Research, links and quotes that might be useful:

http://www.meao-cfs.on.ca/about_me/symptoms.shtml

"Myalgic Encephalomyelitis is not depression. Myalgic Encephalomyelitis is not hysteria. Myalgic Encephalomyelitis is not a conversion disorder nor is it a somatization disorder. Myalgic Encephalomyelitis is an acute onset diffuse injury of the brain. Psychiatrists should not ever be placed in charge of diagnosis and treatment of M.E. patients. It is simply not their area of expertise and their meddling has at times caused great harm to M.E. patients. Also, during the 20 years that I have investigated M.E. patients I have yet to see a single case of real M.E. that has responded to psychiatric pharmacological treatment." ~ Byron Hyde


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From: Chronic Fatigue Syndrome : The Limbic Hypothesis

"In some studies the CFS panic disorder, particularly in those patients with no premorbid moon disorders seems to be somewhat different. The anticipatory anxiety seems to be much more autonomous, as if it were being generated by a neurotransmitter disorder, as one might see in a post-viral syndrome. Once again, most CFS symptoms do not usually resolve when panic and anxiety are reduced or even eliminated. This clinical observation supports the hypothesis that a limbic encephalopathy is involved with most cases of CFS, and that one aspect of this process would be panic disorder.

"It is hypothesized that the prefrontal cortex generates agoraphobia by stimulus generalization as a result of random panic attacks. I prefer to interpret agoraphobia as being a dysfunction of heteronmodal and paralimbic input to limbic structures and not to restrict agoraphobia to the prefrontal cortex. However, a "panic disorder circuit has been proposed from the medullary reticular area to the locus ceruleus, through the dorsal ascending bundle to the limbic lobe and prefrontal cortex and back to the nucleus reticularis gigantocellaris, which gives primary stimulatory input to the locus ceruleus. My view would inovle more cortical structures. This ceircuit would include structures found to be hypoperfused in CFS brain SPECT scans, the anterior temporal lobe and the dorsolateral prefrontal cortex.

"There is a genetic tendency to develop panic attacks. There may also be a learned tendency to catastrophize from geteromodal/paralimbic information, thereby provoking panic attacks. This neuroanatomical hypothesis makes sense for panic disorder, but not for the multitude of CFS symptoms that would be difficulty to fit under the panic disorder aegis. Anti-kindling medications are not particularly effective in CFS, and benzodiasepines rarely affect symptoms other than anxiety, vertigo, or IBS (for which they are effective).

"Calcium channel blockers have anti-anxiety effects, but only nimodipine is of much value in CFS. Nifedepine has been used in epilepsy. A possible use for them would be in combination with acetazolamide and magenesium to interfere with ecitotoxin release after cell injurty, cause by various possible factors, especialy viruses. Magnesium itself has been reported to prevent panic attacks in the so called "neuronal hyperexcitability syndrome" as well as anxiety and somatization. Depression was not affectied."


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Acta Neurologica Scandinavica. 96(3):158-162, September 1997.
Lindal, E. 1; Bergmann, S. 2; Thorlacius, S. 2; Stefansson, J. G. 1

"Abstract:
Objective: In order to clarify the lifetime likelihood of developing psychiatric disorder following the Akureyri disease, we have investigated 55 well documented cases of the Akureyri disease.


"Materials and methods: All participants were interviewed and diagnosed as to psychiatric disorders according to DSM-III.

"Results: Of the 55 subjects included in this analysis 53 were women. The mean age of the participants was 67.7 years. The most common problem was agoraphobia with panic attacks 12.7% (P<0.0001); agoraphobia without panic attacks 21.8% (P<0.0001); social phobia 14.5%(P<0.001); simple phobia 18.1% (P<0.05); schizophrenia 3.6% (P<0.01); and alcohol dependence 5.4% (P<0.05).

"Conclusion: Prolonged chronic fatigue most commonly results in anxiety disorders. Following the infection, the more serious psychiatric disorders do not seem to play a major role in the long run."


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ME patients are more prone to anxiety than depression.
Lindal E et al. Anxiety disorders: A result of long-term chronic fatigue - the psychiatric characteristics of the sufferers of Iceland disease. Acta Neurologica Scandinavica, 1997, 96, 3, 158-162.

The aim of this study was to assess the likelihood of developing psychiatric disorder following the outbreak of Akureyri disease (i.e. epidemic ME).

The researchers investigated 55 well documented cases of Akureyri disease who were still experiencing symptoms. All participants were interviewed and the results were compared to those of 421 members of the general population.

Of the 55 subjects included in this analysis, 53 were women. The mean age of the participants was 67.7 years. The following disorders were found more commonly among the patients than the controls: agoraphobia with panic attacks 12.7%; agoraphobia without panic attacks 21.8%; social phobia 14.5%; simple phobia 18.1%; schizophrenia 3.6%; and alcohol dependence 5.3%. The rate of recurrent major depression was also higher than in the controls (5.4%) but the difference did not reach significance.

When the patients were compared with 10 people suffering from systemic lupus erythematosus (SLE), the only significant difference was in the prevalence of lifetime generalised anxiety.

The researchers conclude that prolonged chronic fatigue most commonly results in anxiety disorders, particularly those relating to social conspicuousness. In other words, patients may become afraid of not being able to manage a whole social encounter etc. This is also found in people with SLE. "Following the infection, the more serious psychiatric disorders do not seem to play a major role in the long run."