Che-Chuan Wang

Hyperbaric oxygen effects on neuronal apoptosis associations in a traumatic brain injury rat model

BACKGROUND The neuroprotective mechanisms of hyperbaric oxygen (HBO) therapy on traumatic brain injury (TBI) remain unclear, especially neuronal apoptosis associations such as the expression of tumor necrosis factor alpha (TNF-α), transforming growth-interacting factor (TGIF), and TGF-β1 after TBI. The aim of this study was to investigate the neuroprotective effects of HBO therapy in a rat model of TBI. MATERIALS AND METHODS The experimental rats were randomly divided into three groups as follows: TBI + normobaric air (21% O₂ at one absolute atmosphere), TBI + HBO, and sham-operated normobaric air. The TBI + HBO rats received 100% O₂ at 2.0 absolute atmosphere for 1 h immediately after TBI. Local and systemic TNF-α expression, neuropathology, levels of the neuronal apoptosis-associated proteins TGIF and TGF-β1, and functional outcome were evaluated 72 h after the onset of TBI. RESULTS Compared to the TBI control groups, the running speed of rats on the TreadScan after TBI was significantly attenuated by HBO therapy. The TBI-induced local and systemic TNF-α expression, neuronal damage score, and neuronal apoptosis were also significantly reduced by HBO therapy. Moreover, HBO treatment attenuated the expression of TGIF but increased TGF-β1 expression in neurons. CONCLUSIONS We concluded that treatment of TBI with HBO during the acute phase of injury can decrease local and systemic proinflammatory cytokine TNF-α production, resulting in neuroprotective effects. We also suggest that decreased levels of TGIF and increased levels of TGF-β in the injured cortex leading to decreased neuronal apoptosis is one mechanism by which functional recovery may occur.

Hyperbaric Oxygen Effects on Depression-Like Behavior and Neuroinflammation in Traumatic Brain Injury Rats

OBJECTIVE The aim of this study was to determine whether hyperbaric oxygen (HBO) therapy causes attenuation of traumatic brain injury (TBI)-induced depression-like behavior and its associated anti-neuroinflammatory effects after fluid percussion injury. METHODS Anesthetized male Sprague-Dawley rats were divided into 3 groups: sham operation plus normobaric air (NBA) (21% oxygen at 1 absolute atmosphere [ATA]), TBI plus NBA, and TBI plus HBO (100% oxygen at 2.0 ATA). HBO was applied immediately for 60 min/d after TBI for 3 days. Depression-like behavior was tested by a forced swimming test, motor function was tested by an inclined plane test, and infarction volume was tested by triphenyltetrazolium chloride (TTC) staining on days 4, 8, and 15. Neuronal apoptosis (terminal deoxynucleotidyl transferase dUTP nick-end labeling assay), microglial (marker OX42) activation, and tumor necrosis factor (TNF)-α expression in microglia in the hippocampus CA3 were measured by immunofluorescence methods. RESULTS Compared with the TBI controls, without significant changes in TTC staining or in the motor function test, TBI-induced depression-like behavior was significantly attenuated by HBO therapy by day 15 after TBI. Simultaneously, TBI-induced neuronal apoptosis, microglial (marker OX42) activation, and TNF-α expression in the microglia in the hippocampus CA3 were significantly reduced by HBO. CONCLUSIONS Our results suggest that HBO treatment may ameliorate TBI-induced depression-like behavior in rats by attenuating neuroinflammation, representing one possible mechanism by which depression-like behavior recovery might occur. We also recommend HBO as a potential treatment for TBI-induced depression-like behavior if early intervention is possible.

The increased risk of stroke in early insomnia following traumatic brain injury: a population-based cohort study

OBJECTIVE Insomnia, a common symptom after traumatic brain injury (TBI), may be a pre-symptom for developing stroke. This study aims to investigate whether insomnia is a potential risk factor for stroke after TBI, especially early insomnia. METHODS Taiwans Longitudinal Health Insurance Database 2000 from 1999 to 2013 was used in this cohort study. TBI patients with insomnia were selected based on the ICD-9-CM code (TBI: 801-804 and 850-854; insomnia: 307.4, 327, and 780.5). The outcome we were interested in was stroke (ICD-9-CM: 430-438). The incidence rate ratio of stroke between TBI with insomnia and the general population with insomnia was calculated by Poisson regression. The relative risk adjusted for potential confounding variables was estimated by Cox regression. RESULTS For 1174 TBI patients with insomnia and 5870 general patients with insomnia, TBI patients have 209.85 incidence risk of new-onset stroke if they have insomnia. TBI patients have 2.28-fold (95% CI: 1.70-3.06) risk of new-onset stroke compared with the general population, even when controlling for age, gender, socioeconomic status, and comorbidities. The hazard ratio of new-onset stroke among different phases of new-onset insomnia after TBI surgery is 1.95-fold (95% CI: 1.05-3.62), 2.75-fold (95% CI: 1.73-4.37), and 2.66-fold (95% CI: 1.68-4.21) at ≤3, 3-12, and 12-24 months, compared with the general population with insomnia, respectively. CONCLUSION TBI patients with insomnia have a higher risk of stroke compared with the general population with insomnia. Early new-onset insomnias after TBI will have higher risk of stroke. Therefore, we consider that insomnia could be a signal of the development of new-onset stroke in TBI patients.

Brain abscess associated with cerebral amyloid angiopathy and hemorrhage.

PURPOSE We want to report an extremely rare condition, brain abscess associated with cerebral amylid angiopathy and hemorrhage. CASE REPORT We report on a 64-year-old woman who presented initially with moderate fever and headache. She was initially misdiagnosed with a bleeding tumor or arteriovenous malformation rupture and treated without antibiotic therapy. The mass was surgically drained due to neurological deterioration on day 14 after admission. Streptococcus virdians was isolated from the pus culture. The pathology evaluation showed cerebral amyloid angiopathy. She received intravenous antibiotic therapy for 4 weeks. She was eventually discharged home with left quadrantanopia. CONCLUSION This case reminds us early recognition of brain abscess formation at the site of intracerebral hemorrhage is very important for prompt and appropriate treatment to improve the overall prognosis.

Distal Anterior Cerebral Artery Aneurysm: An Infrequent Cause of Transient Ischemic Attack Followed by Diffuse Subarachnoid Hemorrhage: Report of a Case

We report a 54-year-old female who presented with a wide-based saccular aneurysm distal to the junction of the right pericallosal and callosomarginal arteries, showing acute onset of transient ischemia stroke initially, followed by diffuse spontaneous subarachnoid hemorrhage and supracallosal, intraventricular hemorrhage. Rotational 3-dimensional digital subtraction angiography clearly indicated the aneurysm location and shape. Pre-operatively, her Hunt and Hess grading was IV. Craniotomy with aneurysm trapping was performed in the acute stage. Postoperatively, her consciousness gradually improved but left hemipsresis remained. This clinical presentation, to our knowledge, has not been previously reported. We would like to emphasize that in patients with transient ischemic attacks presenting with hemiparesis, the possibility of a distal cerebral arterial aneurysm should be taken into consideration for prompt and appropriate management.

Trauma-related True Aneurysm of the Superficial Temporal Artery: Report of a Case

Trauma-related aneurysm of the superficial temporal artery is rare. We report a 23-year-old man who developed a painless pulsating temporal mass on his previously contused area four weeks after blunt trauma. Preoperative investigation including duplex ultrasound and enhanced brain tomography suggested a pseudoaneurysm. Surgical resection of the mass via proximal and distal artery ligation was performed. Pathological examination of the mass revealed a true arterial aneurysm. The pathogenesis of the true aneurysm formation in this case could be related to the arterial wall degenerative change due to trauma. We suggest that surgeons encountering similar cases consider sampling a small segment of ”unsual” artery near the aneurysm to investigate the possibility of pre-existing dysplastic blood vessels.

A Growing Pre-existing Juxta-facet Cyst after Lumbar Laminectomy: Report of a Case

The growth of a pre-existing lumbar juxta-facet cyst after a laminectomy is a rare condition. Here we report a 60-year-old woman who presented with acute severe buttock pain and recurrent left L5 radicular pain one month after a laminectomy for L4-5 spinal stenosis and a herniated intervertebral disc. Magnetic resonance imaging (MRI) revealed that a cyst extending from the facet joint to the spinal canal compressed the left L5 nerve root. Without surgical intervention, the patients condition improved after analgesic medication, bed rest and the fitting of a lumbar corset. At the 6-month follow-up, the MRI showed spontaneous resolution of the cyst with no narrowing of the spinal canal or root compression. The pathogenesis of the cyst could have been related to the degenerative mobile spine after the decompressive laminectomy. This case demonstrates that post-laminectomy recurrence of radiculopathy may result from the growth of a pre-existing juxta-facet cyst. Furthermore, conservative treatment may be the first therapeutic option because spontaneous resolution of such a cyst is known to be possible.