Hypersensitive Processes: Are Fibromyalgia and Environmental Illness Kissing Cousins?

by Cort Johnson | Nov 4, 2014 | Homepage | 18 comments

Of all the disorders commonly allied with Chronic Fatigue Syndrome and Fibromyalgia, chemical sensitivity or Environmental Illness (EI) probably gets the least respect and certainly gets the least funding. It was astonishing to hear Dr. Clauw, an FM doctor and researcher who has battled disparaging attitudes toward Fibromyalgia for decades, make a belittling comment about environmental illness at a Pain Symposium.

Environmental illness has had trouble getting respect, but researchers are providing some clues.

That’s the way it often goes, though, for Environmental Illness, a condition that gets little research funding. EI is not just associated with ME/CFS and FM but with PTSD, depression, anxiety, and asthma as well. Unlike ME/CFS and FM, it’s not clear whether mood disorders precede or follow EI, but if EI follows its counterparts (and why wouldn’t it?), mood disorders will be found to be a result of rather than a contributor to EI. Right now EI with its poor funding is open to all sorts of interpretations.

Environmental Illness: A Short Overview

In the “Allergic To Life” story in the Nov 2013 issue of Discover magazine, Jill Neimark asked EI expert Claudia Miller what she thinks causes chemical sensitivities. Her answer indicated she believes EI is a sister disorder not just to Chronic Fatigue Syndrome and Fibromyalgia but to disorders like epilepsy and chronic regional pain syndrome (CRPS).

She presented two models of EI:

The One Trigger Model

Several models propose how triggering factors can set off environmental illness

In the one trigger model an intense exposure “tilts” the central nervous system into over-reacting not just to that substance but to other substances as well. This general process – a single stressor that triggers a hypersensitive response to future stimuli – is seen in Fibromyalgia, but is most dramatically demonstrated in CRPS, where a small injury triggers excruciating pain and immune changes that spread from the site of the original injury.

The Intermittent Trigger Model

The intermittent stimulation of the limbic region of the brain that explodes into an epileptic seizure may be another model for EI. In this model, toxicants traveling straight from the nose to the limbic regions of the brain may, in susceptible individuals, trigger a state of limbic system hyperactivity.

Interestingly, a study of genes involved in detoxification suggested that problems detoxifying the offensive chemicals was probably not the issue. Dead ends in immune and olfactory studies have pointed to activation of a highly sensitive and excitable limbic system as a prime suspect.

[We should note, though, that Dr. William Rea, an environmental illness specialist in Dallas, has successfully used a combination of desensitization (allergy shots), detoxification (sauna) and immune factors to treat EI as well as some people with Chronic Fatigue Syndrome.]

Amazingly electroshock therapy worked for one severe EI patient. Other practitioners such as Dr. Rea use less “shocking” methods..

The idea the EI may be a central nervous system disorder was buttressed in the dramatic fashion when a person with almost off the charts sensitivity (QEESI score of 95/100) returned to near normal levels after he participated in electroshock therapy (ECT). By the third treatment his EI score was 30/100. The shock therapy apparently allowed his central nervous system to reset itself.

Take the QEESI Chemical Sensitivity Questionnaire Here

The parts of the brain that odors activate in people with EI read like a short list of brain regions associated with ME/CFS and FM: the insula, hypothalamus, thalamus, prefrontal cortex, somatosensory cortices and the limbic system. That suggests perhaps chemical sensitivities may be to people with EI what pain is to people with Fibromyalgia: different stimuli, but a similar overactive brain response.

Are chemicals and pain tweaking the brain in similar ways in EI and FM? A Swedish study used a functional MRI (fMRI) to examine how the brains of women and healthy controls responded when presented with very low levels of odor in women.

Let’s see what they found out.

The Study

Brain responses to olfactory and trigeminal exposure in idiopathic environmental illness (IEI) attributed to smells — An fMRI study. Linus Andersson, Anna-Sara Claeson, Lars Nyberg, Berndt Stenberg, Steven Nordin. Journal of Psychosomatic Research, November 2014

The bar for entrance into this Swedish study was not set particularly high. It was a women-only study because, like FM and ME/CFS, women are much more likely to have EI. The selection criteria said participants had to report that smells that didn’t bother others tended to bother them, and they had to have two symptoms at least once a week for the past three months. Twenty-five odor-sensitive women and twenty-six healthy controls participated.

As they were given increasing doses of a banana smelling odorant, a functional MRI (fMRI) assessed their brain activity. An odorless trigeminal nerve stimulant was also applied. The doses were very low – lower than had been assessed in EI patients before.

The Findings

“The lower BOLD signal in the prefrontal cortex and higher signal in the thalamus in the IEI group may thus be interpreted in terms of an inability to inhibit salient, attention grabbing, and arousing stimuli.”

The very low doses of the banana smelling odor caused the thalamus to spring into action in the environmentally sensitive group and knock down activity in a portion of the prefrontal lobe (the superior frontal gyrus) compared to the healthy controls. Since the thalamus processes and relays sensory stimuli between the lower and upper parts of the brain, the increased activity there suggested the thalamus of the EI-sensitive participants may be hitting the prefrontal cortex with a barrage of stimuli.

The prefrontal cortex and thalamus acted differently in people with EI when exposed to an odor

The prefrontal cortex is known for its importance in planning complex actions and decision-making, but it also processes sensory stimuli. In a recent hypothesis paper Japanese researchers proposed that damage to the prefrontal cortex (DLPFC) played a major role in ME/CFS including difficulty processing sensory inputs (physical sensations, over-stimulation), causing high emotional lability and problems with attention span and working memory.

The reduced activation of the prefrontal cortex during the odor test could reflect a similar situation, and indeed, anybody with significant chemical sensitivities will recognize the emotional lability, difficulty concentrating, and short-term memory problems that occur after being exposed to too many chemical odors.

The two findings suggest people with EI may have a thalamus that pounds the prefrontal cortex with chemosensory signals when they’re exposed to chemicals, and a prefrontal cortex that lacks the resources to process them properly. Ever feel like you can’t get “outside” of or push aside chemical odors? That you can’t concentrate in the face of them? The kind of reduced prefrontal cortex activation seen in this study has been associated with an increased focus on external stimuli.

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The PRC – the seat of executive functioning – should be mostly helping us decide, plan, and organize our day. But if your PFC is getting hijacked by “chemosensory” signals, it may not have the wherewithal to make decisions or plan your next moves.

Fibromyalgia, ME/CFS, and EI

Do prefrontal cortex problems link EI, FM and ME/CFS?

Could a similar process be occurring in Fibromyalgia and Chronic Fatigue Syndrome? With regards the prefrontal cortex – possibly. FM imaging studies often show enhanced activation of pain processing regions such as the somatosensory cortices, ACC, and insula in conjunction with decreased activation of the prefrontal cortex. A study finding “weaker coupling” between the pain regions of the brain and the prefrontal cortex in FM suggested poor control of the pain circuits was present. Another study found that the prefrontal processes healthy people use to reduce pain were disrupted in FM.

No studies I was able to find suggested that increased activation of the thalamus plays a role in FM. However, increased levels of neuroinflammation in the thalamus of ME/CFS patients was found to be associated with increased pain levels in ME/CFS in the recent Japanese neuroinflammation study.

Is the PFC a weak link in FM, Environmental Illnesses and ME/CFS? Time will tell.

Klimas Group Opens Environmental Health Program

Just as this blog was being produced came word that Dr. Klimas’ Institute for Neuro-Immune Medicine at Nova Southeastern University is creating an Environmental Health program to treat and presumably research the connection between environmental exposures and Gulf War Syndrome (GWS) and ME/CFS patients. Advertisements for a Fellowship and a Faculty appointment just went out.

This is, to my knowledge, the first ME/CFS research center to explicitly focus on environmental illness and ME/CFS. It’s a welcome addition.

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