Jen-Tsung Yang

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

BACKGROUND Microvascular 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. METHODS Among 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. RESULTS Over 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. CONCLUSIONS An 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.

Predictors of early clinical deterioration after acute ischemic stroke

The measurements for predicting early deterioration of stroke patients is controversial. We studied laboratory measurements and previously identified risk factors to identify factors or predictors of early deterioration after stroke. A prospective observational study of 196 patients with first-time acute ischemic stroke was performed. Demographic data, patient histories, laboratory measurements, and initial stroke severity assessments were recorded. Patients with early deterioration in National Institutes of Health Stroke Scale scores (increase ≥3 points within 3 days) were defined as having stroke-in-evolution (SIE). Thirty patients were diagnosed with SIE. An initial National Institutes of Health Stroke Scale score of 12 or higher, a Glasgow Coma Scale score of 12 or lower, d-dimers more than 1000, or blood urea nitrogen/creatinine (BUN/Cr) ratio higher than 15 were more frequent in SIE patients. After multivariate analysis, only a BUN/Cr higher than 15 was independent predictor of SIE. These patients were 3.41-fold more likely to have SIE (P = .008). These findings suggest that BUN/Cr may be a novel predictor of SIE, potentially useful in emergency departments.

Expression of brain-derived neurotrophic factor immunoreactivity and mRNA in the hippocampal CA1 and cortical areas after chronic ischemia in rats

We studied the expression of brain‐derived neurotrophic factor (BDNF) immunoreactivity and mRNA in the ischemia‐vulnerable cerebral hippocampal CA1 and cortical areas after permanent occlusion of bilateral internal carotid arteries. Four groups of rats were studied, including 1) young normotensive Wistar‐Kyoto (WKY) rats, 2) aged normotensive WKY rats, 3) young spontaneous hypertensive rats (SHR), and 4) aged SHR. Each group contained rats from sham operation and 1 week, 4 weeks, and 8 weeks after cerebral ischemia (n = 3–5 at each time point). Hematoxylin and eosin staining and in situ apoptosis detection showed no neuronal damage from 1 week to 8 weeks in all the ischemic rats. Immunohistochemistry and Western blot showed that BDNF immunoreactivity increased only at 1 week in the CA1 area of young WKY rats (P < .001) and SHR (P = .002) and decreased only at 8 weeks in the cortical area of aged WKY rats (P = .02). In situ hybridization and TaqMan real‐time RT‐PCR showed that BDNF mRNA decreased consistently from 1 week to 8 weeks in both CA1 and cortical areas in young SHR (P < .05 and P < .01, respectively) and in aged WKY rats (P < .01 and P < .05, respectively) but was not changed in young WKY rats or aged SHR (P > .05) compared with the sham‐operated rats. Our study demonstrates an expression disparity of BDNF immunoreactivity and mRNA in the hippocampal CA1 and cortical areas, especially in the young SHR and aged WKY rats after mild cerebral ischemia. Our study suggests that, under permanent occlusion of bilateral internal carotid arteries, aging and the level of blood pressure may have influence on the expression of BDNF.

Foramen ovale cannulation guided by intra-operative computed tomography with integrated neuronavigation for the treatment of trigeminal neuralgia

BackgroundRadiofrequency rhizotomy of the Gasserian ganglion for the treatment of trigeminal neuralgia via percutaneous cannulation of the foramen ovale is facilitated by various localization modalities. In our preliminary study, we described the feasibility of computed tomography (CT) using an integrated neuronavigation system to cannulate the foramen ovale.MethodsAnalysis was performed on 42 consecutive patients who underwent cannulation of the foramen ovale for radiofrequency trigeminal rhizotomy guided by CT using an integrated neuronavigation system. The reproducibility and safety of the neuronavigation-guided procedure were evaluated.ResultsOverall, the average dimension of the foramen ovale was 7.1 (1.5) × 4.7 (1.1) mm, and it was successfully cannulated by neuronavigation guidance in 31 (73.8%) patients with a mean cannulation time of 3.1 (0.7) min and an overall procedure time of 68.2 (16.4) min. The remaining 11 (26.2%) patients required subsequent CT guidance for successful puncture of the foramen ovale.ConclusionsThese data demonstrate that neuronavigation-guided cannulation of the foramen ovale can be executed both quickly and safely on an outpatient basis. Additionally, the use of CT with integrated neuronavigation technology provides superior visual-spatial information compared to conventional fluoroscopy, the process of CT scanning, object planning, and neuronavigation-guided intervention can be completed in the same locale, and its application is easy to master and has the potential to enhance procedure tolerability of awake patients.

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.

Dexamethasone reduces brain cell apoptosis and inhibits inflammatory response in rats with intracerebral hemorrhage.

Spontaneous intracerebral hemorrhage (ICH) is associated with high rates of mortality and morbidity. Thus, the identification of novel therapeutic agents for preventing strokes and attenuating poststroke brain damage is crucial. Dexamethasone (DEX) is used clinically to reduce edema formation in patients with spinal cord injury and brain tumors. In this study, we sought to elucidate the effects of DEX treatment on apoptosis and inflammation following ICH in rats. A high dose of DEX (15 mg/kg) was administered immediately following ICH induction and again 3 days later. The inflammatory and apoptotic responses in the rat brains were evaluated by using hematoxylin‐eosin, terminal deoxynucleotidyl transferase dUTP nick end labeling, Nissl, and neurofilament‐H staining. Levels of phosphorylated neurofilaments and apoptosis‐related proteins such as B‐cell lymphoma 2 (Bcl‐2), Bcl‐2 associated X protein (Bax), caspase‐3, and P53 were analyzed by Western blotting. This study shows that rats without ICH that received DEX treatment had a fourfold higher expression of Bcl‐2 than sham‐operated rats. ICH causes an increase in Bax, cleaved caspase‐3, and P53 proteins from 4 hr to 7 days following ICH induction. In comparison with the ICH rats, the ICH/DEX rats showed significantly decreased apoptotic cell death and increased neuron survival and maintained neurofilament integrity in the perihematomal region. DEX increased the Bcl‐2/Bax ratio and lowered the expression of cleaved caspase‐3 at 12 hr and 5 days. The ICH rats were accompanied by activation of the inflammatory response, and DEX treatment modulated the expression of a variety of cell types and then decreased ICH‐induced apoptosis.

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.

Bun/creatinine ratio-based hydration for preventing stroke-in-evolution after acute ischemic stroke

BACKGROUND Blood urea nitrogen (BUN)/creatinine (Cr) ratio was recently reported to be an independent predictor of stroke-in-evolution (SIE) among patients who had suffered acute ischemic stroke. We aim to determine if providing hydration therapy to patients with a BUN/Cr ≥15 reduces the occurrence of SIE after acute ischemic stroke. METHODS This prospective interventional study included 189 patients (hydration group, n = 92; control group, n = 97) with acute ischemic stroke and a BUN/Cr ≥15. Hydration group received intravenous bolus (300-500 mL) saline followed by a maintenance saline infusion (40-80 mL/h for the first 72 h), while control group received maintenance saline infusion (40-60 mL/h for the first 24 h and 0-60 mL/h for 24-72 h). The study endpoint was the proportion of patients who developed SIE within the first three days of emergency department admission. RESULTS There were no significant differences in demographic or clinical characteristics between both groups. Patients in the hydration group received a significantly larger (all P < 0.001) median volume of infused saline than patients in the control group on Days 1 (2400 vs 1440 mL), 2 (1440 vs 0 mL), and 3 (1000 vs 0 mL). The proportion of patients who experienced SIE was significantly lower in the hydration group (9/92; 9.8%) compared with the control group (21/97; 21.6%) (Fig. 1, P = 0.026). CONCLUSIONS Our preliminary findings suggest that providing patients with acute ischemic stroke hydration therapy on the basis of their presenting BUN/Cr ratio may help reduce the occurrence of SIE and therefore improve prognosis.

Dural metastasis from prostatic adenocarcinoma mimicking chronic subdural hematoma

Dural metastasis is rare. In most reported cases, brain CT scan findings are mistaken for subdural hematoma or meningioma. We present here a 72-year-old male with a history of headache and progressive mental status changes. Brain CT scans suggested chronic subdural hematoma. However, the only surgical findings were diffuse thickening of the dura and sclerosis of the temporal bone. Histopathology revealed metastatic prostatic carcinoma. As the surgical approach and prognosis of chronic subdural hematoma and metastatic tumors are completely different, the differential diagnosis of these diseases is very important. A contrast-enhanced brain CT scan is recommended for patients who could possibly have dural metastases.