition to free-running electromyography of the bulbar muscles, brainstem auditory evoked potentials or corticobulbar motor evoked potentials could be combined to prevent injury of the cranial nerves or nucleus. IOM for cerebral tumors can adopt direct cortical stimulation or direct subcortical stimulation to map the corticospinal pathways in the vicinity of lesion. IOM is a diagnostic as well as interventional tool for neurosurgery. To prove clinical evidence of it is not simple. Randomized controlled prospective studies may not be possible due to ethical reasons. However, prospective longitudinal studies confirming prognostic value of IOM are available. Furthermore, oncological outcome has also been shown to be superior in some brain tumors, with IOM. New methodologies of IOM are being developed and clinically applied. This review establishes a composite view of techniques used today, noting differences between adult and pediatric monitoring.

• Journal of Chest Surgery
• /
• v.41 no.4
• /
• pp.405-416
• /
• 2008

Background: Spinal cord ischemic injury during thoracic and thoracoabdominal aortic surgeries remains a potentially devastating outcome despite using various methods of protection. Neuronal voltage-dependent sodium channel antagonists are known to provide neuroprotection in cerebral ischemic models. This study was designed to compare the neuroprotective effects of phenytoin with those of hypothermia in a rabbit model of spinal cord ischemia. Material and Method: Spinal cord ischemia was induced in New Zealand white rabbits by means of infrarenal aortic cross clamping for 25 minutes. Four groups of 8 animals each were studied. The control group and the hypothermia group received retrograde infusion of saline only ($22^{\circ}C$, 2 mL/min); the normothermic phenytoin group and the hypothermicphenytoin group received retrograde infusion of 100 mg of phenytoin at different rectal temperatures ($39^{\circ}C$ and $37^{\circ}C$, respectively) during the ischemic period. The neurologic function was assessed at 24 and 72 hours after the operation with using the modified Tarlov criteria. The spinal cords were harvested after the final neurologic examination for histopathological examination to objectively quantify the amount of neuronal damage. Result: No major adverse effects were observed with the retrograde phenytoin infusion during the aortic ischemic period. All the control rabbits became severely paraplegic, Both the phenytoin group and the hypothermia group had a better neurological status than did the control group (p < 0.05). The typical morphological changes that are characteristic of neuronal necrosis in the gray matter of the control animals were demonstrated by means of the histopathological examination, whereas phenytoin or hypothermia prevented or attenuated these necrotic phenomena (p < 0.05). The number of motor neuron cells positive for TUNEL staining was significantly reduced, to a similar extent, in the rabbits treated with phenytoin or hypothermia. Phenytoin and hypothermia had some additive neuroprotective effect, but there was no statistical significance between the two on the neurological and histopathological analysis. Conclusion: The neurological and histopathological analysis consistently demonstrated that both phenytoin and hypothermia may afford significant spinal cord protection to a similar extent during spinal cord ischemia in rabbits, although no significant additive effects were noticed.