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If you are a woman between ages 20 and 44 years and suffer from migraine headaches you may have an increased risk for ischemic stroke. In this type of stroke the brain cells do not get enough oxygen, usually because either the vessel itself has narrowed-which may be a temporary condition-or the blood vessel is blocked by a clot or plaque. The lower level of oxygen causes cells to die. Symptoms, including migraines, vary according to the part of the brain affected.

A family history of migraines also increases your risk for both ischemic and hemorrhagic strokes even if you do not have them yourself. Hemorrhagic stroke occurs when a vessel breaks, allowing blood to bleed into the brain. This deprives cells upstream of an oxygen supply and they die. If enough blood escapes and puts pressure on other vessels, circulation and oxygen will be cut off to other areas of the brain

High blood pressure, use of birth control pills, and/or smoking increase this risk significantly because they cause blood vessels to constrict and limit blood flow to the brain. Changes in frequency or type of migraines were not found to be a predictor of stroke in study participants who use birth control pills. However, if taking birth control pills you should tell the physician prescribing them about your migraines or any other type of headache you experience.

Up to 40 percent of strokes occurring in women with migraines may develop directly from this type of headache.

The discovery of a feedback system that’s active during a migraine headache has researchers at the University of Iowa questioning some of the traditional theories about migraine headaches.

The team found that inflammatory agents released during a migraine seem to signal certain nerve cells (neurons) in your brain to increase production of a neuropeptide, calcitonin gene-related peptide, or CGRP. One result of CGRP’s presence is to stimulate your brain tissue to release more inflammatory agents. The new inflammatory agents send more signals to the neurons to release more CGRP, the cycle continues, and so does your migraine.

At present, the most effective migraine medication on the market is sumatriptan, which provides relief for 50 to 75 percent of the people who use it. Even though scientists know it works, they don’t understand why or how.

While studying the drug, the Iowa researchers discovered that sumatriptan keeps calcium levels high in the neurons. In most cases, a high-calcium level also means a high level of neuropeptides in the affected neurons. However, when the participants took sumatriptan, CGRP didn’t increase, which may be one reason why this drug works so well against migraines. If the CGRP doesn’t increase, then the inflammatory agent-CGRP cycle described earlier is broken.

Interestingly, the same signal (calcium release) can give two different reactions depending on the strength and duration of the signal. A short, fast burst of calcium causes an increase in the CGRP, which continues the cycle and your headache. However, if the calcium increase is a slow, steady rise, it actually lessens the amount of CGRP that is released. Researchers believe it is this second type of calcium increase that sumatriptan brings about.

As a follow-up to this study, researchers will look for the exact mechanism for the initial release of CGRP, with the hope that blocking this action would divert the migraine.

Those who suffer cluster headaches may have non-painful warnings that the headaches are going to occur anywhere from several days to several weeks before their onset, according to a study done by researchers at the Universidad Nacional de Rosario in Argentina.

Four patients in the study described various symptoms that preceded the onset of cluster headaches. The first patient’s symptoms were described as “eye discomfort,” a heightened state of anxiety, and a feeling of having “something inside my head.”

The second patient complained of eye discomfort that was aggravated by reading or noise. The third patient reported feeling numbness in the left temple about a week before the onset of the headaches. And the last patient described discomfort on the right side of the head.

Cluster headaches are similar to migraines and occur as often as two or three times a day over a period of weeks. They come on suddenly, and sufferers experience throbbing pain behind the nostril and one eye. The attacks rarely last longer than two hours, and it may be weeks or months in between attacks.

This study is important, said researchers, because it demonstrates that “changes occur in the nervous system that anticipate the autonomic (self-controlling) and painful manifestations.” Also, recognizing that warning symptoms can occur before the severe pain strikes is the first step in developing preventive treatment and a better understanding” of the cause of cluster headaches.

When brain images are taken of people who experience primary headaches, they’re normal. This has led scientists to believe that headaches come from dysfunction rather than an abnormality in the structure of the brain. However, researchers from the National Hospital for Neurology and Neurosurgery in London are suggesting that this conclusion may have been made in error.

Headaches not directly due to injury or disease are called primary headaches. Included in this category are tension, migraine, and cluster headaches. Magnetic resonance imaging (MRI) or computed tomography (CT) scans have consistently shown no structural abnormality in these people—until now.

With a new type of imaging called voxel-based morphometry, British researchers have conducted a study that shows that people with cluster headaches have an abnormality in the part of the brain called the hypothalamus. The hypothalamus lies deep in the brain and is responsible for maintaining a constant internal environment, including temperature and wakefulness, and carrying out certain behavior patterns—sexual behavior, physical expression of emotions, and pain and pleasure. It affects the nervous system directly and through hormones.

Researchers compared the brain images of 25 people with cluster headaches to the brain images of 29 people in the control group. Fourteen of the headache sufferers had a headache during the test.

The tests showed that all the people with cluster headaches had a greater density of grey matter in their hypothalamus. Researchers then compared the two groups using positron emission tomography (PET). The PET scans showed both structural and functional abnormalities in this same area of the hypothalamus.

Now that an exact area of the brain has been identified with cluster headaches, researchers are hoping to develop more effective treatments for these and other types of primary headaches.

However, they can’t say that the extra grey matter actually causes the headache, just that all the participants with cluster headaches had this hypothalamic density. Perhaps the increased density is the result of the headaches, not the cause. Further testing will be needed to explore the exact association between primary headaches and hypothalamic abnormality.

More than 16 percent of patients with epilepsy conceal seizures from their doctors, according to a recent study. Previous research has reported that many people with epilepsy hide it to avoid social stigma and loss of employment or driving privileges.

Researchers, from the University of East Anglia in Norwich, England, and at King’s Fund in London, distributed two identical questionnaires to 111 adult patients who’d had epilepsy for an average of 21.5 years. The first questionnaire was completed with the general practitioner at an office visit, and the second was completed anonymously by the same patients about two weeks later. The researchers compared the two questionnaires for each patient.

Forty-two patients (38 percent) told their doctors that they’d had a seizure within the past year. Sixty patients (54 percent) admitted this on the anonymous questionnaire. The researchers suggest that an important reason for not telling the doctor is to keep driving privileges. In England, patients must be seizure-free for 12 months to drive. Six of the 42 patients who told their doctors about seizures still had a driver’s license, compared to 24 of the 60 who admitted anonymously to having seizures.

Another reason for concealing seizures may be to maintain employment. About 47 percent of the patients who told their doctors about seizures were unemployed, compared to 17 percent of those who concealed their seizures.

Patients who’d had seizures in the past year, whether or not they’d told their doctors, were also significantly more likely to be anxious or depressed or to feel stigmatized, than those whose epilepsy was controlled.

Writing in the January 8, 2000, issue of the British Medical Journal, the researchers conclude that while concealing seizures may prevent these patients from getting the best care, many consider that price worthwhile if it allows them to keep driving and working.

The researchers also point out that the doctor’s role in determining whether patients with epilepsy can drive or participate in other activities hampers their ability to provide appropriate care for those patients. They suggest that driving regulations for people with epilepsy be changed. They noted that in Wisconsin, which has a low accident rate, epileptics only need to be seizure-free for three months to drive.

The authors also call on general practitioners to explain to their patients that they must report their seizures if they want to receive optimal care.

If your epilepsy doesn’t respond to any anticonvulsant medications or treatments, perhaps you don’t have epilepsy after all. Researchers from the Manchester Heart Centre and the David Lewis Centre for Epilepsy in the United Kingdom believe many people diagnosed with treatment-resistant or atypical epilepsy may actually be suffering from a cardiovascular disorder.

The study included 88 participants, ages 16 to 75, who experienced recurrent seizure-like episodes that had been diagnosed as epilepsy. Each was given tests designed to diagnose recurrent fainting. During these tests, they were monitored with electroencephalogram (EEG), which traces the electrical activity of the brain. In addition, some participants had a small cardiac-monitoring device implanted under the skin that served as a continual electrocardiogram (ECG), which traces the electrical activity of the heart.

The cause of seizures in 43 of the 88 participants was not epilepsy at all. In 26 cases, a cardiovascular problem was found to be the cause. In the remaining 17, the attacks were found to have a psychological origin.

The use of the implantable cardiac monitor aided in the diagnosis by helping to differentiate between an epileptic seizure and a convulsive fainting episode. The former is caused by abnormal electrical activity in the brain and the latter by an interruption in normal blood flow to the brain. Diagnosing this condition can be very difficult because the interruption only shows up on a test if a person is actually experiencing an attack during the test. Using the implantable device allows monitoring to continue for over a year, increasing the chances that an attack will occur during monitoring.

If the cause of your seizures is determined to be due to a cardiovascular problem, treatment with the proper medication or insertion of a pacemaker may be able to eliminate your episodes. The anticonvulsant medications used for epilepsy are not effective in treating seizures due to cardiovascular problems.

Epilepsy is estimated to affect more than four million people in the United States and Europe. The researchers estimate that approximately one-third of them have been misdiagnosed.

A conservative estimate is that more than 100,000 people with epilepsy in the United States alone have uncontrolled seizures and could benefit from surgery. Most of them have seizures that arise from a problem in a temporal lobe of the brain, and the most common operation to treat refractory epilepsy is anterior temporal lobectomy. This is a procedure with a proven record of efficacy, eliminating or greatly reducing the prevalence of seizures in trial after trial. A group of researchers at the University of Pennsylvania and Dartmouth University decided to delve deeper into the impact of this procedure on the lives of patients in the first five years after lobectomy.

The test subjects were 89 volunteers, ranging from 10 years old to 60, all suffering persistent seizures at least once a month for at least one straight year. All had elected to have surgery after at least three different antiepileptic drugs (AEDs) and one attempt at combination therapy failed to improve their condition. Neurologists had confirmed in each case that their seizures probably arose from a single temporal lobe and could therefore be addressed by its excision; all those patients whose seizures originated in more than one site, or in a site other than the temporal lobe, were excluded from surgery because of the obvious undesirability of removing large or valuable pieces of brain tissue. Surgery does not immediately cancel the need for medication; patients were initially advised to continue taking their AEDs at moderate doses for two years after study, and this was later extended to five years.

The results of surgery

The most basic yardstick for measuring the value of any surgery aimed at reducing seizures is obviously the impact on seizure frequency. This was documented at two weeks, two months, six months, and again at one year after surgery. Follow-up continued every year in those patients who were seizure-free to see how long they stayed that way. Patients were grouped into four categories according to the degree of improvement. Class One patients were seizure-free after surgery, or currently seizure-free for at least one year (exceptions were made for isolated seizures associated with withdrawal of medication). Class Two patients were those who still had occasional seizures, but no more than three in a year – a significant improvement in a group that had previously averaged at least eight seizures per month. Class Three patients had more than three seizures in a year, but still registered a post-surgery reduction of over 80% in seizure frequency. Finally, Class Four patients included all patients whose seizures had become less frequent, but by less than 80%, and those who had registered very little improvement or none at all.

By any standards, the surgery was very effective. After five years, 62 patients (70%) were in Class One, a further eight (9%) were in Class Two, and 10 more (11%) were in Class Three. Thus, 90% of patients had achieved significant relief from their seizures, and most of them were effectively cured. Only five patients (6%) had fallen into Class Four, while four (4%) had died of various causes, none of them related to surgery. More than half of all patients never had another seizure following surgery. (This does not include those seizures that sometimes follow immediately after the operation, which are caused by the trauma to the brain inherent in surgery, and do not reflect any permanent epileptic condition.)

Lobectomy does not impair intelligence

One common misconception about lobectomies (arising, no doubt, from the connotations of the similar word lobotomy) is that it can reduce intelligence. IQ tests administered to patients before and one year after surgery showed no change in verbal scores and a noticeable improvement in the performance score, especially among those who had left (as opposed to right) temporal lobectomies. Both left and right-side patients (especially left) raised their average overall IQs. Thirty-minute visual memory and facial memory were also improved. Most importantly, the patients showed greatly reduced scores on standard tests of depression and anxiety; they were happier and more relaxed.

These changes could not be expressed more clearly than in the improvements that those patients who became seizure-free achieved in their own lives over the five years following surgery. Before the operation, only 34% of all patients were working full-time and 24% were unemployed. Five years later, 63% were working full-time and only 11% were unemployed. Full-time employment rose even higher in the majority who became seizure-free, and unemployment in Class One patients dropped to 3% – below the national average. The psychological, social and material benefits of having a paying job, which can hardly be overestimated, are among the biggest dividends of successful treatment of seizures.

Rarely does a medical procedure offer such a clear and long-term improvement to the well-being of patients as temporal lobectomy. In the face of such encouraging findings, the researchers recommend that patients with epilepsy focused in the temporal lobe be encouraged to consider surgery as soon as the failure of drug treatment becomes apparent. Much unnecessary suffering and marginalization could be avoided and thousands of people rescued from the trap of epilepsy if this procedure were applied in more cases.

Research has come a long way in providing effective treatment for people with epilepsy, but for some, it just is not enough. Despite adequate and therapeutic doses of medication, many still continue to experience several seizures a month. But according to researchers from the University of Michigan, a drug called oxcarbazepine may provide relief to those who continue to have a type of seizure known as a partial seizure, even if they have already been through the gamut of other medications.

In their study, researchers found that oxcarbazepine, sold under the brand name of Trileptal, was safe and effective for this population. They followed 87 patients, some as young as 12 years old, who had partial seizures that remained uncontrolled despite the fact that they were on medication. The study participants were first tapered off of their regular drug regimens, and then they were divided into two treatment groups. One group received a low dose of 300mg/day and the other group a much higher dose of 2,400 mg/day of oxcarbazepine. (The drug’s manufacturer currently recommends a daily dose of 1200 mg/day.)

The results, says study author Ahmad Beydoun, M.D., associate professor of neurology and director of the Comprehensive Epilepsy Center at the University of Michigan, are encouraging and he believes that the patients responded well to this drug. In the group receiving 2400 mg/day, 12 percent remained free of seizures and almost half had a 50 percent reduction in the number of seizures they were experiencing. The results were less encouraging for those on the lower dose — none of the patients became seizure free.

Epilepsy is a neurological disorder and affects more than 2.3 million American adults and children. It is characterized by seizures, which occur when specific brain cells release high amounts of electrical energy and in turn, trigger a sudden loss of control over movement, thought or awareness.

There are many types of seizures, and experts have divided them loosely into generalized and partial seizures. The most common type is the partial seizure, which occurs when the disturbance takes place in just one area of the brain, and affects whatever physical or mental activity that particular region controls. The generalized seizure happens when a massive burst of electrical energy occurs throughout the brain at one time, causing unconsciousness, convulsions and other severe effects.

“In epilepsy drug therapy, tolerability and efficacy are often closely related,” says Beydoun. “One of the challenges in treating this disorder is the side effects associated with the standard antiepileptic drugs.” Many patients cannot control their seizures because they are unable to tolerate high enough doses of their medication. For the most part, oxcarbazepine was well tolerated by the people in the study, and the majority of them were able to reach the highest recommended dose, which may partially explain why it worked so well for them.

Some epilepsy drugs are given in combination with other drugs, while some are used alone in what is called monotherapy. This study examined the efficacy of oxcarbazepine as a monotherapy, and it has been approved by the FDA to be used alone. However, Carmel Armon, MD, a professor of medicine at Loma Linda University in California and a Fellow with the American Academy of Neurology, is not yet ready to switch his patients over to oxycarbazepine. He believes that a closer look is needed at this drug, particularly if it is going to be used as monotherapy.

The four-month trial period, he points out, was not long enough to test the long-term efficacy of oxcarbazepine. “Even though it’s very gratifying that 12 percent had a chance to go seizure free on this medicine, the study design is not such that it would tell us how long that benefit would be sustained,” he says. Often a patient may do well initially on a new drug, but then after a few months, the same problems emerge. A much longer period of time is needed to truly test the efficacy of a drug, Armon believes.

Sometimes, just a change in a medication regimen can temporarily reduce the number of seizures, Armon points out, and so the reduction in seizures seen in the study could be partially attributed to that. “It’s frequently seen that when you make a change, a small percentage of your patients will be seizure free and then relapse, ” says Armon, who specializes in treating patients with epilepsy. “And in fact, many of my patients will give me a story that every change I’ve made seems to be a change for the better, and then they broke through.”

Armon believes while the study did demonstrate some effectiveness as a monotherapy in treating partial seizures, the results were just not that striking. Only a small percentage of the patients became seizure free, and since the study followed them for just four months, it is unknown how long the effect will last.

“Based on this knowledge,” says Armon, “They may better off working with the drugs that they are currently taking, and using oxcarbazepine as an add-on or addition to their current medication regimen.”