Ali Gorman, R.N.

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October 3, 2011 (WPVI) -- Ron Reigner has spent most of his life working at his family store, Passmore Service Center, helping people get parts and equipment. Related Content
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For the past 25 years, his life has been interrupted by pain from migraines. "At least one day a week, I was in bed, and couldn't do anything. A lot of pressure behind the eyes. My jaw and my neck would hurt" said Reigner Doctors believe migraine pain is caused by a complex chain of events in blood vessels and nerves on the lining of the brain. Nerves fire wildly, like lightning in a storm. Medicine helps many sufferers but never worked long for Reigner. At times he was too nauseous from the migraines to take medication at all. About four years ago, he enrolled into clinical trials testing a new device called the Genesis stimulator A small generator is implanted on the hip sending mild electrical pulses to the nerves on the back of the brain. The frequency and intensity of the pulses can be adjusted. Dr. Stephen Silberstein of the Jefferson Headache Center says so far trials done in the United States have worked for many patients. "In fact, we had one patient who after the stimulator was put in, there was an 80 percent reduction in his headaches," said Dr. Silberstein. Overall, the makers of the device report a 28 percent decrease in headache frequency in patients with the device after 12 weeks, compared to a four percent drop among patients tested with a placebo. Still Dr. Silberstein says not all patients in the Genesis trial were happy. A quarter of them said they would not try the stimulator again. Reigner, however, says it turned his life around. "Once a month, I may get a headache, but the intensity isn't there," said Reigner. The stimulator is said to be only for people who have exhausted all other options. The Genesis device was approved in Europe this summer. The FDA is expected to make a decision whether it will be approved in the U.S. sometime next year. (Copyright 2011 WPVI-TV/DT. All Rights Reserved.)

Glutamate: A New Key To Migraine Treatment?

Glutamate: A New Key To Migraine Treatment?
by Teri Robert, Lead Expert Information presented at the 61st Annual Meeting of the American Academy of Neurology (April, 2009) indicates that glutamate receptors may play a role in Migraine treatment. Trial Phase IIa data showed Addex Pharmaceuticals' ADX10059, an investigational glutamate receptor inhibitor, could prove helpful for Migraine prevention. Other early trials have shown ADX1005 to be an effective abortive treatment for acute migraine attacks. Glutamate is a neurotransmitter, a chemical occurring naturally in the brain that transmits messages from one nerve cell to another. A theory under investigation is that since glutamate receptors are found in regions of the brain involved in Migraine, inhibiting transmission through glutamate receptors could lead to Migraine treatments. Dr. Peter Goadsby of the UCSF Headache Center and investigator in the study commented: "Medication is available to prevent migraine but these treatments are often secondary uses of the drug and come with potentially limiting side-effects... New therapies specifically developed for migraine prevention are urgently needed especially for the substantial proportion of migraine sufferers who have frequent attacks and have significant disability in their daily lives. Targeting mGluR5 (glutamate) signaling with ADX10059 is an interesting approach that is showing significant promise in early clinical evaluation."2 and "It wasn't a great effect, but it confirms that glutamate is a legitimate target... It's generally quite clear that there is glutamate-mediated transfer of pain signals in migraine... The question is how to take advantage of it."1 According to Goadsby, ADX10059 works by "toning down" the receptors as opposed to totally blocking them.

The trial showed:

Pain-free response two hours after taking ADX10059 was significantly greater than placebo. Only 10% remained pain-free at 24 hours with ADX10059, compared with 3.1% for placebo, a difference that was not statistically significant. ADX10059 was not as well tolerated as placebo, causing central nervous system adverse events such as cognitive effects and fatigue more commonly than placebo (71% versus 14%).
(Page 2)

Even in the face of these less than stellar results, Dr. Goadsby said he remained hopeful that these compounds have potential for the prevention of migraine, and he is involved in a trial of the compound for this effect, adding that using lower doses over longer periods of time for prevention might avoid the side effects observed in this trial. Summary and comments: At this time, there are no medications on the market that were developed specifically for Migraine prevention. All of the 100 plus medications in use are "hand-me-down" medications, medications that were originally developed for other purposes. The possible development of a new class of medications is exciting and hope inspiring.

Even though ADX10059 showed problems in this phase IIa trial, it's still early. Hopefully, it will prove to be a safe and effective preventive even if it doesn't work out as a Migraine abortive medication.

Course # 9042 Seizures and Epilepsy Syndromes CASE STUDY 1

The events of a complex partial seizure have been described as follows: The patient suddenly stopped talking and stared at the ground. Her head moved slowly to the side and she began rubbing the table with one hand, as if she was smoothing down a piece of paper. Her movements were slow and appeared deliberate. I asked the patient to remember "purple elephant." I asked the patient to lift one foot off of the floor, but there was no response. The event lasted 90 seconds. The patient moved back to her previous position in the chair with her head in a neutral position and her hand in her lap. She looked at me, with a groggy expression, and stated repeatedly, "I'm ok." The patient was slow to respond and lethargic for several minutes. After she was alert, she could not recall the event or the phrase "purple elephant." The patient complained of a headache and fatigue. After a period of rest, she was able to resume her usual activities.

CASE STUDY 2
The following is an example of a patient with non-epileptic pseudoseizures: Patient E is a man who experiences pseudoseizures after serving in the Vietnam War. A witness described the patient's pseudoseizure: "He began by crying, then becoming very withdrawn and quiet. He slowly leaned against the wall and slumped gradually to the floor onto his back. His eyes rolled around and his mouth was moving as if he was speaking without any words. Movements began in his left shoulder then proceeded down his arm, then throughout his entire body. His arms and legs flayed around, as if he were running away from something." Further questioning about the movements of the extremities revealed that the patient's arms moved independently of each other, in a smooth, nonrhythmic fashion. His legs had a kicking and running movement to them. Although this description does not automatically discount an epileptic seizure, there are some details that are not consistent with a common epileptic seizure. One of the most obvious inconsistencies is that the event does not follow a neuroanatomic pattern. Movements during a pseudoseizure may have personal symbolic significance to the patient.

CASE STUDY
Patient R is a female, 38 years of age, with a history of seizures since birth. She is otherwise in good health. Her current diagnosis is temporal lobe epilepsy. Patient R experiences complex partial and secondarily generalized seizures. She states that she is aware that a seizure is going to occur because she has a very brief "strange sensation." This sensation is her aura. After the aura, the patient cannot recall any other events until the postictal period. During the postictal time, Patient R is fatigued and confused and often experiences headaches. Witnesses have noticed a typical pattern to Patient R's seizures. First, she becomes very quiet and blank. She will not communicate or respond to other individuals. She experiences vocalizations and yells in a very loud voice, "Jesus help me." During the vocalizations, Patient R will experience automatisms that include pulling at her clothing. Usually, the seizure ends after approximately 60 seconds, and she regains consciousness within several minutes. At other times, the seizure will progress, and she will experience tonic posturing followed by clonic movements. The tonic-clonic phase is quite severe and may last several minutes. The postictal period after the secondarily generalized seizure is prolonged and may last for several hours. Patient R experiences disorientation, confusion, and somnolence. She has experienced status epilepticus twice in the past. At times, Patient R's seizures occur almost every day. However, some days will be seizure free, and she may have several days at a time with no seizure events. Unfortunately, this does not occur consistently. Most days she will experience at least one seizure, and often she has several during the same day. She has been on a number of AEDs in the past, including phenytoin, phenobarbital, valproic acid, and experimental medications. Her current medications include carbamazepine and topiramate, with lorazepam as needed. She also takes an over-the-counter multivitamin and, occasionally, acetaminophen for headache. Her sister has been

instructed on administering lorazepam when Patient R is experiencing several consecutive seizures that occur over a 15-minute period or after her second secondarily generalized seizure for the day. Her sister administers the lorazepam approximately once every 2 weeks. However, Patient R's seizures are quite variable with no known pattern. One week, she may not require any lorazepam; the next week, she may require it several times. Patient R is very compliant with her medications. She uses a pillbox and can correctly describe her daily medications and doses. She has used a seizure calendar method of tracking her seizures for years. Each day she records the number of seizures she has and describes them. Patient R has no family history of epilepsy, and she has not had any surgical treatments. During Patient R's physical examination, her physician discovers that the patient had difficulty with coordination. There are deficits in cognitive processes, such as calculation and abstract thinking. The exam is otherwise unremarkable. Patient R has a twin sister who is neurologically normal. The twin sister provides a large amount of social and emotional support and is always present to accompany the patient at her visits. Patient R is a very independent woman who lives in an assisted living center and wears a protective helmet. She has completed the 5th grade. She does not use nicotine products, drink alcohol, or use illicit substances. She has experienced difficult situations in the past related to a divorce and loss of her only child. The patient has been involved in the trial of several new experimental AEDs with varying success. The latest study she participated in had a positive effect on her seizure frequency. Unfortunately, the pharmaceutical company discontinued the medication from the study. As a result, other alternatives were sought. Her current healthcare providers evaluated Patient R and placed her in the epilepsy monitoring unit for simultaneous EEG/video monitoring. In the epilepsy monitoring unit, Patient R's AEDs are slowly withdrawn. She begins to experience her typical events, including vocalizations. During these events, a large amount of motor activity is exhibited and EEG readings are difficult to ascertain. The medical team suspects a diagnosis of pseudoseizures. The patient completes the neuropsychological testing, and the evaluation continues for several days. The patient experiences a secondarily generalized seizure, and the EEG readings clearly reveal epileptogenic changes. Sphenoidal electrodes are placed to obtain localizing information. Patient R continues to have a large number of seizures and requires frequent administration of intravenous benzodiazepines to maintain seizure control. After more than a week of monitoring, a seizure focus is determined. Unfortunately, multiple focal areas exist in the bilateral temporal and frontal lobes, eliminating the surgical option. The patient is restarted on her AEDs and stabilized, and alternative treatments are discussed. The patient and healthcare team agree that a vagus nerve stimulator would be a positive option. Alterations in the medication regimen are discussed. The patient and sister are offered the option to attempt dosing with felbamate with close monitoring. Patient R doe not want to attempt felbamate and opts for slowly removing the topiramate and attempting a trial with lamotrigine while awaiting the vagus nerve stimulator placement. This medication is somewhat helpful, but the vagus nerve stimulator provides substantial relief.

Vagus nerve stimulation is a procedure that sends electrical impulses into your brain in an effort to improve depression symptoms. Sometimes called vagal nerve stimulation, vagus nerve stimulation is one of a few newer brain-stimulation methods designed to treat chronic depression when other treatments haven't worked. There's one vagus nerve on each side of your body. Each nerve runs from your brainstem through your neck and down to your chest and abdomen. With vagus nerve stimulation, a device called a pulse generator is surgically implanted in your chest. A wire threaded under your skin connects the pulse generator to the left vagus nerve in your neck. The pulse generator sends out electrical signals along the vagus nerve to your brain. These signals affect mood centers of your brain, which may improve depression symptoms.

Why it's done

By Mayo Clinic staff

Vagus nerve stimulation

Antidepressant medications, psychological counseling (psychotherapy) or electroconvulsive therapy (ECT) can improve depression in most people. But everyone's different, and for some people these standard depression treatments don't work very well. In such cases, vagus nerve stimulation may be added to standard treatments to help relieve symptoms. When vagus nerve stimulation may be a good option The Food and Drug Administration (FDA) has approved vagus nerve stimulation for people who: Are adults (age 18 or older) Have chronic, hard-to-treat depression (treatment-resistant depression) Haven't improved after trying four or more medications or electroconvulsive therapy (ECT), or both Continue standard depression treatments along with vagus nerve stimulation Vagus nerve stimulation doesn't always relieve depression Vagus nerve stimulation has been used for treatment-resistant epilepsy for over a decade and is known to produce good results. The benefits for depression aren't so clear.

The possibility that vagus nerve stimulation might work to treat depression was identified when it was being studied in people with epilepsy. Researchers noticed that some people who were getting vagus nerve stimulation had an improved mood. This led to further studies, which have produced mixed results. For most people, vagus nerve stimulation doesn't significantly ease depression symptoms. However, it does seem to make a significant difference for some people. However, results vary from person to person. Some mental health experts don't recommend its use for depression at all, and most health insurance companies don't cover the procedure for depression treatment. This can be a concern, as the vagus nerve stimulation device and surgery to implant it is expensive.

Risks
By Mayo Clinic staff For most people, vagus nerve stimulation is safe. But it does have some risks, both from the surgery to implant the device and from the brain stimulation. Surgery risks Surgical complications with vagus nerve stimulation are rare and are similar to the dangers of having other types of surgery. They include: Pain where the cut (incision) is made to implant the device Infection Damage to the vagus nerve Breathing problems Nausea Heart problems Incision scarring Vocal cord paralysis, which is usually temporary in some people it has been caused by fiddling with the transmitter under the skin after implantation Side effects after surgery Some of the side effects and health problems associated with vagus nerve stimulation can include:

Voice changes (this occurs in over half the people who have the procedure) Hoarseness Throat pain Cough Tingling Neck pain Chest pain or spasms Breathing problems, especially during exercise Difficulty swallowing Tingling or prickling of the skin For most people, side effects are tolerable. They may improve over time, but some side effects may be bothersome for as long as you use vagus nerve stimulation. Adjusting the electrical impulses can help minimize these effects. If side effects are intolerable, the device can be shut off temporarily or permanently. Other complications In some cases, complications of vagus nerve stimulation can include:

Pulse generator malfunction or movement, which may require additional surgery Worsening of depression Suicidal thoughts or behavior

How you prepare

By Mayo Clinic staff Because vagus nerve stimulation is a relatively new depression treatment, carefully consider the pros and cons before using it. It's not known precisely how stimulation of the vagus nerve may improve depression. The long-term effects of vagus nerve stimulation are still being studied, and not all side effects may be known yet.

Make sure you know what all of your other treatment choices are and that you and your doctor both feel that vagus nerve stimulation is the best option for you. Ask your doctor exactly what you should expect during surgery and after the pulse generator is in place. Before surgery, your doctor will do a physical examination. You may need blood tests or other tests to make sure you don't have any health concerns that might be a problem. Your doctor will have you start taking antibiotics before surgery to prevent infection. You may need to stop taking certain medications ahead of time, and your doctor may ask you not to eat the night before the procedure. When you set up your surgery appointment, make sure you're clear on exactly what steps you need to take.

What you can expect

By Mayo Clinic staff During the surgery Surgery to implant the vagus nerve stimulation device is done either on an outpatient basis, allowing you go to home that same day, or on an inpatient basis, requiring an overnight stay in the hospital. The surgery usually takes one to two hours. You may remain awake but have medication to numb the surgery area (local anesthesia) or you may be unconscious during the surgery (general anesthesia). The surgery itself doesn't involve your brain. The pulse generator is implanted in the upper left side of your chest. The device is meant to be a permanent implant, but it can be removed if necessary. The pulse generator is about the size of a stopwatch and runs on battery power. A lead wire is connected to the pulse generator. The lead wire is guided under your skin from your chest up to your neck, where it's attached to the left vagus nerve through a second incision. After the procedure The pulse generator is turned on during a visit to your doctor's office a few weeks after surgery. Then it can be programmed to deliver electrical impulses to the vagus nerve at various durations, frequencies and currents. Vagus nerve stimulation usually starts at a low level and is gradually increased, depending on your symptoms and side effects. Stimulation typically lasts for 30 seconds and occurs every five minutes. You may have some tingling sensations or slight pain in your neck during episodes of nerve stimulation. You'll be given a hand-held magnetic device so that you can control the stimulation yourself. This enables you to temporarily turn off the vagus nerve stimulation, which may be necessary when you do activities such as public speaking, singing or exercising, or when you're eating if you have swallowing problems.

You must visit your doctor periodically to make sure that the pulse generator is working correctly and that it hasn't shifted out of position.

What are late signs of increased intracranial pressure?

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Cushing's triad: increased intracranial pressure, hypertension, bradycardia or tachycardia (bradycardia is late sign). Cushing's triad is a late sign. Do not assume the brain is OK if you do not see hypertension & bradycardia.