Surgical Neurology最新文献

Background

With the combination of microsurgery and microinjection techniques, we investigated the development of motor neurons in the spinal cord of fetal rats with spina bifida occulta by injecting the retrograde trace FG into the levator ani muscle.

Methods

The fetal rats were divided into 3 groups. On the day 9 of gestation, 6 mature Wistar rats (weighing 250-300 g) in the control group (group 1) were subcutaneously injected with 0.5 mL of normal saline at their hind limbs at 9:00 am and 4:00 pm. At these 2 time points, 15 rats in the treatment group (group 2 and group 3) were subcutaneously injected with 20% sodium valproate solution (400 mg/kg of body weight) at their hind limbs, too. On the day 20 of gestation, pregnant rats were anesthetized with 10% chloral hydrate (300 mg/kg of body weight) intraperitoneally, and then fetal microsurgery and microinjection were performed to expose the levator ani muscle, whereas 5% FG was administered with microinjector. Twenty-four hours later, transcardial perfusion of 4% paraformaldehyde in phosphate-buffered saline (PBS) was given to the operated fetus. After the spine sample was stained with Alcian blue GX, the image of stained spine was measured using a computer system for the distance of the 2 cartilaginous ends of the vertebra arch. Then, the lumbosacral spinal cord was cryopreserved in 20% sucrose in PBS for a later serial transverse cryosection after 24 hours. The FG-labeled motor neurons were visualized with a wide-band ultraviolet-fluorescent filter, and the number of the FG-labeled motor neurons was recorded. Nine fetal rats survived in group 1. Eighteen fetal rats survived in the treatment group, including 7 (with no malformation) of 18 fetuses in group 2 and 11 fetuses with spina bifida occulta in group 3.

Results

The FG-labeled motor neurons in the ventral horn of normal spinal cord clustered at the dorsolateral and dorsomedial corner of the ventral horn. The FG-labeled motor neurons in the ventral horn of deformed spinal cord were less than that of normal spinal cord, and the motor neurons were scattered around the space between the dorsomedial and dorsolateral corners. The number of FG-labeled motor neurons was 244 ± 41 in group 3, 426 ± 36 in group 1, and 397 ± 20 in group 2. The data were stastistically significant if P < .05.

Conclusion

The motor neurons that innervate the levator ani muscle in fetal rats with spina bifida occulta are fewer than the normal fetal rats, and they are arranged in abnormal distribution.

Background

Brain tissue scarring (gliosis) was believed to be the major cause of epileptic focus after brain injury, and prevention of scarring could reduce the incidence of seizure. We tried the HA coating onto the cortical brain defect of Spraque-Dawley rats to reduce the marginal glial scarring.

Methods

A 4 × 2 × 2 mm³ cortical defect was created in the brain of Spraque-Dawley rats. Three percent HA gel was coated onto the lesion for the experimental groups and normal saline solutions for the control groups. The brain was retrieved 4, 8, and 12 weeks after treatment. The brains were then sectioned and processed for H&E and GFAP staining, and the thickness of the scarring and the number of GFAP+ cells were analyzed.

Results

The thickness of cutting marginal gliosis was significantly decreased in the HA groups. The 12-week HA group showed the smallest thickness of gliosis, whereas the 12-week control group exhibited the largest thickness of gliosis. The significant difference in the thickness of gliosis was also noted between the HA and the control groups 8 weeks after treatment. The number of GFAP+ cells was also significantly decreased in the HA groups when compared to the respective control group 4, 8, and 12 weeks after the surgery.

Conclusion

The results support the hypothesis that HA inhibits glial scarring not only by decreasing the thickness of gliosis but also by reducing the number of the glial cells. Furthermore, our results suggest that HA might be used to reduce glial scar formation in central nervous system surgery, which subsequently prevents the post-operation or posttraumatic seizure incidence.

Background

Parkinson's disease, affecting at least 1% of population older than 65 years, is the most common neurodegenerative movement disorder. Up to now, no evidence has demonstrated that biochemical changes in CSF occur preceding the onset of Parkinson's symptoms. In this study, we tested the hypothesis that biochemical changes in CSF precede behavioral deficits in Parkinsonian animals.

Methods

We infused different doses of 6-OHDA into the MFB of rats bilaterally and examined the animals' movement behaviors, biochemical alterations in CSF, and dopaminergic neuronal number in the SNpc 1 week later.

Results

Our results indicated that animals with over 70% dopaminergic neuronal loss in the SNpc exhibited behavioral bradykinesia and rigidity, and a decrease of HVA in CSF. In contrast, animals with about 42% dopaminergic neuronal loss in the SNpc showed normal movement behaviors, but displayed a drastic decline of HVA in CSF. Furthermore, the number of dopaminergic neurons in the SNpc was positively correlated with the HVA level in CSF.

Conclusions

Our findings demonstrate that biochemical alteration in CSF foreruns behavioral deficits and the HVA level in CSF is positively correlated with the number of dopaminergic neurons in the SNpc of Parkinsonian rats induced by 6-OHDA. Our results strongly suggest that additional studies are needed to evaluate usefulness of monitoring the HVA level in CSF for early detection of the loss of dopaminergic neurons in the SNpc that precedes the onset of Parkinsonian symptoms in humans.

Background

Severe TBIs are major causes of disability and death in accidents. The Brain Trauma Foundation supported the first edition of the Guidelines for the Management of Severe Traumatic Brain Injury in 1995 and revised it in 2000. The recommendations in these guidelines are well accepted in the world.

There are still some different views on trauma mechanisms, pathogenesis, and managements in different areas. Individualized guidelines for different countries would be necessary, and Taiwan is no exception.

Methods

In November 2005, we organized the severe TBI guidelines committee and selected 9 topics, including ER treatment, ICP monitoring, CPP, fluid therapy, use of sedatives, nutrition, intracranial hypertension, seizure prophylaxis, and second-tier therapy. We have since searched key questions in these topics on Medline. References are classified into 8 levels of evidence: 1++, 1+, 1−, 2++, 2+, 2−, 3, and 4 based on the criteria of the SIGN.

Results

Recommendations are formed and graded as A, B, C, and D. Grade A means that at least one piece of evidence is rated as 1++, whereas grade B means inclusion of studies rated as 2++. Grade C means inclusion of references rated as 2+, and grade D means levels of evidence rated as 3 or 4.

Overall, 42 recommendations are formed. Three of these are rated as grade A, 13 as grade B, 21 as grade C, and 5 as grade D.

Conclusions

We have completed the first evidence-based, clinical practice guidelines for severe TBIs. It is hoped that the guidelines will provide concepts and recommendations to promote the quality of care for severe TBIs in Taiwan.

Background

Patients with SAH often experience cognitive decline. Previous studies used normal volunteers, published normal test values, and orthopedic patients as controls to identify factors for postoperative cognitive decline. The present study excluded the effects of surgery by comparing cognitive function after surgical repair in patients with aneurysmal SAH and patients with unruptured intracranial aneurysm.

Methods

This study recruited 117 patients with SAH due to ruptured aneurysm and 39 patients with incidentally found unruptured intracranial aneurysms. The cognitive test battery consisted of the Japanese translation of the WAIS-R, the Japanese translation of the WMS, and the recall trial of the ROCF. Postoperative neuropsychological test scores for the patients with SAH and control subjects were compared using group-rate and event-rate analysis. The relationship between clinical variable and postoperative cognitive decline in the patients with SAH was evaluated by univariate analysis using the Mann-Whitney U test or χ² test.

Results

Group-rate analysis showed that the WAIS-R and ROCF scores were significantly lower in the SAH group than in the control group. Event-rate analysis demonstrated that the incidence of cognitive decline in the patients with SAH (73 [62.4%] of the 117 patients) was significantly higher than that in the control subjects (12 [30.8%] of 39 patients). The Hunt and Hess grade was significantly higher in patients with postoperative cognitive decline.

Conclusion

The cognitive function after SAH was significantly correlated with Hunt and Hess grade on admission when using patients with postoperative unruptured intracranial aneurysm as the control group.