The initial acute phase illness most often occurs in summer with a 3-5 day incubation period and during this period is said to be highly infectious.
Generally from then, the initial presentation takes one of two forms: a severe, incapacitating prolonged illness, or an apparent remission followed by increasing relapses until the patient is forced to recognise exertional limitation. The most common initial symptoms reported are: Pain in the spine, neck or head; mild fever and ‘flu-like symptoms; nausea or vomiting; flaccid muscle weakness; and muscle pain or tenderness. For some people, ME is triggered by Hepatitis B vaccination [M.E. Association Survey Report, 2010], blood transfusion, or chemical poisoning, although it is now thought organophosphate poisoning is a different illness.
The later course of ME is difficult to predict, and may either become consistently severe, improve to a plateau, or be markedly relapse-remitting. In some, even prolonged severe incapacitation can be relieved by unpredictable remission, although relapse is always possible. The degree of impairment and complexity depends on the degree of diffuse brain injury and end organ involvement.
The evidence for subgroups is strengthened by research using heterogenous CFS criteria, although this artificial heterogeneity also hampers consensus. It is likely that subtypes exist within the ME milieu based on the clinical findings, history, and perhaps gender of patients.
Factors triggering a relapse
ME relapses are often a result of overactivity, but can occur without warning with no obvious inciting factors. Exposure to increased sensory information in light, sound, and movement can provoke a sensory storm which has been termed “The Mall Effect” due to its particular provocation by the stimulus of a busy shopping mall.
Infections, such as the common cold, influenza, and gastroenteritis, also increase the risk for a relapse. Heat and cold can transiently increase symptoms.
Pregnancy can directly affect the susceptibility for relapse. Later pregnancy appears to offer a natural protection against relapses, and there are anecdotal reports of post-partum remission. However, pregnancy does not seem to influence long-term disability.
Although much is known about abnormalities in myalgic encephalomyelitis, the reasons why they occur is not known. There are two ME conferences held in the UK each year attended by international research luminaries, and other conferences held worldwide.
Myalgic encephalomyelitis is a complex disease in which the immune and neurological systems appear dysregulated and in conflict, producing a wide variety of findings.
The problem is that most of the research in recent years has been conducted on people with CFS. This is a heterogeneous population, and includes patients with psychiatric disorders, as well as vitamin and nutritional deficiencies (especially vitamin D) and post-viral states such as ME.
According to a strictly immunological explanation of CFS, the inflammatory processes triggered by T-cells create leaks in the blood-brain barrier (a capillary system that should prevent entrance of T-cells in the nervous system). These leaks, in turn, cause a number of other damaging effects such as swelling, activation of macrophages, and more activation of cytokines and other destructive proteins such as Rnase-L. A reduced ability to move metabolites in and out of cells (channelopathy) has been implicated in this process. This may also be applicable to ME.
Some evidence shows viral infection of muscle and brain in at least a proportion of sufferers. This triggers inflammatory processes, stimulating other immune cells and soluble factors like cytokines and antibodies.A model for late ME has been proposed analogously to post-polio syndrome in which repaired nerve tissue forms inappropriately [The Late Effects of ME: Can they be distinguished from the Post-polio syndrome?]. Radiological research on ME has shown hypoperfusion of the brain stem and an abnormal response to exertion, but research on CFS is often inconsistent and must be interpreted with caution. For example, a reduced volume of grey matter may be a result of a lack of activity and is reversible with cognitive behaviour therapy.
An inquest into the death of Sophia Mirza from ME found inflammation of the dorsal spine ganglia and liver abnormalities. However, she had comorbid disorders.
Hemodynamic abnormalities are widely found, including serum and RBC hypovolemia, NMH, cerebral hypoperfusion. Vascular and endothelial abnormalities have been published by MERUK. However, none of these studies used research criteria for ME so the results may not be applicable to ME.
Some cardiological features such as cardiac insufficiency, inverted T-waves and myofiber disarray have been reported in CFS and recently added to by findings of reduced Q-value. This has lead clinician and researcher Dr. Paul Cheney to posit that CFS is form of partially compensated cardiomyopathy in which orthostatic intolerance and rapid fatiguability are secondary protective mechanisms. Due to the heterogeneity of the population, a single cause is unlikely, but one third of people with ME have abnormalities when tested with Holter monitors.