Silent neuritis (Quiet Nerve Paralysis)

Leprosy Mailing List – March 9th, 2012 

Ref.:    Silent neuritis (Quiet Nerve Paralysis)From: H Srinivasan, Chennai, India

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Dear Dr Salvatore Noto,

Ref.: Query by Dr Narayanakumar (Kumbakonam, India) about “Silent neuritis”

Thank you, Dr Narayanakumar. My response is as follows :-

The term “Silent neuritis” is used by many to refer to the occurrence of nerve function deficit (NFD), usually motor paralysis, without concurrent or immediately antecedent episode of acute neuritis.  I preferred the term “Quiet Nerve Paralysis” (QNP) to refer to this phenomenon.

While leprologists were aware of its occurrence, I drew attention to the fact that it was associated with the occurrence of deformity in a significant proportion of patients [1].  Here I will not go into the reasons why I preferred the term ‘Quiet Nerve Paralysis’ to ‘Silent Neuritis’.  Interested colleagues may refer to reference [2].  

During the course of my investigations, in the field and in the sanatorium, on the origin and progress of deformities in leprosy patients, I found that motor paralysis and associated deformity was five times more common in patients giving a history of remembered attack(s) of acute neuritis of the concerned nerve trunk than in those not giving such a history.  However, I also found that such patients accounted for only about 20% to 25% of those showing paralytic deformity.  Even allowing for faulty memory, it appeared that a sizable proportion of patients developed deformity without developing acute neuritis.  We designated such patients as having ‘Quiet Nerve Paralysis’.

This group of patients comprised:
1). untreated or inadequately treated patients;
2).Patients adequately treated in the past and discharged as ‘cured’; as well as
3).patients still under treatment.
We hypothesized that uncontrolled leprosy was the cause of nerve paralysis in the first group and instituted proper anti-leprosy therapy in them.  We considered QNP as the manifestation of relapse of leprosy in the second group and treated them again with anti-leprosy treatment of the day.  As for the third group, we felt that, in the absence of other explanations, they probably had “subclinically operating reactional pathology” in them and so treated them with a standard course of prednisolone for three to four months or more depending on their response.  Varying proportion of patients showed partial or complete restoration of nerve function in all the three groups, indicating that our conjectures were probably correct, at least in those patients.  Those in the first two groups who did not show any sign of recovery of nerve function after three months of anti-leprosy therapy were given a standard course of steroid therapy for what it was worth.  If I remember right, there was no clinical evidence suggestive nerve compression in these patients and so nerve decompression was not offered to them.

We subsequently tried to carry out a prospective trial of steroid therapy for QNP in the field, but the results were not reliable due to operational problems.

I should also point out that the patients were from South India, and the study was done during the ‘dapsone era’ when dapsone monotherapy was the standard anti-leprosy treatment.  I do not know what the situation is like in present conditions of years of intensive coverage of the patient population with MDT and fewer cases of active leprosy in the environment.

H Srinivasan FRCS
Surgeon (Retd.)
25, First Seaward Road
Chennai - 600 041
India

[1] Srinivasan H, Rao KS, Shanmugam N (1982).  Steroid therapy in recent “quiet nerve paralysis” in leprosy. Leprosy in India  54(3) :  412 – 419.
[2] Srinivasan H, Gupte MD.  Experiences from studies on Quiet Nerve Paralysis, Ch. 3  in The Peripheral Nerve in Leprosy and Other Neuropathies, (pp 30 – 35), Ed. by Noshir H Antia & Vanaja P Shetty, Delhi, Oxford University Press, 1997.