Chen-Nen Chang

Factors affecting graft infection after cranioplasty.

The aim of this study was to identify the risk factors associated with bone grafts infection after cranioplasty. Eighty-four cranioplasties were performed on 75 patients between 2002 and 2006. Cryopreserved bone grafts were used as graft material in group 1 and polymethylmethacrylate (PMMA) was used in group 2. Risk factors including age, gender, time intervals between craniectomy and cranioplasty, mechanism of injury, number of procedures, graft material, and the Glasgow Coma Scale score were compared between groups. Swab culture results and bone graft infection were assessed in group 1. Multiple procedures before cranioplasty and an inadequate time interval between craniectomy and cranioplasty increase the risk of infection after cranioplasty. Swab culture results, age, gender, mechanism of injury, graft material and Glasgow Coma Scale score are not related to infection. The use of PMMA was associated with a relatively low risk of infection (6.25%). Risk of graft infection was not associated with the choice of graft material in the present study. Multiple procedures and insufficient time intervals increase the risk of infection. Interrupting the wound healing process may be the cause of infection. PMMA is a safe material for cranioplasty regardless of previous infection.

Reoperation for recurrent trigeminal neuralgia after microvascular decompression

BACKGROUNDnMicrovascular decompression (MVD) is an effective technique for those who have trigeminal neuralgia (TN) but cannot tolerate, or show no response to medicine. Though the initial success rate is high, some patients may develop severe recurrent neuralgia, especially after a longer period of follow-up. The efficacy of reoperation needs to be evaluated. To know the possible risk factors of recurrence after initial MVD is mandatory to the management of recurrent TN.nnnMETHODSnAmong the 80 cases of TN treated with MVD, five cases showed severe recurrent symptoms within a follow-up period from 9 months-4 years. The symptoms recurred on the same side of the face, and were unresponsive to medical treatment. Brain computed tomography (CT) and magnetic resonance imaging (MRI) may reveal the etiology of recurrence. Repeat decompression of the trigeminal nerve was the main goal of reoperation, which was done via a suboccipital approach.nnnRESULTSnOver the past 17 years, 80 MVDs for TN have been performed at Chang Gung Memorial Hospital. There were five cases of serious postoperative recurrence, which could not be relieved by medicine. Recurrence occurred 1 day-12 months after the initial surgery. Three cases were due to vascular compression, while two were caused by the local effect of Teflon felt. Reoperation produced complete remission in four patients, and partial remission in one.nnnCONCLUSIONSnAn increasing number of patients may experience severe recurrent TN after initial MVD during a long period of follow-up. Reoperation is safe and beneficial for these patients, but the results are dependent on the etiology of the recurrence. Further vascular compression of the trigeminal nerve can be relieved by MVD. Otherwise, in cases of severe adhesion caused by Teflon, complete microneural lysis can achieve satisfactory results.

The properties of SBS-g-VP copolymer membrane prepared by UV photografting without degassing

The grafting of 4-vinylpyridine (VP) onto styrene-butadiene-styrene triblock copolymer membrane (SBS) was induced by UV-radiation without degassing to obtain the SBS-g-VP copolymer membrane. The graft copolymer membrane was characterized by electron spectroscopy for chemical analysis (ESCA) and scanning electron microscope (SEM). The tensile strengths and elongations of dry and wet SBS-g-VP copolymer membranes were measured. The contact angle of dry and wet SBS-g-VP graft copolymer membranes with different amount of grafting were determined. By using Kaelbles equation and the contact angle data, the surface energy of dry and wet SBS-g-VP graft copolymer membranes were determined. The protein absorption of fibrinogen and albumin on the SBS-g-VP membranes were evaluated. It was found that the oxygen content in the SBS-g-VP copolymer membrane increased with increasing grafting degree which resulted from the UV photografting without degassing. The tensile strength of dry SBS-g-VP membrane increased with increasing degree of grafting but the elongation decreased. The tensile strengths and elongations of wet SBS-g-VP were significantly lower than those of SBS. The surface energy of dry and wet SBS-g-VP were determined by using Kaelbles equation and the contact angle data. It was found that the surface energy of SBS-g-VP membrane increased. The surface energy of wet SBS-g-VP was higher than that of dry SBS-g-VP. The absorption of albumin and fibrinogen decreased with increasing grafting degree and then levelled off.

Dexamethasone enhances NT-3 expression in rat hippocampus after traumatic brain injury.

The cellular events in traumatic brain injury (TBI) are complicated, and the factors mediating neurotrophins to protect and repair the injured brain cells are only beginning to be identified. This study examined the effect of dexamethasone (DEX) on neurotrophin-3 (NT-3) expression following TBI. Levels of NT-3 mRNA and protein in rat hippocampus were measured using in situ hybridization and immunohistochemistry, respectively. After TBI, the NT-3 mRNA expression was down-regulated during the first 24 h. DEX reversed the post-traumatic reduction of NT-3 mRNA expression at 2, 4, 6, and 12 h in the hippocampus, and also decreased the cell death in hippocampal hilum and supraventricular cerebral cortex after 7 days. The NT-3 protein levels generally corresponded to the mRNA levels in the hippocampal region. DEX enhanced the NT-3 expression after TBI, indicating that post-traumatic neuroprotection in the hippocampus is at least partially mediated by NT-3 and thus can be modulated by DEX treatment.

Effect of dexamethasone on the expression of brain-derived neurotrophic factor and neurotrophin-3 messenger ribonucleic acids after forebrain ischemia in the rat.

Objective To determine whether a large dose of dexamethasone affected brain damage induced by concurrent cerebral ischemia, we used in situ hybridization to examine the expression of brain-derived neurotrophic factor and neurotrophin-3 messenger ribonucleic acids (mRNAs) in rats with and without dexamethasone administration after transient forebrain ischemia. Design Prospective experimental study in rats. Setting Experimental laboratory in a teaching hospital and university. Subjects Eighty adult rats. Interventions Twenty minutes of transient forebrain ischemia was induced by occlusion of four vessels in lightly anesthetized rats. Thirty-six animals received dexamethasone (15 mg/kg, intraperitoneally) after initial reperfusion. Thirty-six dexamethasone-control rats were injected with saline, and the remaining animals underwent sham surgery but no ischemia or dexamethasone. Measurements and Main Results Using in situ hybridization, we determined hippocampal brain-derived neurotrophic factor and neurotrophin-3 mRNA expression 2, 4, 6, 12, and 24 hrs and 2, 3, 4, and 7 days after brain ischemia. Additionally, hippocampal CA1 region cell death was measured with Nissl stains. Both brain-derived neurotrophic factor and neurotrophin-3 mRNA exhibited a biphasic response after ischemia. Brain-derived neurotrophic factor mRNA showed two peaks of 4.07-fold and 2.84-fold increases relative to sham operation at 6 hrs and 2 days, respectively. Neurotrophin-3 mRNA initially decreased to 59% of sham levels at 4 hrs and then increased to 146% at 3 days before it returned to basal levels. When the ischemic rats were treated with dexamethasone, the elevation of brain-derived neurotrophic factor mRNA and the reduction of neurotrophin-3 mRNA level were prevented within the first 24 hrs, and hippocampal CA1 neurons were protected from ischemia-induced cell loss 7 days after brain ischemia. The protein levels of both brain-derived neurotrophic factor and neurotrophin-3 in general correspond to the mRNA levels in the hippocampal region. Conclusions Dexamethasone modulates the intriguing temporal and spatial expression of brain-derived neurotrophic factor and neurotrophin-3 that predominantly supports neuronal innervation at different times after brain ischemia and also may provide specific trophic support for various neurons in the central nervous system.

Dexamethasone inhibits ischemia-induced transient reduction of neurotrophin-3 mRNA in rat hippocampal neurons.

DEXAMETHASONE (DEX) increases the expression of neurotrophin-3 (NT-3) in normal rat hippocampal neurons, whereas transient forebrain ischemia reduces the NT-3 mRNA level. The effect of DEX on the expression of NT-3 mRNA in injured brain cells after ischemia has not been investigated, however. Using in situ hybridization and ribonuclease protection assay methods, we studied NT-3 mRNA expression in rats with and without DEX administration after transient forebrain ischemia. Without DEX treatment, NT-3 mRNA was down-regulated in the hippocampal neurons at 2, 4, 12 h and returned to basal levels 24 h following ischemia. With DEX treatment, however, NT-3 mRNA showed no change at 2, 4 and 12 h and increased 24 h after ischemia. The results indicate that DEX inhibits ischemia-induced NT-3 mRNA down-regulation during the first 12 h and up-regulates NT-3 mRNA 24 h after ischemia. DEX administration might be effective in influencing some of the pathophysiological effects of ischemia in the hippocampus.

Hyperbaric oxygen treatment decreases post-ischemic neurotrophin-3 mRNA down-regulation in the rat hippocampus

The therapeutic effect of hyperbaric oxygen (HBO) on ischemic injury was investigated using in situ hybridization to detect the mRNA expression of neurotrophin-3 (NT-3), which is thought to play a crucial role in protecting against neuronal death induced by brain ischemia. The rats under investigation were subjected to 10 min transient forebrain ischemia, and subsequently exposed to HBO (100% oxygen, 2.5 atm absolute) for 2 h. Levels of NT-3 mRNA in the CA1, CA2 and CA3 regions, and the dentate gyrus of the hippocampus were measured after various reperfusion periods. Neuronal death in the hippocampal CA1 region was also measured by Nissl staining, seven days post ischemia. The results demonstrated that HBO treatment significantly reduced the ischemia-induced down-regulation of the NT-3 mRNA level at 4 h post ischemia, and significantly increased cell survival 7 days after reperfusion. The findings suggest that an HBO treatment maintaining the NT-3 mRNA level in the hippocampus can be beneficial to the ischemic brain within a certain time frame.

Dexamethasone enhances upregulation of nerve growth factor mRNA expression in ischemic rat brain

Nerve growth factor (NGF) is well-established as a trophic factor that plays a crucial role in neuroregeneration and plasticity after brain insults. Dexamethasone (DEX), a powerful glucocorticoid steroid, has long been used in the clinical management of neurological disorders. We examined the relationship between NGF and DEX after an ischemic insult to the brain. In situ hybridization was used to measure NGF mRNA expression in the rat hippocampus after 20 min of transient forebrain ischemia. Immunostaining for NGF protein was performed using the avidin-biotin peroxidase method. Immunohistochemistry for glial fibrillary acidic protein (GFAP) was also used to study the astrocyte reaction in the hippocampal CA1 area. Ischemic brain from rats not treated with DEX had a 2 and 3 fold increase in NGF mRNA compared to sham-operated rats at 4 and 6 h after ischemia, respectively. The NGF mRNA expression returned to basal levels 12 h to 7 days post-ischemia. Treatment with DEX potentiated the ischemia-induced increase of NGF mRNA to 4 times that of sham-operated rats at 6 h following reperfusion and NGF protein expression was similarly elevated. Additionally, the number of GFAP positive astrocytes in the CA1 region in the ischemic rats was markedly increased. These data suggest that DEX may play a role in modulating NGF mRNA expression in the hippocampal neuronal response to brain ischemia.

Cigarette smoking decreases neurotrophin-3 expression in rat hippocampus after transient forebrain ischemia

Stroke is a common cause of death and severe disability among adults in developed countries. Cigarette smoking adversely affects human health in many ways and is considered to be a risk factor for a stroke. However, the mechanism that determines the relative importance of neurotrophins in this process remains unclear. To study the effect of chronic cigarette smoking on ischemic stroke, in situ hybridization and immunohistochemistry were employed to detect the mRNA and protein expression of neurotrophin-3 (NT-3), respectively, which is thought to play a critical role in protection against neuronal death in brain ischemia. Rats, with or without chronic cigarette smoking, were subjected to 20 min of transient forebrain ischemia. Distribution and quantification of mRNA and protein of NT-3 in the whole hippocampus and the cell death in the hippocampal CA1-CA3 regions were determined in these rats. Experimental results show that chronic cigarette smoking produces a significantly delay and persistent down-regulation of ischemia-induced NT-3 mRNA and protein changes at 6-24h post-ischemia, and seemingly increases neuron death 7 days after reperfusion. These experimental results indicate that by influencing NT-3 expression, directly or indirectly, chronic cigarette smoking has a potentially harmful effect when acute brain ischemia attacks.

Corpus callosum involvement and postoperative outcomes of patients with gliomas

Corpus callosum involvement is associated with poorer survival in high grade glioma (HGG), but the prognostic value in low grade glioma (LGG) is unclear. To determine the prognostic impact of corpus callosum involvement on progression free survival (PFS) and overall survival (OS) in HGG and LGG, the records of 233 glioma patients treated from 2008 to 2011 were retrospectively reviewed. Preoperative magnetic resonance (MR) images were used to identify corpus callosum involvement. Age, sex, preoperative Karnofsky performance scale, postoperative Eastern Cooperative Oncology Group (ECOG) score and extent of resection (EOR) were evaluated with respect to PFS and OS. The incidence of corpus callosum involvement was similar among HGG (14xa0%) and LGG (14.5xa0%). Univariate analysis revealed that PFS and OS were significantly shorter in both WHO grade II and grade IV glioma with corpus callosum involvement (both, pxa0<xa00.05). Multivariate analysis showed that grade II glioma with corpus callosum involvement have shorter PFS (pxa0=xa00.03), while EOR, instead of corpus callosum involvement (pxa0=xa00.16), was an independent factor associated with PFS in grade IV glioma (pxa0<xa00.05). Corpus callosum involvement was no longer significantly associated with OS after adjusting age, gender, EOR, preoperative and postoperative performance status (pxa0=xa00.16, 0.17 and 0.56 in grade II, III and IV gliomas, respectively). Corpus callosum involvement happened in both LGG and HGG, and is associated with lower EOR and higher postoperative ECOG score both in LGG and HGG. Corpus callosum involvement tends to be an independent prognostic factor for PFS in LGG, but not for OS in LGG or in HGG.