Dr G Heuser-The Role of the Brain and Mast Cells in MCS

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The Role of the Brain and Mast Cells in MCS

http://www.ei-resource.org/articles/multiple-chemical-sensitivity-articles/the-r\

ole-of-the-brain-and-mast-cells-in-mcs/

by Gunnar Heuser, MD, PhD, FACP

Multiple Chemical Sensitivity (MCS) was first described in the 1980s, yet it

has remained controversial. The resistance to the concept of MCS has come

from scientists who pointed out the lack of solid scientific diagnostic

tests. It has also come from the industry which has trouble accepting the

proposition that their products make a great number of people sick.

My personal experience (I have evaluated several thousands of chemically

injured patients) has convinced me that MCS is based on a physiological and

not on a psychological mechanism. This is why I have been interested in

finding objective evidence for MCS. In this paper I will present a mast cell

hypothesis, a limbic system hypothesis, and an office approach to objective

testing for MCS.

Mast Cell Disorder and MCS

Patients with mastocytosis can be exquisitely sensitive to even small

amounts of chemicals. When mast cells discharge histamines and other

compounds, patients often develop flushing and a metallic taste in their

mouth

..

A few years ago I decided to test some of my patients for mast cell disease.

Some of these patients with MCS actually turned out to have mastocytosis.

Other patients were found to have a mast cell disorder.

All diagnoses were made on the basis of skin biopsies done in an area which

on inspection and palpation, showed no evidence of abnormality. It was also

made on the basis of an elevated tryptase (an enzyme produced by mast cells)

level. If mast cells were present in excess and/or if tryptase levels were

elevated we would make a diagnosis of mast cell disease or disorder, if the

clinical picture was also consistent with that diagnosis. In a few patients

we also used a bone marrow biopsy to assist in the diagnosis.

Mastocytosis is considered to be a very rare disease. Yet, I have

accumulated more then 20 patients with that diagnosis in a matter of two to

three years.

At this time our testing is done on a random basis. We are now developing a

protocol by which we will introduce a challenge (e.g. perfume, nail polish,

chemicals found in a carpet store, etc.) and then test at a time when the

patient is symptomatic from that challenge.

We also hope to work with the Mastocytosis Society1 in further developing

diagnostic approaches to the overlapping syndromes of mastocytosis and MCS.

At this time the diagnosis of MCS is considered justified only in the

absence of diseases such as mastocytosis and porphyria.2 This exclusion will

require that all patients with MCS be tested for mast cell disorder and

porphyrinopathy. I believe that this indeed should be done.

In summary I postulate that chemical injury can trigger a mast cell disorder

which in turn can cause MCS. This concept was recently published.3

Limbic Hypermetabolism and MCS

Patients with MCS often show emotional instability during their reactions to

small amounts of chemicals. This has been likened to the epileptogenic

effects of kindling which is particularly effective in the limbic system of

the brain. Yet no proof of this concept has come forward to date.

We started doing PET brain scans on some of our patients with MCS and found

that the limbic, hypothalamic and brain stem areas are hypermetabolic (in

terms of their radioactive glucose uptakes) and therefore hyperactive

(almost as seen during focal seizure activity).

Since the limbic system contributes emotional reactions and interpretations

to sensory input, and since patients with amygdaloid (the amygdala is part

of the limbic system) seizures can develop panic and related attacks during

an amygdaloid seizure, our data appear to explain the emotional instability

during a reaction to chemicals.

The previously mentioned structures also serve memory and cognitive as well

as neuroendocrine and autonomic nervous system functions, all of which can

be deranged in a patient with MCS.

In summary, I have shown that patients with MCS can develop hyperactivity in

deep structures of the brain and that this may explain their emotional

instability which therefore develops on a physiological rather than

psychological basis.

It should be mentioned at this time that patients who are impaired and/or

disabled from chemical injury and resultant MCS often become depressed. This

depression would obviously be a natural reaction to their impairment and/or

disability and therefore be a secondary depression.

Our findings were first published in 19994 and will soon be published5 in

proceedings of a meeting on Chemical Intolerance. In this volume, kindling

and related mechanisms are also discussed.

Challenge Testing in the Medical Office

A few years ago, at a meeting on MCS, testing of patients in an

environmental chamber was suggested as the most scientific approach to

proving MCS. This suggestion proved impractical which is why so few

publications exist which provide a protocol for testing a patient for MCS.

In my office we have developed a protocol by which a patient first undergoes

baseline testing of pulmonary and immune functions as well as 24-hour urine

collection for porphyrin fractions. Then the patient voluntarily inhales

(via mouth and nose) nail polish, perfume, or exposes himself/herself to a

chemical environment. Once symptomatic from that exposure, the patient

undergoes follow-up testing of the same parameters and of course, undergoes

a follow-up physical examination

with special attention to neurological abnormalities and/or changes on

auscultation of the lungs.

Ideally, the patient brings a non-sensitive person (age and sex matched) who

undergoes the same testing. Patient and volunteer (control) are carefully

observed by my office staff who make detailed notes.

Table 1 shows comparison of some immune parameters with regard to the

above-mentioned tests. So far, we have found that MCS patients indeed

respond more to chemical exposure than their controls. This is also true of

pulmonary function which is more impaired when the patient becomes

symptomatic after exposure to a small amount of chemicals (see table 2).

We addressed elevation of TA1 (CD3+CD26+) cells in an earlier publication. 6

Our data on T3+ (CD3) cells are unpublished. These cells can, in my opinion,

be used as indicators of reactions to chemicals although they do not seem to

contribute to any symptomatology.

We are in the process of adding additional measurements (e.g. cerebral blood

flow, tryptase blood levels, and others) to our protocol. Naturally, we do

challenge testing only when the patient needs to prove MCS to Social

Security, insurance carriers (long-term disability) and the courts. We are

slowly accumulating data for future publication in a peer-reviewed journal.

If other interested physicians were to use our approach, data would quickly

accumulate and hopefully become statistically significant much sooner than

using an environmental chamber approach in an academic setting.

In summary, I have shown approaches to MCS which in my opinion are promising

and will help to further define the mechanisms underlying the development of

MCS.

Tables:

(see link)