Washington State has one of the high est stroke mortality rates in the nation. To improve this situation, acute intervention al therapies for stroke are being employed to restore circulation to ischemic brain tissue that surrounds areas of completed infraction, while avoiding risk of hemor rhage due to reperfusion of large areas of infracted brain tissue.
Urgent thrombolysis with intrave nous alteplase is the only therapy known to improve clinical outcomes following acute stroke. Unfortunately, alteplase has had limited usage because many patients arrive in an emergency department after the three-hour treatment window. The FDA has also approved two clot removal devices based on the ability to restore circulation. These devices are used up to eight hours after symptom onset. Several approaches to improved acute stroke care are now under way, including extension of the thrombolysis window to 4.5 hours, identification of safer thrombolytic agents and research identifying brain at risk of in farction following a stroke.
A recent European study demonstrat ed the efficacy of alteplase up to 4.5 hours after ischemic stroke in patients younger than age 80 years who have neither dia betes mellitus or prior stroke. The safety profile during this longer window for these patients appears similar to that at three hours.
Another promising advance employs a new thrombolytic agent called des moteplase.
Since its introduction in 1982, transcranial doppler ultrasound (TCD) has evolved into a portable, multimodality, noninvasive method for real-time imaging of intracranial vasculature.
The detection of cerebral microemboli is among the more remarkable capabilities of TCD. Emboli create countable signals in the ultrasound display due to the higher reflection of sound waves compared to the blood cells. Experimental models have shown a high sensitivity and specificity for detection of a variety of substrates, including thrombotic, platelet and atheromatous emboli.
Microembolic signals (MES) within the intracranial vasculature are most frequently identified in patients with large-vessel atherosclerotic disease, such as carotid stenosis. They have also been reported in intracranial arterial stenosis, arterial dissection, cardiac disease and atheroaortic plaque. Additionally, they have been seen in arteries distal to coiled aneurysms.
There is strong evidence that MES detection predicts future ipsilateral stroke risk in patients with symptomatic carotid stenosis (Markus HS, et al.; King A, et al.). A recent study of patients with asymptomatic carotid stenosis demonstrated that MES predicted subsequent ipsilateral stroke and TIA, and also ipsilateral stroke alone, and that it is helpful in selecting patients who will benefit from carotid endarterectomy (Markus, HS et al.).
Identification of active embolization provides crucial pathophysiological information to the neurologist and can also aid in the selection of tailored therapy aimed at reducing the risk of stroke. Emboli from different sources have unique compositions and require specific therapy, such as antiplatelet agents for emboli from large artery atherosclerotic plaque and anticoagulants for cardiac emboli.
Future advances in TCD technology will permit full automation and better identification of the composition and size of circulating embolic materials, thus improving its value for patients with cerebrovascular disease.
Contact Colleen Douville, RVT, at firstname.lastname@example.org or 206-320-4080, for more information about TCD for detection of cerebral microemboli.
Intracranial aneurysms are present in up to 4 percent of the population. These potentially dangerous vascular lesions are being detected with increasing frequency in asymptomatic patients by advances in noninvasive imaging techniques, such as magnetic resonance angiography (MRA). Appearing like blisters on the wall of the brain’s blood vessels, aneurysms develop when the blood vessel’s native repair ability is exceeded by the mild, but constant, injury created by flowing blood under high pressure. The five most common risk factors for developing an aneurysm are: smoking, female gender, high blood pressure, middle age and family history.
Intracranial aneurysms are complex lesions that require a highly specialized, multidisciplinary approach that is individualized for each patient. Key members of the care team for these patients include endovascular neuroradiologists, neurosurgeons with special expertise in aneurysm surgery and neuroanesthesiologists. Availability of dedicated neurocritical care units is an essential care component. A consensus recommendation by these specialists may include close observation, obliteration of the aneurysm with a surgical clip, or filling the vascular outpouching with filamentous coils that are introduced by endovascular microcatheters via an artery in the leg. This latter process is called “coiling.”
The Swedish Neuroscience Institute (SNI) at Swedish Medical Center in Seattle, Washington, is committed to improving the delivery of neurologic care through evidence-based protocols, research and education. SNI offers advanced training through five fellowships:
- Cerebrovascular Fellowship
- Epilepsy and Functional Fellowship
- Complex and Minimally Invasive Spine Fellowship
- General Neurosurgery Fellowship
- Skull Base Fellowship
Applications are reviewed as received, with fellowships beginning bi-annually on January 1 and July 1. For one hundred years Swedish has been the premier health-care provider in the Pacific Northwest and a trusted resource for people when it truly counts. As a high-volume, urban medical center located at the epicenter of the Puget Sound area, Swedish attracts nationally recognized physicians and scientists, and provides a broad population base that enhances the patient care, research and education efforts at SNI. Applying for an SNI fellowship You can also email your inquiries to SNIFellowships@swedish.org
Bilateral 8th cranial nerve tumors, also known as vestibular schwannomas or acoustic neuromas (see figure), are pathognomonic of a fascinating syndrome called central neurofibromatosis or neurofibromatosis type 2 (NF-2). NF-2 is a rare, autosomal-dominant disease with an incidence of 1 in 30,000 live births. The mechanism by which the genetic changes underlying NF-2 produce these tumors of a cranial nerve remains a mystery. Interestingly, two other associations are also sufficient to make a diagnosis of NF-2. These are unilateral VS at early age (< 30 years) plus two other specific lesions (meningioma, schwannoma other than VS, glioma or pre-senile cataract), and unilateral VS at early age with an affected first-degree parent, sibling or child. Patients with NF-2 usually present between the ages of 18 and 24 years with tinnitus, hearing loss and balance difficulties. Symptoms of unilateral tinnitus, asymmetric hearing loss or unresolving vertigo or imbalance warrant a gadolinium-enhanced MRI with a neurotological consultation to rule out brainstem pathology.
NF-2 is caused by inactivation of the NF-2 tumor suppressor gene on chromosome 22 (22q12.2) which encodes the "Merlin" protein. Like a double negative, inactivation of a tumor suppressor gene produces an autosomal-dominant inheritance pattern identical to classical activating mutations.
When a diagnosis of NF-2 is entertained, evaluation should include a complete family history; a detailed head and neck and neurological examination with attention to cranial nerve deficits, and an MRI of the brain with dedicated images to detect bilateral VS, meningiomas and optic gliomas. Spinal MRI with gadolinium should be performed to look for spinal meningiomas or schwannomas, and ophthalmologic evaluation should be obtained in cases with visual loss or with suspicion of juvenile cataracts.
Unilateral VS and NF-2