Thursday, December 27, 2007

Vitamin B3 Test results

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.

Monday, November 26, 2007

Patient Update Nov 23, 2007

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.

Tuesday, November 20, 2007

vitamin B12 deficiency

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

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

Some updates & observations

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).

Sunday, November 18, 2007

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.


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

Wednesday, November 14, 2007

Hospital Visit

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

Thursday, October 11, 2007

Patient Update October 11, 2007

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.

Monday, July 16, 2007

Patient Update July 16 2007

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/

Wednesday, May 23, 2007

Patient Update May 23 2007

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

Patient Update May 22 2007

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.)

Friday, May 18, 2007

Patient Update May 17 2007

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.

Wednesday, May 16, 2007

Patient Update May 16, 2007

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.

Tuesday, May 15, 2007

Patient Update May 15, 2007

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.

Friday, May 11, 2007

Patient Update May 11, 2007

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

Thursday, May 10, 2007

Patient Update May 10, 2007

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

Monday, May 7, 2007

Patient Update May 7, 2007

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.

Sunday, May 6, 2007

Patient Update May 6, 2007

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.

Tuesday, May 1, 2007

Time for a Specialist

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

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

Monday, April 30, 2007

Lamotrigine Info - Medication Candidate for seizure relief

Lamotrigine Message boards-

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

Patient Update

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.

Thursday, April 26, 2007

Patient Update April 26, 2007

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

Sunday, April 22, 2007

Patient Update April 22, 2007

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

Saturday, February 24, 2007

DHEA, Melatonin, Seizures

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

Thursday, February 15, 2007

Phosphatidylserine (PS)

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

Friday, February 9, 2007

Patient Update February 9, 2007

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

Friday, January 19, 2007

Patient Excitotoxins

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

Thursday, January 18, 2007

PRODH Deficiency

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

Tuesday, January 16, 2007

Balancing mood with L-Theanine

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

Monday, January 15, 2007

Patient Update January 15, 2007

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

Wednesday, January 10, 2007

Patient Update January 10, 2007

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