The following subgroups are currently subsumed under the heading of CFS. However, I believe that some, if not all, could be entities in their own right. Given the available evidence, it might be useful to study these groups separately, thus enabling researchers to compare them with both CFS and other subsets. In my view, it is becoming increasingly difficult to support the argument that all fatigue states have the same aetiology and that they can therefore be treated in the same way.
The diagnosis of ME is based on descriptions by Ramsay (e.g. 1978, 1988) and the London criteria (research).
1. Loss of muscle power during minimal exertion plus a delay in the return of muscle power after exertion. Recovery of muscle strength usually takes at least 24 hours (cf. Paul et al 1999).
2. Impaired circulation, e.g. pallor or cold extremities.
3. Evidence of central nervous system involvement, e.g. disequilibrium, visual disturbances, unusual headaches, emotional fragility, neurally mediated hypotension etc.
Patients frequently report intolerance to
alcohol (see also OP subgroup below).
The fact that several studies on CFS have failed to document a delay in the recovery of muscle strength following exertion supports the view that ME is not identical to CFS.
Enteroviruses and herpes viruses. Possibly a
combination of pathogens. Onset more common from May to November.
ME affects young to old but peaks occur late
thirties and forties.
Links with infection means that ME tends to be
clustered. Prevalence varies both geographically and from year to year.
ME is difficult to distinguish from post-viral fatigue syndrome, if the definition of the latter links fatigue with exertion (e.g. Ho-Yen 1990).
ME is an acute illness which has a tendency to
become chronic (cf. Ramsay).
Lack of support may lead to adrenal dysfunction
and the symptoms associated with chronic stress.
Cold viruses.
Splenic enlargement (rare).
Fever (if present, tends to be low grade.)
Pacing of activities.
Sound diet (low sugar, low fat).
Emotional support.
Stress may lead to secondary problems, low
cortisol, etc, so worth avoiding.
Possible supplements: antioxidants.
If relevant: antiviral drugs, immune modulators.
Antidepressants in low doses may be useful for
'brain fog', sleep disturbances, pain, e.g. amitripyline, fluoxetine.
No alcohol.
Description by Pedersen (1959).
Vertigo is typically triggered by a cold. Most recover within days or weeks but 10-15% become chronic. It's often accompanied by fatigue, anxiety and depression. Attacks become less frequent over months but sequelae may persist for years.
Movement of head and neck or rapid changes of posture.
Linked with CFS (e.g. Chaudhuri and Behan 2000), but vertigo dominates the clinical picture. Unclear whether this is a primary vestibular disorder or subset of CFS (Ash-Bernal et al 1995).
Possible link with brainstem dysfunction and reduced blood flow.
Likely source of chronic stress.
Onset is less common in Summer.
Drugs for vertigo.
Emotional support.
Effect of vestibular exercises is unknown.
Infection caused by Epstein-Barr virus.
Diagnosed using a blood test (OHCM 1998).
Fatigue, sore throats, malaise, swollen and
tender glands. There may be a fever for 7-10 days. Recovery is often protracted
but most will recover within one year (if managed correctly).
Youth (teens and early twenties).
Depression.
Polio (cf. ME).
Neurological symptoms less common than in ME.
Rest.
Avoid alcohol.
Formerly known colloquially as a 'nervous breakdown' or 'burn-out'.
Currently not classified as an entity in DSM-IV-TR. Ongoing stress relates not so much to pressures on individuals but their inability to cope with them.
Fatigue, fear, irritability, anger, indigestion, disturbed sleep, sweating, pain in muscle and joints, sensitivities to foods, poor concentration, initially high, then low cortisol levels (e.g. Edwards and Bouchier 1991, Yehuda et al 2000, Pruessner et al 1999).
Patients may become increasingly exhausted and become more prone to ordinary infections (colds, flu). They may find it difficult to deal with normal stress. These changes are possibly mediated by cortisol deficiency.
Major life events.
Active lives.
Poor coping plus personality traits which lead
individuals to push themselves rather than rest when tired.
Alcohol intolerance is less common than in ME.
Patients may become tired-all-the-time (i.e.
show fewer fluctuations linked to exertion).
More apathy than in ME?
Patients may fulfil criteria for Generalized Anxiety Disorder if anxiety is major symptom. Many will meet criteria for neurasthenia.
Epidemics.
Psychotherapy or counselling to identify
stressors.
Good diet.
Relaxation.
Supplements e.g. licorice (increases cortisol
levels), kava kava.
Sufficient rest with graded activities.
Possibly drugs.
Oxford criteria or CDC criteria '94 plus irrational beliefs about activity and avoidance behaviour (Wessely et al 1998). Excessive rest leads to deconditioning and feelings of weakness and faintness on standing. The latter often respond favourably to a programme of graded activity (three months).
Fatigue, normal headaches, indigestion, sleep disturbances, pains and other symptoms which can be linked to lack of physical fitness, stress and mood disorders. Patients may be tired-all-the-time. They show no or few signs of immune activation and severe cognitive impairment found in ME and strictly-defined CFS. Neurological symptoms are generally limited to dizziness, fainting, trembling hands or tingling sensations in hands and feet.
Misinformation
Fear
Hyperventilation
Onset may be any time of year and affect any age
group. This subgroup is generally not clustered.
Patients tend to meet criteria for neurasthenia.
Maladaptive avoidance can complicate and
perpetuate many post-viral states.
Ongoing disease or infection.
Alcohol intolerance.
This subgroup is less 'neurological' than ME.
CBT plus graded activity.
Emotional support.
Psychotropic drugs (full dose are more likely to be tolerated than in ME).
These patients present with symptoms suggestive
of CFS but on examination are found to have somatoform disorders, phobias,
fibromyalgia, hypothyroidism, cancer, pesticide poisoning etc (e.g. Richardson
2000, Wilson et al 1994).
Unexplained fatigue, pain, and various other
symptoms.
Depends on primary diagnosis, e.g. fibromyalgia
patients will report more pain than other CFS patients. Individuals with SD
or their relatives may admit to 'gains' associated with ill health.
Minimal exertion.
Cognitive deficits documented in ME.
Epidemics.
Depends on primary diagnosis.
Symptoms which are caused by vitamin D
deficiency and which are alleviated when taking the appropriate supplements.
(Hock 1997).
Fatigue, aches and pains, and other symptoms
typical of CFS.
Vitamin D.
Minimal exertion.
Intolerance to alcohol.
Epidemics.
Supplements.
Symptoms which disappear while avoiding certain
foods.
Unexplained fatigue, dizziness, pains, anxiety
and other symptoms of CFS.
Gut dysbiosis?
Nutritional deficiencies and stress, hence may
be secondary to any of the above.
Ongoing viral infection.
Epidemics.
Minimal exertion.
Some cases of Gulf War Syndrome (Haley et al
2000).
Effects of exposure to organophosphates (Davies
et al 2000).
Sub clinical hypothyroidism (Skinner et al
2000).
Back problems (e.g. Perrin 1993).
All the above may present with chronic fatigue
and other symptoms suggestive of ME.
NB. Having one of the above does not make an individual immune to other fatigue states. Thus ME can lead to or coexist with chronic stress disorder or hypothyroidism.
Do fatigue states other than ME/PVFS show the
typical reduction in muscle power during minimal exertion plus the prolonged
recovery times?
Are fatigue states other than ME/PVFS associated
with cognitive deficits (replicate Scholey et al 1999) and immune
activation? Which are associated with low cortisol levels?
How many patients in each subset show evidence
of HHV-6 infection?
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With thanks to Drs. Trudie Doorduin.
Copyright EM. Goudsmit, PhD C. Psychol.
November 2000 ©
Editor ME and CFS Capita Selecta Quarterly
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