ME/CFS, Depression and Infection - A Family History (Sept. 2007)
This e-mail came from a graduate student with ME/CFS who wishes to
remain anonymous.
Differentiating ME/CFS from Depression. -
As you have recently published a newsletter
commenting on the definitional controversy in ME/CFS, I
thought I would add my two cents. I vehemently disagree with Dr.
Jason's assertion that ME/CFS
can be reliably distinguished from major depression or any other fatiguing
illness on the basis of symptoms alone. I would be very happy with you
if you would post my commentary on your website for others to think about.
I believe this so strongly because it is true of every other medical
disorder. Even the most talented clinician cannot, on interviewing a
patient with extreme exhaustion and other symptoms, reliably tell whether
the patient has "hypothyroid fatigue" or "cancer fatigue" or "Addison's
disease fatigue" or "heart fatigue" or "autoimmune disease fatigue" on the
basis of the patient's complaints (or by scores on instruments like the
SF-36). Despite the fatigue in the above conditions tending to be a
bit different, it is not enough different for the doctor to distinguish the
disorders based on symptoms alone. Medical testing is a MUST to
distinguish them.
The same is true of ME/CFS
and depression. First of all, it is under acknowledged by
CFS
advocates that major depression itself has a physical basis and that people
with primary depression people do have 'real' fatigue and pain, not simply
reduced motivation due to their mood. Whether the depression is
'melancholic' or not, depressed people as a group have evidence of chronic
inflammation that correlates with the mood symptoms. This is evidenced
by evidence of increased pro-inflammatory cytokines and by the fact,
confirmed in multicenter prospective studies, that currently depressed
people have a 3-fold risk of heart attack or stroke
AND
this risk disappears if and only if the depressed person achieves remission
with antidepressant treatment.
CFS
advocates also need to realize that melancholic depression is a SMALL
subgroup of people with major depression, accounting for 10-15% of cases.
The melancholic subgroup is the one most strongly associated with elevated
cortisol levels and with the most evidence of genetic causation.
People with 'atypical' depression (where there is hypersomnia, reactive mood
and increased appetite), have lower cortisol levels than controls.
These two subgroups respond to different types of antidepressants.
Thus, the argument that
CFS
and depression are clearly distinguishable based on cortisol responses is
simply not true.
An
ME/CFS Family
History.
Further, if you remember my e-mails to you discussing my family, where all
four of us have an ME/CFS
diagnosis, I strongly believe that the underlying disease process in ME/CFS
may cause purely psychiatric presentations in addition to ME/CFS.
As a child I had childhood major depression, severe developmental
coordination disorder, selective neurocognitive abnormalities, ADHD,
tantrums, irritability, and social problems (avoidant personality disorder
of childhood). I did not have any persisting fatigue or pain.
What made my psychiatric disorder different from a typical one was (1)
unequivocal onset following a series of infections at age 4, (2) very
atypical symptom pattern leading to a slew of psychiatric diagnoses instead
of a few, (3) clear , measured neurologic and cognitive changes, (4)
laboratory evidence of virus infection (low WBC, glucose, neutrophils,
elevated monocytes, evidence of previous EBV exposure by age 3 and
reactivated EBV by early antigen at age 9).
My psychiatric symptoms remitted by early teens, then I developed ME/CFS
at age 20. I continue to have very high EBV titers in the spinal
fluid, in addition to unequivocal HHV-6A infection and c. pneumoniae.
The same lab test pattern was detected with my adult-onset ME/CFS
Now, listen closely, EBV mononucleosis clearly initiated my dad's classical
ME/CFS
in 1984 (the year I was born).
Both he and my mother both had multiple
episodes of reactivated EBV measured by early antigen in the 1980s and, for
my dad, by
PCR
in the 1990s, when my father started seeing Dr. Peterson.
My mother suffered from severe episodes of treatment-refractory major
depression, which DID correlate with the finding of reactivated EBV, from
the late 1980's until 2004 when she finally became bedridden with severe
ME/CFS. However, she showed laboratory evidence consistent with ME/CFS back
when she was still able to tolerate aerobic exercise and her only symptom
was severe depression. In 1998 she was having odd neurological complaints
(skin crawling sensations) that didn't fit with the clinical picture of
depression. Dr. Peterson sent a research nurse to draw her blood free of
charge; she showed an NK cell function of ZERO, elevated Rnase-L, and
evidence of reactivated EBV and c. pneumoniae. Because she was so depressed
and pessimistic she refused his recommended treatment (Ampligen) and denied
the tentative ME/CFS diagnosis. When she became bedridden five years later
she showed active HHV-6 infection. She has not since responded well to any
treatments, and the opportunity to get Ampligen is no longer available to
her. She is not bedridden but is housebound with very poor quality of
life."
Regarding
CFS
I agree with Reeves that reduced activity OR fatigue may be characteristic. When a person with mild ME/CFS
paces themselves appropriately, they may stop being aware of fatigue.
My sister, for instance, who was bedridden by ME/CFS
acutely at age 14, substantially improved over time and no longer complains
of either fatigue or pain. However, she does have serious depressive
symptoms and a quite restricted activity level. This fall, she
attempted a full time college load and developed severe fatigue within 5
weeks of attempting a normal activity level. For the past 4 years, she
had denied having 'CFS'
and blamed her reduced activity on emotional issues such as severe
depression, obsessions, and phobias. But AS SOON AS she overcame the
emotional problems and tried to live a normal lifestyle, --boom, the
exhaustion comes back.
CFS
is clearly distinguishable from major depression on the basis of course and
outcome over time and certain objective tests but NOT by symptoms alone!
ME/CFS and ADHD (Attention Deficit Hyperactivity Disorder) - Two
Similar Dilemmas.
Disorders in
psychiatry (depression, ADHD, schizophrenia) are DEFINED BY SYMPTOMS and are
necessarily heterogeneous and subjective. They always are and always
will be until the definitions are changed. They will always be
controversial. Until the ADHD definition principally includes
objective measurements of attention span, response to ADHD medications, and
underlying neurobiological abnormalities, and it continues to be defined
ad-hoc based on parent/teacher/doctor ratings of whether the child seems to
have trouble with attention and hyperactivity, it will always remain
controversial (with arguments raging over whether ADHD is a 'real' disorder
or whether society is choosing to overmedicate and control problem
children).
Medical disorders are DEFINED BY FINDINGS. For example, MS is
diagnosed by objective evidence of two demyelinating events by (1)
of brain or spine, OR (2) oligoclonal bands in CSF, OR (3) abnormal visual
or auditory evoked potentials.
Wresting ME/CFS
From Obscurity: Defining it Physically -
ME/CFS is not a psychiatric disorder BUT it is currently being
defined and studied as if it were. There are only a few medical conditions
defined only by symptoms, such as migraine. But, migraine has very specific
symptoms, whereas ME/CFS symptoms are all over the map. It is no wonder
uneducated doctors don't think it is "an illness".
The only
way to wrest ME/CFS
from the hands of psychiatric obscurity is to define it IN TERMS OF its
physical findings, not by endless debates about what symptoms are "real ME/CFS".
If we want ME/CFS to be accepted by doctors, then we have to tell
them what tests to run in order to evaluate the disease as opposed to
evaluating "complaints".
