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Adult Mouse Venous Hypertension Model: Common Carotid Artery to External Jugular Vein Anastomosis.

The understanding of the pathophysiology of brain arteriovenous malformations and arteriovenous fistulas has improved thanks to animal models. A rat model ...

University of California, San Francisco

Traumatic internal carotid artery dissection is a serious condition that may cause ischemic stroke in young patients. It has been under-diagnosed in the past. We present three cases of traumatic internal carotid artery dissection. The clinical manifestations include hemicrania, hemiparesis, partial Horner's syndrome and cranial nerve palsy. Diagnosis is with carotid color Doppler ultrasound, CT angiography of the neck and conventional angiography. The outcome may be poor with hemiparesis, persistent vegetative state and death. We review the literature and discuss the clinical presentation, diagnosis, grading and treatment choices for traumatic internal carotid artery dissection and stroke.

Traumatic internal carotid artery dissection.

Optimally, internal carotid artery (ICA) injury associated with craniofacial trauma should be treated soon after diagnosis. However, diagnosis is difficult and often delayed. The typical symptoms and signs for diagnosis of traumatic ICA injuries are sometimes easily neglected. Clinically, some patients were initially diagnosed by craniofacial fracture nearby the course of ICA. This investigation retrospectively reviews clinical experience in patients with traumatic ICA injury with a focus on the importance of craniofacial fracture nearby the course of ICA observed on brain or facial bone computed tomography. Eighteen patients with traumatic ICA injury were diagnosed at Chang Gung Memorial Hospital, Taiwan, from June 1998 to April 2004, including 10 patients with pseudoaneurysm formation, seven patients with occlusion, and one patient with laceration. Brain or facial bone computed tomography was reviewed retrospectively. The sample included 14 (78%) patients with skull base fractures involving the intracranial course of ICA and three (17%) patients with mandibular and cervical spine fractures near the course of extracranial ICA. Only one (5%) patient did not have evident fracture. Fractures involving the carotid canal were noted in three (17%) patients. Eight patients received interventional treatments. No further interventional treatments for traumatic ICA occlusion were performed as a result of good collateral flow from contralateral ICA or large infarction noted when diagnosed. Three patients with pseudoaneurysm received expectant management. One patient with arterial laceration with extravasation received no further management. Through meticulously evaluating routine brain and facial bone computed tomography, craniofacial fracture involving intracranial or extracranial course of ICA may be an adjuvant indicator of traumatic ICA injury for early diagnosis.

Diagnosis of traumatic internal carotid artery injury: the role of craniofacial fracture.

Traumatic aneurysms of the anterior cerebral artery (ACA) were retrospectively reviewed in an effort to identify patients at high risk of ACA aneurysm.

Traumatic anterior cerebral artery aneurysm following blunt craniofacial trauma.

Massive epistaxis following blunt craniofacial trauma should alert clinicians to possible traumatic internal carotid artery (ICA) aneurysm. This article describes a case of a 46-year-old female patient with traumatic ICA pseudoaneurysm presenting similar to a sphenoid sinus mass lesion. Massive bleeding occurred during the endoscopic procedure. Brain angiography revealed two lobulated ICA pseudoaneurysms over a cavernous segment. The patient successfully underwent endovascular stent assisted coil embolization. Timely diagnosis and treatment of the ICA psuedoaneurysm produced a favourable outcome.

Traumatic internal carotid artery pseudoaneurysm mimicking sphenoid sinus tumor.

Metastases to the spine are a common problem in the large oncology center and represent a challenging problem in oncology practice. Patients with osteolytic metastases often experience intractable local and/or radicular pain. Therapeutic intervention can alleviate pain, preserve or improve neurologic function, achieve mechanical stability, and improve quality of life. Percutaneous polymethylmethacrylate vertebroplasty is an effective and relatively easy method of relieving patients' pain.

Percutaneous polymethylmethacrylate vertebroplasty in the treatment of pain induced by metastatic spine tumor.

A retrospective study to detect patients with new-onset compression fractures following vertebroplasty.

Repeated and multiple new vertebral compression fractures after percutaneous transpedicular vertebroplasty.

A rat model of jugular venous reflux (JVR) is widely used in studies of cerebral arteriovenous fistula, cerebral venous hypertension and chronic cerebral hypoperfusion. However, methods to validate the effectiveness of the operation are needed.

Validation of the jugular venous reflux animal model by three-dimensional time-of-flight MRA with a clinical scanner.

Aging is the most significant non-modifiable risk factor and hypertension is the most significant modifiable risk factor for ischemic stroke. We used magnetic resonance imaging (MRI) to investigate the evidence of ischemic susceptibility after aging and hypertension. Four groups of rat were studied: young normotensive Wistar-Kyoto (WKY) rat, aged normotensive WKY rat, young spontaneously hypertensive rat (SHR) and aged SHR. Brain images were acquired at a 3.0T Tim-Trio MRI system. For diffusion-weighted images, apparent diffusion coefficient (ADC) was measured. Relative cerebral blood flow (CBF) was also calculated. Cerebral ischemic susceptibility was examined by using ischemic model of bilateral common carotid artery occlusion. In the MRI study of non-ischemic rat, aged SHR had significantly higher ADC (P<0.01) and significantly lower CBF (P<0.01) in the parietal cortex, but aged WKY rat had only significantly lower CBF (P<0.01) when compared with young WKY rat. The ADC/CBF ratio in the parietal cortex was significantly higher in aged SHR when compared with young WKY rat, young SHR and aged WKY rat (P<0.01, P<0.05, P<0.05, respectively) suggesting a significant diffusion-perfusion disparity in aged SHR. After bilateral common carotid artery occlusion, there was significantly larger damage in the parietal cortex of aged SHR when compared with young WKY rat, young SHR and aged WKY rat (all P<0.05), but not in the hippocampus and thalamus (P>0.05). Our study demonstrated a significantly increased ADC value and reduced CBF in the ischemia-vulnerable cortical area. This cerebral diffusion-perfusion disparity is seen mainly in aged rat and can be more evident if associated with hypertension indicating an increased susceptibility of brain tissue to ischemic injury.

Effects of aging and hypertension on cerebral ischemic susceptibility: evidenced by MR diffusion-perfusion study in rat.

Stroke, or brain attack, is the third leading cause of death and the leading cause of adult disability worldwide. There is a great demand for intervention therapy. Unfortunately, although more than 700 drugs that target neuroprotection showed beneficial effects in preclinical animal studies, none of them proved efficacious in treating stroke patients. There is recent interest in understanding mechanism for post-ischemic angiogenesis in the penumbra area, and correlation of the extent of angiogenesis with survival in stroke patients. It is postulated that besides replenishing oxygen and nutrients to ischemic tissue, angiogenesis may play a crucial role in neural protection and tissue recovery. Consequently, therapeutic agents to promote angiogenesis and formation of new vessels after stroke can offer promising approach. Several large population epidemiological and clinical studies have revealed a reciprocal relationship between intake of phytochemicals and incidence of stroke. However, the detailed cellular and molecular mechanisms leading to these beneficial effects remain to be elucidated. In this article, we review the current knowledge on phytochemicals and post-ischemic angiogenesis, and discuss the possibility of a combinatorial treatment, including neuroprotection, angiogenesis, neurogenesis, and phytochemicals regimen for stroke.

Stroke, angiogenesis and phytochemicals.

Primary Leptomeningeal Melanoma Mimicking Meningitis: A Case Report and Literature Review.

Astragaloside (AST) is traditionally prescribed for the prevention and treatment of cerebrovascular diseases. We directly tested the therapeutic effects of AST in a rat model of traumatic brain injury (TBI). One hour after the onset of TBI rats were given Saline (1 ml/kg) or AST (20-80 mg/kg) via i.p. injection. AST causes the attenuation of TBI-induced cerebral contusion, neuronal apoptosis, and neurological motor dysfunction. TBI-induced microglial activation evidenced by the morphological transformation of microglia (or ameboid microglia) and the microglial overexpression of tumor necrosis factor-alpha was reduced by AST. Our results indicate that AST may protect against brain contusion and neuronal apoptosis after TBI by attenuating microglia activation in male rats.

Astragaloside improves outcomes of traumatic brain injury in rats by reducing microglia activation.

Recent epidemiology studies have indicated that traumatic brain injury (TBI) can increase the risk of developing neurodegenerative diseases such as Alzheimer's disease (AD). Amyloid-β (Aβ) plaques and neurofibrillary tangles are pathological indicators of AD. The accumulation of Aβ is considered the first step of AD pathophysiology. Compelling studies have supported the hypothesis that TBI accelerates the formation and accumulation of Aβ. These findings could link TBI with AD, although the research that reported these findings had limitations, particularly regarding mild TBI (mTBI) patients. The effects of mTBI on Aβ accumulation remain uncertain because of a lack of mTBI pathology data. Using amyloid-positron emission tomography (amyloid-PET), researchers can help to determine whether mTBI increases the accumulation of Aβ, which might be involved in the pathophysiological mechanisms of mTBI in AD, and could be a target for the treatment of neurodegenerative diseases associated with TBI. In this study, we recruited 27 mTBI patients with mTBI in mean 6years before this study (21 mTBI patients without cognitive impairment, 6 mTBI patients with cognitive impairment,) and 10 controls. All of them underwent mini-mental state examination, apolipoprotein E (APOE) genotyping, and amyloid-PET. The results show an increase of amyloid accumulation and allele frequency of APOE4 in the mTBI patients with cognitive impairment. These findings indicate that amyloid accumulation is an important indicator of cognitive impairment, and amyloid-PET should be a safe and useful tool for diagnosing amyloid-related cognitive impairment. APOE allele might play a role in the occurrence of cognitive impairment after mTBI. The contribution of mTBI to the amyloid accumulation requires further study, and mTBI patients should be recruited for longitudinal research with repeated amyloid-PET studies.

Shun-Tai Yang

Department of Anesthesia and Perioperative Care and Center for Cerebrovascular Research

University of California, San Francisco

Adult Mouse Venous Hypertension Model: Common Carotid Artery to External Jugular Vein Anastomosis.

Shun-Tai Yang

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Anesthesia and Perioperative Care and Center for Cerebrovascular Research

University of California, San Francisco

Adult Mouse Venous Hypertension Model: Common Carotid Artery to External Jugular Vein Anastomosis.

Department of Anesthesia and Perioperative Care and Center for Cerebrovascular Research