Multi-Chemical Sensitivities and CFS

Discussion in 'Fibromyalgia Main Forum' started by fairydust39, Feb 17, 2005.

  1. fairydust39

    fairydust39 New Member

    I found this to be good info. Hugs Shirley
    Brain Injury CFIDS and MCS

    The following is a transcript from a presentation given by Dr. Jay Seastrunk at the 1997 CFIDS Awareness Conference held at Saddleback Hospital in Laguna Hills, CA, June 1, 1997.

    Dr. Jay Seastrunk is a Psychiatrist who used to practice in the state of Texas and had one satellite office in Southern California. He no longer is in private practice.

    He has determined that many of those afflicted with CFS can attribute their illness to focal brain injury

    Dr. Seastrunk began by stating he has seen about 400 folks with CFS and Multiple Chemical Sensitivities (MCS). The majority of the people he had seen had history of head trauma. About 2 million people experience head trauma and 25% require hospitalization. Whiplash can also cause focal brain injury. Focal brain injury can be inherited and is the cause of non-traumatic brain injury such as hypoxia (insufficient oxygen to the brain) and hypoglycemia (insufficient sugar). Frontal lobes are most commonly injured. In CFS, in the least, is left frontal lobe brain injury. In MCS, it can be in multiple areas. Vascular disease, toxic conditions, substance abuse, infections (mycoplasma incognitus, Herpes, chlamydia pneumonia), high fevers, MS, Alzheimer's, ALS, tumors, and/or brain malformations can all be associated with brain focal dysfunction.

    Usual testing includes the use of Magnetic Resonance Imaging (MRI). Most of the time MRIs are normal. The patients will need better tests; Functional MRI (FMRI) measures blood flow; Magnetic Resonance Spectroscopy (MRS) used to identify chemicals in the brain; PET scanning; and Computerized EEGs. Most of the time regular EEGs are interpreted as being normal, so the patient will need the better EEG.

    If the MRI shows abnormality, it will show atrophy and injury, primarily in the frontal lobes, but also in the posterior temporal parietal and occipital lobe locations. Bilateral circumlinear atrophy in the frontal temporal lobe and frontal parietal lobe tips. Also, deep white matter focal hyper-intensities on T2 weighted MRIs.

    These are the kinds of things you see in micro-vascular injury and MS. MS can generally be differentiated from micro-vascular injury with using MRS.

    By placing the magnet of the MRS on certain areas of the brain and through the use of special computer software, graphs of the chemicals present in that area will be displayed. Chemicals such as lactate will become elevated with immune dysfunction. N-acetyl-asparite (NAA), a marker of neuronal presence. Dr. Seastrunk described a patient, a physician, who has a severe case of CFIDS and showed his MRS. He had an area of tuberous sclerosis, left frontal lobe had a marked increase in choline and glutathione peak, glutamic acid, frequently seen in people with CFS. Left frontal lobe is worse but right frontal lobe can also have damage but not as bad. Often, nerve endings from the left frontal lobe will cross over and report to the right frontal lobe.

    Liver proton MRS is often used along with brain MRS to help in identifying if toxic issues are important. Abnormal liver spectroscopy in an individual with Multiple Chemical Sensitivities indicated a marked increase in glutamine (as a toxic by-product) and also had a high choline peak (associated with tumor, in this case a thyroid tumor). Liver proton MRS of a person with CFS indicated a lot of noise because the liver is hardened and shows a marked decrease of water necessary to give a good picture. In this CFS profile, there is a marked increase in choline peak (patient also had a tumor) and an increase in fatty acids.

    MRS usually has creatine as a standard but with CFIDS, creatine cannot be used as a standard because it is markedly abnormal in CFS/MCS/FM patients. With Single Photon Emission Computerized Topography (SPECT), decrease in blood flow and function in the left frontal lobe can be measured.

    Why does brain injury become a factor years later? CFS is not a psychological illness but is physical with psychological overlays such as stress. Brain dysfunction is associated with abnormal behavior. Dr. Seastrunk developed a questionnaire, called the organic evaluator, for his patients that includes questions involving abnormal olfactory hallucinations (smells and tastes that aren't there); visual distortions (colors, spots, sparkles in outer portion of visual field which he said indicates the temporal lobe is injured); oscillopsia (vibration or oscillation of visual field); unable to understand when people are talking to you (left temporal lobe dysfunction); wrong word is used during conversation or go blank in the middle of the sentence; auditory hallucinations (hear noises, clicks, or someone calling your name while the television is on or while taking a shower or using a hair dryer); dizziness (temporal lobe dysfunction); and gastrointestinal dysfunction. 95% of the CFS/MCS patients who take Dr. Seastrunk's questionnaire have demonstrable brain pathology.

    Autonomic dysfunction such as abnormal feelings of hot, cold or itch is also seen in CFS/MCS patients. Assuming menopausal symptoms, many doctors will prescribe Estrogen for this but it will often make it worse because it sets off brain injury. Progesterone will make it better.

    Cognitive dysfunction is a right temporal lobe phenomena. Multiple mood swings, trouble sleeping are all temporal lobe abnormalities.

    Temporal lobe is responsible for understanding what we hear, retrieving and restoring our memories even though the patient may feel they have difficulty with their memory. The problem is actually the retrieval of this information. The card catalog is there but the CFS/MCS/FM patient can't find the right word. Not being able to find the word or forgetting what you are going to do, or blocking, is a left temporal lobe phenomena.

    30% of people with panic disorder have focal brain injury as a cause, according to Dr. Seastrunk's tests.

    Deja Vu, the feeling of having been there before, is a temporal phenomena. Jamais Vu, the feeling of being lost while driving your usual way home, is also a temporal lobe phenomena (the temporal lobe has misfired).

    Migraine or migraine equivalents may also be a result of brain injury.

    Kindling is when exposure to small amounts of chemicals or toxic exposure can cause the brain injury to fire. In 1949, Pope described the Mirror Focus Phenomena. In animals and man you can produce an epileptic focus on one side by producing an injury. Within a period of time, an identical firing will occur in the exact same location in the other hemisphere. When the original injury is stopped the mirrored injury will continue to fire even though it is not injured. In 1969, Goddard named it kindling, where a permanent change in brain function resulting from daily electrical stimulation will occur subliminally after repeated exposures. Repeated applications of irritants or stimulation, either chemical or electrical, to a particular brain area will eventually produce abnormal firings or seizure, even though each stimulation by itself is incapable of producing the firing. A stimulus to the brain, if repeated over and over, can produce significant changes in both behavior and electrical activity. The repeated stimulus is called a chronic irritant and the result and effect is called a kindling response.

    In following Vietnam vets with head injury, it took 15 years for psychosis to develop.

    Smell can become a trigger mechanism to set off a brain injury. The limbic system organizes information into understandable categories whether sensory, imaginative, autonomic, etc. The limbic system can trigger emotions, memories, and behaviors. Researchers of epilepsy have long known that the olfactory limbic system is particularly vulnerable to kindling. But this also can apply to non-seizure behavior. Cognitive thinking, autonomic nervous system response, vestibular response, and emotional responses are all connected and can be affected by a single intense exposure, trauma, or injury. You can get cross sensitization so that when one chemical begins to fire you become sensitive to all of them or most of them.

    Dr. Seastrunk contradicted some of the statements Dr. Vojdani stated earlier. He stated that chemicals trigger the nerve cells in the nose that go into the brain and begin this firing process which activates the focal brain injury. Detoxification is not needed because the chemicals are not actually inside the brain unless gross evidence suggests mercury in the brain.

    Once a person experiences a brain injury, subsequent brain injuries are likely to occur.

    Women are more sensitive to smells and thus makes them more predetermined to have smells be a triggering mechanism for their focal brain injury.

    Stress activates seizures and focal brain injury. Sleep deprivation activates focal brain injury. Dr. Seastrunk believes that immunity is secondary to the brain dysfunction. Corticotropin releasing hormone is controlled by the brain and tells the adrenals what to do.

    Decreasing stress is helpful in decreasing the effects of the illness. His experience is that after treatment for three months of the focal brain injury, the immune mechanism is normalized. Treat the brain, you don't have to treat the immune system. The brain will correct the immune system on its own. CFS symptoms are a manifestation of the brain injury and brain dysfunction. Continued exposure of individuals without appropriate intervention is sure to increase the symptoms and debilitation in the affected person.

    The cornerstone for treatment is the anticonvulsant Neurontin (gabapentin). It is a pure amino acid that people thought would act like GABA, an inhibitory neurotransmitter. It doesn't. Neurontin was developed by the Japanese as an anti-spasmodic. It was sold to Parke-Davis who discovered its anti-epileptic properties. In the trials, the dosage used was too low so that they only got efficacy as an adjunct to other anti-convulsant. They are in the process in doing studies with it as a single agent. Commonly used in the US today as a single agent with a dosages ranging from 3,000 to 6,000 mg/day with many people taking as high as 9,000-10,000 mg. It is not toxic.

    Dr. Seastrunk has never seen anybody allergic to Neurontin. The chemical structure of Neurontin is almost identical to that of L-Leucine, a necessary amino acid the body needs to have. The body has a mechanism to absorb Neurontin very readily into the blood through the L-Leucine transport system and then from the blood into the brain. But Neurontin is lost very quickly as well, that is the problem. It is not metabolized in the body, it is not protein bound, there are no cross reactions with other medicines, there are no toxic level, it is very safe. [One of the reasons that it works so well for MCS patients is that] it treats chronic glutamate toxicity by inhibiting branch chain amino acid transferase. It is transferred by the system L amino acid, the L-Leucine transport system, to the blood in the brain. It enhances the breakdown of the toxic product of glutamic acid by decreasing glutamic acid decarboxylytes.

    Neurontin has its own receptor in the central nervous system, however it is blocked by magnesium. Do not take magnesium while taking Neurontin. Neurontin is water soluble and it is easily absorbed with food.

    Bioavailability is 51-59%, in low doses, peak is 1-3 hours. Half-life is 3 hours when first started but after steady state (stabilized round the clock dosing) is 5-7 hours. Steady state is reached in 2 days.

    Side effects tend to occur when you first start the medicine but are gone in 2 weeks. Symptoms include dizziness, drunk feeling, drowsiness, sleepy, ataxia and fluid retention. You can offset fluid retention with a diuretic.

    People with poor kidney function require less Neurontin. People on renal dialysis will reach therapeutic levels with 200-400 mg/day.

    When Neurontin is started its half-life is very short. Dr. Seastrunk uses about 12 different dosage schedules. If a person is scared of taking medications, they will start at 100mg every three hours, and take 200 mg at bedtime. Neurontin must be taken first thing in the morning and right when you go to bed because the blood level drops overnight. Once at a stable dose, he will have them take more at bedtime and more the first thing in the morning to maintain blood level. Basically, Dr. Seastrunk likes to get the patient to 3200mg daily at a minimum as quickly as possible. Some people start at 400 mg at night and increase 400 mg every day. Others start at 400 mg three times a day and increase by 400 mg each day until they are on 800 mg four times a day. Once on 3200 mg for two days, blood level is checked to see how much is getting in the bloodstream. There is no therapeutic level established for Neurontin. He looks for blood levels to come back at 8-18. Experts feel that therapeutic level may be around 40. Benefit increases linearly up to 3,200 mg and then it levels off and little improvement is seen beyond 6,000 mg. Benefit is correlated by how much one takes. If you take too much you will feel drunk. Usually, doses are increased every 2-3 days as they're getting the patient on the drug. Maximum dose, based on blood level and symptoms, typically ranges from 3,600 - 4,200 mg/day. It will take two years to get effect.

    Some people get migraines or migraine equivalents while taking Neurontin. If so, they will increase the Neurontin to see if it stops (sometimes this works). If not, they treat with Depakote (an anticonvulsant) which has a labeled use for migraines (1,500 to 2,000 mg/day). If this doesn't work they go to Parlodel (2.5 mg before meals).

    A certain portion have this illness show improvement with Neurontin but they continue to have sickness. These people are having something that continues to injure their brain. This could be mycoplasma incognitus (fermantens), chlamydia pneumonia, [Lyme Disease, or one or more of the Herpes viruses) organisms that gets into the lining of the blood vessels. This could explain the blood flow problems seen in the MRS. Fifteen to twenty percent of his 400 patients treated are in complete remission and are back to normal. Some have been bed-bound for 17-19 years. Eighty percent of the people achieve significant improvement. They aren't completely well but they continue to improve. Improvement will start to show-up within three months. Ten percent have not shown improvement. Quitting Neurontin can be done by backing off 400 mg each day or by taking another anticonvulsant.

    Other treatments for brain injury include serotonin reuptake inhibitors (SSRIs), Norepinephrine reuptake inhibitor, dopamine (Parlodel) for apathy. First step is Neurontin. Effexor, an antidepressant, SSRI and Norepinephrine inhibitor, is also used quite frequently if the patient can tolerate the drug. The problem is only 40% of the individuals can tolerate taking Effexor, others cannot handle the increase in Norepinephrine. If you can tolerate it, it is a wonderful drug and it fine tunes the cognitive focusing and increases energy level. It has fewer side effects and less P450 cross reactions than the other SSRIs. Typical dose of Effexor is 75-225mg/day. The PDR states that Effexor can increase blood pressure but this won't happen until you exceed 225 mg/day. Even so, it is recommended the patients have their blood pressure checked periodically.

    The next best treatment is Zoloft. Zoloft does have some P450 cross reactions but they are 20 times less than Prozac and Paxil. Typical dose for Zoloft is 100-150 mg/day. The recommended treatment for sleep aid is Trazadone (Desyrel). Recommended dosage is 25-50 mg/night, half-life is 3 hours, no hangover in the morning. If you like an antihistamine, Doxepin (Sinequan), a tricyclic antidepressant, is recommended at 25-50 mg/night. Doxepin is a powerful antihistamine, 1 mg = 200 mg Benadryl. The benzodiazepines, such as Xanax, are not recommended because they are habit forming. If you really need one of the benzos, Klonopin is probably the one to choose.

    A problem with Zoloft and Effexor is that they can cause sexual dysfunction. Frequently, approximately 50% of the time, treat the sexual dysfunction with one morning 75 mg dose of Wellbutrin. Wellbutrin., on its own, works in a different way from the other SSRIs [by also being a dopamine reuptake inhibitor] and is not as good as the other SSRIs but it does help some.

    Parlodel, a dopamine agonist, is used in treating Parkinson's disease. A dopamine agonist means that it works like dopamine, fires the dopamine receptor, but it isn't dopamine. Dopamine is one of our very important neurotransmitters and is the one which is lacking in Parkinson's disease, and it is metabolized to Norepinephrine. Dopamine will help with apathy due to brain injury and it will provide an energy boost.

    Neurontin is expensive; average cost for 3200 mg/day will run about $400/month. However, if you make less than $16,000/year as an individual or $25,000/year as couple, and you do not have a drug card or state insurance, the company will provide any amount of Neurontin for $3/month. If you don't have insurance, the company will provide any amount of Neurontin for ~$138/month regardless of your income.

    Dr. Seastrunk could not find anyone (including Parke-Davis) to fund a study for CFS because it is such a controversial entity. They may have a chance with multi-centers to perform a study in the future.

    Transcript reedited by Marilyn K. 7/10/01