I'm
not posting this because I am a disciple or follower of Dr Hyde but because not having any knowledge on the subject, I would like some idea of how much of the info is true or feasible.
He writes:
"
The possible role of genetic susceptability in M.E.-like patients
Ehlers Danlos Syndrome (EDS)
One of the more severe forms of acute onset vascular M.E. is Ehlers
Danlos Syndrome. There is not one Ehlers Danlos Syndromes but at
least 8 varieties. Some cause such severe anatomical and physiological
changes that the child does not survive infancy. Probably each of the
EDS variants are all genetic based illnesses although I have never seen
a genetic study published on each of the subtypes. One of these EDS
subtypes is important in any discussion on the subject of M.E., which I
will now briefly outline.
I have only seen Ehlers Danlos in women. Their illness tends to be
severe and often misdiagnosed. Whether this is a variant of M.E. only
time will tell but if it is not it should be placed in this group for the
moment. The patient usually falls ill sometime after the age of 16-18.
Up until this moment there is no indication of any M.E. or CFS like
abnormality. It is possible they may have previously been diagnosed
with hyper-reflexia or as a child they may have amused their friends
by their double joint manifestations. Probably all EDS have abnormal
connective tissue in their blood vessels. These patients all seem to have
fallen ill immediately after an untyped infectious episode or following
an immunization. I believe these women have a genetic disease and it
is either turned on by a specific virus or alternatively by some aging
trigger.
These hyper-reflexive EDS patients tend to be light sensitive, and
suffer from severe Dysautonomia with one or more of the following:
POTS (orthostatic tachycardia syndrome), IST (inappropriate sinus
tachycardia, and NMH (neurally mediated hypotension).
Marfan Syndrome
Marfan syndrome in its extreme form is quite easy to recognize and is
due to an inherited genetic trait of the connective tissue. The classical
Marfan patient is a tall thin, thin-headed individual with long limbs
hands and fingers and long narrow feet. In the extreme form the
patient develops severe aortic and valvular pathology that today can be
replaced where previously many of these patients died before reaching
20-30 years. These patients are easily recognized by their parents and
their physicians. Wikipedia has an excellent review of the pathological
findings in these extreme patients.
Our problem is not the classical easily diagnosed Marfan individual but
in the wide variety of expression of this genetic illness. These milder
disease forms of patients often are missed and not diagnosed as Marfan
syndrome but present with a history of gradual onset fatigue syndromes
and as with its close cousin, Ehlers Danlos Syndrome they should be
considered in the differential diagnosis
In my patient physical examination check-list, I have a triad of
progressive illnesses. Hyper-extensive syndrome, Ehlers Danlos and
Marfan disease. All three are associated with fatigue syndromes and
dysautanomia. The three are not related but they do form a progressive
cause of the dysautanomia family of pathologies. My check-list of
Marfan features is as follows:"
taken from
http://www.hfme.org/Other/DefinitionBooklet_Sept_2011.pdf
if it is a load of twaddle I will gladly delete it.
