Posts Tagged 'MD'

Expecting the Best in Pregnancy and MS

 Pavle Repovic, MD, Ph.D, Neurologist, Multiple Sclerosis, Swedish Neuroscience Institute

Considering that multiple sclerosis (MS) affects primarily women of childbearing age, it comes as no surprise that for many patients MS and pregnancy often occur together. The issues to consider when discussing pregnancy and MS include:

• How pregnancy affects MS

• How MS affects pregnancy

• How MS treatment should be managed throughout pregnancy

The Pregnancy in MS (PRIMS) study of 254 patients revealed that pregnancy is generally protective against MS relapses, in particular during the third trimester. In contrast, the same study found a rebound of relapses during three months post delivery, with 30 percent of women experiencing a relapse within three months after delivery. Several strategies have been proposed to avert the risk of postpartum relapse, including the use of prophylactic IVIG or corticosteroids. More recently, exclusive breast-feeding has been found to offer some protection against postpartum MS activity; however, this finding was disputed in a subsequent study.

There is no evidence that MS impairs fertility or leads to an increased number of spontaneous abortions, stillbirths or congenital malformations. MS also does not increase a woman’s risk of preeclampsia or premature rupture of membranes. Pregnant women with MS are 1.3 times more likely to undergo antenatal hospitalization and to have a Cesarean delivery, and they are 1.7 times more likely to have infants who are small for gestational age 6.

Except for glatiramer acetate, all MS disease-modifying treatments (DMT) have documented in utero harmful effects in animal studies and are therefore FDA pregnancy category C agents. Glatiramer acetate is a category B agent and is not known to have harmful effects in animal studies, although human studies are lacking.

For these reasons, the National MS Society and most MS specialists advise women who intend to become pregnant to discontinue therapy. Given their pharmacokinetics, we suggest the following schedule based on the type of therapy: one month (glatiramer), two months (fingolimod) or three months (interferons, natalizumab) prior to anticipated conception. It is less clear when to resume the therapy following the delivery.

Because only a minuscule amount of medications is excreted in mother’s milk, some MS specialists advise patients to resume therapy – with the exception of fingolimod or natalizumab – as soon as possible, even in women who intend to breast-feed. In the event of an MS relapse during or after the pregnancy, treatment with high dose intravenous methylprednisolone is generally considered safe for both mother and baby.

Questionable Hope for CCSVI

James Bowen, MD, Neurology, Multiple Sclerosis, Swedish Neuroscience Institute 

Once again, multiple sclerosis patients’ area buzz over a new theory and treatment for the disease. The theory is called chronic cerebrospinal venous insufficiency (CCSVI); and, this time, social media is driving the patient excitement.

CCSVI is based on a controversial idea that impaired venous drainage of the brain due to blockage in venous structures causes MS. Increase in venous pressure promotes leakage of blood across capillaries, with inflammation resulting from the iron deposition into the brain. In 2009 Paolo Zamboni, M.D., reported that virtually all MS patients in a study had abnormalities in the jugular or azygous veins, whereas no control patients had such findings. The Zamboni, or Liberation, procedure involves either angioplasty or stenting of the abnormal vein. Many MS patients are understandably enthusiastic about this theory and treatment.

There are, however, a number of problems with the CCSVI theory that patients and MS neurologists should consider.

• Diagnostic criteria for CCSVI are not standardized or accepted

• CCSVI does not seem to explain the distribution of white matter lesions or the relapsing and remitting course that most patients experience

• CCSVI does not explain the presence of inflammation in MS lesions

• Iron in MS lesions is contained within macrophages, not erythrocytes or free, as predicted by the CCSVI theory

• Other diseases with increased venous pressure do not resemble MS

• Venous drainage is highly redundant, so stricture of a vein usually does not increase venous pressure in the brain

• Changes in muscle tone or posture from neurological disease may explain some venous blockages; and neurological disease can lead to lower venous blood flow due to circulatory auto regulation

Studies that have been performed to date have not supported the CCSVI theory. Preliminary results from the Buffalo Neuroimaging Analysis Center at the University at Buffalo, The State University of New York, found 56 percent of patients with MS, 42 percent of those with neurological diseases other than MS, and 23 percent of controls met criteria for CCSVI. This group found a decrease in cerebral venous volume in MS patients compared to normal, whereas blockage in venous flow would be expected to induce vascular dilation and increased venous volume. At the recent ECTRIMS (European Committee for the Treatment and Research of Multiple Sclerosis) meeting in Sweden, groups from Gotteborg, Berlin, Padua, Amsterdam and London found no evidence for venous obstruction in MS patients compared to controls. A study from London, Ontario, found that venous blockage increased with age in both MS and controls. A study from Beirut, Lebanon, found venous changes in only 9 percent of patients after their first MS attack, increasing to 92 percent with advanced MS, possibly suggesting a late finding that is unrelated to the cause of the disease. Nevertheless, as anecdotal reports continue to circulate of individual patients with dramatic responses to treatment of CCSVI, the theory has been of great interest among MS patients and has become the subject of a significant number of studies.

Before CCSVI can be considered as contributing to MS, three criteria should be required.

1. Venous blockage must be shown to be increased in MS patients relative to healthy controls and other neurological diseases. This would demonstrate an association between CCSVI and MS, but not prove causation.

2. Treatment of CCSVI should stop the progression of MS symptoms in placebo controlled, blinded, multi-center studies. This would prove that CCSVI contributes to MS, but not prove causation.

3. MS should develop in humans or animals with venous blockage.

The scientific community is taking CCSVI very seriously. Most of the studies currently under way are testing whether MS patients have venous blockage. The National MS Society and the MS Society of Canada funded seven 24-month studies in June 2010, totaling $2,400,000 of ultrasound, MRI and angiographic techniques to determine whether venous blockage is specific to MS patients in both adult and pediatric populations. The MS Society of Italy is contributing £900,000 (nearly $1.3 million) to study the question. The Buffalo Neuroimaging Analysis Center is conducting a study of venous imaging, as well as a small treatment trial. Saskatchewan and MS Research Australia have also initiated large studies.

The risks of the Liberation procedure in MS are not entirely understood, though stent migration and fatal intracerebral bleeding have already been described. Only controlled studies will teach us the true complication rate. In the meantime, most MS neurologists are recommending that patients await the results of current studies before proceeding with this controversial treatment. 

Advances in thrombolysis

Bill Likosky, MD, FAAN, FAHA, Director for Stroke and Telestroke, Swedish Neuroscience Institute

 

 

Washington State has one of the high­est stroke mortality rates in the nation. To improve this situation, acute intervention­al therapies for stroke are being employed to restore circulation to ischemic brain tissue that surrounds areas of completed infraction, while avoiding risk of hemor­rhage due to reperfusion of large areas of infracted brain tissue.

Urgent thrombolysis with intrave­nous 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 in­farction following a stroke.

A recent European study demonstrat­ed the efficacy of alteplase up to 4.5 hours after ischemic stroke in patients younger than age 80 years who have neither dia­betes 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 des­moteplase. Derived from the saliva of the vampire bat, this agent has a longer half life than alteplase and does not break down basement membranes, leading to a lower risk of hemorrhagic complica­tions. The Swedish Stroke Program is part of an international effort to test this drug in a nine-hour window.

Todd Czartoski, M.D., and Bart Keogh, M.D., Ph.D., are collaborat­ing with the stroke team at Stanford University to identify patients with vi­able ischemic tissue regardless of time from onset of symptoms. Perfusion MRI identifies impaired blood flow in brain (the “penumbra”) surrounding an infarct. In cases where there is a large area at risk, the use of alteplase or clot retrieval may prove beneficial long after the three-hour window has elapsed.

Telestroke is another important development in acute stroke care. This program enables the timely alteplase treatment of patients in emergency rooms around the Pacific Northwest that lack onsite neurological expertise.

For more information about the Swedish Stroke Program, contact Sherene Schlegel, R.N., FAHA, at 206-320-3484. For information about telestroke, contact Tammy Cress, R.N., MSN, at 206-320-3112.

Options widening for wide-necked aneurysms

 

Yince Loh, MD, Interventional Neuroradiology, Neurosurgery, Swedish Neuroscience Institute 

 

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.”

Those aneurysms that have a balloon-like opening, or neck, from the parent vessel are typically good candidates for coiling. Not infrequently, however, the aneurysm’s shape does not permit safe coiling. When the aneurysm’s neck is wide, it appears more like a molehill than a balloon. A molehill configuration is often referred to as a “wide-necked aneurysm.” The wide neck allows an unwanted protrusion of coils back into the artery. This can lead to a number of problems, including failure to obliterate the aneurysm and stroke. Thus, in situations where an aneurysm is not surgically accessible or the patient cannot undergo surgery, no therapeutic options can be offered.

Until recently, wide-neck aneurysms could not be treated by coiling. The U.S. Food and Drug Administration, however, has approved a tubular device called an intracranial stent to be used for such situations.

Once a stent is deployed across the neck of the aneurysm, coils are placed into the aneurysm through the stent wall. The stent struts prevent the coils from falling back into the artery by essentially creating a “chain link fence” across the neck of the aneurysm.

Stenting, however, produces another set of problems. A stent is a foreign body that can promote the formation of a blood clot inside the vessel, which is why patients are placed on two antiplatelet medications to thin the blood, usually aspirin and clopidogrel (Plavix®), after placement of a stent. The length of time required to thin the blood after stent placement is unclear, although stents may become incorporated into the vessel wall and covered with endothelium within weeks.

Multimodal Treatment of Spinal Tumors symposium

Join us next week!
Multimodal Treatment of Spinal Tumors symposium
Friday, February 25, 2011
 
 
 
 Course Chair: Rod J. Oskouian, Jr., M.D, Neurosurgery, Spine Surgery, Swedish Neuroscience Institute.
 
 
 
 

 Today, health-care providers who treat patients with spinal tumors are able to offer a myriad of treatment options that were essentially non-existent in the recent past.  Internationally renowned speaker, inventor, entrepreneur and neurosurgeon, John R. Alder, M.D., will present the keynote presentation at this year’s symposium and initiate our discussion of  the technical and therapeutic options available for spinal tumor patients.

For full course information and to register: http//www.swedish.org/spinaltumors2011

 
 

Pediatric Neuroscience Center receives “Tuberous Sclerosis Complex (TSC) Clinic” Designation

February 3, 2011. The Tuberous Sclerosis Alliance announced today that it has designated the Swedish Pediatric Neuroscience Center (SPNC) at SNI as a TSC Clinic. Marcio Sotero, MD, medical director of SPNC, is the director of the new center. This designation is an important step forward in the regional delivery of care to patients with tuberous sclerosis, as the TSC Clinics closest to Seattle are located at the Barrow Neurological Institute in Phoenix and Children’s Hospital in Oakland, CA.

TSC is a genetic disorder that causes tumors to form in many different organs, primarily in the brain, eyes, heart, kidney, skin and lungs. Seizures are a very common manifestation, and some people with TSC experience developmental delay, mental retardation and autism.

SNI Grand Rounds Series 2010 – Extending the Window for Stroke Therapy: The Role of Imaging

Thursday December 16, 2010
7:30am – 8:30am
Swedish Education and Conference Center, Room B

 Gregory W. Albers, M.D., Professor of Neurology, Stanford University

 

 

 

 

Objectives:

At the conclusion of this session, attendees will have an increased ability to:

  • Discuss options for expanding the treatment window for acute ischemic stroke
  • Review the role of neuroimaging for identification of salvable tissue in stroke patients 
  • Discuss the results of the DEFUSE trial and the study design of the ongoing DEFUSE 2

SNI Grand Round Series is every 1st and 3rd Thursday of each month.