A Review of Therapeutic Nerve

Decompression for Neuropathy in Hansens

Disease with Research Suggestions
D. Scott Nickerson, M.D.,1 and David E. Nickerson, B.A.2

ABSTRACT

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Nerve decompression surgery for leprosy neuritis has a long history and large
literature. New understanding of the high frequency of spontaneous recovery from nerve
function impairment requires re-evaluation of the value of decompression in acute nerve
dysfunction with strong evidence-based protocols. Several reports and theoretical consid-
erations suggest research avenues that might offer hope for prevention of long-term
complications and relief of impairment and disabilities.

KEYWORDS: Leprosy, surgery, nerve decompression, neuritis, impairment

HISTORICAL PERSPECTIVE treated have enduring disfigurement and disability.2

Leprosy has been a scourge to mankind since before
biblical times. The identification of those infected who
must be isolated from the community as unclean is
detailed in the Old Testaments Leviticus, Chapter 13.
The destructive skin lesions of leprosy and its crippling
neuritis with deformity, numbness, traumatic wounds,
and secondary infections have been greatly feared. To
this day, there is great stigma attached to those infected,
who often face prejudice and marginalization.
The bacterial nature of this disease was recog-
nized by Dr. Armauer Hansen in 1873,1 the second
disease so documented after Koch had first identified the
bacillus causing anthrax. Effective antibiotic therapy was
first available in 1943 with the sulfa antibacterial dap-
sone, diamino-diphenylsulfone, but problems with drug
resistance soon became manifest. The addition of rifam-
picin and clofazimine in a multiple drug therapy (MDT)
protocol eventually allowed consistent bacteriologic cure
of Hansens disease. Cure of infection is not cure of
disease, however, because an estimated 25% of those
Prevention of residual impairment and recovery of func-
tion are the continuing challenges in leprosy treatment
today. Surgeons may play a significant role in this effort.
PATHOPHYSIOLOGY
Leprosy, or Hansens disease, is a chronic skin and nerve
disease caused by Mycobacterium leprae. The complex
molecular and biochemical aspects of its pathophysiol-
ogy as currently understood have been reviewed by
Scollard3 and Harboe et al.4 The germ enters the body
via the respiratory tract and travels by hematogenous
spread to distant sites, causing granulomatous lesions of
the integument and peripheral nerves. M. leprae directly
attacks the Schwann cell, binding to the G domain of the
a-chain of laminin 2 (found only in the peripheral
nerve). Both humoral and cell-mediated immunity are
elicited, causing nerve injury, axonal atrophy, inflamma-
tion, and eventual demyelinization and cell death.
Humans exhibit an astonishing variety of both cellular

1
Northeast Wyoming Wound Clinic, Sheridan Memorial Hospital,
Big Horn, Wyoming; 2University of Washington School of Medicine,
Seattle, Washington.
Address for correspondence and reprint requests: D. Scott
Nickerson, M.D., Northeast Wyoming Wound Clinic, Sheridan
Memorial Hospital, PO Box 278, Big Horn, WY 82833 (e-mail:
thenix@fiberpipe.net).
J Reconstr Microsurg 2010;26:277284. Copyright # 2010 by Thieme
Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001,
USA. Tel: +1(212) 584-4662.
Received: September 8, 2009. Accepted: November 21, 2009.
Published online: February 8, 2010.
DOI: http://dx.doi.org/10.1055/s-0030-1248237.
ISSN 0743-684X.
277
278 JOURNAL OF RECONSTRUCTIVE MICROSURGERY/VOLUME 26, NUMBER 4
and humoral immunologic response, ranging from
complete resistance to infection in most people to
overwhelming disease. The spectrum of severity is char-
acterized by the World Health Organization as pauciba-
cilliary (PB) to multibacilliary (MB). The RidleyJopling
clinical diagnostic schema classifies the spectrum of in-
creasing severity of disease states as progressing from
indeterminate to tuberculoid, borderline and lepromatous
forms corresponding to increasing humoral and decreas-
ing cellular immune competence. The response to in-
fection may continue for at least 15 years, progressing
even after antibiotic treatment achieves bacteriologic
cure. This ongoing evolution is thought to be due to
the persistent presence of residual bacterial antigen and
the bodys continuing attempts to neutralize it.
In the course of infection and treatment, Hansens
disease can exhibit sudden storms of immune attack
known as reversal reactions (Type 1) or erythema nodo-
sum leprosarum (ENL, Type 2).5 These exacerbations
can occur before, often during, or even years after anti-
biotic treatment and presumptive biological cure. It is at
this time that peripheral nerve trunks are most at risk for
onset and rapid progression of nerve function impair-
ment (NFI). NFI frequency is 15 to 55% at the time of
diagnosis,6 and 40% of MB patients can develop new
NFI during antibiotic MDT treatment.7 PB cases are at
less risk. The escalation of pain, numbness, and func-
tional loss during reversal reactions are frequently the
symptoms that first lead the patient with Hansens
disease to medical care.
CLINICAL PRESENTATION OF NEURITIS
It is well recognized that clinically leprosy neuritis
preferentially involves the facial, greater auricular, ulnar,
median, radial, peroneal, and posterior tibial nerves. The
physical examination finds them to be enlarged, hard-
ened, and tender to varying degrees. The superficial
subcutaneous location of these nerves in slightly cooler
tissue temperatures apparently favors growth of bacteria
at these specific sites.8,9 A key contribution to under-
standing the neuritis of leprosy was Dr. Paul Brands
recognition,10 expanding Virchows observations,11 that
pathologic neural changes were concentrated in certain
nerves and usually in only a few anatomical areas where
peripheral nerve traversing joints is passing through
unyielding fibro-osseous tunnels. These fascial slings
serve to tether the periarticular nerve near the axis of
rotation and guide the gliding nerve motion occurring
with flexion and extension movements. When bacterial
attack occurs here, constricting external compression is
generated as the nerve becomes edematous within a
confined space. This local external entrapment of the
enlarged nerve trunk is combined with internal pressure
elevation generated by intraneural swelling from the
inflammatory reaction to infection and immune attack
2010
to form a vicious circle of edema, vascular obstruction,
and ischemia, with blockage of axoplasmic flow.12
Physically, the nerve suffers local crush, plus stretch
and rub from joint movement.13 The result is pain,
numbness, motor loss, and autonomic dysfunction of
leprosy neuritis and eventual terminal nerve fibrosis.
Anatomically, the carpal tunnel, cubital tunnel,
Guyons canal, the peroneal fibular tunnel, tarsal tunnel,
and medial and lateral plantar or abductor tunnels are
well-known areas of potential peripheral nerve trunk
entrapment. In Hansens disease, the claw hand, monkey
hand, foot drop, and claw toe effects of severe nerve
damage are common stigmata. The lagophthalmos re-
sulting from facial nerve attack can lead to blindness. All
these symptoms and signs could theoretically benefit
from timely surgical decompression of peripheral nerve
in areas of constriction.
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MEDICAL TREATMENT OPTIONS
FOR NEURITIS
Both anti-inflammatory drugs and surgery have been
used to improve sensory and motor function and relieve
pain in leprosy neuritis. Success rates of around 50% are
usually reported for each. The rationale for corticoste-
roid use is that therapeutic effects of reduced inflamma-
tion should decrease intraneural edema, reduce
intraneural pressures, improve vascular and axoplasmic
flow, and allow recovery of nerve function. Beneficial
effects at the molecular biochemical level are presumed
but neither defined nor demonstrated.
Short courses of adrenocorticotropic hormone or
cortisol were suggested in 1952 by Lowe,14 and later
Pearson15 recommended longer courses at a higher dose.
Prednisolone in doses of 30 to 40 mg/day with biweekly
tapered 5 mg reductions over 12 to 16 weeks has been
standard medical therapy for significant new onset neu-
ritis for several decades.16,17 Thalidomide is sometimes
of use in ENL cases.5 Suspicions that much longer
duration of treatment was necessary were borne out
recently18 in a controlled, blinded prospective study
showing that best results required 20 weeks of treatment
and 60 mg prednisolone daily, yet failed in 24% to
achieve resolution without dose increases or prolonga-
tion of therapy. Leprologists continue to use predniso-
lone but have come to believe that higher doses and
individualized increases in dose, delays in tapering, and
longer treatment periods are necessary to achieve best
overall results.
SURGICAL DECOMPRESSION
FOR NEURITIS
Surgery for swollen nerves was suggested early for treat-
ment of the Hansens disease ravages when little else was
available. Hansen and Looft in 189519 reported incising
 A REVIEW OF THERAPEUTIC NERVE DECOMPRESSION FOR NEUROPATHY IN HANSENS DISEASE/NICKERSON, NICKERSON
the swollen nerves in leprosy, or what would today be
called epineurotomy. The rationale for decompression of
nerve is that the edema responsible for initial physical
effects of inflammation, fibrotic strangulation, and ob-
struction to axoplasmic flow can be reversed by removing
the physical chokepoint of intraneural scar and the
unyielding fibro-osseous tunnel.
But therapeutic surgeries were not widely prac-
ticed until after World War II. Brand in 195210 sug-
gested that anatomically localized neural damage was
responsible for the sensory and motor impairment caus-
ing typical extremity deformities, unrecognized wounds,
foot ulcerations, and bone loss of leprosy. He used the
erratic patterns of muscle sparing and involvement to
begin application of tendon transfers for functional
reconstruction and rehabilitation using unaffected
muscles to replace function lost to leprosy paralysis.
Others quickly found in this localized pathology a
rationale for therapeutic decompression of fibro-osseous
tunnels and the enlarged nerves themselves.11,2025
Dr. Brand was never enthusiastic about this decompres-
sive approach, holding until his death the opinion that
risk of damage to nerve circulation and nourishment
outweighed potential benefit.26 No published reports
demonstrating such damage have been found. These
attitudes were formed in an era before successful devel-
opment of segmental nerve grafting, neurotization, the
gap-bridging neurotube, and other techniques that
separate nerve tissue from direct vascular nourishment.
Nonetheless, Brands reticence has strongly colored
leprologists attitudes, leaving the debate on the value
of nerve decompression (ND) in Hansens disease un-
settled for 50 years.
A 2009 Cochrane Review surveyed the many
reports since 1950 of surgical decompression in patients
with Hansens disease.27 The extensive bibliography is
strongly recommended to those interested in an in-depth
study. Almost all published articles report retrospective
descriptive series recounting that patients have been
relieved of pain and had varying degrees of recovery of
strength and motor function after ND. Only two small
studies used prospective design and control groups to
compare ND plus steroid treatment to steroid treatment
alone.2830 Half a centurys retrospective reports of ND
surgery in leprosy can be summarized as follows:
 Pain is predictably relieved.
 Ulnar, median, radial, peroneal, facial, and posterior
tibial nerve ND procedures have all been reported to
show benefit.
 Motor and sensory recovery are frequent but vary in
degree.
 Authors agree that external release is mandatory, but
differ on the advisability, necessity, or indications for
medial humeral epicondylectomy, anterior ulnar nerve
transfer, epineurotomy, selective meshing of epineu-
279
rium,31 perineurectomy, and interfascicular dissec-
tion.32
 Nerves that have multiple areas of potential entrap-
ment, such as the ulnar nerves cubital tunnel and
Guyons canal and the posterior tibial nerve tarsal
tunnel and abductor tunnels, should have all locations
decompressed.33
 Decompression surgery early in the neuritis course
gives better strength and sensation return, and action
within 3 months of onset seems best.
 Even in late NFI, functionality may be improved by
microsurgical internal neurolysis of electrically iden-
tified areas of dysfunction.34
 PB and MB cases may show different results.
 Large randomized, controlled prospective studies
comparing surgery to antibiotic treatment alone or
to sham surgery, or combined surgery/steroid treat-
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ments to steroid treatment alone do not exist.
TECHNIQUES OF DECOMPRESSION
It is theoretically attractive to combine the intraneural
medical decompression of anti-inflammatory steroid
with external and internal benefits of surgical decom-
pression using external neurolysis to open the napkin
ring constriction of fibro-osseous anatomical structures,
epineurotomy to eliminate surface constriction, and
interfascicular neurolysis for internal scarring. Several
techniques have been used to accomplish this,35 includ-
ing medial humeral epicondylectomy, anterior ulnar
nerve transfer, epineurotomy, selective meshing of epi-
neurium,31 partial or subtotal perineurectomy, and in-
terfascicular decompression.36,37 Timing of intervention
is likely to be important, because fibrosis and axonal
death accumulate as time passes, despite prolonged
retention of the physiologic capability for functional
recovery and nerve regeneration. Malaviya,38 in partic-
ular, decries the relegation of surgical decompression to
last-resort usage in situations where all else has failed
and months of impairment have accumulated. Just as late
steroid treatment for NFI has been shown to have little
value, belated surgery when fibrosis has replaced edema
has odds stacked against its success.
RECOMMENDED SURGICAL INDICATIONS
Applying what is known from publication of past results
of surgery, several authors have tried to develop a
rational approach to using surgical intervention.
Virmond39 Srinivasan,40 Pandya,41 Malaviya,38 Kazen,42
and Bernardin and Thomas43 reviewed published reports
and made recommendations based on extensive personal
surgical experience. Combined, the indications are:
 Increasing pain while receiving MDT and cortico-
steroid treatment for NFI.
280 JOURNAL OF RECONSTRUCTIVE MICROSURGERY/VOLUME 26, NUMBER 4
 Failure of NFI to respond to initial prednisolone
therapy within several weeks, particularly in cases
presenting with symptoms of >3 months duration.
 Deteriorating motor function while under neuritis
treatment with prednisolone.
 Chronic pain after MDT with unimpaired motor and
sensory function.
 Recurring neuritis in reversal reaction or ENL.
 Plantar area (posterior tibial nerve) sensory loss put-
ting the patient at risk of foot ulcer.
 Medical complications or contraindications prevent-
ing steroid use.
 Pregnancy, with its frequent onset of reversal reaction
and silent neuritis.
 Psychiatric or travel difficulties complicating a super-
vised medical course.
SPONTANEOUS RECOVERY FROM NFI
Reports after 2000 began to document an unexpected
phenomenon, that of spontaneous recovery from signifi-
cant documented NFI.44,45 The Tripod 3 study46 defin-
itively confirmed this unsuspected outcome, finding that
half the patients in the placebo control arm with MB and
NFI of 6 to 24 months duration had recovery in an
efficacy study of standard corticosteroid regimens. The
Tripod 2 report47 describes similar findings in the con-
trol group of a study of standard steroid treatment for
16 weeks as neuritis prophylaxis in newly diagnosed
MB patients with mild sensory impairment. There was
around 75% recovery at 1 year in both the treatment and
placebo groups, and a delay but no demonstrable reduc-
tion in risk of reversal reactions or NFI for the treatment
group at final (12 month) evaluation. Prophylaxis with
prednisolone did not diminish the risk of the eventual
appearance of new NFI during MDT in those initially
presenting with normal nerve function.48
Now that the extent of spontaneous NFI resolu-
tion has been documented, we can understand that the
retrospective descriptive reports of the past, without
placebo groups or untreated controls, would be incorpo-
rating the spontaneous improvement cases to the credit
of the treatment. There has to be a significant question
whether the 50% statistical improvement in NFI found
in both the corticosteroid and surgical ND literature
reflects a therapeutic benefit of the intervention, or is
primarily a result of scientifically weak study designs
lacking proper control groups.
STATE OF THE CURRENT SCIENCE
Bringing this question directly to the fore, van Veen et al
have led two recent studies that thoroughly review the
literature on both the chemotherapeutic49 and surgical
decompression27 approaches to the treatment of NFI.
These reviews found only a handful of reports on either
2010
treatment using prospective, randomized protocols with
control groups that would be considered Level I or Level
II in terms of evidence-based medicine.50
For medical corticosteroid treatments they con-
clude, Evidence from randomized controlled trials does
not show a significant long-term effect. Randomized
controlled trials are needed to establish their effective-
ness, the optimal regimens and to examine new thera-
pies, and with decompression surgery, Evidence from
randomized controlled trials does not show a significant
added benefit of surgery over steroid treatment alone.
Well-designed randomized controlled trials are needed to
establish the effectiveness of the combination of surgery
and medical treatment compared to medical treatment
alone.
Clearly, we need to begin anew to scientifically
justify either corticosteroid anti-inflammatory drugs or
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surgical ND with well-designed prospective, controlled
investigations.
RESEARCH OPPORTUNITIES
Let us consider the protocol or study characteristics
necessary to produce strong, evidence-based results
that will allow science to guide any recommendations
for ND surgery in Hansens disease. Ideally these
would include prospective design, randomization,
tight cohort definition, control groups, well-defined
therapy and specific endpoints, objective outcome
measures, thorough complication reporting, and ex-
tended follow-up.
Several difficulties complicate the design of such
surgery studies. The variability of patients nerve involve-
ment and immune status make cohort definition, selec-
tion, and enrollment challenging. In view of the findings
by Rao et al18 and with an appreciation of the frequency
of spontaneous resolution of NFI, perhaps the most
fruitful study cohort would be those patients failing
initially to respond well in the first 4 to 6 weeks of
higher dose 60 mg/day prednisolone therapy.
These patients could then be randomized to a
control group continued on corticosteroid and compared
with a study group treated with surgical ND while
continued on the standard tapering prednisolone proto-
col. The decompression group could be subdivided to
evaluate the various decompression techniques listed
above. Further patient groups on standard tapering
high-dose therapy whose NFI relapsed and required
reversion to full-dose corticosteroid, or subsequently
recurred, could later enter the study cohort and be
randomized. This would produce three control sub-
groups for analysis: the poor early responders, those
relapsing under treatment, and those recurring after
satisfactory completion of an initial steroid course. An
additional study might evaluate an NFI patient cohort
with contraindications to steroid use randomized into
 A REVIEW OF THERAPEUTIC NERVE DECOMPRESSION FOR NEUROPATHY IN HANSENS DISEASE/NICKERSON, NICKERSON
either decompression surgery or a not-operated control
group.
Objective measures are needed to eliminate the
requirement for observer and patient blinding. Standard
outcome measures51of monofilament or ballpoint pen
sensation testing and motor function by the Medical
Research Council strength grading scale are semisubjec-
tive, requiring an evaluation and report from either
patient or observer. Perhaps grip or pinch dynamometer
use could be standardized for strength evaluation in
research protocols. Use of the Pressure Specified Sensory
Device or an electronic aesthesiometer may improve
accuracy and reproducibility of sensory evaluation.52,53
Electrodiagnostic recording can accurately measure
nerve activity, although this has not been directly corre-
lated with sensory or motor function. Still, these are
protocol features to be targeted to achieve strong levels
of scientific evidence.
Improved study designs and protocols with stron-
ger outcome measures should be applied to answer these
open questions about treatment of acute and chronic
NFI:
 Are there differing roles and indications for ND
via epineurotomy, selective meshing of epineurium,
fibrous perineurectomy, internal neurolysis, medial
epicondylectomy, and anterior ulnar nerve transpo-
sition?11,35,37,54
 Should nerves with multiple known sites of entrap-
ment always have multiple-site decompression33,55 to
minimize double crush effects? For example, ulnar
nerve releases at cubital tunnel plus Guyons canal;
median nerve at carpal tunnel plus pronator arcade;
and tibial nerve at tarsal and abductor tunnels plus
soleus sling.56
 Do the eventual surgical recommendations apply to
silent neuritis without skin lesions, particularly in
pregnancy?57
 Is relief of severe or residual pain alone an adequate
indication for ND?37,58
 Is there potential benefit to surgery in long-standing
NFI when modern microsurgical techniques are com-
bined with intraoperative evaluation of nerve electrical
function?34
 Is there any prospect for restoration of protective
sensation to hands and feet with the Norris technique,
resecting damaged nerve segments, and autografting
conduits of freeze-thawed skeletal muscle?59
 Can posterior tibial decompression restore protective
sensation in feet with plantar sensory loss and prevent
wound complications, accelerate foot ulcer healing, or
minimize ulcer recurrence?
 Might acral bone resorption in fingers and toes and
the tarsal bone degeneration of leprosy be, like dia-
betic Charcot foot, a neurally mediated dysfunction
amenable to treatment with bisphosphonates or ND?
281
ADDRESSING CHRONIC NFI
AND ITS COMPLICATIONS
The inability to offer patients with Hansens disease any
hope of recovery with longer duration NFI is a frustrat-
ing disappointment. This group comprises several mil-
lion individuals and is at continual risk of a cascade of
complications including wounds, ulcers, chronic infec-
tion, amputations, and blindness due to their loss of
protective sensation. There is tantalizing published evi-
dence or theoretical justification suggesting that, in the
last four of the above questions, ND might be an avenue
for reversal or prevention of some of these long-term
complications.
Interfascicular Dissection Guided by
Intraoperative Electrodiagnostics
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Turkof et al34 have described skip lesions scattered
throughout the facial nerve. Using intraoperative elec-
trodiagnostics to identify all areas of abnormal impulse
transmission, intrafascicular decompression was able to
restore gentle eye closure and improve electrical function
in half of longstanding (2 to 15 years) facial nerve
impairments. The lesser involved side served as control
nerve in this non-crossover interventional internally
controlled cohort of 10 patients with bilateral facial
nerve disease in borderline-type leprosy. Richard et al60
described similar diffuse involvement and skip lesions in
the tibial nerve at locations other than fibro-osseous
tunnels. Six of their nine long-term NFI patients recov-
ered muscle mass after interfascicular neurolysis of af-
fected segments. The results serve as preliminary
evidence that fascicular dissection does not threaten
neural nourishment to an extent that precludes nerve
survival and recovery. This challenges the idea that ND
can serve no purpose after 6 months of chronic NFI and
surgical interference risks important damage to blood
supply.61
Denatured Muscle Nerve Conduits
Miko et al62 have demonstrated that severely damaged
nerves retain the capacity of regeneration for at least a
decade. Pereira et al63,64 attempted to take advantage of
this potential by resection of damaged nerve segments
and autografting regeneration conduits of freeze-thawed
skeletal muscle using the technique of Norris et al.59
There is but minimal literature on this technique and its
results. One might postulate that the grafted segment,
being free of Schwann cells, could be resistant to re-
current immune attack.
Foot Protection and Amputation Prevention
The leprosy literature includes reports35,42,55,6568 of
sensory or autonomic recovery and improved ulcer
282 JOURNAL OF RECONSTRUCTIVE MICROSURGERY/VOLUME 26, NUMBER 4
healing after posterior tibial ND. Prospective reporting
on ND in the similar situation of diabetic foot neuro-
pathy, without control groups, noted reduced ulcer risk,
recurrence rates, amputation risk, and foot-related
hospitalizations in comparison with the literature.69
Restoration of protective sensation to the insensate
foot in Hansens disease might in theory produce
similar benefits.
Skeletal Bone Change Arrest
Acral bone resorption and the tarsal midfoot collapse of
Hansens disease are well described but have received
minimal research attention.70,71 Undoubtedly, sensory
loss and bony deformity combine to play a part in plantar
ulcerations, infections, hospitalizations, and amputa-
tions. The Charcot neuroarthropathy of diabetes melli-
tus is much better studied and may offer some guidance
to students of the Hansens disease equivalent. It is now
hypothesized that the aggressive bone resorption of
diabetes is a neurally mediated process in a denervated
foot72,73 with adequate circulation. In the diabetic
Charcot process, biochemical markers of bone turnover
are known to correlate with foot temperature normal-
ization when bisphosphonate treatment is used for
Charcot neuroarthropathy,74 and a few cases of rapid
radiographic resolution after ND are reported.75 A
longitudinal radiological study followed patients with
leprosy from the time of cure for 2 to 15 years and found
that 20% had new or progressive bone lesions despite
completed antibiotic treatment and presumed bacterio-
logic cure.76 This suggests processes other than direct
bone infection, perhaps damaged nerve,77 may also
mediate the Charcot Foot of Hansens disease. Studies
of bone turnover markers in leprosy and their changes
with ND could reveal whether common processes are
operating in the two neuroarthropathies.
CONCLUSION
Surgical decompression for NFI has a long history in
Hansens disease. It has not been widely applied in the
past due to limited infrastructure, questions about its
safety and effectiveness, and wide availability of inex-
pensive steroid anti-inflammatory drugs, which seemed
to produce similar benefits. The value of both the
standardized corticosteroid regimens and ND is called
into question by the recent elucidation of the frequency
of spontaneous recovery from early, mild, and even more
persistent NFIs of up to 2 years. Future research needs to
control for spontaneous recovery in evaluating the bene-
fits of either therapy. Several newer approaches might
find ND surgery useful to reverse chronic, longer-term
NFI and prevent the complications of neuromuscular
impairment, wounds, infection, tarsal disintegration,
ulcers, amputations, and blindness.
2010
ACKNOWLEDGMENTS
The invitation and encouragement of Professor A. Lee
Dellon to undertake and publish this review was crucial
to its completion. No financial arrangements supported
this work.
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