Frontal Temporal Dementia - FTD - Formerly Orthomolecular Schizophrenia Protocol

FTD Information Links

2009-04-13T16:39:00.003-05:00

FTD Genetics: http://www.ftd-picks.org/?p=learnmore.genetics

Genetic Defects for some cases of FTD: PGRN, MAPT: http://www.ftd-picks.org/?p=research/200608_ResearchAdvance

Patient Update March 26, 2009

2009-03-26T13:11:00.004-05:00

This will be a brief update to be followed by more detail soon.

Patient is recovering on a ventilator for more than 90 days now. Recently began using eyes. After the 1st 40 days of Patient being on anticonvulsants, they were discontinued at the request of the Family because the progress had not changed. At day 80 (approx.) Patient was said to not be responding (no brain activity) when tested while still (mistakenly) prescribed anti-convulsants during a recent week long hospital visit. But in the weeks before and after the anticonvulsants there are signs of progress. It was the opinion of the ICU neurologist that anticonvulsants were required despite no seizures EVER being recorded or witnessed while Patient is lying in bed. What impact has this had on the recovery of the Patient. We can prove it caused SEVERELY delayed recovery, which for many families in this situation, would have convinced your family members to listen to doctors and to turn off the machines. more to come....

Patient Update December 23, 2008

2008-12-23T04:47:00.003-05:00

Patient was taken to hospital December 16 by ambulance. Six resuscitations were performed in a time period of about 40 minutes. Patient is now stable breathing assisted. Acute cause: seizure followed by aspiration, seizure, respiratory distress, heart failure. Swallowing difficulty and saliva were becoming factors in the two weeks leading up to this event.

Family is pleading with researchers working on discoveries in Frontal Temporal Dementia to contact us with a comment and your contact information and we will moderate the comment (all posts are first moderated) and not post the contact info to the blog.

Valproate is being administered by iv.

Current Diagnosis - FTD

2008-11-21T14:18:00.007-05:00

The most recent diagnosis made is FTD ( aka fronto-temporal lobe dementia).
The details of this disease appear to explain Patient's symptoms over the past years. A key determining factor involves the age range of people with this disease. Patient's age falls into the category, which is why Patient cannot be diagnosed with the more common/general type of dementia (which strikes those of an older age group).
The drugs prescribed when beginning symptoms unfolded, are commonly prescribed for people diagnosed with this illness.

The disease has reached an advanced stage which involves weight loss, difficulty walking, carrying on conversation, and poor memory and cognitive abilities, excessive saliva perhaps due to poor swallowing function.
We are still open to forms of treatment for possible improvement of functioning ability.
It is not clear what caused this illness, however there is some speculation that it was a result of inflammation that was not caught/diagnosed sooner.
Patient's mother had some form of dementia.

Patient is no longer taking Lamictal, Zyprexa or any of the drugs in this category because the side effects were overwhelming difficult to deal with. Doctors informed us that this could potentially happen.
Patient recently started using Exelon, a small patch daily for memory.

Seizure Frequency and Diet

2008-09-23T15:08:00.004-05:00

The following excerpt can be found at this site:
http://dogtorj.tripod.com/id21.html

"In addition to successfully managing the epileptic, the dietary solution provides insight into the wide variety of presentations of this elusive condition. For instance, the typical age of onset in the dog ranges from six months to six years. If this is simply a genetic defect of some sort, why does that first seizure occur over such a wide range of ages? Also, why is it often a progressive condition in the afflicted individual, beginning with milder seizures and longer intervals but changing into more violent attacks that are closer together? This suggests that the cause of the seizures is getting worse over time, doesnt it? The idea that there is a lessening of the epileptics ability to handle the glutamate by a progressive deficiency in the reductase enzymes just makes sense. As the glue-induced malabsorption in the gut worsens, the individuals ability to process the rising glutamate in the brain becomes impaired by the dropping reductase levels. This explains both the variance in age of onset and the shrinking intervals between seizures. In addition, the attacks get more violent, especially once we institute anticonvulsant therapy thereby allowing the levels of glutamate to reach more toxic levels."

Gluten Intolerance? Celiacs?

2008-09-22T09:46:00.004-05:00

"I am currently off of all seizure & pain meds & doing GREAT!

When I went low gluten (only the hidden trace sources) I stopped having seizures. I am walking w/o even a cane. Sleeping in regular bed now w/ lots of pillows"

Read this post by cybermommy/Deb on the following website:

http://www.glutenfreeforum.com/index.php?showtopic=32311

2008-09-22T09:17:00.006-05:00

"Neurological conditions eg. multiple sclerosis, motor neurone disease,epilepsy, memory loss.

--Associated with Gluten

Diagnosis of Gluten intolerance in elderly patients is disproportionately high. This is because it is misdiagnosed and under-diagnosed by doctors. Some Gluten intolerance is identified in children.
But for others, it is not until much later in life that Gluten intolerance is actually suspected.

Frequently it is triggered by some life event like divorce, job loss or serious illness.

The symptoms of both Non-Celiac Gluten Sensitivity (NCGS) and Celiac Disease (CD) become worse with age if left undiagnosed.

Many people suffer from headaches, mouth ulcers, weight gain or weight loss, poor immunity to disease, and skin problems like dermatitis and eczema.

But the common and well-known Gluten intolerance symptoms are gastro-intestinal (diarrhoea, flatulence, bloating etc.)

However sufferers improve dramatically within weeks on a Gluten-free diet.

After a few weeks on a gluten-free diet, newly diagnosed Gluten sensitive people find they are free of a raft of other symptoms as well which for years had compromised their lifestyle: flatulence, abdominal cramps, tiredness and their tendency to catch ‘bugs’ and viruses easily.

It is surprising how quickly the small intestine actually heals. Soon you will begin to absorb nutrients from food more effectively. The digestive tract gets back to doing its job normally and you will start feeling well again."

information taken from: http://www.foodintol.com/celiac.asp

Naturopathic Body Scan

2008-07-11T11:46:00.003-05:00

Patient will be undergoing a Naturopathic body scan within the next 10 days by a Naturopathic Doctor to see if results reveal any new/compelling information that is helpful in determining the cause of Patient's problems.

Medication Frustration

2008-07-09T12:33:00.004-05:00

Here is a recap of what we've seen so far with two medications.

10mg of Zyprexa + 150mg Lamical twice daily = The worst combination so far -- INCREASED physical problems (the worst/really bad--bent over to the ground, pain), INCREASED hallucinations/psychosis. This was the treatment upon leaving early June hospital visit. It was also discovered that Patient was administered HALDOL (dosage not released) during the hospital visit!! This is very upsetting to the family and we know that Patient was in really bad shape upon returning home from the hospital.

7mg of Zyprexa + 150 Lamictal twice daily = Major Dehydration, INCREASED physical problems, INCREASED psychosis.

5mg of Zyprexa + 100mg Lamictal twice daily = REDUCED physical problems, REDUCED hallucinations, INCREASED fainting/seizures.

5mg of Zyprexa + 125mg Lamictal twice daily = INCREASED physical problems, INCREASED paranoia. REDUCED fainting/seizures. (The current prescribed treatment)

75mg of Lamictal twice daily = some relief with back pain, suicidal thoughts, loss of appetite

35mg of Lamictal twice daily = loss of appetite, suicidal thoughts

In sum, Patient is not getting enough relief and there appear to be too many problems. This raises questions as to whether or not Patient should even be taking these drugs. And how much damage has been caused by these drugs?

Questions of concern:
Why does a drug for psychosis increase psychosis for Patient (Zyprexa) when the dosage is increased?

Why does a drug for seizures increase psychosis for Patient when it is increased?

Why are physical problems expected to reduce when Lamictal dosage is raised but physical problems and psychosis increase?

Why are Doctors recommending Zyprexa if there are serious warnings for those taking it that could be suffering from dementia?
Anyone who does a search on Zyprexa will see that " Zyprexa is not for use in psychotic conditions that are related to dementia." If Patient was given a suspected dementia diagnosis based on symptoms, shouldn't Patient go off of this drug, regardless of the dosage? Seems like even just a little (5mg) should be considered too much if there are any doubts about this drug related to Patient's condition. This is very disturbing.

Are seizures happening because of the overuse of anti psychotic medications?

Is patient experiencing drug-induced Parkinson's symptoms?

What if Patient goes off of Lamictal & Zyprexa for a length of time (return to baseline) and is evaluated and treated for nutritional deficiencies/problems using vitamin therapy?

Important findings of B-12

2008-07-08T12:34:00.003-05:00

Vitamin B12:
Vital Nutrient for Good Health

By Sally Fallon and Mary G. Enig, PhD

"Vitamin B12 works with folic acid in many body processes including synthesis of DNA, red blood cells and the insulation sheath (the myelin sheath) that surrounds nerve cells and facilitates the conduction of signals in the nervous system. Severe depletion manifests as pernicious anemia, which was invariably fatal until the discovery of B12 in liver. But long before anemia sets in, other conditions may manifest, most often neurological problems (numbness, pins and needles sensations, a burning feeling in the feet, shaking, muscle fatigue, sleep disorders, memory loss, irrational anger, impaired mental function and Alzheimer’s) or psychological conditions (dementia, depression, psychosis and obsessive-compulsive behavior).

"Because the absorption process is so complicated, and therefore subject to various blocks, many people--particularly the elderly--may develop deficiencies even though they are taking in plentiful B12 in their food. Fortunately, the body absorbs about 1-5 percent of free B12 by a process of passive diffusion. Thus supplementation with large doses of crystalline B12 or with foods extremely rich in B12 can successfully treat deficiencies caused by compromised protein digestion or lack of R-protein, intrinsic factor or pancreatic enzymes. Supplementation with the coenzyme forms methylcobalamin and adenosylcobalamin (the forms found in the cells) can overcome B12 deficiency in the cells caused by lack of, or malfunction of, conversion enzymes.

B12 is found almost exclusively in animal foods such as liver, kidney, meat, fish, shellfish, milk products and eggs but the original source of B12 in nature is bacteria, the only creatures able to manufacture this vitamin. In humans and animals, these bacteria produce B12 in the colon; however, little if any is absorbed across the colon wall so we must get our B12 from animal foods. Bivalves such as clams, mussels and oysters contain high levels of B12 because they siphon large quantities of vitamin B12-synthesizing microorganisms from the sea.³ Production of B12 supplements involves fermentation procedures similar to those used for penicillin and other antibiotics.

[Patient has a known allergy to penicillin]

"A surprising source of cobamides is bacterial overgrowth in the small intestines, which can produce B12 analogs.¹³ The use of antibiotics, or a diet high in refined carbohydrates, can encourage the proliferation of bacterial overgrowth and lead to B12 deficiencies.

"Yet another area for concern is multivitamin products! The late Victor Herbert, a noted B12 researcher, maintains that many multivitamin products contain spurious and even dangerous analogs of B12 possibly formed when crystalline B12 interacts with other nutrients in multivitamin products, such as vitamin C, iron and copper.¹⁴

"High levels of folic acid can accelerate neuropsychiatric complications in persons with B12 deficiency.¹⁵Since folic acid intakes of vegetarians tend to be high (from green vegetables and from grain products that have been fortified with folic acid), those following a vegetarian lifestyle may be at increased risk of neurological and psychological problems.

"The body stores considerable B12 in the liver. Thus a delay of 5-10 years may separate the beginning of a vegetarian diet (or absorption problems) and the onset of deficiency symptoms. Interestingly, the body can recycle over 75 percent of the B12 it uses.¹⁶ Used B12 is excreted in bile and then reabsorbed in the small intestine by the same complex process described earlier. Some people have a more efficient recycling system than others and hence can go longer on a vegetarian diet without signs of deficiency. However, more B12 is excreted in the presence of high levels of fiber, a common feature of vegetarian diets.¹⁷

MEASURING B₁₂ DEFICIENCY

"American medical opinion defines blood levels lower than 200 pg/mL as an indication of deficiency. This number is based on the level associated with the most severe manifestation of deficiency, pernicious anemia. In contrast, the lower limit in Japan and some European countries is 500-550 pg/mL, the levels associated with psychological and behavioral manifestations such as dementia and memory loss. Physicians in these countries consider blood levels of 500-1300 to be the normal range.¹⁹

"According to Dr. John Dommisse, an expert in B12 deficiency, the acceptance of high levels as normal in Japan, and the willingness to readily treat psychiatric symptoms with B12 explains the low rates of Alzheimer’s dementia in that country--as well as the reason for the very high rates of Alzheimer’s in the US.²⁰

"Even with the very low cutoff currently considered the risk point, large numbers of Americans are deficient. In the ongoing Framingham Offspring Study, involving 3000 men and women in the town of Framingham, Massachusetts, researchers found that 39 percent had B12 levels in the so-called "low normal" range, that is below 258.²¹ Had the researchers chosen the optimal range of 1100-1300 as a measure of B12 status, very few would have qualified as B12 replete.

"One of the most surprising findings of this study was the fact that the youngest group (26 to 49 years old) had about the same B12 status as the oldest group (65 and up), an indication that deficiencies are becoming more common.

SYMPTOMS OF AGING

"B12 deficiency mimics many of the features of old age--ataxia (shaky movements and unsteady gait) muscle weakness, spasticity, incontinence, slowed reactions, memory loss, disorientation, depression and confusion can all occur when B12 levels are low.

"Whether or not Alzheimer’s disease constitutes a condition of B12 deficiency is the subject of considerable debate among physicians. A recent and fascinating study of a family in Wales provides convincing evidence that low levels of B12 and Alzheimer’s are linked.²²

"Research shows tremendous potential for B12 to reverse mental decline in elderly patients. In one study, 61 percent of patients with mental impairment had complete recovery with supplementation; investigators speculate that those that did not recover had suffered from deficiency so long that damage to the nervous system had become irreversible.²⁴²⁵ Thus, routine early testing for B12 has the potential to prevent mental decline in the vast proportion of the elderly. By the time Alzheimer’s is conclusively diagnosed, it may be too late for supplementation to be effective. Supplementation results in little improvement for those who have had full blown Alzheimer’s symptoms for greater than six months.

NERVOUS DISORDERS

"One condition that would seem obviously correlated with B12 deficiency is multiple sclerosis (MS), a disease characterized by demyelination of the central nervous system. Yet many studies indicate that those with MS have normal blood levels of the vitamin. Japanese researchers have found that in MS patients, there is a decrease in the binding capacity of B12, thus inhibiting the transport of B12 into the cells, even in patients with normal levels in their blood.³³ Even so, they were able to achieve some improvement with high-dose supplementation.

"The benefit of B12 for depression may be due to B12’s ability to activate a substance called tetrahydrobiopterin (BH4), a compound which in turn helps activate "feel good" neurotransmitters like serotonin and dopamine.³⁴
Surprisingly, B12 has also proven successful in treating diabetic neuropathy, possibly because the condition of diabetes deranges B12 metabolism.³⁵

"Recurrent seizures may be a manifestation of B12 deficiency. One study found that individuals who suffered from seizures had low B12 levels.³⁶

Other neurological problems associated with B12 deficiency include urinary incontinence³⁷ and migraine headaches.³⁸ In one case history, B12 worked better than steroids as a treatment for Bell’s palsy.³⁹ Another case study reports that shaky leg syndrome responds well to B12 injections.⁴⁰

AN EXCEPTION TO OUR RULE

"In these pages, we have consistently advised obtaining vitamins from food (including superfoods) rather than with vitamin supplements. One good reason to avoid supplements derives from research indicating that they can interfere with B12 uptake, exacerbate the symptoms of B12 deficiency or even cause the creation of B12 analogs that increase the body’s need for B12.

"However, when it comes to B12 itself, supplementation with isolated B12 is often necessary and appropriate. The many factors in our modern lifestlye that block the complicated uptake pathways of this important nutrient--from nutrient deficiencies to exposure to toxins to factors in processed foods that cause reduced stomach acid, autoimmune disease and enzyme disruption--make it difficult to obtain sufficient quantities from our normal diet; and since vitamin B12 in supplements is produced in exactly the same way as B12 in nature, that is, by bacterial fermentation, the danger of high doses in most cases is negligible.

The authors wish to acknowledge the contribution of Lee Clifford, MS, CCN, for providing her extensive files on vitamin B12.

http://www.westonaprice.org/basicnutrition/vitaminb12.html

2008-07-07T11:17:00.001-05:00

We need to revisit the blog post that was dated 11/20/07 and explore it further.

Current Diagnosis.

2008-07-07T10:09:00.004-05:00

Patient has been given two diagnosis - one by the Neurologists, the other by the Psychiatrists: Temporal Seizure vs. Frontotemporal Dementia. However, it is important to note that even though Patient's symptoms were classified as frontotemporal dementia, there is no enlargement of the frontal temporal, which is commonly associated with this dementia. This raises the question of whether or not Patient truly has that disease, or the symptoms brought on as a result of the medication.
Also, it is important to note that Patient did not experience current type of seizures prior to going on psychiatric medications.

Perhaps testing and evaluation performed by a holistic doctor would be worth considering at this point and that some damage could be reversed.

Notes for followup

2008-07-04T17:09:00.000-05:00

http://en.wikipedia.org/wiki/Ketogenic_diet

http://addspouse.proboards29.com/index.cgi?board=comorbid&action=display&thread=760

http://www.dr-bob.org/babble/20070719/msgs/772724.html

Patient Overview

2008-07-03T17:30:00.010-05:00

A recap of Patient's history is highly beneficial/crucial at this point.

Around the time patient was turning 50 years old, patient tried to communicate to daughter that a problem in the brain was occurring, yet little explanation or details were given about what exactly was happening. Patient mentioned something about issues involving confusion or other supposed cognitive issues, yet there appeared to be no concern or cause of alarm from the family. No symptoms were visible from members of the family. Patient was convinced of having cancer, yet no confirmed reports ever surfaced from doctors. Patient appeared to have some sort of psychosis related theory.

At age 53 Patient experienced a blow to the head after being struck by a steel parking lot gate. No hospital visit occurred - patient did not lose consciousness.

Patient did experience at age 56 some depressing feelings when daughter moved away and got married.

Patient received positive mood lifts from taking DHEA, however use was discontinued due to hair loss.

A few years went by and then patient began to show signs of paranoia that family misunderstood to be a relationship conflict pertaining to a family member. Then, hallucinations, delusions and disturbing paranoia all began to surface and become very stressful for Patient and noticeable by family members. When evaluated by a doctor, Patient was given medication for supposed depression. The drug, Celexa was prescribed but it did not reduce patients paranoia, rather it sent Patient into a heightened, very paranoid state.

Celexa was halted and then switched to a different medication (an anti-psychotic).

Patient experienced continued paranoia and hallucinations while on Abilify.

On Respirdal, Patient's cognitive functioning was significantly reduced along with diminished personality. Patient also suffered from Tardive like symptoms, in which Patient's eyes would continuously close/want to stay closed involuntarily. This occurred within days of taking the drug. It was then halted due to these alarming/disturbing side effects.

Patient also tried Seroquel, which also produced negative side effects.
When seizures were suspected, Patient tried Tegredol and Keppra. Patient had a serious reaction to Keprra, which involved increased anger and paranoia.

In looking back on everything the past few years, one of the most crucial factors to point out is that as soon as Patient began treatment with psychiatric drugs as well as anti-seizure drugs, PATIENT HAS SLOWLY DECLINED IN MANY AREAS. PERSONALITY HAS DIMINISHED, THINKING ABILITY, RATIONALIZING, REMEMBERING DETAILS -- HAVE ALL BECAME A STRUGGLE. PATIENT'S HALLUCINATIONS AND DELUSIONS HAVE NOT GONE AWAY. Patient became less involved in social activities and has in the past 6 months suffered physical symptoms and episodes that the Family has never before witnessed in Patient.

Patient has not improved but clearly is struggling from something that is affecting the ability to live a normal life. Those who know Patient well can see that Patient is not the normal self they once knew.

Some friends have even described Patient to appear to be in a "drugged like state."
Patient is aware of some of the problems that are occurring with speaking, getting up, walking, pain side effects, etc and is very discouraged. At times the Patient's personality does seem to surface with moments of laughing and emotion expressed. Yet Patient has suffered so many physical symptoms it has interfered with many daily activities.

While on Zyprexa and Lamictal Patient has experienced decline in energy, fainting episodes, dehydration, dizziness, sleep disturbances, trouble carrying on conversations, troubles with word finding, memory disturbances, delusions, hallucinations (some related to smell). back pain, leg pain, weight gain.

When physical problems related to getting out of a chair or bed began to surface, family members noted that Patient could get up with no help if a motivation had occurred like the phone ringing. However, if Patient was sitting and then decided to get up, Patient would have difficulty initiating that act and gaining the muscle strength to rise out of a chair. In the past couple of months, Patient has needed more and more help getting out of a chair or bed regardless of a stimulant/outside motivation present.

At this point it is hard to know whether or not the physical problems and night time issues are due to an undiagnosed disease or condition, or a result of being medicated by the WRONG drugs. Patient has suffered MORE BURDENSOME/NEGATIVE side effects than one should undergo for drugs that should be providing relief from a suspected problem/illness.

Since patient's psychiatric symptoms did not significantly improve on medication, there appears to be no clear behavioral illness or psychiatric illness. From a common sense standpoint, if psychiatric illness was the main health problem, drugs should have done a much better job of correcting Patient's symptoms, especially after undergoing treatment with several types of psychiatric drugs. Also, medical professional has indicated that behavioral illness onset is rare for Patient's age group.

Regardless of what the real problem is, the Family has witnessed a gradual decline.

We can say with assurance that Patient was significantly altered once Anti-psychotic medications were introduced for treatment and has not returned to normal self -- the self that Patient's family remembers.

Members of the family still suspect that there could be an allergy, or chemical imbalance/deficiency that could have produced the initial symptoms of paranoia a few years back. Patient has suffered stomach/gastrointestinal upset on a regular basis for many years.
Perhaps there is a link that to this day, has still not been identified.
Likewise, the Family is interested and open to the natural medicine approach, as it may provide a valuable/added evaluation that has not been considered by all of the doctors involved up to this point.

Patient has not been clearly diagnosed, yet the journey continues and the family has not given up on finding the right treatment for Patient.

Currently, patient is being evaluated and tested again for seizures.

Patient Update

2008-07-03T17:15:00.003-05:00

Since being released from the last hospital stay in early June, patient has been experiencing on-going physical problems that make it difficult to get out of bed or out of a chair without assistance. Patient has experienced frequent sleep walking episodes throughout the night in which patient has difficulty moving around without falling/passing out. Patient grumples/groans during these episodes. Cannot recall these episodes the next morning.

Upon leaving the hospital, Patient was prescribed a higher dosage of Zyprexa (10mg) and 150mg of Lamictal, whereas patient was previously taking 7mg and 150mg respectively (no increase). Patient had severe problems walking around and complained of pain in the legs. Could not stand up straight without discomfort. Hallucinations and delusions had not improved. Upon hearing of this, the doctor decreased the medication down to 5mg Zyprexa and 100mg Lamictal. Psychiatric doctor believes patient has been suffering from a temporal lobe problem and has suspected seizures to be a culprit, therefore has prescribed these medications.

Since being reduced to 5mg, the problems with walking decreased. The degree of hallucinations and delusions reduced as well but did not completely go away. Fainting spells started to occur more often. Patient experienced 4 episodes in one day. Patient has been unable to sleep throughout the night for months.

Patient Update June 21 2008

2008-06-21T11:27:00.003-05:00

Received report that Patient experienced 4 drop attacks a day after beginning DHEA, RALA and ZINC. Two of the drops occurred without the Patient's knowledge. In the preceeding year, drop attacks have not been experienced prior to starting supplements. Recommended DHEA be withheld and followup discussion Saturday evening on progress. Patient is on dose of 100mg Lamictal and 5mg dose of Zyprexa daily. Patient was on unknown dose of furosemide since stay in hospital and has discontinued use. Flurosemide was prescribed because of severe ankle swelling at the time of the recent event leading to the hospitalization.

Pfeiffer Treatment Center, Warrenville, Illinois

2008-06-14T15:00:00.004-05:00

The Pfeiffer Treatment Center was recommended by a reader.

"The Pfeiffer Treatment Center is a not-for-profit medical research and treatment facility in Warrenville, Illinois specializing in research and treatment of biochemical imbalances."

"PTC takes a unique, integrative approach to identify and treat the root metabolic causes of these symptoms with a multi-disciplinary clinical team involving physicians, nurses, dietitians, pharmacists and other clinical specialists."

Patient Update June 14 2008

2008-06-14T14:12:00.003-05:00

One year on Lamictal. Patient was hospitalized for a week for an event that was classified as severe dehydration. The medication was not being managed by the family, but by the Patient. Upon release from hospital, the family requested the dose being reduced to 100mg daily and an effort to wean Patient off of Lamictal. Family also requested dose reduced for Zyprexa to 5mg. Patient's condition after a year on these two drugs can be characterized as "drug suppressed" and not making any progress towards improving condition. Drugs controlled Patient's bad symptoms (paranoia and mania) while also robbing patient of experiences of joy in life. Patient is not getting quality sleep, may be sleep walking now, was seen urinating in corner of bedroom at 3AM, and walking around without eyes open. Beginning course of low histamine treatment based on past experience with not responding well to SAMe. Asked family to provide the Patient DHEA, ZINC and R-ALA for the next week.

"Histamine Metabolism"

2008-06-14T12:54:00.004-05:00

Histamine Metabolism

What is histamine and why is it so important? Carl Pfeiffer studied more than 20,000 people with schizophrenia and determined that 90% of them fell into three bio-chemical subgroups: high histamine, low histamine, and pyrroluria - hence the term “The Schizophrenias” (Pfeiffer, 1970; Walsh, 1997b). Histamine is a reflection of neurotransmitter availability. Histamine is integral in balancing the electrical activity of the nucleus accumbens, which is an area of the brain responsible for behavioral responses, filtering incoming sensory information, and communicating with the hypothalamus, ventral tegmentum, and amygdala (Shoblock & O’Donnell, 2000; Otake & Nakamura, 2000; Chronister et al, 1982). A plethora of research has determined that people with schizophrenia have poor ability to filter incoming sensory information. It has also been reported that 15-20 % of people with schizophrenia have high whole blood histamine levels and another 30-40 % of people with schizophrenia have low whole blood histamine levels (Heleniak, 1999; Pfeiffer, 1988; Heleniak, 1985; Chronister & DeFrance, 1982; Rauscher et al, 1977; Pfeiffer, 1972a).

A person with schizophrenia who has high histamine is under-methylated (Walsh, PTC- Ref. B; Heleniak & Frechen, 1989). A person with schizophrenia who has low histamine is over-methylated (Walsh, PTC- Ref. B; Heleniak & Frechen, 1989). Taking detailed patient histories is key (Jackson et al, 1998; Edelman, 1996; Jaffe & Kruesi, 1992; Pfeiffer, 1988; Walsh, PTC - Ref B). People with high histamine have been found with typical symptoms of high intelligence, thought blanking, low grade hallucinations, and thought disorder, perfectionism, competititiveness, obsessions, compulsions, suicidal and seasonal depression, defiance, and phobia.

High histamine individuals are inherently high in folic acid. Although folic acid is used along with B-12 in the production of methoionline it is also involved in histamine production along with B-12. Consequently B-12 and folic acid are strictly avoided in high histamine patient care. These patients need to avoid multi-vitamins.

People with low histamine have been found with typical symptoms of under-achievement, more severe thought disorder and hallucinations, paranoid thoughts with less pronounced obsessions, suicidal depression, cyclic or suicidal depression, and anxiety. (Jackson et al, 1998; Edelman, 1996; Jaffe & Kruesi, 1992; Walsh, PTC - Ref. B).

Excess copper and zinc defiiciency, discussed below under heavy-metal overload, are typical low histamine traits that need to be addressed (Sandstead, 1994; Wallwork, 1987; Pfeiffer & Braverman, 1982; Walsh, PTC - Ref. B)

Metal Imbalance

Metal imbalance is associated with schizophrenia, behavior disorders (including ADHD), and hormonal depression (Walsh, PTC- Ref.C).

Copper excess causes brain dopamine levels to rise in low histamine schizophrenia. “Copper poisoning with zinc deficiency will explain the present dopamine theory of simplistic schizophrenia since this condition occurs only in one-half of patients labeled schizophrenic”, that is, in low histamine schizophrenia (Pfeiffer, 1987b). Paranoia is also associated with elevated copper (Pfeiffer & Iliev; Walsh, 1997b). Copper oxidizes catecholamines such as dopamine and therefore propagates neurotoxin formation (compare "Niacin Section" above). Zinc imbalance is associated with central nervous system disorders such as schizophrenia and autism and several other pathologies (Walsh & Usman, 2001a; Ebadi, 1995; Walsh, PTC- Ref. C).

Some nutrients help remove heavy metals but environmental exposure must be addressed. This includes restrictions on diet and the elimination of environmental factors such as copper tea pots, copper sulphate (jacuzzi or swimming pool water), bad drinking water, prenatal vitamins, copper IUD’s, etc. (Walsh, PTC- Ref.B). Drugs such as neuroleptics, antibiotics, antacids, cortisone, tagamet, zantac, diuretics, and birth control pills, etc. may exacerbate copper overload. (1)

Vitamin B3 Test results

2007-12-27T23:23:00.000-05:00

Patient has received test results back from primary care doctor showing that patient is extremely deficient in vitamin B3 (Niacin). Since hearing the news, patient is back on Niacin supplements. Deficiency may be explanation behind behavioral symptoms, weakness, bowel problems, forgetfulness and insomnia. We are waiting for the results from the other mineral & metals that were evaluated.

Patient Update Nov 23, 2007

2007-11-26T14:58:00.000-05:00

A full week before admittance to the Epilepsy center at Henry Ford hospital, the Patient decided to discontinue prescribed 150mg of Lamictal -- only taking half and stopped taking Zyprexa. After the hospital visit, the doctors encouraged Patient to go back to taking the full 150mg dosage for seizure prevention. However, within a few days of taking ONLY Lamictal as prescribed, profound negative effects became obvious in Patient. Patient was struggling to maintain any type of focus: appeared to be in a total fog. Cognitive ability was extremely compromised. Patient was in constant motion wither going to sit or going to lay down, could not get comfortable, making 6 trips per hour to lay down. Patient could not understand easy questions and was feeling nausea, poor appetite, profound weakness being unable to get up from sitting position without assistance, poor posture, standing in place staring for extended periods of up to 10 minutes. It was so bad we were almost going to take patient to the hospital. On Nov. 21 Patient resumed taking Zyprexa prescribed dose and stopped Lamictal. Within 24 hours, Patient regained muscle strength, cognitive ability returned, nausea absent, appetite normal, 90% of excess sitting and standing absent. @48 hours emotions improved, cognitive speed improved, posture improved.

We should request Patient see a cardiologist for the orthostatic hypotension, and determine if current Psychiatrist can refer her to one. We have an appointment for Patient's B 12 levels and Thyroid to be tested. We would like to know Patient's histamine, copper, methylation, homocystene levels to specifically find vitamin deficiency and behavior subtyping. (There's a hospital outside of Chicago that treats patients based on these results).

We would like to know if there are any other specialized doctors that can be recommended for further testing or evaluation for underlying medical issue.

vitamin B12 deficiency

2007-11-20T16:02:00.005-05:00

We are curious if there could be an underly medical condition with
dementia-like symptoms such as vitamin B12 deficiency.
(Patient's symptoms appear in bold font below. Symptoms are either
current or experienced at one point or another)

Neuropsychiatric Manifestations of Vitamin [B.sub.12] Deficiency:
Peripheral nervous system involvement.
Symmetric peripheral neuropathy, beginning with
symmetric parasthesias of the lower extremities,
can ascend to eventually involve the upper extremities;

hyporeflexia may be present; occasionally autonomic
neuropathy occurs, which can present as orthostatic hypotension.

Spinal cord involvement.
Dorsal column involvement: loss of position and vibration sense,
ataxia,  broad-based gait, and, occasionally, Lhermitte's sign.
Lateral column involvement: weakness and spasticity
(spastic paraparesis), urinary and fecal incontinence,
impotence, hyperreflexia, clonus, and
Babinski reflex may be present.
Subacute combined degeneration.
Spinal cord involvement and peripheral neuropathy.
Visual impairment.
Retrobulbar neuritis, optic atrophy, and pseudotumor cerebri.

Psychiatric manifestations.
Dementia, hallucinations, 
frank ("megaloblastic madness"),
paranoia, depression, violent behavior, and 
change in personality

Above information taken from
http://findarticles.com/p/articles/mi_m0689/is_n6_v41/ai_17913640

2007-11-20T16:00:00.000-05:00

"Vitamin [B.sub.12] deficiency is thought to be a continuum with five stages.[9] These stages include: I, normality; II, negative vitamin [B.sub.12] balance; 111, vitamin [B.sub.12] depletion with possible clinical signs and symptoms (reversible neuropsychiatric findings); IV, vitamin [B.sub.12]-deficient erythropoiesis with possible clinical signs or symptoms (potentially reversible neuropsychologic symptoms); and V, vitamin [B.sub.12] deficiency anemia with probable clinical signs and symptoms, including irreversible lateral column involvement."
http://findarticles.com/p/articles/mi_m0689/is_n6_v41/ai_17913640

2007-11-20T15:54:00.001-05:00

http://www.postgradmed.com/issues/2001/07_01/dharmarajan.htm

Some updates & observations

2007-11-20T12:46:00.001-05:00

Patient and other members of the family admitted that Patient was dealing with orthostatic hypotension-like episodes several years back before Patient went on any psychiatric meds. Patient said thyroid testing in the past revealed over-active thyroid.
Patient is currently suffering from memory problems and cognitive impairment.
Patient scored low in neuropsychological testing taken in the epilepsy unit of the hospital by the neuro psychology department. Doctors evaluating patient recommended a complete neurological work-up. Suspects there could be dementia symptoms. Doctors also suspected there could be an issue with the autonomic nervous system, with regard to the orthostatic hypotension. Patient's heart beat is normal, no other heart irregularities found. Some of our research on dementia indicates patients struggling with dementia-like symptoms could actually be suffering from a vitamin B-12 deficiency.

"Because the symptoms are almost identical, many health problems are often mistaken for Alzheimers and other age related dementia. But, the problems causing the symptoms are usually treatable if detected early enough. Prescription drugs interactions and side effects, vitamin B12 deficiency and dehydration most commonly produce false symptoms of dementia. (According to Consumer Reports on Health, "Any new health problem in an older person should be considered drug induced until proven otherwise.")In other words, symptoms that some people (including many doctors) often dismiss as a "normal part of aging" — really aren't. "
http://www.aging-parents-and-elder-care.com/Pages/Age_Dementia_Next_Steps.html

The following tests should be administered:

The tests may involve some or all of the following, many of which are designed to rule out other possible causes for your loved one's problems:

An evaluation of memory and mental skills.
A physical exam, including a review of family medical history, to detect other medical problems, including possible interactions between prescription drugs, over-the-counter medications, herbal supplements, vitamins and/or mineral supplements. Many foods can also cause unexpected interactions with prescription medications.
A nutritional evaluation to determine if dietary problems or improper eating habits may be causing the problem.
Blood tests, including tests for vitamin B12 and folic acid deficiencies, thyroid hormone imbalances, anemia, etc.
EEG (electroencephalogram).
A neurological exam to rule out other disorders of the brain such as Parkinson's disease, hydrocephalus (fluid accumulation in the brain), prior strokes and mini-strokes, brain tumors, etc.
Brain Scan (CT or MRI).

Patient Update November 18, 2007

2007-11-18T16:50:00.000-05:00

ORTHOSTATIC HYPOTENSION was the only condition to come out of 8 days of tests at a Henry Ford Hospital epilepsy center. We have not had a full briefing from the doctors yet. Patient is returning home tomorrow. We are looking at information regarding blood pressure and blood supply to brain now.

Note that low blood pressure is a possible Zyprexa side effect - Patient has been off Zyprexa since a week before Hospital stay.

Entry: quote from "Amalgam Illness diagnosis and treatment" by Dr. Andrew Hall Cutler PhD PE

PAGE 159
"Methyl donors and compounds involved in methlyation metabolism help the liver transport fats, help with one part of phase 2 metabolism, and have other effects in the body - most notably antidepressant effects through increased brain serotonin."

... "Methylation both increases and controls histamine levels. Your body cannot make methyl groups - it needs to get them from your diet. SAMe, choline, TMG, folate and B12 all have similar effects via methyl metabolism, and lecithin, phosphatidylcholine and phosphatidylserine can sometimes also act as methyl donors in the brain."

links

http://www.latitudes.org/forums/lofiversion/index.php?t2056.html
http://www.diagnose-me.com/cond/C376825.html
http://www.diagnose-me.com/cond/C447056.html
http://www.ebiologynews.com/1523.html
http://www.ebiologynews.com/2754.html
http://health.yahoo.com/nervous-overview/drop-attack/healthwise--hw214611.html
http://www.alternativementalhealth.com/articles/walshQZ.htm
http://www.vitaminstuff.com/vitamin-b9-folic-acid.html
http://www.vitaminstuff.com/vitamin-b9-folic-acid-2.html

http://www.drugdigest.org/DD/DVH/HerbsSideEffects/0,3925,552122%7CLecithin,00.html

Hospital Visit

2007-11-14T10:09:00.000-05:00

Patient is undergoing a week long hospital visit in the hospital unit that specializes in the treatment and evaluation of seizures. Patient has stopped medication to return to baseline and is being monitored with medical equipment. Behavior is also being monitored as well. Current team of doctors are looking for possible causes of seizure and psychological symptoms.

Info on aspartame & seizures, psychiatric symptoms:
http://www.mpwhi.com/aspartame_and_psychiatric_disorders.htm
http://www.holisticmed.com/aspartame/adverse.txt

Patient Update October 11, 2007

2007-10-11T15:37:00.001-05:00

Many thanks to a reader for comments regarding the histamine levels method of determining the right vitamins and supplements. You can read the comments in the July 16 2007 post. Of interest to me now is the histamine levels and how our information should be split along those histamine levels. I am researching this now and have some links and notes to post here for our own reference later:

http://www.ionchannels.org/showabstract.php?pmid=2425593

http://www.ctds.info/5_13_magnesium.html

http://www.answers.com/topic/histamine?cat=health

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&list_uids=4336944&cmd=Retrieve&indexed=google

http://www.raysahelian.com/ps.html

The Patient began taking soy-phosphatidylserine again a week ago. There's info available which states it would "influence the release of histamine, glucose uptake in the brain" and "when both phosphatidylserine and calcium were added histamine secretion was remarkably stimulated, apparently through the effect of phosphatidylserine on calcium transport across the plasma membrane."

Patient Status: Positive improvement. Interest in religious activities greatly improved/normal and may indicate healing in condition. Trouble finding words occasionally but flow of thought and conversation improved.

Patient Update July 16 2007

2007-07-16T09:18:00.000-05:00

Patient spent the past week in hospital under supervison and all tests were renewed. Seroquel has been abondoned. Seizures had been increasing up to the time of hospitalization. Hallucinations are now treated with Zyprexa. Initial observations of Patient following release are much better mood and memory as well as the range of topics in conversation significantly improved.

Meal Medication & Dosage

Breakfast: Lamictal 150 mg (1) Pill

Lunch: (No Medication)

Dinner: Lamictal 150 mg (1) Pill

Bed Time: Zyprexa 7.5 mg (1) Pill

Important info about Zyprexa http://www.eff.org/legal/cases/zyprexa/

Patient Update May 23 2007

2007-05-23T08:32:00.000-05:00

Spoke with Patient at 9 AM. Thoughts were clear. Patient seemed excessively concerned about feelings or mood.

Patient Update May 22 2007

2007-05-23T08:12:00.000-05:00

Patient experienced confusion and drowsiness after a full day on increased dose of meds. (150mg Seroquel at 11PM, 100mg Lamictal 11AM & 5PM) Doctor was called. Patient spoke to Doctor. Decision was made to not change meds yet for a few days.

Patient fell with dizziness at about 1AM (a couple hours after evening meds.)

Patient Update May 17 2007

2007-05-18T08:33:00.000-05:00

Patient reported having hallucination again at about 3AM and woke up other family member a few times. This may occur as a result of having taken the drug at 4PM instead of bedtime by mistake. Patient reports today no known side effects from doubling dose of Lamictal.

We should mention that information is available which suggests that Seroquel can lower seizure thresholds and theres a possibility the Neurologist in consult with Psychiatrist prescribed Lamictal as a prevention.

Patient began using a spreadsheet with daily checklist for medications.

Patient Update May 16, 2007

2007-05-16T23:30:00.000-05:00

Patient begins double dose of Lamictal on May 17th which becomes 50mg at 11AM and 50mg at 5PM.

Had video conference with Patient for an hour this evening. We discussed how the Patient mistakely took the 100mg Seroquel at 4PM today May 16th and as a result fell asleep between 7-8PM and planned to go to sleep at 11PM for the night. Conversation started at 8PM by phone. We discussed a hallucination that was experienced at 3AM today. We also discussed the hallucination from 3 weeks ago that involved a police visit to the house and the trip to the hospital. It is the same concern for the family member which is being experienced. The hallucinations were being stated as factual events and no fear was associated with the memories of the events during the discussion.

It appears that at least the Psychiatrist has allowed for the possibility that seizure treatment could improve the outcome. Since our posts about Lamotrigine and requests for trials for the Patient largely went ignored up to this point, we are satisifed that the current Psychiatrist perhaps has some prior experience with this matter. During the first consult after release from the hospital the family requested Lamictal samples and this Psychiatrist agreed and provided them. It was just a few days later when the Neuorlogist who had, even as recently as the day before, been stating that seizures were not present, that all the symptoms we have previously posted in the blog were not seizures, the next day prescribed the anti-convulsant Lamictal (Lamotrigine.) And prescribed the increasing dose 25mg x 2, 50mg x 2, 75mg x 2 over the coming weeks. If you've been following the history of this blog up to this point, lets pause for a moment.... Ok, enough said.

Observations of the Patient's progress can be summarized as follows:
1. Clearer thought and speech as compared to Risperdol & Abilify.
2. No motor impediments yet noticed as compared to Risperdol & Abilify.
3. Sleep cycle appears healthy and day wake hours appear normal and longer than without medication.
4. expression of emotion returns.
5. thought disorder which previously occured daily after meals has become very infrequently very late at night near time of night dose of Serquel is due.
6. Patient feels clear thinking enough to drive a vehicle early in the day.
7. Patient has conversations by phone that go without any searching for words and feels this is significant progress.
8. Long conversations are now possible extending beyond an hour where before 5 minutes would have been the limit.
9. Optimism has increased regarding outlook, that we may find a solution and slow or stop the decline and not end up in the same condition as mother at the same age.
10. Patient recalls memories and brings them up in conversation instead of only being able to answer questions.
11. Patient askes fewer questions of family members and experiences less confusion and less thought disorder.
12. Patient experinces little worry where before worry would consume the entire day and be present with serious fears.
13. Patient no longer experienceing leg or muscle weakness.
14. Patient appears to be mentally less affected by blood sugar fluctuations around meal times.
15. Patient remarks being tired of changing drugs (referring to the side effects), and wants the current drugs to work.

Patient Update May 15, 2007

2007-05-15T10:33:00.000-05:00

Patient is taking 100 mg of Seroquel at bedtime and 25 mg of Lamictal at 11AM & again 5PM. Patient's psychosis appears to be less frequent.
Patient has initiated conversation more frequently and is able to 'small-talk'. Patient still struggles at times to express complete thoughts/sentences, but not as problematic as previously when at hospital on Atavan, Tegredol, Seroquel.

Both Neurologist and Psychiatrist have agreed that Patient should continue taking the Lamictal, we aren't certain what common conclusion they came to, just that they told Patient to take it instead of just taking Seroquel alone. Patient described having a feeling of a seizure coming on this past Saturday, however Patient said it did not manifest itself into a full seizure. Patient said a feeling/sensation originated in midsection but then wore off before escalating into anything further.

We were told that Seroquel was missed on Friday evening because Patient mistakenly thought it was taken at 4PM and didn't want to over do it at regular time. As a result, Thought disorder was experienced by 10 AM the following morning and significantly at 10PM that next day.

Patient has started to bring up topics related to patient's Christian faith and has expressed the importance of holding onto that faith and remembering it during Patient's struggles. Before, Patient almost seemed removed from this religious/spiritual aspect of Patient's life. The fact that Patient is returning to these thoughts is a sign of improvement. Also, Patient experiences a wider range of deeper emotion now. Patient also expresses care for the feelings of other family members.

Patient Update May 11, 2007

2007-05-11T23:00:00.000-05:00

Neuorolgist calls to prescribe anti-convulsant Lamictal and reports that current Psychiatrist was consulted.

Patient Update May 10, 2007

2007-05-10T22:00:00.000-05:00

Neurologist calls in AM to discuss diagnosis. Claims that seizures are not present (despite reporting seizure activity from 2nd EEG results in Nov 2006.)

Patient Update May 7, 2007

2007-05-07T22:44:00.000-05:00

Patient visits with new Psychiatrist. Seroquel dose is raised to 100mg before bed. During Dr. visit a family member requests Lamictal trial.

Dr. begins seziure discussions with Patient. It become clear at this point the seizure information is completely new information which was not provided by other doctors from the same hospital system with 3 previous EEG tests showing possible activity.

Lamictal is provided as 25mg AM and 25mg PM for two weeks.

Patient Update May 6, 2007

2007-05-06T21:00:00.000-05:00

Patient is still experiencing psychosis to the same degree of what it was before hospital visit. Fifty mg of Seroquel has been taken at bedtime since being released from the hospital. Psychosis symptoms were noticeable on Thursday evening, 3 days following release from hospital. Patient also communicated feelings of depression Thursday evening. Psychosis / thought disorders were continous throughout the day on Saturday and Sunday. Patient sees doctor May 7th for first consult after hospital release by Psychiatrist in same hospital system, once previously visited before the Keppra event. Patient has experienced headaches in the upper/back region of her skull. Auditory hallucinations have occurred since being home from the hospital.

Obervations are that the hospital medicines which were tested or tried are now worn off and Seroquel is the only medication being used at this point.

Time for a Specialist

2007-05-01T10:49:00.000-05:00

As a result of our in depth research coupled with our understanding of the Patient and medical history, we are dissatisfied and frustrated with the current situation and how the doctors have handled Patient. We feel as though the doctors have only scratched the surface and have shown little concern or desire to dig deeper and consider other angles.

Based on Patient's unique symptoms and poor response to medications prescribed up to this point, and nothing hopeful from Patient's doctors, we have reached a point of frustration. it appears we've exhausted our options locally with respect to finding a Physician with expertise in dealing with Patient's unique blend of symptoms. Considering the delicate nature of the situation with respect to potential damage occurring from taking wrong medications, we cannot afford to keep Patient on current medication for psychosis for long when we know Patient's seizures aren't being addressed and cognitive abilities are being strongly compromised by the current drug.

We need to find a doctor as soon as possible who can help transition Patient off of the risky medication currently being used for psychiatric treatment.
At this point we feel it would be beneficial to find a Specialist familiar with the connections between Neurology and Psychiatry. We are looking into brain doctors with experience dealing with people suffering from similar problems as Patient (those dealing with patients whose case has been passed back and forth between neurologist and psychiatrist). We will be in contact with the insurance company to determine if two doctors in consideration participate with Patient's insurance. Depending on results we may need to perform further research to find a few more Specialists that deal with seizure patients with psychosis. We are open to recommendations. Please comment with known name of doctor practicing in this field of medicine.

CRITICAL INFORMATION ABOUT SEIZURES WITH PSYCHOSIS SYMPTOMS AND RISK OF MIS-DIAGNOSIS:
http://www.psychiatrictimes.com/p950927.html

For Further Consideration

2007-05-01T00:30:00.000-05:00

In doing research, I found this information which may be beneficial. One patent was diagnosed with with CP TLE with evidence of bipolar disorder caused by TLE. This patient was given 2500mg of Depokote (aka Valproic acid) and 50mg of Seroquel. This patient claimed that after suffering affects of this disorder for 20 years, never felt better since treatment with these medications.

Refer to this article later with regards to how it deals with glutamate toxcicity:

http://www.nature.com/tpj/journal/v4/n5/abs/6500269a.html

Refer to this article regarding Valproic Acid:

http://en.wikipedia.org/wiki/Valproic_acid

Lamotrigine Info - Medication Candidate for seizure relief

2007-04-30T23:21:00.000-05:00

Lamotrigine Message boards-

http://www.bluelight.ru/vb/archive/index.php/t-208772.html

Patient Update

2007-04-30T22:21:00.000-05:00

April 30, 2007

Patient is now home following the 8 day hospital stay.
It is evident that the doctors have decided to focus their attention on treating our family member as a psychiatric patient by perscribing a neuroleptic medication, Seroquel to control psychosis even though patient's EEG results show seizure activity in the temporal lobe.

Doctors we have dealt with in psychiatric field have been quick to medicate the behaivoral symptoms. Seizures could be causing the psychosis, but the psychiatrists are not addressing that. Patient was given seizure medication during hospital stay but we suspect it was discontinued toward the middle of hospital stay.

Patient was not sent home with any seizure medication even though Patient has experienced distinct symptoms that mirror those of temporal lobe epilepsy, including overwhelming/intense emotion connected to episodes of psychosis experienced from time to time, in this case emotion has consistently been fear. Periods of depression and lack of motivation have been common in between episodes of fear/psychosis.

Instead of leaving hospital with seizure medication, patient left with neuroleptic medication. Neuroleptics are known to induce seizure activity.
Patient is currently experiencing extreme inability to carry on a conversation, difficulty processing information quickly, much trouble with articulating thoughts. Patient's symptoms from Seroquel are strikinly similar to ones experienced in previous use of Respirdal. Overall cognitive functioning has decreased significantly to a pathetic level. Patient's cognitive problems are worse with Seroquel.

The neurologist with EEG results has been unable to come up with a diagnosis. We suspect patient is suffering from temporal lobe epilepsy with psychosis appearing symptoms. We feel patient should be treated for seizures, not psychosis. Patient experienced seizures as an infant and suffered from a head injury within the past 10-15 years and complained of undisclosed symptoms following that. Patient recently experienced episodes of passing out, blacking out, minor shaking and episodes of dizziness and tingling. Patient's psychosis symptoms consistently involve intense feeling of fear in every episode with periods of depression, lack of motivation, lack of energy experienced in between. Patient has mentioned a sensation of motion rising up from midsection (evidence of aura/partial seizure). Patient has experienced smells and tastes that were out of the ordinary.

Patient Update April 26, 2007

2007-04-26T22:01:00.000-05:00

Prescribed meds update. This list was provided Thursday April 26 by the hospital. Most of this information is from the Wikipedia.

Ativan (Lorazepam) 1MG/6hrs possesses all five principal benzodiazepine actions (sedative/hypnotic, muscle relaxant, anxiolytic, amnestic and anticonvulsant), but to different extents. Lorazepam also has found use as an adjunct anti-nausea drug. Lorazepam is a potent drug and its unique pharmacological properties underlie both its drawbacks and its advantages. Lorazepam may be safer than many other benzodiazepines in patients with impaired liver function because it does not require hepatic oxidation, which means that, similar to oxazepam, it is less likely to
accumulate to an extent where it causes adverse reactions.[2] On regular use, lorazepam builds up to maximum serum levels after only 3 days and longer term use does not result in further accumulation. Similarly, on discontinuation of regular use, lorazepam serum levels become negligible after 3 days and undetectable after a week. Lorazepam is thought to bind more strongly to GABA receptors. Lorazepam is thus more predictable when used intravenously for status epilepticus, both in regard to its more prolonged anti-seizure effects and in less drug accumulation in the patient's body (causing prolonged sedation after effects), such as is seen when diazepam injections have needed to be repeated when their effects wore off. Lorazepam's inactive metabolite is another advantage over diazepam in this setting.

++Acute therapy of catatonic states either alone, or preferably together with haloperidol as lorazepam can have paradoxical effects). Long-term treatment of otherwise resistant forms of petit mal epilepsy. Short-term treatment of insomnia, particularly if associated with severe anxiety. Treatment of anxiety disorders (especially Panic Disorder)

--Benzodiazepines in general may sometimes unmask suicidal ideation in depressed patients (indirectly, through disinhibition or fear reduction, rather than through any known direct effect). Though relatively non-toxic, the concern is that benzodiazepines may inadvertently become facilitators of suicidal behaviour. Lorazepam should therefore not be prescribed alone in depression but only together with an appropriate antidepressant and at the minimal dose required. Long term therapy may lead to cognitive deficits, especially in the elderly, who may already be more prone to forgetfulness, but this is reversible after a period of discontinuation. The likelihood of abuse, dependence and withdrawal symptoms is thought to be substantially greater with lorazepam relative to other benzodiazepines because of its particular properties: (a) Lorazepam binds relatively strongly to the GABA receptor complex. (b) Lorazepam has a short serum half-life and its effects wear off quicker due to it having no active metabolite, in contrast to diazepam. (c) Lorazepam is highly potent, making even 0.5 mg a significant dose reduction. In the UK the smallest available tablet strength is 1 mg, accentuating this problem.

Addiction is not a unique problem to lorazepam but for the reasons given above lorazepam is best used short-term to minimise this risk. Coming off lorazepam is more realistically achieved by, first, gradually changing over to an equivalent dose of diazepam and, secondly, stabilizing the patient on diazepam before contemplating dose reductions. This stabilization period is important since lorazepam levels (and effects) fluctuate more than those of diazepam: anxiety symptoms are more noticeable when lorazepam wears off and symptom relief more drastic when taking another dose, which may reinforce psychological dependence. Diazepam is here best administered once daily to tackle this aspect of dependence. The dose is reduced gradually over a period of months or years, depending on prior dose and duration of use.

Seroquel (Quetiapine) 25MG/PM which acts antagonist on - D1 and D2 dopamine and 5-HT1A and 5-HT2 serotonin receptor. Also has an antagonistic effect on the histamine H1 receptor.

Quetiapine has the United States Food and Drug Administration (FDA) and international approvals for the treatment of schizophrenia, treatment as an adjunct to either Lithium or Divalproex, and acute mania in bipolar disorder. Additionally, in October 2006, Seroquel was approved by the FDA for the treatment of depressive episodes associated with Bipolar I (or Bipolar-II) Disorder.[1][2] Currently, Seroquel is the only agent approved for this indication—as a single agent monotherapy. It is also used off-label to treat other disorders, such as post-traumatic stress disorder, restless legs syndrome, autism, alcoholism, hallucinations in Parkinson's disease patients using ropinirole, Tourette syndrome,[3] and as a sedative for those with sleep disorders or anxiety disorders.

--may lower the seizure threshold,the development of diabetes, significant risk of development of the incurable neurological disorder tardive dyskinesia with any prolonged use. Constipation, headache, and mild weight gain. Less common side effects (less than 2% of patients) include: abnormal liver tests, dizziness, upset stomach, substantial weight gain, a stuffy nose, and increased paranoia. Of note is the somnolence/sedation that occurs with Seroquel - as this side effect is most pronounced within the first 7 days of treatment and decreases over time thereafter. There is a significant risk of development of the incurable neurological disorder tardive dyskinesia with any prolonged use of any neuroleptic drug. However, quetiapine is believed to be less likely to cause tardive dyskinesia[7][8] somewhat less often than typical antipsychotics based on the data sources which point to placebo-level incidence of extrapyramidal side effects (a claim that only Seroquel can make, based on current research). The rare, but life-threatening, neuroleptic malignant syndrome. Weight gain can be a problem for some patients using quetiapine, by causing the patient's appetite to persist even after meals. However, this effect may occur to a lesser degree compared to some other atypical antipsychotics such as olanzapine or clozapine. Like other atypical antipsychotics, there is some evidence suggesting a link to the development of diabetes, however this remains unclear and controversial.

Tegretol (Carbamazepine) 200MG/12hrs an anticonvulsant and mood stabilizing drug, used primarily in the treatment of epilepsy and bipolar disorder. It is also used to treat schizophrenia and trigeminal neuralgia.

Mechanism of action is relatively well understood. Voltage gated sodium channels are the molecular pores that allow brain cells (neurons) to generate action potentials, the electrical event that allows neurons to communicate over long distances. After the sodium channels open, to start the action potential, they inactivate, essentially closing the channel. Carbamazepine stabilizes the inactivated state of sodium channels, meaning that fewer sodium channels are available to open, making brain cells less excitable.

--drowsiness, motor-coordination impairment and/or upset stomach. cardiac arrythmias, blurry or double vision and/or the temporary or mild loss of blood cells or platelets. Underactivity of the thyroid gland may be provoked, so thyroid function tests are advisable every year or two. Small reductions in white cell count and serum sodium are common. reports of a bizarre auditory side effect, whereby patients perceive musical notes about a semitone lower than their actual pitch.

AND...

may aggravate juvenile myoclonic epilepsy, so it is important to mention any history of jerking, especially in the morning, before starting to take this drug.

Desyrel (Trazodone) 50MG/PM serotonin reuptake inhibitor and is also a 5-HT2 receptor antagonist.

--Episodes of complex partial seizures have been reported, possibility of discontinuation syndrome if the medication is stopped too quickly. Care must therefore be taken when coming off the medication, usually by a gradual process of tapering down the dose over a period of time. Elevated prolactin concentrations have been observed in patients taking trazodone. Skin rash, itching, edema, and, rarely, hemolytic anemia, methemoglobinemia, liver enzyme alterations, obstructive jaundice, leukocytoclastic vasculitis, purpuric maculopapular eruptions, photosensitivity and fever. Aching joints and muscles, peculiar taste, hypersalivation, chest pain, hematuria, red, tired and itchy eyes. Decrease and, more rarely, increase in libido, weight gain and loss, and rarely, menstrual irregularities, retrograde ejaculation and inhibition of ejaculation. Rare cases of idiosyncratic hepatotoxicity have been observed, possibly due to the formation of reactive metabolites. Nausea, vomiting, diarrhea, gastrointestinal discomfort, anorexia, increased appetite. Orthostatic hypotension, hypertension, tachycardia, palpitations, shortness of breath, apnea, syncope, arrhythmias, prolonged P-R interval, atrial fibrillation, bradycardia, ventricular ectopic activity (including ventricular tachycardia), myocardial infarction and cardiac arrest. Dry mouth, blurred vision, priapism, diplopia, miosis, nasal congestion, constipation, sweating, urinary retention, increased urinary frequency and incontinence. Drowsiness, fatigue, lethargy, psychomotor retardation, lightheadedness, dizziness, difficulty in concentration, confusion, sex drive increases.

OH, it gets better...

Tremor, headache, ataxia, akathisia, muscle stiffness, slurred speech, slowed speech, vertigo, tinnitus, tingling of extremities, paresthesia, weakness, complex partial seizures, and, rarely impaired speech, muscle twitching, numbness, dystonia and involuntary movements. Death by deliberate or accidental overdosage has been reported. There is no specific antidote for Trazodone.

thoughts...

We plan to contact the insurance company to discuss seeing a specialist which may actually cost them less than the current path. We have one lined up. Also, a discussion with the current assigned Dr. regarding why we are diagnosed Psychosis NOS when we have identified Drop Attacts, Seizures, Declining IQ that these neuroleptics are likely to further worsen the condition. And why Lamotrigine was not tested first when it is indicated for all the symptoms. Patient was visited today by sw/gwh at 7PM and was clearly in an Abilify-like state.
Patient experiencing emotion, but poor energy, poor social interaction, heavily druged. We suspect a new drug was introduced in the past 24 hours or began to take effect. Patient was responding much better the previous day via phone conversation and more in touch with feelings.

--gjh

Patient Update April 22, 2007

2007-04-22T20:09:00.000-05:00

Patient spent 4 days in hospital as a result of calling police to the home for poisoning. Police realized this was 5th time visiting residence for psychosis. We had asked Patient to return to neurologist for checkup EEG and possible alternative meds for seizure. Patient was failing to make appointment. At this point I am livid. Here's why...

Dr. (original neurologist) had nothing to go on - although aware of seizures, no diagnosis. Had another EEG taken.

The Patient was delivered psych hospital last night at 11:00PM involuntary status.

The egotistical Dr. calls into question our desire to be involved with monitoring the quality of the Patient's care and does not comment on the faxed study or questions about prescribing Lamotrigine - ignored.

It now appears that a social worker at the hospital and a dr. at the psych hospital were involved in the transfer. Damaging meds are prescribed that took the patient three months to recover from. The family has provided the psych hospital system this warning - to HALT RISPERDAL IMMEDIATELY. They claim to have not seen the fax the next day. Three days later during a visit a member of the family sees the fax in a binder a RN is flipping through. Hmmm.

RN calls SW and says following this evening:

*Patient signed info release on paper to allow family status info.

*Patient is prescribed the following meds:

*Ativan (like Valium) anti-anxiety

*Tegretol (carbamazepine) Tegretol is an antiepileptic drug. Types of seizures treated with Tegretol include: grand mal, focal, psychomotor and mixed (seizures that include complex partial or grand mal seizures). Absence seizures (petit mal) do not respond to Tegretol.

*unknown antibiotic

*Risperdal at bed time! - caused Patients tardive and syptoms which included:
hallucinations audio and visual
had no dynamic conversation
had severe dizziness
had poor balance
had severely slowed motor movement
had severe tardive symptoms, eyes felt clamped shut, arms protruding in front of body
had no personality
had inability to discern emotion and social cues
had trouble making sentences
never started conversation
had inability to keep her eyes open
had nausea
and considering patients taking Risperdal are 50% risk for Diabetes - the family is demanding immediate halt of Risperdal. If the goal is to heal Patient, it must be stopped.

AND Patient presently being held involuntarily. Now ask yourself what happens to "second opinion"

-edited Friday 27th with updates
--gjh

DHEA, Melatonin, Seizures

2007-02-24T03:05:00.000-05:00

I'm returning to the DHEA topic. Patient has taken a two week break from DHEA after taking for a couple months. One problem Patient has battled with lately is not having a regular sleep schedule, despite continuing Melatonin. Patient has typically been very tired around 7-8PM and gone to bed only to wake up at 1-2am.

While looking at possibilities to get the schedule under control I have decided to give DHEA a shot at it. Will request Patient take DHEA 2.5mg in late afternoon. Idea being that Patient will get a small burst of energy/activity boost to carry into evening hours for a target 10-11pm sleep time. Six to seven PM has also been typically when Patient has delusional thoughts so I want to see how DHEA affects this time of day.

I suggest you read the following links for a better understanding of the role of these hormones within the body.

"...It is this rebound response that is the large area of stimulated nerves
that cause the seizures. Once the brain has stimulated sufficient DHEA, then the seizure stops." (1)

(1) http://www.bio.net/bionet/mm/neur-sci/2000-April/043570.html

http://www.bio.net/bionet/mm/neur-sci/2000-April/043570.html

http://www.bio.net/hypermail/neuroscience/1998-January/030264.html

I've updated the protocol on right side of page with info about max levels of DHEA. I should add that it is estimated that males levels naturally are 10-15 mg daily, female levels are up to 20% less than male levels. Upregulation does not occur when DHEA is taken orally, so do not exceed the natural levels. Why on earth would anyone take 25, 50, 100mg ???

--gjh

Phosphatidylserine (PS)

2007-02-15T11:00:00.000-05:00

I found an excellent brief on Phosphatidylserine located at the link below. I did not find anything to suggest it would increase seizure activity, so I may introduce it for its list of benefits.

"PS is a fat-soluble nutrient and would be expected to require at least several days' dosing to build up in the nerve cell membranes." "PS appears in the blood at about 30 minutes. After a few more minutes uptake begins into the liver and, later, the brain." "Given orally, PS is rapidly absorbed and readily crosses the blood-brain barrier to reach the brain. There, its sites of action appear to be exclusively in cell membrane." "Structurally, PS protected the hippocampus (a major memory center) from the loss of dendrite connections that normally occurs with aging (see Nunzi et al, 1987)." "Nunzi and co-workers (1992) found that in the rat hippocampus, a fall-off in nerve growth factor receptor density occurs with aging. PS reversed this receptor density decline and seemed to enhance NGF production." "PS given to these athletes prior to starting exercise produced an impressive degree of down-regulation of the stress hormones"(1)

Regarding dosing: "A reasonable supplementation strategy with PS is to begin at 300 mg per day with meals for a month, then go into a maintenance mode at a lower level of intake (100 to 200 mg daily). There is no indication of potential problems from long-term supplementation with PS."(1)

"As a general rule, because PS is so safe the more severe the subject's problems the more aggressive can be the supplementation strategy. Patients with severe memory problems can be kept on all their other supplements and medications, and be given PS with their meals at 300 to 500 mg per day on an ongoing basis. Subjects afflicted with motor problems may respond better at 500 mg per day. Mood problems may require a starting dose of 400 mg per day. For age-related cognitive decline (ARCD), a daily intake of 300 mg may be appropriate. "(1)

(1) "Phosphatidylserine, A Remarkable Brain Cell Nutrient"
http://www.springboard4health.com/books_online/ps/phosphatidylserine.html

--gjh

Patient Update February 9, 2007

2007-02-09T21:10:00.000-05:00

Patient has not followed supplement protocol over the period of past week and reports from family about paranoia and psychosis have been relayed. Work schedule and vacation interferes with daily updates. I decided daily updates will not be necessary for blog at this time.

Had conversation with Patient about options: supplements or drugs. Since I am not seeing a significant reverse of paranoia or psychosis or memory deficit baseline behavior without heavy supplementation, I am ready to test a drug.

Based on the findings of the PRODH deficiency study, I have faxed a 24 page document to the Neurologist requesting a review and comment on the study as well as recommendation for a test period of Lamotrigine (drug.) I provided the study and info from wikipedia about the drug which I had been searching for over the past few weeks since finding the study details.

Here's my Letter to the Doctor:

I am providing information for your review and comment regarding prescribing Lamotrigine for Patient (blank). I have been keeping a blog (web journal http://orthosz.blogspot.com) of research and daily progress for Patient. Based on the findings of a study and what I have learned by controlling diet and supplements and monitoring daily, I would like to have you review the attached information for comment and possible prescription to target the regulation of glutamate. The findings of the study essentially report the following:

1. glutamate toxicity factor - loss of PRODH gene function directly causes hyperactivity of nerves that use glutamate to signal other nerves.
2. dopamine toxicity factor - loss of PRODH gene function causes upregulation of COMT gene responsible for encoding the enzyme that breaks down dopamine.
3. upregulation of COMT gene is not possible in patients with 22q11 microdeletion which causes toxic buildup of dopamine {and psychosis/paranoa in Patient.}
4. PRODH deficiency increases release of glutamate at synapses in hippocampus and inhibits LTP, important step in forming memories.
5. Lack of glutamate regulation due to loss of PRODH contributes to learning difficulties.

Over the period of time since our last visit I have learned that the supplement L-Theanine (apparently) has a direct boost effect on Dopamine and for this Patient, caused paranoia and psychosis. We have known for a long time that excess sugar in the diet has also triggered the psychosis and paranoia, just not as quickly as Theanine (a green tea extract.)

Lamotrigine would target the glutamate regulation, help to control the seizures, and control the drop attacks. I am hopeful that it may prevent the chain reaction of Dopamine toxicity as well. If the glutamate release at hippocampal neurons is presently toxic, this drug may help improve the memory which at is a steady, slow deficit currently.

Patient's mother suffered from seizures that eventually robbed her of memory. Patient has been experiencing daily morning dizziness. I am aware that for many people seizures occur in the twilight sleep just as they begin to wake up. We have used a GABA enhancing supplement called Kavinace (Phenibut, Taurine) which eliminated seizures and dizziness during the day. However, this is smoke and mirrors if what is broken has to do with regulating glutamate. Even with morning and evening doses of Kavinace we did not prevent the morning dizziness that occurred when first getting out of bed-possibly a partial seizure.

end of Letter

Patient Excitotoxins

2007-01-19T17:11:00.000-05:00

This post (incomplete-to be updated) serves as a reminder for family meal planning, Patient supplement, environmental and diet NO-NOs:

_________BAD__________________________
Dopamine boosters

L-Theanine, Green Tea

Nicotine

_________BAD__________________________
Glutamate boosters

MSG - monosodium L-glutamate, (Seen as ingredient NATURAL FLAVORS in processed foods) Hydrolyzed Protein Sodium Caseinate or Calcium Caseinate, Autolyzed Yeast or Yeast Extract, Gelatin, Hydrolyzed Oat Flour

aspartame (nutrasweet),
candy, glutamic acid, glutamine, aspartate, and cysteine.
Mercury and aluminum trigger glutamate release.

hypoglycemia, or low calorie/starvation conditions stimulate release of glutamate and reduce the ability to remove excess levels of glutamate from the brain. Excess glutamate reduces glutathione levels - antioxidants found in the body which protect neurons from damage. Reduced Glutatione leads to the death of additional neurons.

Food Item	Free Glutamic (mg/100g)	Free Aspartic (mg/100g)
Tomato	140.0	35.0
Fresh tomato juice	260.0	60.0
Processed tomato juice	230.0	60.0
Grapefruit, white meat	11.5	87.1
Grapefruit juice	18.6	130.0
Orange juice	21.0	89.0
Nectarine, fruit	9.0	200.0
Peach juice	32.0	212.0
Plum, yellow fruit	7.9	185.0
Prunes (California)	14.4	185.5
Prunes, dry	18.6	518.4
Grape, red Malaga	184.0	12
Grape juice	258.0	16.8
Strawberry	44.4	60.1
Potato	102.0	-
Broccoli	176.0	40.0
Parmesan Cheese	1,200.0	-
Gruyere Cheese	1,050.0	60.0
Mushroom (Psalliota campestris)	180.0	30.0

(1.)

Food Item	Bound Glutamate (mg/100g)
Parmesan Cheese	9,847
Eggs	1,583
Chicken	3,309
Duck	3,636
Beef	2,846
Pork	2,325
Cod	2,101
Mackerel	2,382
Salmon	2,216
Peas	5,583
Corn	1,765

(1.)

Food Item	Glutamate (mg/g N)	Aspartate (mg/g N)
Potato	639	775
Sweet Potato	541	825
Beet	946	1,131
Apple	700	1,300
Apricot	372	1,300
Avocado	769	1,413
Banana	575	656
Fig	600	1,500
Orange	760	880
Pear	540	2,800
Strawberry	920	1,400

(1.)

(1.) http://www.autismanswer.com/articles/yasko/approach_to_reversing.html

--gjh

PRODH Deficiency

2007-01-18T00:26:00.000-05:00

Patient had extra 100mg of L-Theanine today and within 90 minutes had elevated paranoia and panic. I've read that L-Theanine increases dopamine levels. Now when you read this genetic explanation, this entire blog/Patient history seems to parallel the information in the article.

The link below may be the genetic explanation for what may be happening with this Patient. The description of problematic neurotransmitters and the cause of the imbalance of glutamate and dopamine seems to match our findings with foods, supplements, drugs and behaviors of Patient history.

(1.) http://www.innovations-report.com/html/reports/life_sciences/report-52499.html

"Disruption of gene interaction linked to schizophrenia

Results of studies with laboratory model of PRODH deficiency demonstrate the role of COMT in compensating for overactive dopamine signaling, according to St. Jude

Disruption of the normal interaction between the genes PRODH and COMT contributes directly to major symptoms of schizophrenia by upsetting the balance of the brain chemicals glutamate and dopamine, according to a group of investigators that includes a scientist now at St. Jude Children’s Research Hospital.

The investigators developed a model of schizophrenia that provides a way to study and understand how the loss of both PRODH and COMT gene activity contributes to the symptoms of schizophrenia.

The insights they gained into the disease with this model are important because the loss of the PRODH gene causes the imbalance in the levels of both glutamate and dopamine; and this imbalance contributes directly to the symptoms of schizophrenia, according to Stanislav Zakharenko, MD, PhD, an assistant member of the Department of Developmental Neurobiology at St. Jude.

The team investigated the roles of PRODH and COMT because these genes are located in the q11 region of human chromosome 22. Previous work by other scientists showed that a mutation in this region--the 22q11 microdeletion--is one of the major risk factors for developing schizophrenia.

The study’s findings linked changes seen at the molecular level directly to symptoms of schizophrenia seen in humans, said Zakharenko, who is a co-author of a report on this work that appears in the November 15 issue of Nature Neuroscience. The work was completed by Zakharenko and his colleagues at Columbia University (New York), Rockefeller University (New York) and the University of Utrecht (the Netherlands). Zakharenko is continuing his work on the molecular causes of schizophrenia at St. Jude.

The key finding in the current study was that the models of PRODH deficiency had increased COMT activity in the frontal cortex of the brain. "This might reflect a response to the increased dopamine activity caused by PRODH deficiency," Zakharenko said. "And it shows that when PRODH is lost, the additional loss of COMT due to the 22q11 mutation may worsen the symptoms of schizophrenia by allowing dopamine levels to rise." The prefrontal cortex is the part of the brain involved in complex cognitive functioning (e.g., thinking and reasoning).

In the same issue of Nature Neuroscience, another group of investigators reports that their study of adolescents with the 22q11 deletion showed that low activity of COMT is a risk factor for loss of volume of the part of the brain called the prefrontal cortex; and that this same mutation also puts adolescents at risk for developing psychotic symptoms.

Using their model of schizophrenia, Zakharenko and collegues first discovered that the loss of PRODH function directly causes hyperactivity of nerves that use glutamate to signal other nerves in the brain. Next, they found that disruption of PRODH gene activity causes the upregulation of the COMT gene, which encodes for the enzyme that breaks down dopamine. Upregulation is the increase in the rate at which a gene is decoded so the protein it codes for can be manufactured by the cell.

Prior research had already shown that PRODH makes an enzyme that breaks down proline, an amino acid that mimics the action of glutamate on most nerves in the brain. When PRODH activity is low, proline levels are high, creating an excess of excitatory activity leading to overall hypersensitivity of nerve cells to stimulation that might contribute to some schizophrenia symptoms. "Our model of schizophrenia was particularly useful because it lacked only a part of PRODH gene, so the level of proline rose to approximately that seen in individuals with schizophrenia," Zakharenko said.

Although dopamine and glutamate systems were suspected to contribute separately to the development of schizophrenia, researchers had not found a clear connection between them, according to Zakharenko. However, the present study clearly shows this connection. Specifically, when PRODH activity is low, proline levels are high, and there is excess in dopamine activity, he said. The subsequent increase in COMT compensates for the increased release of this dopamine caused by PRODH deficiency. "This finding shows why loss of COMT activity is linked to symptoms of schizophrenia," Zakharenko said.

The study also showed why patients with schizophrenia who also have the 22q11 microdeletion are especially disadvantaged. "COMT upregulation appears to be a response that brings the level of dopamine signaling back to normal," Zakharenko said. "So patients with the 22q11 microdeletion are unable to compensate for their PRODH deficiency by upregulating COMT."

The team further showed that PRODH deficiency increased the release of glutamate at synapses formed by CA3 and CA1 neurons in the part of the brain called the hippocampus. These synapses are routinely used as models of specific types of brain activity responsible for learning and memory. A synapse is the gap between an incoming nerve and its target cell across that gap. Signals pass from one cell on one side of the gap to another cell on the other side. The increased release of excitatory chemicals glutamate and proline due to PRODH deficiency inhibited the ability of the synapse to undergo a change called long-term potentiation (LTP)--a long-lasting strengthening in the connection between two nerve cells. LTP is an important step in forming memories, and disruption of this process interferes with the ability to store information.

Another study using the PRODH-deficiency model showed that the drug D-amphetamine causes exaggerated movement similar to that caused by amphetamine in humans with schizophrenia, according to the researchers. A PRODH deficiency caused lab models to have problems remembering how to respond to an audible tone in a way that was previously learned.

"These observations showed that lack of regulation of glutamate levels due to loss of PRODH function contributed to learning difficulties similar to those found in schizophrenia," Zakharenko said.

Moreover, the researchers showed that PRODH deficiency caused a reduction in the levels of three proteins that, in combination, are associated with dopamine function in the frontal cortex. Because these proteins cooperate with COMT to regulate the overall dopamine activity, the microdeletion 22q11 is likely to contribute to schizophrenia symptoms by eliminating PRODH. "This finding is further evidence that PRODH and COMT interact to control dopamine levels and further explains why the 22q11 microdeletion is associated with schizophrenia," Zakharenko said.

Finally, the investigators used the drug D-amphetamine to stimulate release of dopamine, while blocking COMT activity with a drug called tolcapone. Blocking COMT activity significantly increased the effect of D-amphetamine in PRODH-deficient models, proving that disruption of COMT disrupts the brain’s ability to rein in dopamine activity.

"This genetic model offers a way to make additional predictions about how specific gene defects in addition to PRODH and COMT deletions contribute to the development of schizophrenia in patients with 22q11 microdeletions," said Zakharenko. "Further studies using this model will likely help to answer many more questions about this disease."

Other authors of the study include Joseph A. Gogos, Maria Karayiorgou, Marta Paterlini, Wen-Sung Lai, Jie Qin, Hui Zhang, Jun Mukai, David Sulzer, Paul Pavlidis and Steven A. Siegelbaum (Columbia University and Rockefeller University) and Koen G.C. Westphal and Berend Olivier (University of Utrecht)." (1.)

--gjh

Balancing mood with L-Theanine

2007-01-16T10:35:00.000-05:00

L-Theanine information

Increasing L-Theanine from 100mg to 200mg today. Asked Patient to take one 100mg with AM meal and one 100mg with PM meal. The effects take approximately 30 minutes.

L-Theanine creates alert relaxation (non-drowsy) and stimulates production of Alpha brain waves, creating a deep state of relaxation similar to a massage or hot bath. Also plays a role in production of GABA.

(Updated 1-18-07) And unfortunately for this Patient it also appears to significantly increase Dopamine levels which elevates the SZ symptoms. Theanine is placed on hold in the supplement line up now.

CHANGED TO AVOID from ON HOLD 2-5-07

--gjh

Patient Update January 15, 2007

2007-01-15T19:00:00.000-05:00

Patient reported January 14th that taste buds started working (normal flavors) the day the L-Carnosine was reduced to 250mg.

Additional L-Carnosine info:

Study that showed "Acceleration of metabolism of stress-related substances by L-carnosine."

--gjh

Patient Update January 10, 2007

2007-01-10T20:11:00.000-05:00

Patient has been on Am and PM 475mg Kavinace daily for second week, first week PM only daily. Dizziness under control. Keeping the routine and the schedule on track is supportive for controlling the dizziness. Exercise on treadmill is daily for 10-15 minutes.

Minimum required exercise is 3 times a week for generating new brain cells. Challenging those cells with new learning and socialization helps integrate them permanently.

During the past week, 1,000 mg L-Carnosine (500mg am / 500mg pm) was taken and Patient had elevated levels of paranoia. L-Carnosine is said to have support affect on serotonin and dopamine. In the past, this Patient had elevated paranoia while on antidepressents. The 1,000mg has been reduced to 250mg once in AM for the next week. The intention was to have 500mg in AM, not 1,000mg which the Patient self administered. If paranoia reduces on the 250mg L-Carnosine, it will remain, otherwise it will be dropped to 100mg or eliminated. (update 1-13-07: Patient reported on 1-12-07 having difficulty exhaling, having tight chest - during the week long period of 1,000mg and this symptom is no longer present on 250mg after one day.)

L-Theanine 100mg has also been taken during the past week and will continue once in AM daily with regular supplements. (UPDATE 2-24-2007 Theanine caused elevated dopamine levels and paranoia so we have discontinued Theanine for this Patient.)

Sorry for the long delay in posting updates. Daily progress checks have been handled by phone over the period without posts. The progress has been consistent, slow, and positive. Mood appears to be improving. Still, there are good days and bad days for paranoia symptoms, but especially elevated over the past week on large 1,000 mg L-Carnosine-now reduced.

--gjh

Patient Update December 24, 2006

2006-12-24T03:25:00.000-05:00

Exciting Information... Finally located a company that may be able to
help us at www.neurorelief.com. They seem to understand the need for
testing and addressing deficiencies and food allergies.

Food Allergy Testing Link http://www.neurorelief.com/index.php?option=com_content&task=view&id=241&Itemid=46

Basic Info http://www.neurorelief.com/index.php?option=com_content&task=section&id=7&Itemid=49

We will definitely be contacting them regarding getting Patient's levels tested and devising a more targeted therapy.

note: important supplements: L-Theanine, Taurine, L-Carnosine

--gjh - very excited!

Patient Update December 23, 2006

2006-12-24T02:45:00.000-05:00

SW reported Patient doing well in AM.

Phone call with Patient at 6PM revealed morning dizziness, dizziness after lunch. 2 Neuro Optimizer pills taken at lunch, 1 at dinner, 1 before bed. (Discontinued, see below)

Family members living with Patient aren't interested in tracking progress and have decided to not contribute to the record, despite repeated
requests. Therefor, each update posted is information gathered as a
result of a phone call with Patient. Relying on the information provided by the Patient only is not providing an accurate record on some days.

Neuro Optimizer contains Acetyl L-Carnitine, which has warnings for seizure prone individuals. For this reason, we may need to halt Neuro Optimizer if the dizziness continues. (UPDATE 2-24-2007 Neuro Optimizer has been discontinued for this Patient due to elevated levels of paranoia AND seizure possibly caused by L-Carnatine in the combined supplement. Negative effects were seen within 48 hours or less, tested twice.)

I will likely introduce some testing of the Taurine blends found at neurorelief.com and I have new found hope we will eventually get something in the protocol that stabilizes the Patient.

--gjh

Patient Update December 22, 2006

2006-12-24T02:42:00.000-05:00

Patient started Dr. recommended Neuro Optimizer supplement. Took two with evening meal.

Patient Update December 19th 2006

2006-12-19T19:29:00.000-05:00

Patient sounded alert and normal (7:40PM) and started conversation. Reported dizziness after getting out of bed. Exercised in AM. Turkey and Cheese sandwhich. Pumpkin pie today after lunch. Had spaghetti for dinner

--gjh.

Patient Update December 18th 2006

2006-12-18T22:46:00.000-05:00

Spoke to at 9:00 PM, Patient sounded very tired, alertness increased slightly during 30 minute conversation. Family reported psychosis in the early evening which included voices and banging on something. Patient reported having cereal in morning, banana, spaghetti for dinner.

--gjh

Patient Update December 17th 2006

2006-12-17T15:31:00.001-05:00

Patient felt light-headed shortly after consuming decaf coffee with a small amount of sugar.

Patient reported voices in walls, concern about some vehicles in the early evening.

Patient Update December 16th

2006-12-17T15:28:00.000-05:00

Patient experienced minor paranoia at 4:45pm. Patient had not eaten anything since noon.

Patient Update December 15, 2006

2006-12-16T17:24:00.000-05:00

Patient experienced minor psychosis late afternoon and revealed that a candy bar had been eaten an hour before. Discussed with Patient the possibility of sugar metabolism problem and requested elimination of unnecessary, excessive sugar.

Neurologist conference called at 4PM. Decision was made to schedule Endocrinologist before starting any new seizure medication. Family has observed Patient has been seizure free, with no complaints of dizziness.

Decision was made to include DMG supplement in protocol. Patient has been visiting family, away from home for past 4 days in effort to reduce stress factors of psychosis.

Endocrinologist will be consulted Monday regarding appointment.

--gjh

Dimethylglycine (DMG) links

2006-12-15T15:39:00.000-05:00

http://www.autismwebsite.com/ARI/newsletter/dmg1.htm

(to be udated later)

Hyperthyroidism

2006-12-15T14:49:00.000-05:00

This link has information of what to look for in blood tests to see presence of hyperthyroidism:

http://www.emedicine.com/NEURO/topic371.htm

Supplements and Epilepsy

2006-12-15T14:47:00.000-05:00

Check this link out when more time is available.
Touches on supplements and nutrients recommended for seizures.
Also states the following:
"About 10 to 20% of epilepsy patients do not respond to drug therapy and may require surgery."

http://www.vitacost.com/science/hn/Concern/Epilepsy.htm#Condition-Symptoms

Magnesium and the Brain

2006-12-14T09:33:00.000-05:00

"Magnesium Calms the Brain
People don't need to become severely deficient in magnesium for the brain to become hyperactive. A new study confirms earlier reports that a marginal magnesium intake overexcites the brain's neurons and results in less coherence--creating cacaphony rather than symphony--according to electroencephalogram (EEG) measurements. During half of the six-month study, 13 women consumed 115 milligrams of magnesium daily--or about 40 percent of the Recommended Dietary Allowance (RDA). During the other half, they got 315 mg daily--a little more than the 280 mg recommended for women. After only six weeks on the marginal intake, EEG readings showed significant differences in brain function.

"Magnesium is the fourth most abundant element in the brain and is essential in regulating central nervous system excitability. Clinical studies of people severely deficient in this essential element have reported epilepsy-type convulsions, dizziness and muscle tremors or twitching as well as many psychological symptoms, including irritability, anxiety, confusion, depression, apathy, loss of appetite and insomnia. While the marginal intake in this study did not produce such severe symptoms, it did hype brain activity.

"This is the first experimental study in which magnesium intakes were tightly controlled and EEG measurements were analyzed by computer so they could be statistically compared. Good sources of magnesium include whole grains, nuts, peanut butter, cottonseed, peanut and soybean flours, green leafy vegetables and spices. It's better to get magnesium from foods rather than supplements because high doses have a laxative effect--the body's way of preventing toxic levels."
http://www.ars.usda.gov/is/np/fnrb/fnrb1095.htm

Sugar Cravings

2006-12-14T09:23:00.000-05:00

"When any carbohydrate is eaten, it is broken down into glucose by the body and is known as blood sugar. Insulin is a hormone secreted by the pancreas that takes the glucose from the blood and brings it into the body’s cells where it can be used for energy. However, if there is too much glucose in the blood from eating too many refined carbohydrates, then the body’s cells can stop responding to the insulin. This is called carbohydrate intolerance or insulin resistance.

"The problem does not stop there, because the glucose can not get into the cells for energy and the cells essentially starve. This has profound effects on the body, especially the brain, whose only source of energy is glucose. If the brain is not getting the necessary energy, it signals the body to crave more dietary carbohydrates. This begins a vicious cycle of low energy, sugar cravings, and increased consumption of dietary carbohydrates.

"But poor nutrition is not the only cause of this cycle. Chronic stress is also responsible. When the body is under continued stress, the stress hormone cortisol is continually produced. One of cortisol’s effects is to increase insulin production. This produces the same effect as eating too many carbohydrates.

"Carbohydrate intolerance can directly lead to obesity, diabetes, heart disease or stroke. But the good news is that the vicious cycle of carbohydrate intolerance can be broken through dietary and stress management."
http://carolinanewswire.com/news/News.cgi?database=columns.db&command=viewone&id=258&op=t

2006-12-12T15:39:00.000-05:00

Patient will see Dr. Margolis on Thursday.

Supplements for Seizure Control

2006-12-12T03:12:00.000-05:00

Here's a post I found regarding Diet and Supplements for Seizure control. - (UPDATE) we HAVE changed our nutri-supplement protocol for dealing with seizures, we are still researching and making adjustments but, at this time we feel strongly that Kavinace was instrumental in controlling seizures for Patient.

The Post...

"
THE PROGRAM
Vitamins & Supplements prescribed by a Nutritionist MD
Eliminated Food Allergens (Grains, Dairy, Beans, Seeds, Peanuts, Sweeteners, Alcohols)
Along with the AEDs (Tegretol XR & Depakote ER), the anti-depressant (Prozac), and the anti-psychotic (Respirdal). {YIKES DRUGS!}

MY DIET
Eggs (hard boiled, scrambled, fried)
Fruit (raw)
Vegetables (raw & steemed)
Potatoes (mashed, boiled, baked, fried)
A Variety of Cooked Meats (Beef, Turkey, Chicken, Clams)
Juices (fresh squeezed)
Water (bottled or purified)
Prescribed Supplements & Medications

VITAMINS
B6 (Pyridoxal-5-Phospate)
Zinc
Evening Primrose Oil
Taurine w/p copper
Vitamin D3
Magnesium Gyconate
Vitamin C (ascorbic acid)
Folate
B12 (methylcobalamin)
Calcium Citrate
L-Tyrosine
L-Lysine
5-HTP
Potassium Iodide
Magnesium Citrate
Chromium Citrate
Molybdenum Citrate
Potassium Citrate
Boron Citrate
Vanadium Citrate
Digestive Enzymes
Multi-vitamin w/ lots of vegetables
As well as Chinese herbal & homeopathic remedies"(1.)

(1.) http://brain.hastypastry.net/forums/showthread.php?t=2727

L-Carnosine

2006-12-12T02:42:00.000-05:00

One of the previous posts refers to L-Carnosine. This post will be updated with related info on L-Carnosine.

http://www.ethosplan.com/l-carnosine-information.asp

http://www.cherab.org/information/dietaryeffects/carnosine.html

http://cat.inist.fr/?aModele=afficheN&cpsidt=14508390

http://www.1stvitality.co.uk/az/carnosine/carnosine_an_antioxidant.htm

http://www.1stvitality.co.uk/az/carnosine/carnosine.htm

--gjh

AMPAKINE Structures

2006-12-12T02:08:00.000-05:00

I'll reaserch what I can find on AMPAKINE Structures as they relate to seizures (not SZ)

--gjh

Patient Update December 11, 2006

2006-12-12T00:26:00.000-05:00

Patient experienced "Keppra Anger" and psychosis side effects today. Patient was belligerent and almost violent. Made emergency call to Dr's office and spoke with neurologist. Result - Patient must stop Keppra today, evening dose was not taken. Side effects appeared about 4 days after starting medication (a couple pills were skipped due to poor memory and other emergencies attended by family. :( The dose was 250mg AM 250mg PM. Follow up call scheduled for Friday.

Patient had not had any seizures/dizziness since starting Keppra.

We think that we should see an endocrinologist and confirm we haven't missed something. Patient was said to have been hyperthyroid in the past.

--gjh

Patient Update December 9, 2006

2006-12-09T18:09:00.000-05:00

Patient had no dizzyness after lunch (rare), second day on drug Keppra. Noticed Patient speaking slower, perhaps both are indication that drug is already affecting GABA receptors.

No dizziness reported after evening meal.

--gjh

Aspartame Poisoning (Equal®, Nutrasweet® and Spoonful®) - seizures, memory loss, methanol poisoning

2006-12-09T17:43:00.000-05:00

Whoops! YIKES! Did not know that! I suggest you read these links.

http://www.sweetpoison.com/aspartame-information.html

http://www.mercola.com/article/aspartame/hidden_dangers.htm

http://www.holisticmed.com/aspartame/adverse.txt

http://nccn.net/~wwithin/aspartame.htm

http://www.aspartamesafety.com/

http://aspartametruth.com/aspartamedotorg/

Questions to ask doctor

2006-12-08T18:27:00.000-05:00

Should we have more tests taken to determine if patient has epilepsy?

What is Patient's measured CSF glutamate level presently? (1.)

What are Patient's compared DHEA to Cortisol Levels? (& melatonin)(2.)

What are Patient's food allergies, Dairy, Gluten, Sugar?

Is Patient Hypoglycemic? (3.)

(1.) http://www.worldwidehealthcenter.net/category.php?prod=659

(2.) http://www.blackwell-synergy.com/links/doi/10.1111/j.0013-9580.2005.59704.x/abs/

(3.) http://www.medhelp.org/forums/neuro/archive/14681.html

Patient Update December 8, 2006

2006-12-08T17:52:00.000-05:00

Patient began Keppra in AM Experienced minor dizziness again after eating lunch.

Patient may be experiencing transient ischemic attack (TIA), or "mini-stroke" - dizzy spells have been how Patient described the experience. However, on at least two of these events the Patient fell to the ground and was seen shaking just before falling.

Patient's mother also had these at similar age. Patient also had seizures as a baby during high fever.

Patient Update December 7, 2006

2006-12-07T16:50:00.000-05:00

Neurologist prescribed Keppra for 2 weeks.

Researching L-Glutamine, GABA, Zinc, ALA as mentioned previously.

Patient needs tests for levels: zinc to copper (update later)

--gjh

Sleep-related Epilepsy

2006-12-07T16:05:00.000-05:00

"In a review of 100 consecutive cases of nocturnal frontal lobe epilepsy [16], 28% occurred in sleep stages 3 or 4, and only 3% during REM. Clear epileptiform abnormalities on routine EEG occurred in less than half of patients. Forty-two patients showed a clear ictal discharge on polysomnography."(1.)

"O'Regan et al. [19] studied 25 children with an acquired disorder of communication and seizures, but not strictly meeting criteria for LKS. EEGs were uniformly epileptiform, usually (16 of 25 patients) worsening with sleep. Magnetic resonance imaging (MRI) was typically normal, but single photon emission computed tomography (SPECT) was abnormal (22 of 25 patients). Most were considered to have a receptive aphasia. Language deficits have been hypothesized to result from the persistent epileptic discharges, as evidenced by hypometabolism on SPECT [19]."(1.)

(1.)Sleep-related Epilepsy
Carl W. Bazil, MD, PhD
Current Neurology and Neuroscience Reports 2003, 3:167-172
Current Science, Inc. ISSN 1528-4042
Copyright © 2006 by Current Science, Inc.
http://www.current-reports.com/article.cfm?PubID=NR03-2-3-01&Type=Article&KeyWords=

Seizure Recovery Story - a natural approach

2006-12-07T14:23:00.000-05:00

"Absorbing as much of the information as she could, she decided that she wanted a change for her son. She found the scientific information referenced in the article, “absolutely amazing”, and she was determined to try a natural approach. On her own she began giving her son supplements that were discussed in the article. She started him on 1000 mg of omega-3, 400 IUs of vitamin E, 500 mg L-Carnosine, 500 mg L-Glutamine, selenium, Vitamin C, zinc, and B-complex."(1.)

"She made changes in his diet, eliminating dairy and wheat and all processed food, which Jonathan frequently ate. “Now that I look back at it he had an awful diet.” She switched to all organic food and began using filtered water. She also started reducing the amount of Jonathan’s medication."(1.)

"Within two weeks Jonathan started showing some amazing changes. Denise noticed improved eye contact and increased “clarity”. He suddenly became more focused and articulate. He had more patience playing games and wasn’t as angry. Jonathan also began singing, something that he never really did before. Denise was happy and surprised, “He’s actually singing! Oh my God he’s singing!”(1.)

(1.) http://www.healthsentinel.com/org_news.php?id=111&title=Reversing%20autism%20and%20seizures%20?%20Jonathan?s%20story&event=org_news_print_list_item

--gjh

Glutamine and GABA

2006-12-07T09:52:00.000-05:00

"The action of the heart is under considerable control of the nervous system, and the pathways involved in the neural control of cardiovascular function happen to rely on glutamate and GABA. If the brain has a faulty glutamine / glutamate / GABA metabolism, we can expect the development of cardiovascular dysfunction as well. In addition, glutamine serves as a substrate for the synthesis of a special type of beta-endorphin, glycyl-l-glutamine. This dipeptide appears to be important for the regulation of blood pressure and prevention of cardiorespiratory depression. Glycyl-l-glutamine is also important for the immune response, since it enhances the activity of the natural killer (NK) cells."(1.)

"The synthesis of glutamine protects the body, and the brain in particular, from ammonia toxicity. In fact, the synthesis of glutamine from glutamate is the key pathway for detoxifying ammonia. Excess ammonia is a crucial factor in the development of neurodegenerative diseases, since ammonia interferes with the oxidative metabolism of neurons and thus reduces the production of ATP, our "energy molecule." In addition, ammonia gives rise to very harmful nitrogen-based free radicals."(1.)

"In the brain, glutamine is a substrate for the production of both excitatory and inhibitory neurotransmitters (glutamate and gamma-aminobutyric acid, popularly known as GABA). Glutamine is also an important source of energy for the nervous system. If the brain is not receiving enough glucose, it compensates by increasing glutamine metabolism for energy-hence the popular perception of glutamine as "brain food" and its use as a pick-me-up. Glutamine users often report more energy, less fatigue and better mood."(1.)

"Glutamine also plays a part in maintaining proper blood glucose levels and the right pH range. The body has an exquisite mechanism for maintaining pH homeostasis. If the pH of the blood is too acidic, more glutamine is directed to the kidneys, where a certain type of glutamine results in the release of bicarbonate ions to correct acidosis. If the pH is too alkaline, more glutamine is sent to the liver, where a different kind of metabolism releases hydrogen ions to correct alkalosis."(1.)

"And there is still more. Due to its dependence on sodium transport, glutamine is one of the amino acids that control the volume of water in the cells, and the osmotic pressure (osmoregulation) in various tissues. Glutamine also plays a vital part in the control of blood sugar. It helps prevent hypoglycemia , since it is easily converted to glucose when blood sugar is low. In addition, glutamine regulates the expression of certain genes, including those that govern certain protective enzymes, and helps regulate the biosynthesis of DNA and RNA. Recently it has been discovered that glutamine is important for the cardiovascular system as well."(1.)

"The glutamine cycle in the brain is simple and elegant. Glutamine readily crosses the blood-brain barrier. Neurons take up glutamine and convert it to glutamate or GABA (through the additional step of decarboxylating the glutamate). Some glutamate is used for energy, some for synthesis of glutathione and niacin, some as neurotransmitter. After either glutamate or GABA are released into the synaptic junction, the supportive cells called glia, with their high supply of glutamine synthase, take up the glutamate or GABA and resynthesize glutamine, detoxifying ammonia in the process. The glutamate that is not converted to glutamine is used by the glia as a source of energy, and also to produce energy nutrients alanine and alpha-ketoglutarate, which are then released to the neurons."(1.)

"If excess glutamine accumulates through the action of the glia, the brain donates it to the body. Normally, however, very little glutamine is released by the brain, in contrast to muscle and adipose tissue, which donate a lot. In the brain, it's pretty much an internal affair. What we see is the glutamine glutamate GABA glutamine cycle."(1.)

"If the glia are dysfunctional due to reduced aerobic metabolism, or the release and/or activity of the glial glutamine synthase is inhibited in any way (free-radical damage, toxins, certain drugs), not only glutamate, but GABA as well might accumulate in excess, possibly causing lethargy and cognitive dysfunction. It has been suggested that this too is one of the phenomena we see in the aging brain. On the one hand, glutamate excitotoxicity damages or destroys some neurons, leading to deficiencies in memory and learning; on the other hand, excess of GABA can lead to lethargy. At the same time, excess ammonia, not detoxified through sufficient glutamine synthesis by the glia, leads to further neural damage."(1.)

"An interesting development related to glutamate is the increasing use of ampakines, a new class of drugs for Alzheimer's disease. Apparently an important factor in the pathogenesis of Alzheimer's disease is stroke or a series of undiagnosed mini-strokes. During stroke, the dying neurons release glutamate, which then unfortunately can cause more neuron death. Furthermore, ischemic episodes damage the glutamate receptors, so that later the glutamate can't work as a neurotransmitter. Without glutamate, there is no memory and no learning. Ampakines amplify the glutamate signal through a yet unknown mechanism, possibly by rebuilding glutamate receptors. In healthy people and in animals, ampakines have been shown to enhance cognitive performance, and can thus be classified as "smart drugs."(1.)

Glutamate

"One current hypothesis is that glutamate is also deficient in schizophrenia, though probably many neurotransmitters are out of balance in neurological disorders."(1.)

"At normal physiological levels, glutamate is beneficial and safe. It is an indispensable neurotransmitter that the brain produces according to need. When the central nervous system is aroused, surprisingly enough we do not see higher glucose consumption. Instead, some of the glucose is converted to glutamate. The other source of glutamate is, of course, glutamine. An abundant supply of glutamine makes it easier for the brain to maintain neurotransmitter balance, by increasing the production of glutamate when required for alertness, learning and memory, and the production of GABA when its inhibitory properties are needed. In fact, some people report feeling more centered and calm after they start taking glutamine. Others report a lifting of depression."(1.)

"Glutamate is our chief excitatory neurotransmitter. It is essential for learning and both short-term and long-term memory. Problems arise only if the normal process of glutamate removal and conversion to glutamine malfunctions and an excess of this excitatory neurotransmitter builds up in the synaptic junctions. Excess glutamate causes excessive influx of calcium ions into the neurons, causing excitotoxicity and ultimately even death of the neurons. It also destroys glutathione, a crucial brain-protective antioxidant. Low levels of brain glutathione are associated with neurodegenerative disorders. Glutathione depletion further leads to neuronal death."(1.)

"Under what conditions do we see excess levels of glutamate at the synapses? Not surprisingly, we see evidence of damage associated with excess glutamate in Alzheimer's disease patients, AIDS patients (the AIDS virus inhibits glutamate uptake by the glia), cancer patients (according to one hypothesis, cancer basically starts with brain dysfunction), and in those who have suffered a severe brain injury. Very high fever or artificially induced hyperthermia can also result in excess glutamate release, leading to seizures."(1.)

"GLUTAMINE--As well as cysteine it is recommended to take the other two aminos that make up glutathione as supplemental glycine and glutamine. Both glutamate and glutamine are forms of glutamic acid, the body easily converts the glutamine to glutamic acid. Glutamic acid readily passes the blood brain barrier and is considered a "brain fuel."(2.)

"In the brain, glutamine is a substrate for the production of both excitatory and inhibitory neurotransmitters (glutamate and GABA). Glutamine is also an important source of energy for the nervous system. Glutamic acid and cysteine are necessary for glucose regulation, and can decrease cravings for alcohol and sugar. If the brain is not receiving enough glucose, it compensates by increasing glutamine metabolism for energy. Glutamine users often report more energy, less fatigue and better mood.(sic.)"(2.)

"Glutamine is the most abundant single amino acid in the blood and in the muscle tissue comprising up to 60% of the amino acid pool in skeletal muscle; and is manufactured and released primarily by the skeletal muscle. Because it is important in the rapid growth of cells more is needed during stress or illness. Glutamine is utilized as a source of energy and for nucleotide synthesis by all rapidly dividing cells, such as the cells of the intestinal lining and certain immune cells thus without sufficient glutamine, the intestines atrophy and the immune function breaks down. Glutamine therapy was found to improve intestinal permeability in AIDS patients."(2.)

"Glutamine serves as a nitrogen donor and a carbon donor, and is thus an important muscle-building amino acid. Glutamine's unique structure, containing two nitrogen side chains makes it responsible for 35% of the nitrogen that gets into the muscle cell. It is anticatabolic, meaning it regulates protein synthesis in muscles, sparing muscle tissue and helps replenish muscle glycogen after exercise. It is also involved in glycogen synthesis in the liver and is a building block of many other amino acids. Glutamine can increase growth hormone levels by 43% thereby slowing aging. It also improves lymphocyte proliferation. Further more it reduces insulin resistance and high blood sugar which also counteracts aging."(2.)

"The amino acid glutamine strengthens the cell lining of both the small and large intestines, provides metabolic fuel for gut cells, brain cells, immune macrophages and lymphocytes. Glutamine has been reported to be helpful in reducing "leaky gut" and "brain fog". Glutamine is important as an energy source for our bodies, and is the primary fuel for the upper intestinal tract. It aids the immune system by increasing the integrity of the intestinal lining preventing toxins and pathogens from entering the bloodstream. Glutamine is also a component of folic acid. There is an association between folic acid deficiency and seizure. Disruptions of the intestinal lining may cause folate deficiency, and consequently lead to seizures."(2.)

"The small intestine uses 40% of the glutamine in the body, it being the primary amino acid for the cells that line the small intestine; it nourishes and repairs them. Insufficient glutamine increases the permeability of the gut leading to leaky gut syndrome. This lets in toxins, pathogens and partially digested molecules into the blood increasing the load on the liver. The large molecules entering the bloodstream stimulate antibody production, and then the liver subsequently has to cope with the waste products of antibodies. Which again increases the demands made on glutathione and other antioxidants."(2.)

"GABA--GABA is made from the amino acid Glutamic acid (Glutamine or Glucose). It reduces anxiety, elevates the pain threshold reduces the blood pressure and heart rate and reduces compulsive behavior. GABA promotes fat loss and stimulates the production of Human Growth Hormone (HGH). GABA can be taken as a supplement (L-Glutamine), produces a calming effect on people who struggle with temporal lobe symptoms like temper, irritability, and anxiety."(2.)

"GLYCINE--Glycine and glucose are the two most common amino acids in the body. Glycine is the simplest amino acid and is the only protein forming amino acid without a center of chirality, that is it is nonpolar. Because glycine has such a small side chain it can fit into many places where no other amino acid can. Hence it is the internal amino acid of a collagen helix, thus collagen is about one-third glycine. Most proteins however only contain a small quantity of glycine."(2.)

"Like GABA, Glycine activates Cl- ion conductance resulting in a hyperpolarization of the neuronal membrane and an antagonism of other depolarizing stimuli. This membrane hyperpolarization makes glycine the major inhibitory neurotransmitter in the brainstem and spinal cord, where it participates in a variety of motor and sensory functions. However in the forebrain it functions in an excitatory way by promoting the actions of the major excitatory neurotransmitter glutamate at the NMDA receptors. Other amino acids, including alanine and taurine, also activate glycine receptors, but with lower potency."(2.)

"Glycine may increase acetylcholine neurotransmission in the hippocampus, the memory center of the brain. This factor could be involved in having "ones life pass before ones eyes" during near death experiences. Increases blood sugar and Growth Hormone. Vitamin B6, magnesium and dimethylglycine are antiseizure and have increased speech in autistic children. Found in many foods, glycine is also synthesized in the human body where, among other functions it helps improve glycogen storage. It is utilized in the synthesis of hemoglobin, collagen and glutathione, and facilitates the amelioration of high blood fat and uric acid levels."(2.)

"It is essential for learning and both short-term and long-term memory. Glutamate, as a neurotransmitter, exists in the extracellular fluid only in very, very small concentrations--no more than 8 to 12 FM (micromoles/liter). When the concentration of this transmitter rises above this level, the neurons begin to fire abnormally. At higher concentrations, the cells undergo a specialized process of delayed cell death known as excitotoxicity; that is, they are excited to death. Some individuals may be especially sensitive and develop severe symptoms and even die suddenly from cardiac irritability, but in most instances the effects are subtle and develop over a long period of time. But, it is free glutamate that is the culprit. Bound glutamate, found naturally in foods, is less dangerous because it is slowly broken down and absorbed by the gut so that the tissues can utilize it, especially muscles, before toxic concentrations can build up. Infusions of MSG are used in mainstream clinical practice to reduce high ammonia levels in the blood (hyperammonemia) by stimulating the conversion of glutamate to glutamine. Both glutamate (as MSG) and glutamine are used by conventional medicine for treating several very serious conditions. Glutamine supplementation has shown better neural energy production and better neuro-transmitter balance are typical results, with improved mental performance and a sense of well-being. The glutamine cycle in the brain is simple and elegant. Glutamine readily crosses the blood-brain barrier. Neurons take up glutamine and convert it to glutamate or GABA (through the step of decarboxylating the glutamate). Some glutamate is used for energy, some for synthesis of glutathione and niacin, some as neurotransmitter."(3.)

"After either glutamate or GABA are released into the synaptic junction, the supportive cells called glia (more specifically, astroglia or astrocytes)--the most abundant type of cell in the central nervous system--with their high supply of glutamine synthase, take up the glutamate or GABA and resynthesize glutamine, detoxifying ammonia in the process. The glutamate that's not converted is used by the glia as a source of energy, and also to produce energy nutrients alanine and alpha-ketoglutarate, which are then released to the neurons. If excess glutamine accumulates through the action of the glia, the brain donates it to the body. Normally, however, the brain, releases very little glutamine, in contrast to muscle and adipose tissue, which donate a lot. During a stroke, ischemic episodes damage the glutamate receptors, so that later the glutamate can't work as a neurotransmitter. Without glutamate, there is no memory and no learning. Glutamate is also deficient in schizophrenia. It's an indispensable neurotransmitter produced in the brain according to need. When the central nervous system is aroused, we don't see higher glucose consumption. Instead, some of the glucose is converted to glutamate. An abundant supply of glutamine makes it easier for the brain to maintain neurotransmitter balance, by increasing the production of glutamate when required for alertness, learning and memory, and the production of GABA when its inhibitory properties are needed."(3.)

"What is the significance of the empty stomach?
Normally the blood-brain barrier protects the brain from excessive
amounts of any single amino acid. However that protection is reduced
dramatically when the amino acid is taken on an empty stomach in
isolation from other amino acids. In fact it is because of the natural
protection of the blood-brain barrier that it is considered necessary
to take glutamine on an empty stomach for purposes of stimulating the
release of growth hormone. If the glutamine is taken as part of
complete proteins, with a meal or on a full stomach, then it will be
forced to compete with other nutrients and amino acids for entrance to
the brain. But that competition between amino acids for entrance to
the brain is the normal state of nature; it ensures that no single
amino acid will flood the brain in isolation. Glutamine works for
stimulating GH release only if we intentionally defeat mother nature's
built-in protections, which in itself is an indication that some risks
are involved."(4.)

"Another concern is that the brain is more vulnerable to excitotoxicity
when the body is fasting. The brain derives most of its energy from
glucose (sugar), and it needs that energy to defend against any sudden
increase in glutamate. The worst time to take large amounts of
glutamine is in the morning before breakfast on an empty stomach, when
the body has been fasting overnight and blood sugar is low."(4.)

(1.) http://www.lef.org/magazine/mag99/sep99-report3.html

(2.) http://biologyofkundalini.com/article.php?story=SupplementList

(3.) Glutamine http://www.tuberose.com/Inflammation_Damage_&_Repair.html

(4.) http://groups.google.com/group/misc.fitness.weights/browse_thread/thread/c86779291cfa2781/a99488e2b334728c%23a99488e2b334728c

--gjh

Patient Update December 6, 2006

2006-12-06T20:53:00.000-05:00

Brief: Patient diagnosed with seizures on the EEG test - details not yet known- appointment scheduled.

We are busy researching GABA, ZINC, etc.. This post is a note pad for some links that need follow up by the Family. We've read seizure can produce effects of SZ.

http://www.sfn.org/index.cfm?pagename=brainBriefings_epilepsyAndGABA

"When GABA is low in the brain, impulsive behaviors are not inhibited (stopped) by logical or reasonable thinking... Low levels of GABA are also associated with epilepsy or seizure disorders.... Low levels of GABA make it easy for the brain to develop seizures which is why seizures are part of the withdrawal syndrome for many substances that work with GABA such as alcohol and tranquilizers. Substances that artificially maintain a high level of GABA, when stopped, create a dramatic drop in GABA levels, thus creating the risk for withdrawal seizures due to the chemical instability that is created."
http://www.enotalone.com/article/4118.html

http://www.nature.com/nature/journal/v376/n6536/abs/376174a0.html

--gjh

Patient has experienced "tonic seizures." There's a possibility that patient's drooping of the eyes is a tonic seizure. Falling episodes could be seizure or low blood pressure.
Patient has also experienced "sensory seizures" that involve having strange tastes in mouth, hearing voices, feeling physical touch, experiencing smells that don't exist, visible hallucinations.
It is not clear yet whether patient's seizures are classified as epileptic or nonepileptic.

--sw

"Psychological causes of NES (non epileptic seizures)

Any experiences that we have, whether good or bad, can have a deep and long-lasting effect on us. Everyone has their own way of dealing with their experiences. For some people, the NES they have are their brain's way of dealing with past painful experiences . . . The causes of NES may be past experiences such as bereavements, divorce, abuse or other emotional difficulties. On-going stress may also cause them, such as work, family or money worries. Some people may not know the cause of their seizures. Some people may not think stress is a possible cause as it may be a normal part of their life."

"NES may be part of post-traumatic stress disorder - a condition that sometimes happens after a traumatic or stressful event."

"A diagnosis of NES means that the seizures the person has are not epileptic. Because the seizures are not epileptic, there is no need to take anti-epileptic medication. Unless someone has both epileptic and non-epileptic seizures, any anti-epileptic drugs that have been prescribed are usually stopped when a diagnosis of NES is made."

http://www.epilepsynse.org.uk/PAGES/info/leaflets/factsnea.cfm

--sw

Food Allergies

2006-12-05T18:51:00.000-05:00

"Food allergies are most often of the delayed type, persisting for some time after the allergic substance has been eliminated and recurring only after repeated daily exposures, once symptoms have improved.
Fixed allergies to gluten containing grains (such as wheat) and dairy products is common, however, and reactions to those foods may persist throughout life, fluctuating in sensitivity from time to time. Viral infections and other illnesses can reactivate food allergies. Allergy is usually the result of repeated exposures to a specific substance or food. The more often the exposure, the more likely it is to provoke an allergic response. For unknown reasons, some foods are tend to be much more allergic than others.
Unless all sensitizing foods are eliminated during the same period of time, for a month or more, there may not be enough time for symptoms to clear. Multiple allergies are additive. Eliminating only one or a few of the sensitizing substances may not be adequate to see improvement, and the diagnosis will be missed.
If symptoms improve and if you feel better on [an elimination] diet, it means that something you eat or drink on a regular basis is either causing or contributing to the severity of symptoms.
You may experience withdrawal symptoms and strong cravings during the first week or two on the diet. Paradoxically, withdrawal and cravings are also symptoms of food allergy. After a few weeks of elimination, cravings for the offending foods will disappear. Cravings are not related to nutritional factors.
Observe carefully for changes in nasal or lung congestion, mucous, fatigue, foggy thinking, digestive disorders, constipation/diarrhea, bloating, gas, fluid retention, pain, mood swings, joint aches, urinary problems, drowsiness after meals, and other symptoms that can be caused by unsuspected food allergies."(1)

(1) http://www.drcranton.com/elimination_diet.htm

Negative effects of sugar

2006-12-04T16:57:00.000-05:00

"Results from four out of five placebo-controlled studies in England, as well as a cross-national analysis of schizophrenia outcomes in relation to national dietary practice, all confirm that an excess of sugar and saturated fat in the diet appears to worsen the long-term outcome of schizophrenia."
Consuming high amounts of sugar and fat cause the brain to produce less of the protein product brain-derived neurotrophic factor (BDNF). BDNF plays an important role in forming new neural growths and synapses.
Dr. Malcolm peet of Swallownest Court Hospital confirms the effects of diet. "It appears that the same dietary factors which are associated with the metabolic syndrome, including high saturated fat, high glycemic load, and low omega-3 PUFA, may also be detrimental to the symptoms of schizophrenia, possibly through a common mechanism involving brain-derived neurotrophic factor."

http://www.schizophrenia.com/sznews/archives/000623.html

Breakfast is critical

2006-12-04T16:24:00.000-05:00

It has been determined that patient should eat breakfast as soon as possible after waking up, and take the supplements at that time also. If food or supplements aren't consumed until noon or later, patient is sluggish and experiences dizziness more frequently. Patient has a difficult time eating three meals per day, but has been very cooperative in following the no-dairy diet. Delusional thinking occured on a day in which no food or supplements were consumed until late afternoon. Spoke with cph to make sure the supplements are being taken in the morning along with breakfast shortly after patient wakes up.

Patient Update Dec 1, 2006

2006-12-01T14:54:00.000-05:00

1:06pm
Just completed phone call with Patient. Patient had an EEG test taken today. Had a bagel and soy milk for breakfast at 8:30 this morning. No dizziness after eating. Patient took all supplements. Slept well last night. Says the dizziness seems to come and go at different times and it's not clear yet what is bringing it on. Has appt. with Dr. Margolis in a few weeks. Patient sounded tired, had not eaten any lunch yet and had not exercised yet. Patient's speaking speed was a little slow today.
Patient possibly concerned about upcoming vehicle purchase. Patient has been experiencing a "fog-like" feeling and says that makes it difficult to do everything patient wants to do. Patient said things were worse when on medication; there was nausea and headaches a lot.

Patient Update November 30, 2006

2006-11-30T13:57:00.000-05:00

Patient had dizziness about 15 minutes after raisin bran and soymilk. Called Dr. to get appointment for checking low blood pressure and high sugar levels. Patient may need a glucose stress test. Patient may need to add sugar or wheat free diet. Asked Patient to have Bagel on Dec 1st instead of cereal. Days that begin with dizzy spell seem to be not as good as days that have no dizziness after the morning meal. Supplements taken today, melatonin taken last night.

Patient remarked that dizziness is fading in strength each day.
-gjh

Patient seems to be improving.
Has exrecised, which helps patient stay alert.
Still takes the supplements and that is helping.
Not much eye drooping as before.
Patient still mentions about hearing things or telling me something is amiss but not as often as in the past.
-gwh

Patient was hearing children in the bedroom (this was after it got dark outside) did not know the time? Just happened to walk into the bedroom and Patient was asking about the voices while cph sat in the chair across the room. This may have occurred after eating dinner?
-gwh

Had cph remove SAM-e dose from pill boxes for now as a result of brain trending towards hyperactivity-possible seritonin or receptor enhancement/anti depression. Perhaps exercise is sufficient mood enhancement.
--gjh

SAM-e for SZ

2006-11-30T12:08:00.001-05:00

"Two independent lines of inquiry have implicated some disturbance of one-carbon cycle metabolism in affective disorders. Folic acid deficiency commonly leads to depression, and S-adenosylmethionine has been reported to have antidepressant properties. Methionine adenosyltransferase has been reported to be underactive in depression and schizophrenia and overactive in mania. This study reports the effects on erythrocyte methionine adenosyltransferase (MAT) kinetics (Vmax) of a 2-week treatment in a population of patients housed on a psychiatric research ward. The drug-free schizophrenic patients and depressives had, upon admission, low Vmax values, and the drug-free manic patients had high Vmax values on admission. After 2 weeks of appropriate treatment, the values for all three patient samples showed significant normalization (i.e., the levels rose in schizophrenics and depressives and fell in manics). We have further shown that pretreatment low levels of erythrocyte membrane phosphatidylcholine in depressives and high levels in manics show statistically significant normalization following 2 weeks of pharmacotherapy. The significance of these results is discussed."(1.)

"SAM-E (also known as SAM or AdoMet) is a derivative of the amino acid, methionine. It's formed when methionine combines with adenosine triphosphate (ATP), a nucleotide present in all living cells. ATP is the major source of cellular energy. The liver uses this process to make SAM-E, as much as 8 grams of it every day, when the liver is perfectly healthy. Liver disease, osteoarthritis and the overuse of prescription drugs or over-the-counter medications can diminish the body's production of SAM-E. A small amount of SAM-E is found in food, but it is highly unstable and an unreliable means of increasing blood levels." (2.)

"As a methyl donor, SAM-E "donates" units called methyl groups, which contain hydrogen and carbon atoms, to other substances. This process is called methylation, and it is one way in which the body protects itself from damage on the cellular level."(2.)

SAM-E facilitates the manufacture of brain neurotransmitters

"Methyl donors help to protect against cancer, heart disease, neurological disorders, and many age-related problems, and facilitate the manufacture of DNA and brain neurotransmitters. SAM-E is involved in more than 50 methylation reactions in the body, including the regulation of various hormones and neurotransmitters such as serotonin, melatonin, and dopamine."(2.)

"Once SAM-E donates its methyl group to choline, creatine, carnitine, DNA, RNA, epinephrine, and other compounds, it is transformed into S-adenosyl-homocysteine, (SAH). SAH donates its sulfur molecule to sulfur-containing amino acids such as cysteine, from which glutathione is formed. SAH then gives up its adenosine molecule to yield homocysteine. Homocysteine is a potentially toxic amino acid and an independent risk factor for coronary disease. Folic acid, choline, or betaine can change homocysteine back to methionine in the presence of vitamin B12, or convert homocysteine into cysteine and glutathione in the presence of vitamin B6. For this reason, it is recommended to supplement your diet with vitamin B12 and B6 when taking SAM-E. SAM-E is particularly important for the liver because glutathione is synthesized from it. Glutathione is crucial for liver function. A good portion of liver SAM-E is turned into glutathione. Glutathione is the liver's natural antioxidant."(2.)

"The synthesis of SAMe is intimately linked with folate and vitamin B12 (cyanocobalamin) metabolism, and deficiencies of both these vitamins have been found to reduce CNS SAMe concentrations. Both folate and vitamin B12 deficiency may cause similar neurological and psychiatric disturbances including depression, dementia, myelopathy and peripheral neuropathy. SAMe has a variety of pharmacological effects in the CNS, especially on monoamine neurotransmitter metabolism and receptor systems. SAMe has antidepressant properties, and preliminary studies indicate that it may improve cognitive function in patients with dementia."(3.)

"Several open and double-blind studies suggest that SAMe may have an anti-depressant effect, and further studies are indicated. SAMe may exert a beneficial effect selectively on endogenous rather than neurotic depression. SAMe crosses the blood-brain barrier. SAMe is involved in several central enzyme pathways relating to transmethylation and folate and monoamine metabolism as well as in membrane function and neuro-transmission." (4.)

Links:

(1.) Abnormalities of one-carbon metabolism in psychiatric disorders: study of methionine adenosyltransferase kinetics and lipid composition of erythrocyte membranes. Smythies JR, Alarcon RD, Morere D, Monti JA, Steele M, Tolbert LC, Walter-Ryan WG. Biol Psychiatry 1986 Dec;21(14):1391-8
http://www.psycom.net/depression.central.same.html

(2.) http://www.healingdaily.com/conditions/sam-e-1.htm

(3.) The clinical potential of ademetionine (S-adenosylmethionine) in neurological disorders. Bottiglieri T, Hyland K, Reynolds EH - Metabolic Disease Center, Baylor Research Institute, Dallas, Texas.
http://www.psycom.net/depression.central.same.html

(4.) S-adenosylmethionine and affective disorder. Carney MW, Toone BK, Reynolds EH - Department of Psychiatry, Northwick Park Hospital, Harrow, England. Am J Med 1987 Nov 20;83(5A):104-6
http://www.psycom.net/depression.central.same.html

--gjh

Lipitor - Glial cell interference

2006-11-29T19:04:00.000-05:00

Lipitor passes the blood brain barrier and interferes with cholesterol's roll in providing synaptic connections between neurons. The brain cannot get cholesterol from the blood supply and relies solely on the cholesterol synthesis production by glial cells in the brain.

Patient was taking Lipitor for 30 days and quit the drug as a result of a muscular side effect.

http://www.spacedoc.net/lipitor_thief_of_memory.html

Heavy Metal Toxicity

2006-11-29T15:53:00.000-05:00

We were told by Patient that at a young age (10), with bare hands, the Patient had played with Mercury from a broken thermometer. So, I am researching what effect Mercury would have on the Patient.

"The "silver" fillings in your teeth - Dental Amalgams - are still widely used by the dental profession in most parts of the world. The "Amalgam" consists of a mix of metals - Generally 50% Mercury, 35% Silver, 15% Tin and other metals. But is it safe to put so much Mercury, the most toxic non-radioactive metal known to man, into the mouth of a person? There is now a growing mountain of evidence that it is NOT safe to do so."(1.)

"Mercury Destroys Brain Cells. Dr. Boyd Haley, Ph.D., a biochemist at the University of Kentucky, is probably one of the world's top experts on mercury toxicity. Hear this fascinating review of the irrefutable evidence that links mercury toxicity to Autism and Alzheimer's disease."(1.)

"Mercury in vaccines - One hundred years ago, children received 1 vaccine (the smallpox vaccine). Forty years ago, children received 5 vaccines routinely (diphtheria, pertussis, tetanus, polio, and smallpox vaccines) and as many as 8 shots by 2 years of age. Children now receive 52 vaccines, in the form of 15 shots, by the time they are 6 months of age if they receive all the recommend shots, including the Prevnar pediatric pneumonia shot. Vaccines contain THIMERSOL (mercury), MSG, aluminum, formaldehyde, sucrose and phenoxyethanol, which is antifreeze, among many other things. Thimerosal, a vaccine ingredient, is nearly 50% mercury. Mercury is a NEUROTOXIN. EPA 'safe' levels are: .1 microgram per 1.0 kilogram of body weight per day. Vaccines contain 12.5 to 25.0 micrograms of mercury, and a 'well baby' visit can see your child have between 50 and 62.5 mcgs of MERCURY injected into their bloodstream. The CDC (US) has found a trend linking autism to mercury laden vaccines. Thimerosal is a registered pesticide with the Department of Pesticide Registration of the Environmental Protection Agency."(1.)

[soon to be completed]

Links of Interest:
http://www.theepochtimes.com/news/6-2-27/38658.html

Mercury Autism http://hatingautism.blogspot.com/2006/10/mercury-caused-autism-epidemic-please.html

(1.) Is Mercury Amalgam Fillings slowly poisoning us?
http://www.shirleys-wellness-cafe.com/amalgam.htm

Oxidative Stress

2006-11-29T14:48:00.000-05:00

OXIDATIVE STRESS AS MARKER OF POSITIVE SYMPTOMS OF SCHIZOPHRENIA - supports the use of Antioxidants in recovery protocol

"Our study also demonstrates a reduction in superoxide dismutase activity and an increase in protein carbonyl concentration in the CSF of tardive dyskinesia patients. Although they did not pass the statistical test, it is important to discuss the findings in the context of the oxidative stress hypothesis of tardive dyskinesia. Superoxide dismutase is an enzyme critical in the of superoxide, a normal byproduct of oxidative metabolism (32). Attenuated activity of superoxide dismutase may contribute to the increase of oxidized protein."(2.)

" The hypothesis of oxidative damage to striatal neurons mediated by neuroleptic enhancement of glutamatergic neurotransmission is supported by reports that vitamin E reverses the symptoms of tardive dyskinesia; the anecdotal reports have been sustained by double-blind, placebo-controlled studies with vitamin E (43-45). Notably, patients are more responsive to treatment with vitamin E earlier in the course of their disorder, consistent with the model that the oxidative damage is cumulative over time and would involve functional impairment before frank degeneration."(2.)

Links:

http://72.14.203.104/search?q=cache:LHVarP96W18J:facta.junis.ni.ac.yu/facta/mab/mab200202/mab200202-05.pdf+peroxynitrite+schizophrenia&hl=en&gl=us&ct=clnk&cd=8&client=firefox-a

(2.) http://ajp.psychiatryonline.org/cgi/content/full/155/9/1207

Update November 29

2006-11-29T10:43:00.001-05:00

4:45pm. Just talked to Patient. Exercised today and attempted to eat a tuna fish sandwich for lunch, but only ate a few bites because it "didn't taste right." Says that there are still lingering side effects of the discontinued medication. Other than that, patient sounded well and was able to carry on a conversation without any hesitation. No experiences today of hearing voices.

Patient slept ok last night - no nightmare and took 1mg melatonin before bed. Patient had breakfast (raisin bran and soymilk without dizziness) & supplements today before 10:30 AM. Spoke clearly and quick thinking.

4PM conversation with Patient responded great, excited, happy. Asked patient about playtime activities when Patient was 10 years old, there was no delay in recalling the memory.

A study published Nov 28 2006 suggests that an area of the brain has been found to have shorter pathways in SZ patients. http://www.annals-general-psychiatry.com/content/5/1/19

The PDF of the study, which you may find on the link above, has diagrams and MRI information.

--gjh

Cerebral Allergies

2006-11-28T15:24:00.000-05:00

Several standing dizzy spells occurred 30 minutes after eating Raisin Bran and soymilk at 12pm. Supplements had not yet been taken.
--sw

No panic or hallucinations reported today. Patient exercised today. Pills found left in todays box at 7pm. Worked with cph to fully manage the pill box and monitor its use. All other supplements have been removed from access by Patient. Multivitamins were found to contain copper and are removed from Patient's access. Discussed these details with Patient by phone. Had not had dinner yet by 8PM. Verified no hallucinations or voices today. Evening meal was antipasto salad - no dizziness.
--gjh

(1)"Dairy and gluten allergies are common to people with schizophrenia," said Carter, who has headed the Schizophrenia Foundation for nearly 20 years. "I've seen many cases when removing them - a majority of the symptoms will abate. These are confirmed by orthomolecular doctors around the world."

(1) Patricia Lefave - "Nuts R Us News" Blog - DONNA NEBENZAHL, The Gazette - Published: Monday, May 08, 2006
http://pistachiopress.blogspot.com/2006/08/conventional-psychiatry-did-not-help.html

Vitamin E

2006-11-28T15:10:00.000-05:00

"Vitamin E consists of eight different compounds — four tocopherols and four tocotrienols (sic...). A varied diet eaten by humans may contain all eight compounds. The most abundant sources of tocotrienols are the oil fractions from cereal grains, including barley, rice, rye and wheat, and the fruit of the oil palm. Commercial quantities of tocotrienols are currently extracted from palm oil and rice bran oil. Tocopherols are also present in these sources but are more abundant in the oils extracted from soybean, corn (maize), cottonseed and sunflower seed, which are now the primary commercial sources for natural vitamin E products.

Y-Tocopherol appears to be more potent than A-tocopherol in increasing superoxide dismutase (SOD) activity in plasma and arterial tissues as well as manganese SOD and copper/zinc SOD protein expression in arterial tissues. SOD is a major antioxidant enzyme" (1.)

"Benefits for cardiovascular health —
The strongest evidence yet for tocotrienols comes from a clinical study conducted by the Kenneth Jordan Heart Research Foundation in New Jersey, USA. The study, now in its fifth year, has been evaluating 50 patients who had stenosis of the carotid artery. It is appropriate here to explain what stenosis is and the problems associated with its treatment. Stenosis means constriction or narrowing — the accumulation of plaque over time causes stenosis of the arteries. Stenosis of the carotid artery can cause stroke. "(2.)

"In addition to enzymes, the animal cell uses many other chemicals to protect against oxygen free-radicals. Vitamin E is the main free-radical trap in the (lipid) membranes. Vitamin C acts as an anti-oxidant in the non-lipid ("watery") portions of cells, between cells and in the bloodstream. Melatonin, a hormone produced by the pineal gland in decreasing quantities with aging, efficiently crosses membranes (including the nucleus) and is effective against hydroxyl radicals." (3.)

(1.) Li, D. et al. (1999) Relative effects of Y- and A-tocopherol on low-density lipoprotein oxidation and superoxide dismutase and nitric oxide synthase activity and protein expression in rats. Cardiovasc. Pharmacol. Ther., 219–226.

(2.) Watkins, T.R. et al. (1998) Tocotrienols: biological and health effects. In: Antioxidant Status, Diet, Nutrition and Health, (see ref. 2) pp.479–496.

(3.) THE FREE RADICAL THEORY OF AGING, Ben Best
http://www.benbest.com/lifeext/aging.html#radical

Melatonin, DHEA for SZ

2006-11-27T17:58:00.000-05:00

In our Patient, TD presents itself as a long closure of the eye lids as if the Patient was asleep. If you engage the Patient in conversation you find the Patient awake and responding and when you discuss a topic the Patient is excited about, the Patient will open the eyes. Patient is aware that eyes are closed and describes them as being clamped shut.
--gjh

"A common side effect of antipsychotic medications used to treat schizophrenia is a condition called tardive dyskinesia, a movement disorder of the mouth characterized by a constant chewing motion and darting action of the tongue. In a study(1.) of 22 people with schizophrenia and tardive dyskinesia caused by antipsychotic medications, those who took melatonin supplements had significantly reduced mouth movements compared to those who did not take the supplements."

(2.) "antipsychotics produce their effect by reducing DHEA." "DHEA naturally begins to decline around age twenty to twenty-five, and this probably occurs earlier in schizophrenics. In addition to this decline, interference with the availability of DHEA may occur because of another adrenal hormone, cortisol, and, beginning at puberty, the hormone, testosterone."

"In my articles on evolution and sleep at this website, I connect the pineal hormone, melatonin, with DHEA. I suggest melatonin may be involved in producing receptors, chemical doorways, for DHEA. For DHEA to produce its growth promoting activities on neurons, it must have a pathway into the neuron. Melatonin stimulates these receptor at night. I think this pathway is reduced in schizophrenics, because nighttime melatonin is reduced in schizophrenia (Biological Psychiatry 1989, 25: 500). Proper amounts of melatonin are necessary for slow wave sleep to occur; the deepest stage of slow wave sleep is stage 4. Lack of stage 4 sleep is documented in schizophrenia. (sic) ...others think reduced melatonin may be involved in some forms of schizophrenia, however, the investigators do not mention DHEA."

"The drugs used to control schizophrenia, I suggest, actually exert their effects by stimulating DHEA production. That is, "...antipsychotic potencies of most neuroleptic drugs closely correspond to their prolactin-releasing potencies at low doses..." (Biological Psychiatry 1990, 27: 1204). Therefore, it may actually be DHEA that ameliorates schizophrenia upon antipsychotic drug administration. Schizophrenia is thought to result from dopaminergic over-activity; essentially all antipsychotic drugs block postsynaptic dopamine receptors. This increases prolactin release. The dopaminergic agonist, bromocriptine, often used as an anti-prolactin agent, produces hallucinations, delusions, and confused thinking when used in excess."

"Schizophrenia results from lack of cerebral hemisphere growth as a result of severe reductions in DHEA and melatonin during brain growth and development. It is triggered by events later in life that reduce DHEA availability and increase the negative effects of cortisol. I suggest treating schizophrenics with melatonin at night and DHEA during the day may help in some circumstances, depending on the level of damage done by prolonged cortisol exposure."

(3.)"Cortisol also inhibits hippocampal neurogenesis, but DHEA has a stimulatory effect. Cortisol can actually kill hippocampal neurons, and does so increasingly with aging and stress, but this effect can be reversed with melatonin and Insulin-like Growth Factor (IGF-1) [THE JOURNAL OF NEUROSCIENCE; Aberg,MA; 20(8):2896-2903 (2000)]."

Useful Links:
http://www.umm.edu/altmed/ConsSupplements/Melatonincs.html
http://www.anthropogeny.com/Schizophrenia.htm
http://www.benbest.com/nutrceut/melatonin.html
http://www.benbest.com/nutrceut/DHEA.html

(1.)Shamir E, Barak Y, Shalman I, Laudon M, Zisapel N, Tarrasch R, et al. Melatonin treatment for tardive dyskinesia: a double-blind, placebo-controlled, crossover study. Arch Gen Psych. 2001;58(11):1049-1052.

(2.)James Michael Howard - http://www.anthropogeny.com/Schizophrenia.htm

(3.) Chapter 3 -- Learning, Memory and Plasticity, by Ben Best
http://www.benbest.com/science/anatmind/anatmd3.html

SZ Subtypes

2006-11-27T11:36:00.000-05:00

Patient took supplements today. No known thought disorder today.

I'm researching subtype of SZ based on memories of Patients past symptoms and pre SZ symptoms. Indications are High Histamine and/or Pyroluria. Patient had history of quick acting, swelling skin reactions to scratches or insect bites. Chronic pre-med SZ symptoms include temper outbursts, delusional thinking, mood swings, anxiety, depression - Patient was misdiagnosed depressed.

useful links:
http://www.hriptc.org/BioTreatment.html
http://answers.yahoo.com/question/index?qid=20061013040917AAWqglK
-gjh

There is a strong possibility that Patient is suffering from an undetected allergy that has affected the brain (a cerebral allergy). Patient experienced highly allergic reaction to eating ice cream 5 years ago and had to go to the hospital. At one point in Patient's past, there was a craving for cottage cheese and frozen yogurt. We've discovered in our research that most often the foods we are allergic to are often times the same foods that we crave. There's a chance that the Patient has become more intensely allergic to dairy products over time and that may have brought on the SZ symptoms because of the body's inability to cope with the allergy. The allergy left undetected may have created what has seemed to appear to be a chronic condition. Dairy molecules can have a negative impact on the brain in those who are allergic to it. Beginning yesterday, consumption of dairy products was stopped for a period of time. We will monitor Patient over the next week or so to see if/how SZ symptoms improve.

Some very interesting allergy information is available at the following link: http://www.springboard4health.com/notebook/health_food_addiction.html
--sw

Blog Launch November 26, 2006

2006-11-26T15:49:00.000-05:00

Natural medicine approach to Schizophrenia - herein referred to as SZ. A daily progress of a family member we refer to as "patient" who is starting the orthomolecular protocol. Entries will be done by family members reporting their observations of the patient.

Patient began assortment of supplements yesterday. Patient reported nightmare from the 1mg Melatonin taken before bed a few days ago and hasn't taken it since. Dream recall may be a positive effect of supplementation whether nightmare or not. The full program began at Day 0.

-7PM Patient questions family about cars missing from driveway (not missing.)

Family Practice Dr.:
Margolis, Steven, MD - Alternacare
43956 Mound Rd., Sterling Heights, MI 48314
Phone: (586) 323-1122

NOTE: This nutritional schedule is under development and is NOT developed or yet reviewed by the family doctor. The information used to create the schedule was pulled from many hours of research. Posts will be updated and corrected when necessary.

Personal note: There is no single source for this information, there is no one person you can talk to, one book you can read, one doctor to visit. This is why we are providing the total information we have found that deals with our unique SZ case. In the event it helps even one family, it will be worth the effort. While it is necessary to accurately document the progress of this method, we will include information that is research oriented for understanding deficiencies, symptoms, and methods for improving the quality of life and restoring the biochemical health. Clearly, the drugs available today (2006) mask the symptoms and present significant risk of serious side effects.
--gjh

useful links:
http://en.wikipedia.org/wiki/Orthomolecular_medicine
http://en.wikipedia.org/wiki/Orthomolecular_psychiatry

In the past, the Patient has taken Miatake, CoQ10, DHEA, copper and Lecithin. SZ is said to be found in people with high copper levels! Patient was taking copper as directed by doctor to help improve a separate health issue. Over a month ago the Patient was still taking Omega 3's, Lecithin and some B vitamins, as well as taking Niacin and small dose of DHEA. Patient has stopped taking copper.

Psychiatric history: Patient developed delusional thinking 2003, with hallucinations occurring 2006. Patient was prescribed Lexapro for depression. Insurance company changed prescription to Celexa. Following administration of Celexa, patient's SZ symptoms became more intense. Patient then visited a different doctor and was diagnosed with Paranoid SZ and prescribed 1 mg of Respirdal. Patient became very lethargic. Thinking and speaking ability slowed down significantly. After 2 weeks of these side effects, patient was switched to 5 mg of Abilify. Strange behaviors and paranoia, audible and sensory hallucinations increased. Then dosage was increased to 20 mg. Eyes began to droop involuntarily. Violent hallucinations experienced. Continuous delusional thinking and thought disorder continued with no relief. Experienced dizziness, backache and metallic taste in mouth often. Ironically, delusional thinking and hallucinations were observed a half hour after patient ingested the Abilify drug (a drug that is supposed to reduce those very symptoms).

20 mg of Abilify was discontinued after 6 weeks. Catatonic demeanor and what appears to be Tardive (heavy eyes, long face-lack of emotion) still present a week later.
--sw

Frontal Temporal Dementia - FTD - Formerly Orthomolecular Schizophrenia Protocol

FTD Information Links

Patient Update March 26, 2009

Patient Update December 23, 2008

Current Diagnosis - FTD

Seizure Frequency and Diet

Gluten Intolerance? Celiacs?

Naturopathic Body Scan

Medication Frustration

Important findings of B-12

Vitamin B12: Vital Nutrient for Good Health

MEASURING B12 DEFICIENCY

NERVOUS DISORDERS

PREVIOUS POST

Current Diagnosis.

Notes for followup

Patient Overview

Patient Update

Patient Update June 21 2008

Pfeiffer Treatment Center, Warrenville, Illinois

Patient Update June 14 2008

"Histamine Metabolism"

Vitamin B3 Test results

Patient Update Nov 23, 2007

vitamin B12 deficiency

Some updates & observations

Patient Update November 18, 2007

ORTHOSTATIC HYPOTENSION was the only condition to come out of 8 days of tests at a Henry Ford Hospital epilepsy center. We have not had a full briefing from the doctors yet. Patient is returning home tomorrow. We are looking at information regarding blood pressure and blood supply to brain now.

Hospital Visit

Patient Update October 11, 2007

Patient Update July 16 2007

Patient Update May 23 2007

Patient Update May 22 2007

Patient Update May 17 2007

Patient Update May 16, 2007

Patient Update May 15, 2007

Patient Update May 11, 2007

Patient Update May 10, 2007

Patient Update May 7, 2007

Patient Update May 6, 2007

Time for a Specialist

For Further Consideration

Lamotrigine Info - Medication Candidate for seizure relief

Patient Update

Patient Update April 26, 2007

Patient Update April 22, 2007

DHEA, Melatonin, Seizures

Phosphatidylserine (PS)

Patient Update February 9, 2007

Patient Excitotoxins

PRODH Deficiency

Balancing mood with L-Theanine

Patient Update January 15, 2007

Patient Update January 10, 2007

Patient Update December 24, 2006

Patient Update December 23, 2006

Patient Update December 22, 2006

Patient Update December 19th 2006

Patient Update December 18th 2006

Patient Update December 17th 2006

Patient Update December 16th

Patient Update December 15, 2006

Dimethylglycine (DMG) links

Hyperthyroidism

Supplements and Epilepsy

Magnesium and the Brain

Sugar Cravings

Supplements for Seizure Control

L-Carnosine

AMPAKINE Structures

Patient Update December 11, 2006

Patient Update December 9, 2006

Aspartame Poisoning (Equal®, Nutrasweet® and Spoonful®) - seizures, memory loss, methanol poisoning

Questions to ask doctor

Patient Update December 8, 2006

Patient Update December 7, 2006

Sleep-related Epilepsy

Seizure Recovery Story - a natural approach

Glutamine and GABA

Patient Update December 6, 2006

Vitamin B12:
Vital Nutrient for Good Health

MEASURING B₁₂ DEFICIENCY