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"We who choose to surround ourselves with lives even
more temporary than our own live within a fragile circle, easily and
often breached. Unable to accept its awful gaps, we still would live
no other way. We cherish memory as the only certain immortality, never
fully understanding the necessary plan."
 Gemma, owned by Lisa Finnie, modeling Dog Boots by Pro-Active Paws
You are their life, their love, their leader. They will be yours, faithful and true, to the last beat of their heart. You owe it to them to be worthy of such devotion." Author unknown
Degenerative Myelopathy (DM) of German Shepherds
is an autoimmune disease. In autoimmune diseases, the patient's
own immune system attacks some part of its body. In DM, the myelin
and axons are attacked. (Myelin is the insulation around nerve fibers
leaving the nerve cell. Axons are long nerve fibers that go from
nerve cells to muscles and other parts. They carry the signals from
the nerve to the muscles.) It is similar to Multiple Sclerosis in
humans.
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The Disease: Written by Dr. Roger Clemmons. Degenerative Myelopathy
(DM) was first described as a specific degenerative neurologic
disease in 1973. Since then, much has been done to understand
the processes involved in the disease and into the treatment
of DM. Hopefully, this will help you understand the problem
and to explain further the steps that can be taken to help dogs
afflicted with DM. The age at onset is 5 to 14 years, which
corresponds to the third to sixth decades of human life. Although
a few cases have been reported in other large breeds of dogs,
the disease appears with relative frequency only in the German
Shepherd breed, suggesting that there is a genetic predisposition
for German Shepherd dogs (GSD) in developing DM. The work presented
here and by others on the nature of DM has been performed in
the German Shepherd breed. Care must be taken in extrapolating
this information to other breeds of dogs. It is currently not
known whether the exact condition exists in other breeds of
dogs. Many dogs may experience a spinal cord disease (myelopathy)
which is chronic and progressive (degenerative); but, unless
they are caused by the same immune-related disease which characterizes
DM of GSD, the treatments described herein may be ineffectual.
The breeds for which there is data to suggest that they also
suffer from DM of GSD are the Belgium Shepherd, Old English
Sheep Dog, Rhodesian Ridgeback, Weimaraner and, probably, Great
Pyrenees. Confirmation of the diagnosis is important in other
breeds before assuming that they have DM of GSD. Diagnosis of
DM is made by a history of progressive spinal ataxia and weakness
that may have a waxing and waning course or be steadily progressive.
This is supported by the neurologic findings of a diffuse thoracolumbar
spinal cord dysfunction. Clinical pathologic examinations are
generally normal except for an elevated cerebral spinal fluid
(CSF) protein in the lumbar cistern. Electromyographic (EMG)
examination reveals no lower motor unit disease, supporting
the localization of the disease process in the white matter
pathways of the spinal cord. Spinal cord evoked potentials recorded
during the EMG do show changes which help determine the presence
of spinal cord disease. Radiographs of the spinal column including
myelography are normal (other than old age changes) in uncomplicated
DM. Unfortunately, myelography can be associated with worsening
of clinical signs and carries some degree of risk for certain
patients. Dogs afflicted with DM have depressed lymphocyte blastogenesis
to plant mitogens. The depression of their cell mediated immune
responses correlates with the clinical stage and severity of
the disease. Furthermore, this suppression has been shown to
be due to the genesis of a circulating suppressor cell. Some
dogs with DM exhibit antigen-binding cells specific to canine
myelin basic protein. Immunoglobulins have been shown to be
bound within lesions within the spinal cords of dogs with DM.
These patients also show increased circulating immune-complexes
in their sera. The antigens in these immune-complexes have been
examined and appear to be markers of inflammation as they have
been found to exist in patients who have other inflammatory
diseases of the central nervous system. 2-Dimensional electrophoresis
of CSF proteins indicates that the elevated proteins in the
CSF of DM patients represent changes which are related to inflammation.
While these changes are not specific for DM, the other conditions
in which the inflammatory proteins have been found in CSF can
be differentiated by clinical signs. The 2-dimensional electrophoresis
of CSF proteins appears to be one of the most specific change
seen in DM. Recently, we have found that CSF levels of the enzyme,
acetylcholinesterase, are elevated in patients with DM. Again,
this occurs in other forms of central nervous system inflammation
in dogs. However, when combined with the history, neurologic
signs, CSF protein concentration and EMG, the elevated CSF acetylcholinesterase
level helps confirm the diagnosis. This allows the inclusion
of DM in the diagnosis, even if other problems are uncovered
during the examination. The gross pathologic examination of
dogs with DM generally is not contributory toward the diagnosis.
The striking features being the reduction of rear limb and caudal
axial musculature. The microscopic neural tissue lesions consist
of widespread demyelination of the spinal cord, with the greatest
concentration of lesions in the thoracolumbar spinal cord region.
In severely involved areas, there is also a reduced number of
axons, an increased number of astroglial cells and an increased
density of small vascular elements. In the thoracic spinal cord,
nearly all funiculi are vacuolated. Similar lesions are occasionally
seen scattered throughout the white matter of the brains from
some dogs, as well. Many patients have evidence of plasma cell
infiltrates in the kidneys on throughout the gastrointestinal
tract, providing a hint to the underlying immune disorder causing
DM. During the past two decades, we, at the University of Florida,
have provided important new insights into the pathoetiology
of DM. The release of antigens during the disease process could
explain the immune deficits seen in DM and suggests that processing
these immune-complexes by circulating macrophages leads to the
development of the circulating suppressor cells that were previously
noted. This provides a logical explanation for the presence
of immune abnormalities in GSD with DM. Electrophoresis of immune-complexes
demonstrates that the proteins present are inflammatory proteins
which increase in inflammatory diseases of the dog nervous system.
It is hoped that working with the antigens present in the immune-complexes
will lead to a major breakthrough in our understanding of DM
and that this also could lead to an early serodiagnostic test
for the condition. However, the development of a serodiagnostic
test will await the availability of antibodies specific to unique
markers within the inflammatory proteins of DM dog immune-complexes.
While the cause of the altered immune system is not known, what
is increasingly clear is that DM is caused by an autoimmune
disease attacking the nervous systems of patients, leading to
progressive neural tissue damage. In many respects, DM is similar
to what has been discovered about the pathogenesis of Multiple
Sclerosis in human beings. In fact, based upon new data concerning
the pathology of MS, we can now say with some degree of certainty
that DM is MS in dogs. We believe that, due to some triggering
factor, immune-complexes circulate. These immune-complexes lead
to endothelial cell damage in the vessels of the CNS. Subsequently,
fibrin is deposited in the perivascular spaces. When this degrades
(point of action of aminocaproic acid), inflammatory cells are
stimulated to migrate into the lesions. The inflammatory cells
release prostaglandins and cytokines (point of action of vitamin
E and C) which leads to the activation of tissue enzymes and
the formation of oxygen free-radicals (point of action of acetylcysteine)
which, in turn, leads to tissue damage. Treatment of DM of GSD,
which we recommend, is directed at these pathologic processes.
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