CEREBRAL
ATROPHY
Introduction
I
do not like to deliver discouraging news. But for many years the
medical world has been dismissing CFS/ME because there has been
no science to say that this illness is serious. Now that scientific
information is pouring in abundantly. Is the medical world going
to continue to maintain that ME/CFS is a trivial psychosomatic problem
of neurotics and hypochondriacs?
In
this issue of the Lyndonville News I would
like to summarize several studies, two of which show the presence
of cerebral atrophy. In lay terms, that means that the brain has
decreased in size, presumably because of death of brain tissue.
The other reviews outline a new study proving the cognitive symptoms
and some older studies demonstrating decreased blood flow to the
brain (cerebral hypoperfusion). In my opinion these issues are connected
or linked.

Literature
Review:
The Presence of Cerebral Atrophy in CFS
Reference:
de Lange F, Kalkman J, Bleijenberg G, Hagoort P, van der
Meer J, Toni I. Gray matter volume reduction in the chronic fatigue
syndrome. NeuroImage 2005;26:777-781.
In this study, the authors studied 28 patients with CFS and 28 healthy
controls using an automated, “user-independent” magnetic
resonance imaging (MRI) voxel-based morphometry (VBM) technique
for measuring brain volume and tissue concentration. They were also
able to quantify the activity reduction of the CFS patients using
a technique called actinometry. For better control they restricted
the study, both patients and controls, to women. They found that
the volume of gray matter of the brain was significantly decreased
in comparison to the healthy controls, (p < 0.001), and amounts
to a reduction in brain tissue of 8% on average, and appears to
be a global phenomenon rather than a local problem. The amount of
brain tissue reduction was correlated to the severity of the activity
limitation. Whether this is a cause or consequence of CFS is not
known.
Reference:
Okada T, Tanaka M, Kuratsune H, Watanabe Y, Sadato N. Mechanisms
underlying fatigue: A voxel-based morphometric study of chronic
fatigue syndrome. BMC Neurol 2004;4:14.
In this study MRI was used allowing “voxel-based morphometry”
of 16 patients and 49 healthy age matched controls. CFS patients
had reduced gray matter volume, primarily in the prefrontal cortex
bilaterally. The authors state, “We observed a significant
reduction in gray-matter volume in the bilateral prefrontal areas
of CFS patients….In comparison to healthy controls, there
was an average of 11.8% volume reduction in CFS patients.”

Literature
Review:
Cognitive Symptoms of CFS
Reference: Lange G,
Streffner J, Cook D, Bly B, Christodoulou C, Liu W, et al. Objective
evidence of cognitive complaints in chronic fatigue syndrome: A
BOLD fMRI study of verbal working memory. NeuroImage 2005;26:513-524.
Many studies have been ambiguous about the cognitive difficulties
in CFS. In this study, the authors, using blood oxygen level dependent
(BOLD) functional MRI imaging show that CFS patients are able to
process challenging information, but utilize more extensive cerebral
networks and must exert greater effort to process auditory information.
They state, “Our findings provide objective evidence for the
subjective experience of cognitive difficulties in individuals with
CFS.”
Comment:
Many standard neuropsychological testing results have been
considered “normal” or “consistent with depression”,
primarily because the areas studied were not the areas of impairment
in CFS. If neuropsychological testing were to be done, the focus
should be on ability to maintain attention, verbal processing speed,
reaction times, and the ability to acquire new information. For
a review of the neurocognitive studies, see Jason L, Corradi K,
Torres-Harding S, Taylor R, King C. Chronic fatigue syndrome: the
need for subtypes. Neuro-psychology Review 2005;15(1):29-58. Hopefully
this study by Lange et al will put to rest the controversy of the
presence of cognitive deficits in CFS, because they can be seen
on fMRI.

Literature
Review:
Abnormal Cerebral
Perfusion in CFS
Reference:
Schwartz R, Garada B, Komaroff A, Tice H, Gleit M, Jolesz
F, et al. Detection of intracranial abnormalities in patients with
chronic fatigue syndrome: comparison of MR imaging and SPECT. American
Journal of Roentgenology 1994;162:935-941.
This
paper was one of the first to look at the incidence of both the
“high intensity” (bright) spots on the MRI scan and
the brain blood flow abnormalities in patients with CFS. The MRI
abnormalities were present in 50% of patients compared with 20%
of controls. The SPECT abnormalities were common in CFS at 81% vs
21% in controls. The authors implied that the SPECT seemed to correlate
with the clinical picture.
There are now many papers on SPECT scans and cerebral perfusion
studies. For a review I would suggest: Jason L, Corradi K, Torres-Harding
S, Taylor R, King C. Chronic fatigue syndrome: the need for subtypes.
Neuropsychology Review 2005;15(1):29-58
Comment:
For many years patients with CFS have said that their cognitive
symptoms are among the most disabling symptoms they experience.
In the early 1990’s Dr. Sandman used the term “CFS dementia”
and everyone was horrified, including me. But it is now clear that
he was correct, depending upon how you define dementia.
Usually,
we associate the term dementia with Alzheimer’s disease, which
over a period of a few years converts a vital, intelligent person
into one unable to recognize family members. This does not occur
in CFS. Over the past twenty years I have heard patients say that
their abilities are more and more limited. I am sure this is true,
but their speech was normal, they were still able to take care of
themselves reasonably well. Because they had adjusted to the ravages
of the illness, some were even doing reasonably well. These observations
are not changed by the recent publications. What we are now seeing
in the medical literature is evidence that CFS is a neurological
disease and some patients have reduction in brain gray matter (cerebral
atrophy).
I
would feel that the results mentioned above are linked to the poor
prognosis seen in many of the CFS long term studies. For those persons
with severe CFS persisting for more than five years, the likelihood
of recovery is slim. I would assume that the neurological damage
that causes the symptoms is also causing the cerebral atrophy, and
that is not likely to be reversed.
What
is causing this cerebral atrophy? We do not know is the simple answer.
But for years we have seen abnormalities in the MRI scans, then
SPECT scans showing reduced blood flow to the brain. Sometimes I
hear neurologists say that the small “hyperintense”
MRI lesions can be due to vascular or embolic phenomena (tiny blood
clots or strokes), and this explanation is consistent with the reduced
blood flow seen on studies. Like CFS, multiple strokes will cause
cerebral atrophy.
Could
it be that the reduced blood flow to the brain is the cause of the
neurologic injury? Is there a hypercoagulable state causing these
problems? Is there “sludging” of the blood flow in the
brain because of reduced circulating blood volume? We don’t
know and it is time that serious research is initiated on scale
that occurred in multiple sclerosis years ago.
If
the cerebral atrophy is due to reduced cerebral blood flow, it is
theoretically preventable by opening the cerebral vessels and increasing
the circulating blood volume. I can be criticized for speculating
here, but I freely say that I do not know. But we need the studies
to find out.
ME/CFS
is a debilitating disease of the central nervous system that causes
widespread disability. Unlike Alzheimer’s disease, ME/CFS
affects young people in the prime of their life and affects children
as well. It should no longer be considered a trivial problem. I
am unhappy with these new research developments, but I find them
hard to refute. But it is even harder to witness a medical world
that continues to speculate whether CFS is “real” or
not.

Disability
Study
A
person I have known for several years is seeking information about
ME/CFSers disability experience. I am wholly in support of her project.
She
writes, "I am a writer seeking contact with CFIDS patients
for an account of CFIDS disability issues. I would like to interview
people willing to share their thoughts and stories concerning any
or all of the following: 1) how your illness has impacted your ability
to work; 2) how having CFIDS has affected your sense of identity
and your capacity to live a normal life; 3) what kinds of experiences
you've had negotiating disability issues with the medical community
and with government and private insurance carriers; and 4) what
kind of reception you've met in publicly disclosing your illness
and in handling its impact upon friendships and family. I can promise
neither fame nor remuneration for your generosity, only my earnest
effort to respect your words, experience, and ideas.
I
taught college English for 27 years and have had CFIDS for over
20 years. I now live on SS disability and the income from a very
small writing business. I will be as timely as possible in my replies
to you. Thanks to all who write: *SCRIBE/P.O. Box 4/Slaterville
Springs, New York/14881."
