State of the Art Answers to 500 Mold Questions
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About this ebook
If you simply want to know what to do to obtain a diagnosis that is accurate and begin therapies that work, 500 Answers is a must read. If you need solid information on how to go about testing your home, school and workplace to see if those buildings could be making you sick, 500 Answers is for you as well.
If you don’t have any experience with human health effects cause by wet buildings, and you are understandably overwhelmed by the fuzzy “science” on the Internet, 500 Answers is your portal to a sharp vision of what is wrong and what needs to be done.
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State of the Art Answers to 500 Mold Questions - Ritchie C. Shoemaker MD
Copyright 2014 by
Ritchie C. Shoemaker, MD
All rights reserved
Permission to reproduce in any form
must be secured from the author.
Please direct all correspondence and orders to
Ritchie C. Shoemaker MD
500 Market St Suite 103
Pocomoke, Md 21851
Printed in the United States of America
ISBN: 9781483533643
TABLE OF CONTENTS
23andme
Absence of HLA susceptibility and illness
Absence of HLA susceptibility and illness due to MARCoNs
Access to care
ACTH, suppression by use of oral cortisone
Activated charcoal
Acute exposure
Acute illness after exposure
ADH
Air conditioners, window units
Air sampling
Alcohol use
Alternative therapies
Ammonia
Androgens, aromatase
Androgens, replacement
Anesthesia
Animals with mold illness
Anti-inflammatory pathways in workplace disputes
Anti-inflammatory pathways, muscles
Aromatase (see androgens)
Aspergillus in sinuses
Autism
Autoimmune response (see T regs)
Avoidance of re-exposure
Bartonella
BEG spray, gentamicin resistant
BEG spray, whole body effects
BEG spray, die-off
Beta glucans
Bibliographies
Bile/gallbladder problems
Bile problems (enterohepatic recirculation)
Biological supplements
Biowarfare
Black tongue
Borax as a cleaning solution
Building testing
C3a
C4a rise from chlorophyll
Candida
Cardiomyopathy
Case definition for mold illness
CD4 and CD25
CD57
CD57 natural killer cells
Celiac disease and HLA
Chiari
Chlorella and mercury
Chlorella, Dr. Klinghardt
Cholestyramine, with liquids
Cholestyramine, re-exposure
Cholestyramine, binding other compounds
Cholestyramine and antibiotics, simultaneous use
Cholestyramine and doxycycline, simultaneous use
Cholestyramine and food
Cholestyramine and mag citrate
Cholestyramine, cessation
Cholestyramine, costs
Cholestyramine dosing
Cholestyramine dosing in children
Cholestyramine intolerance; gastroparesis
Cholestyramine, light
Cholestyramine, long term
Cholestyramine, mixing
Cholestyramine, short duration of Rx not helpful
Cholestyramine, side effects
Cholestyramine treatment before data base
Cholestyramine treatment without a data base
Cholestyramine, use in re-exposure
Cholestyramine, use in (brown) recluse spider bites
Cholestyramine simultaneously with bio-identical hormones
Cholestyramine, used with fatty meals
Cholestyramine, used with non-sweetened almond milk
Chronic inflammatory response syndrome
Cleaning
Climate and CIRS
Coag neg. staph (see MARCoNS section)
Coagulation disorders in CIRS
Cold weather
Colestipol
Colonic irrigation
Communication with other physicians
Consensus statement
Corticosteroids
Crawl space and illness
Crawl space and flooding
Cross contamination
Daughter with 4-3-53 going to college
DDAVP
Demyelination
Denial
Depression
Diagnosis
Diagnosis Lyme, coinfections
Diagnosis, minimum number of laboratory studies
Diagnosis, mycotoxins
Diagnosis, prolonged symptoms after exposure
Diet
Dietary restrictions, carrots
Differential diagnosis
Dishidrosis
Degenerative joint disease
Duration of therapy (See cholestyramine section
Education, patient
ERMI
ERMI/ HERTSMI-2
Erythropoietin
Essential oils
Evaluation of buildings before rental or purchase
Exercise
Exposure, living on a boat
Extreme avoidance
FACT
Flu shots
Food intolerance
Foreign bodies, medical hardware and possible illness
Fungal lung infection
Fungal sinusitis
Gallbladder
Genomics, cure
Genomics, PAXgene tube
Hair loss, catagen versus telogen
Heavy metals #1 (see metals)
HEPA air filtration
HLA#1
HRV/ERV
Hydrocortisone replacement, ACTH suppression
Hypothalamic injury
Hypothyroidism
IgA Nephropathy
Illness, long term
Indoor house plants
Indoor mold versus outdoor mold
Infection from mold
Insurance issues
Intensification
Interstitial cystitis (IC)
IV phosphatidylcholine and IV glutathione
Joint pain
Kidney failure
Labs
Legal
Litigation costs
Lyme, C4a
Lyme disease
MARCoNS
Medication, antidepressants
Melanocyte stimulating hormone (alpha MSH)
Melanotan
Membership
Methylation
Migraines after rifampin and BEG spray combination
Mitochondrial disease
Moisture meter testing
Mold and cancer
Mold and VIP; duration of Rx
Mold in the attic
Mold in cars
Mold growth, winter
Mold illness, concerns
Mold illness, pediatric
Mold in automobiles
Mold in cars
Mold smell on skin
Mold symptoms by mold type
Mold, systemic
Mold testing
Mold versus Lyme
MSH, lab testing
MSH, hypo-pigmentation
MSH, for sale
MTHFR
Multiple chemical sensitivity (MCS)
Multisystem, multisymptom illness
Musical instruments as a source of CIRS
Muscle twitching
Mycology labs
Mycotoxins
Mycotoxins and food
N95 mask
Neuropsychiatric symptoms
NeuroQuant, reading the test results
New home construction
No-amylose diet
Non-porous possessions
Nose bleeds
Obtaining medical advice
Omega 3
Ongoing therapy with ongoing symptoms
Outdoor environmental exposures
Outdoor exposure causing illness
Outdoor illness
OWCP
Ozone
Panchakarma
PANS/PANDAS
Paralysis
Pediatrics
Personal air ionizers and diffusing thieves' oil
Pets and CIRS
Phase I detox compounds
Physician certification
Physician question, cholestyramine endpoint
Physician referral information
Physician request, case management. Case #002
Physician training
Porous materials
Post exertional malaise
Post-remediation testing
Pregnancy and CIRS
Purifier, air
Rashes
Re-exposure comments
Regaining health
Relapse after re-exposure
Remediation, fogging
Rheumatoid arthritis
Scorpion envenomation
Serotonin, melatonin, dopamine
Sicker-quicker
Silicone implants
Skin changes
Smell and evidence of mold
Smell as evidence of water-damaged buildings
Spore trap versus ERMI
Steroids (see corticosteroids also)
Sudden onset of severe symptoms
Supplements
Success rate of remediation
Swiffer testing
Swimming, indoors
Symptoms
Thyroid cancer
Thyroid therapy
Tick bite
Tinnitus
Toll receptors
Tongue, nodules
Toxic black mold
Toxins, storage in fat
Treatment approach
T regulatory cells
Unknown mold
Unusual lab abnormalities
Urinary testing for mycotoxins
Vasculitis
VCS, non-neurotoxins
VEGF, high
VIP, baseline labs
Viruses
Vitamins, binding by CSM
VOC
Weight loss
Welchol
Worms and mold
Zeolite
FOR THE FUTURE
APPENDIX 1 Glossary of acronyms
APPENDIX 2 HERTSMI-2 scoring sheet
Index
PREFACE
Sickened by moldy buildings? Need facts and answers fast? Here is your guide: State of the Art Answers for 500 Mold Questions. Thorough and reliable, 500 Answers
is as current as one can find on a subject where bad information abounds. But, as far as sick people go, what I write here will need to be updated when we finally have genomic information. The world of diagnosis and treatment of chronic inflammatory response syndromes (CIRS) acquired following exposure to the interior environment of water-damaged buildings (WDB) now relies on proteomics and differential diagnosis. Call it mold illness,
if you will. You need to know the latest and best information about human health effects caused by wet, moldy buildings and the importance of understanding human health effects before remediation begins. The time to share what really is going on in sickened people has been with us for nearly 20 years, yet so much just plain wrong information is out there. Our knowledge has reached new levels as therapies like use of vasoactive intestinal polypeptide (VIP) show us where we need to go to reduce reactivity and stop the systemic inflammation of CIRS-WDB.
But, the final frontier of diagnosis and treatment comes from differential gene activation caused by the many entities found in the indoor air of WDB. We know that genomics is such a big deal; how long do we have to wait to add the vitally important gene information? We think the coming scientific revolution will likely happen before Thanksgiving, 2014. We won't just be talking about genetic susceptibility then, but also gene activation and gene suppression. We won’t be focusing just on commensal coag neg staphs but we will be discussing reversal of the known genomic effects these supposedly benign organisms have. We won’t be talking about using pro-biotics as just a good idea
any more; we could be discussing the differential anti-inflammatory effects of such use of bacterial supplements to correct abnormal metabolomics from the gut. Thanksgiving is just five months away.
So why write this compendium now if use of genomics will lead us to an entire new plane of understanding? This answer is simple: at www.survivingmold.com (SM) we are still getting the same Top Ten questions routinely. The information gap between established readers of SM and new visitors tells me that we still have a lot of information and understanding to share with people interested in this increasingly common, and increasingly complex medical problem.
And when genomics arrives, the information gap could become a chasm overnight.
I read comments from mold patients
and mold docs
that tell me that a lot of really bad information about human health effects is still out there. Some ideas are just silly but others are dangerous, as affected patients might actually believe them, spending huge amounts of money and suffering untold medical and social loss as a result. Whether the bad ideas are from the Inspector General of the EPA, the (intentional?) absence of anything useful from the CDC, or from a mold profiteer taking wheelbarrows full of money in exchange for false hope doesn’t matter. False knowledge is dangerous.
Aldous Huxley told us that the key to understanding is casting out false knowledge. We apply his wisdom in this short book of 500 Answers to prepare for the arrival of new knowledge and new understanding from the human genome that is just around the corner.
Based on what we already know about the proteomics of CIRS, the days of ignorance about the pathophysiology of CIRS should be over, but just as we now celebrate useful therapies, we also know that our understanding has been shaped by less than one hundred blood tests. Compare that understanding to what we can mine from data sets of activity of 22,000 genes.
500 Answers includes new discoveries like the information we obtain from NeuroQuant that shows that the inflammation of CIRS causes the development of a distinctive fingerprint of injury to the central nervous system found just in CIRS-WDB patients. Better still, use of NeuroQuant shows us that the ability to correct the inflammatory response will in turn show correction of localized areas of grey matter atrophy in the brain. This result of treatment is unheard of in the world of brain injury. If you want to confirm that your executive cognitive functioning is due to exposure to WDB, do a NeuroQuant as part of the full work up.
If you simply want to know what to do to obtain a diagnosis that is accurate and begin therapies that work, 500 Answers is a must read. If you need solid information on how to go about testing your home, school and workplace to see if those buildings could be making you sick, 500 Answers is for you as well.
If you don’t have any experience with human health effects cause by wet buildings, and you are understandably overwhelmed by the fuzzy science
on the Internet, 500 Answers is your portal to a sharp vision of what is wrong and what needs to be done.
500 Answers has a complete Table of Contents, a roster of the many acronyms used and an index that will help you find out quickly what you want to know. The information in 500 Answers is correct but when we add genomics, the jargon terms and new information is going to require a steep learning curve. We welcome you to learn what you need to know now. We will help you with the new understanding too when the time comes.
Ritchie C. Shoemaker, MD
Pocomoke, Maryland
STATE OF THE ART ANSWERS TO 500 MOLD QUESTIONS
1. 23andme
I have 23andme genetic testing but can’t find a way to understand HLA SNPs vs. the specific tests recommended. Also, I have been told I have protomyxzoa rheumatica infection. Please help.
The future of medicine will include accurate genomic testing. I have little knowledge of the basis for the use of 23andme testing in clinical medicine. I am happy to review any data that you have that supports specificity and sensitivity of these tests underlying clinical illness.
It is my opinion that use of SNP testing is fraught with a significant possibility of error as mere presence of an SNP has nothing to do with gene activation/suppression. Presence of a SNP tells us nothing about regulation of the entire gene by microRNA.
I have never been able to confirm a diagnosis of protomyxzoa infection though I have seen a number of patients who have had testing done by Dr. Fry's lab in Arizona.
I am happy to review any data that you have to confirm this diagnosis with a particular eye to objective proteomic findings separate from findings on peripheral smear.
Please forward these findings to the website so that I may be of assistance to you.
2. Absence of HLA susceptibility and illness
Is it possible to become ill and stay ill without one of the HLA haplotypes associated with susceptibility?
Yes, we see approximately 95% of cases having one of the six HLA haplotypes that in turn comprise 24% of the normal population. That means 5% of ill people (cases) do not have HLA-driven susceptibility. The good statistical news is that for those 5% their prognosis is much better than those of the other 95% of cases. Treatment is still necessary for the non-HLA susceptible individuals. Even though they don’t have the HLA we are accustomed in seeing in cases, they will not self-heal. The standard response to the predictable response of how does HLA alone determine susceptibility
that I have used in the past is that biology is never 100% and HLA research is in its infancy.
That statement is still correct. In order to perform the research needed to show how defective antigen presentation is occurring, we would need a very large prospective study to be done on a multi-site basis.
Don’t forget, once MSH falls to below 35, additional susceptibilities to inflammatory illness develop.
3. Absence of HLA susceptibility and illness due to MARCoNs.
If a non-susceptible individual acquires an CIRS illness, could that condition solely be due to colonization for MARCoNs with its own genomic affects?
This is an interesting question from a reader from Australia. Specifically we are still counting on fingers on one deformed hand the number of people with true MARCoNs without MSH deficiency. If MSH deficiency is the mechanism for MARCoNs colonization (please don’t say infection; it is not an infection) then we can restate your question. Is there a mechanism to get sick solely due to MSH deficiency? That answer is yes. What we don’t see are people ill just from MARCoNs and without low MSH. What this means is that treatment with BEG spray alone will not take care of an inflammatory illness acquired following exposure to an interior environment of water-damaged buildings. Similarly, use of cholestyramine and subsequent protocols will not eradicate the MARCoNs. That treatment is specific for this biofilm-forming commensal.
Please note that researchers from Newcastle University in Australia were among the first to note the importance of MARCoNS first in facial pain first and then in Chronic Fatigue Syndrome. As I recall Dr. Timothy Roberts and Dr. Butts were early and prolific researchers in this field. It has been nearly 10 years since I have spoken with that group and hope that they have adopted use of MSH profiling as part of their susceptibility rosters for acquisition of MARCoNS. We hope to be publishing soon the genomic results of the MARCoNS biofilms study we completed not long ago.
4. Access to care
Is it possible to self-treat using your protocol?
The protocols that I use employ lab tests and diagnostic procedures that must be ordered by a licensed health care professional. I do not agree that it is safe for individual to take on this task without the ability to share what they want to do and what they should be doing with a trained expert. There are multiple physicians who have certified in this protocol listed on this website.
5. ACTH, suppression by use of oral cortisone
I know cortisone can suppress immune system as well as suppress the adrenal output but generally those rebound after cortisone is stopped. How does CIRS change this?
I am uncertain what you mean when you say cortisone can suppress the immune system,
but please recall that both ACTH and MSH are members of a hormone system called melanocortins. There is interaction between ACTH and MSH in the production pathway involving proopiomelanocortin in the hypothalamus.
For those with MSH deficiency, persistent suppression of ACTH following exogenously administered cortisol (or any of the related adrenal steroid compounds) is common and can be an ominous finding. Steroids have an important role in medicine; if the use will bring about needed changes in physiologic parameters, then the risk of suppressed ACTH is not too great. But optional use of prednisone for dermatitis, a mild flare of lung disease or sinus problems, for example, is best avoided.
6. Activated charcoal
My doctor thinks I am too ill to take cholestyramine and wants me to use activated charcoal in the middle of the night instead. Will that be as effective as cholestyramine?
There are a number of questions that we have answered on this website regarding alternatives to cholestyramine. We have abundant objective data showing that Welchol performs the same duties as cholestyramine but to date no other nostrum has been shown to be effective by publication of objective parameters before and after individual use. I am aware that a number of people value use of activated charcoal, particularly since it is not a prescription item. If you are going to use activated charcoal, please be sure to collect a database on inflammatory mediators before you start the medication and after one month to see where you are. Also, please don’t use multiple simultaneous interventions if you are collecting data.
I am uncertain as to why you would take activated charcoal in the middle of the night if you have a chronic fatiguing illness where restorative restless sleep is compromised. As always, of course, your physician has a duty to answer your questions and if your physician feels that taking charcoal in the middle of the night is the right way to go, then by all means you should listen to your doctor.
7. Acute exposure
I went camping this past weekend at Camp Woodlands in Annapolis. Shortly after we turned in for the night, one of my friends developed a significant cough, headache and congestion. Another friend had a flare of her pre-existing asthma. We left after one hour. Should we seek medical care?
Exposure to any number of environments can cause the acute onset of respiratory symptoms without necessarily being an inflammatory response syndrome caused by exposure to the interior environment of a water-damaged building. Classic chronic inflammatory response syndrome is symptomatic for over a month; we cannot say that applies to an exposure of less than 3 hours associated with an illness of less than 3 days.
You mentioned that you are beginning to feel better now several days after your exposure. If you do not have a multisystem, multisymptom illness it would make sense to observe and not initiate treatment. Having said that, if the visual contrast sensitivity (VCS) test is positive at this date, the likelihood that this finding will resolve without treatment is quite low. Having a VCS test done now provides a reasonable basis to look back 2 weeks from now to see whether this is developing into an ongoing syndrome.
I do not object to you having baseline labs done, including C4a and TGF beta- 1, together with MMP-9, as the acute exposure is not likely to have enough time to lower MSH and VIP but did have enough time to drive up inflammatory responses.
8. Acute illness after exposure.
My Mom's house flooded when she was away and it sat soaking for weeks. I went in for six hours scrubbing mold from walls in the home. I now am ill with sinus problems, sore throat and lung congestion. I now am irritable and moody with red eyes and temperature intolerance. Is this serious?
Certainly you have met the requirement for the potential for exposure and you have multiple health systems represented with multiple health symptoms. I would suggest that you take a look at the visual contrast sensitivity (VCS) test to gain a better idea of what all symptoms you might actually have and then to correlate those symptoms with an objective screening test. At some time it would make sense for your physician to evaluate you with the labs that we look at routinely as represented on the physician order sheet in the diagnosis section of this website. You need to have the labs present to secure the diagnosis and initiate treatment. Do not ignore your illness. I think that you have made a good start by contacting us. I hope you will follow through.
9. ADH
After a dose of cholestyramine I find my urinary frequency doubles to approximately 10-12 times per day. What is happening to me?
We would need to look at your level of anti-diuretic hormone (ADH) and simultaneously measured osmolality to get an idea of what is happening to you. Cholestyramine is not absorbed and can not be doing anything directly to ADH; the link to frequent urination is usually inflammatory in origin. Unfortunately, there is no way to answer your question without looking at simultaneously measured laboratory studies before and after your cholestyramine dose. I would look at TGF beta-1, C4a, VEGF, ADH and osmolality before the dose and after the dose over a course of every two hours for a total of three more blood draws.
This is a cumbersome approach in trying to answer a simple question but it's the only way I know to have any data to rely on.
10. Air conditioners, window units
I found mold on the outside window sill and cover of my window air conditioner. Are window air conditioners safe for those with biotoxin illness?
Any air conditioning unit can create problems with condensation and possible microbial growth. Window air conditioners are designed to deliver condensation to the outside world with such delivery enhanced by having a slight angle of the air conditioner with a down hill side directed to the outside. If there is evidence of microbial growth on the inside of your home related to the extra moisture created by the dehumidifier effect of the air conditioner, I would suggest that you have that looked at with a tape lift sample. This procedure costs approximately $35 in a mycology lab. In my experience, the normal organisms found around condensation areas from air conditioners are Cladosporium and Alternaria. These organisms can create some problems with allergy but are not toxin formers.
11. Air sampling
Can you please discuss the spore trap method in detecting mold in a building? Is it reliable and how does it compare to ERMI?
Air sampling for spores was the industry standard for years. Attempts to determine if a building was moldy or not using air sampling, however, is so fundamentally illogical I cannot understand why people still consider these tests to be reliable. They are not.
In this approach to sampling a vacuum device is attached to a filter and then turned on for either five or ten minutes such that air above the sampling device (usually placed in the middle of the room) would be pulled through the filter. Particles smaller then the pore size of the filter would go right through but particles bigger then the pore size would be retained. The pore size was established at 3 microns which made it an effective device to measure large, intact spores. The problem is that for every intact spore, ranging in size from 3 to 8 microns, there will be 99 fragments of spores that sail right through the device, right back into the room to continue to make people sick by inhalation.
An additional problem with spore trapping is that the spores are identified by using light microscopy, often at a mere 200 power. Such microscope work will not distinguish any of the species of the Aspergillus genus; similarly the Penicillium species could not be sorted out. Even worse all Aspergillus itself could not be separated from all Penicillium. What we see in spore trap reports with be 'Asp/Pen,' a classification that wholly ignores the vastly more important role for A. versicolor and A. penicilloides, for example. If particular spores were particularly sticky, as those of Stachybotrys are supposed to be, air samples would often not show any spores of this important mold as spores would not be released from their stuck on
habitat easily. Further, Wallemia has never been reported in any spore trap I have seen.
Using ERMI, a DNA analysis of dust collected not from the air but from areas where dust is settled in a given room, has the opportunity to identify up to 136 species with remarkable accuracy using QPCR. As opposed to guessing about Aspergillus and Penicillium and never even knowing about Wallemia, the QPCR tells us about these very important organisms specifically, inexpensively and rapidly.
Spore trapping has been exposed as inadequate in countless discussions including the World Health Organization report of 2009. WHO suggested that if spore trapping is to be used then multiple samples should be taken from multiple locations in each given room throughout a given day with multiple days per week and multiple weeks per month. The cost of such sampling is prohibitive.
Let's not forget that by using ERMI or HERTSMI-2 you can obtain health information from building information. Such correlation has never been done from air sampling and frankly never can be done reliably given the limitations discussed briefly above. If you are a landlord and want to hide evidence of a moldy building, use a single 5-minute spore trap taken from the middle of a room with the windows open. If you are concerned about health effects of WDB, use ERMI or even better, use HERTSMI-2.
12. Alcohol use
I think I become less tolerant of alcohol when I developed CIRS. Does this happen to other people to?
Changes in alcohol sensitivity is quite variable with the most intolerant being people with ciguatera. As a general rule, use of alcohol does not create an additional burden for affected patients understanding that excessive use of a known chemical toxin is not a great idea.
13. Alternative therapies
I am recently concerned about the possibility that my complex illness is related to mold exposure. We have air samples showing Penicillium and Aspergillus. We have problems with duct work and vents containing excessive moisture.
I have been recommended to use low dose antigens for treatment of mold illness. I am also taking reverse T3 for diagnosis of Wilson Syndrome. My son has an unusual depression and anxiety as well that is ruining his life. I have been told to obtain a SPECT scan. He has had a neurotransmitter test and is being treated with serotonin and norepinephrine.
Over the years I have had a chance to see multiple different approaches to treatment of complex illnesses such as yours and that of your family. I am uncertain as to what antigens are being suggested for you but if you have HLA-based susceptibility, the problem of defective antigen presentation will be a factor that you will need to take into account. We saw a variation of this somewhat ominous idea for treatment stemming from the Lyme vaccine given years ago in the thought that it would help prevent Lyme disease. In the Lyme case, an antigen, OspA, was given intramuscularly on three separate occasions purporting to force the body make antibodies to OspA which would protect against the invading Lyme bacteria. Unfortunately, those with HLA DRB1- 4 (and there were multiple haplotypes that included HLA DRB 1-4, see below) had difficulty processing this antigen. In essence, the Lyme vaccine became an exercise in asking the question, If I give antigen to those who can’t process it, will I create a chronic inflammatory response syndrome in those with given HLA susceptibility?
The answer to this question, of course, was absolutely yes. Needless to say, the Lyme vaccine was a disaster, for those with HLA DR 4-3-53, 4-4-53, 4-7-53 and 4-8-53.
Therefore, please identify which antigens you are going to be given.
I am uncertain as the diagnosis of your thyroid dysfunction. Given that inflammatory responses will down regulate the intracellular enzyme 5'-deiodoinase that converts T4 to T3, I am reluctant to blame unusual thyroid problems on any syndrome in the absence of correction of inflammation. In my experience such correction of inflammation often heals the putative source of the thyroid disorder.
Instead of a SPECT scan, one that shows abnormalities in arteriolar function, and these abnormalities have no bearing on capillary hypoperfusion, I would suggest performance of a NeuroQuant which will give volumetric data in an FDA-cleared program.
Finally, I have not seen any data showing benefit from treatment with norepinephrine and serotonin for alleged neurotransmitter abnormalities. There are