Leprosy mailing list – November 19th, 2005
Ccn: all.
From:
G Warren, Sidney, Australia.
Dear
Salvatore,
Thank
you for your continued email assistance.
I
would be happy to have this sent to Dr Penumaka direct, but as I do
not have her e-mail I would be very happy to have it sent out as
perhaps someone else may have answers to these very common problems.
I
am interested in the request for information on silent neuritis. I will be interested to see
the definition of what Dr Elizabeth Penumaka defines as “Silent
neuritis”. I suppose I
should say what Dr Gelber defines as “silent neuritis”, as she is
studying his charts and, I do not know what he says in them.
The
term silent neuritis only became popular a few decades ago. Yes
everyone accepts that silent neuritis occurs in Leprosy, but many
clinicians do not realize that the nerves are parasitized very early
in leprosy. Therefore every patient with leprosy can be said to have
neuritis and obviously many are silent, for many years at least.
It
is very hard to do research on how to reduce the permanent damage that
occurs in the early days of Lepromatous leprosy, by giving
supplementary medication as well as the routine anti-leprosy
medication, such as MDT. However
that is what I personally feel needs to be done.
In
years of leprosy work in Asia I have found that the addition of simple
medication such as Vitamin B1 and calcium and magnesium do a lot to
reduce paraesthesia not only in leprosy but also in many other
neuropathic disorders. In
many Leprosy endemic areas there are definite deficiencies in some of
these in the diet and an adequate supply makes a lot of difference to
the patient well-being. This is the result of purely
clinical observation and not research testing etc.
I
have asked many neurologists to research the use of these drugs (and
others) in neuropathy; but so far have not found anyone who has
done so. I would be interested to hear of reports on the use of
supplementary drugs in treating any neuropathy.
Having
worked in leprosy for over 45 years I know of many LL patients who
have “done well “ on MDT (or in the early days other anti-leprosy
medication) and never had obvious neuritis in the course of their
treatment. But they develop sensory abnormalities and paralysis
many years after the anti-leprosy medication has ceased. In
Lepromatous leprosy there may be no neurological symptoms for many
years and by the time there is clinical neuritis it is too late to
reverse the damage that has occurred as it is due mainly to the long
slow fibrotic process that occurs in lepromatous and other leprosy of
low resistance type.
I
am distressed to see the number of well-developed Lepromatous patients
who come in with far advanced skin lesions, such as nodules. They may
complain of nerve discomfort, which one discovers is usually numbness
and paraesthesia when carefully questioned. And they are given
steroids to treat “neuritis”.
Yes steroids make them feel good, but in the long term follow
up one finds that they really do not make any appreciable improvement
in nerve function.
Unfortunately some lepromatous patients deteriorate
medically when given long-term steroids. In some LL patients
there is a definite slowing of clearance of AFB (the BI and MI
do not fall as expected) while on steroids. Other patients once
started on steroids like the “feeling of well being” so much that
one has great difficulty in getting them off steroids.
I
have seen LL patients taking steroids for many years while the nerve
function slowly deteriorates due to the ongoing healing of
the nerves that were damaged by “silent neuritis”: in the many
years that the LL had been developing, often before anti-leprosy
medication commenced.
In
the BT, TT of course the silent neuritis progresses till the patient
has clinical neuritis and that is often the clinical presentation that
brings the patient in for care. Yes for these patients there is good
reason in giving steroids in the hope that the steroids will reduce
the oedema and the intraneural anoxia and so in the long
term, save function. If treatment commences early enough it is
sometimes of course possible to reverse the early signs of
neuritis. Hence the
importance of basic nerve function tests at every visit so that the
“silent neuritis” can be detected as soon as possible and
effective treatment instituted.
Of
course many TT and BT patients present long after the silent neuritis
has caused damage that cannot be reversed, but how can one encourage
early diagnosis so that such neural deficits do not occur.
All
the best to her research, I personally will welcome anything that
enables workers to treat silent neuritis before it has caused
irreparable damage.
Grace Warren
Previously
Superintendent of Hong Kong Leprosarium (1960-1974) and
Consultant
in Leprosy and Reconstructive surgery for Asia (1075-1995) for
the Leprosy Mission International.
