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Touch pressure and sensory density after tarsal tunnel release in diabetic
neuropathy
William H. Gondring M.D., M.S.a,*, Prashant K. Tarun Ph.D.b, Elly Trepman M.D.c
a St. Joseph Orthopedics and Heartland Regional Medical Center, St. Joseph, MO, USAb Steven L. Craig School of Business, Missouri Western State University, St. Joseph, MO, USAcDepartment of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, Canada
1.
Introduction
Peripheral neuropathy is a major cause of diabetic foot and
ankle complications including ulcers and Charcot arthropathy
[1,2]. The incidence of sensory neuropathy in diabetic patients is
11-fold greater than in non-diabetic patients [3]. Neuropathic
symptoms affect 3040% of patients with diabetes [4,5]. Non-
healing neuropathic ulcers precede amputation in 84% of lower
extremity amputations in diabetic patients [6], and 1141% of
diabeticpatientsdiewithin1 year of a lower extremity amputation
[1].
The pathogenesis of diabetic peripheral neuropathy and nerve
injurymaybemultifactorial, including (1)metabolicabnormalities
that may cause direct and indirect neuronal damage, such as
hyperglycemia [7], intraneural edema associated with sorbitol,
slowed axoplasmic protein transport, and glycosylation of
endoneurial collagen [8]; (2) microvascular changes that may
cause endothelial dysfunction and ischemia; (3) immunologic and
inflammatory nerve injury [3]; (4) endocrinologic imbalance
including depletion of growth factors and insulin; and (5)
compressive neuropathy, such as entrapment or compression of
the posterior tibial nerve at the tarsal tunnel, resulting in
secondary neuronal edema, inflammatory injury, and symptoms
of diabetic neuropathy [4,9,10].
Nerve entrapment may be caused or aggravated by local
anatomic factors including positional changes in tarsal tunnel
pressure and volume [11,12], tumors, trauma, or fibrosis. In
diabetic patients with symptomatic neuropathy and a positive
Tinel sign at the tarsal tunnel, nerve decompression may decrease
the risk of developing ulcers or incurring an amputation [8].
Furthermore, surgical decompression of the posterior tibial nerve
in diabetic patients may improve pain [13], subjective sensation
[13], and 2-point discrimination [14].
Sensory neuropathy may contribute to the development of
ulcers and Charcot arthropathy because of loss of protective
sensation [2] and impaired balance and proprioception that may
change mechanical stresses [15]. However, sensory impairment
may be complex and may vary with the severity and duration of
diabetes. Quantitative, computerized measurements in the upper
and lowerextremitieshave shown thatdiabeticpatientswith early
nerve entrapment have impaired 2-point discrimination but intact
1-point touch pressure sensation; diabetic patients with late
neuropathy have impairment of both 2-point discrimination and
1-point touch pressure threshold [16,17]. Nevertheless, clinical
evaluation of diabetic neuropathic feet most commonly includes
Foot and Ankle Surgery 18 (2012) 241246
A R T I C L E I N F O
Article history:Received 1 January 2012
Accepted 9 February 2012
Keywords:
Diabetes mellitus
Plantar nerves
Entrapment
Treatment
A B S T R A C T
Background: Limited quantitative information is available about the improvement of protectivesensation after tarsal tunnel release in patients with diabetic peripheral neuropathy.
Methods: Prospective, non-blinded, non-randomized case series of 10 feet in 8 diabetic patients and 24
feet in 22 non-diabetic patients who had tarsal
tunnel release. Preoperative andpostoperative (average,
89 months) anatomic, quantitative sensory testing was done with touch pressure 1-point threshold
(SemmesWeinstein monofilaments) and 2-point discrimination.
Results: There was marked, significant postoperative improvement of mean touch pressure 1-point
threshold, compared with preoperative values, formedial calcaneal, medial plantar, and lateral plantar
nerves in both non-diabetic and diabetic patients. There was minimal improvement in 2-point
discrimination only for the medial calcaneal nerve in non-diabetic, but not in diabetic, patients.
Conclusions: Nerve entrapment at the tarsal tunnel is an important component of diabetic peripheral
neuropathy. Tarsal tunnel decompression may improve sensory impairment and restore protective
sensation.
2012 European Foot and Ankle Society. Published by Elsevier Ltd. All rights reserved.
* Corresponding author at: 1335 Village Drive, St. Joseph, MO 64506, USA.
Tel.: +1 816 233 0211; fax: +1 816 233 8196.
E-mail address: [email protected] (W.H. Gondring).
Contents
lists
available
at
SciVerse
ScienceDirect
Foot and Ankle Surgery
jour nal homepage : www.elsev ier . com/loc ate / fas
1268-7731/$ see front matter 2012 European Foot and Ankle Society. Published by Elsevier Ltd. All rights reserved.
doi:10.1016/j.fas.2012.02.001
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8/11/2019 Touch pressure and sensory density after tarsal tunnel release in diabetic.pdf
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range,420 wks), in part because of difficult geographic conditions
in the midwest region of the United States that affected patient
travel, including large travel distances and stormy weather.
2.2. Quantitative sensory testing
Quantitative touch pressure (1-point) sensory testing was
performed with a series of 20 nylon SemmesWeinstein mono-
filaments (North Coast Medical Inc., Morgan Hill, CA) of different
thicknesses, ranging from 1.65 to 6.65 (logarithmic scale)
corresponding to an applied force ranging from 0.008 to 300 g,
as previously described [18,20]. The monofilaments had been
calibrated by the manufacturer. The examiner applied the
monofilaments to each of the 3 nerve regions (medial calcaneal,
medial plantar, and lateral plantar nerves) perpendicular to the
plantar foot skin with just enough pressure to bend the
monofilament to 908. The monofilaments were applied sequen-
tially from the smallest (1.65monofilament; 0.008 g) to the largest
(6.65 monofilament; 300 g) until the sensory threshold was
determined, defined as the force applied by the smallest
monofilament that the patient could feel at the site tested. Data
recorded included the size of the smallest monofilament sensed by
the patient (sensory threshold force [g]) and anatomic location
(nerve region) [18,21].Quantitative static 2-point discrimination testing was done
with a commercially available device (Dellon-McKinnon Disk-
CriminatorTM, P.O. Box 16392, Baltimore, MD and NexGen
Ergonomics, Inc., 6600 Trans Canada Highway, Suite 750, Pointe
Claire, Quebec, Canada H94 4S2), consisting of an octagonal disk
with pairs of blunt tips that were separated by different distances
(range, from 9 to 20 mm) [22]. The 2-point discrimination testing
was done at each of the 3 nerve regions (medial calcaneal, medial
plantar, and lateral plantar nerves), and the patient was positioned
unable to view the disk in contact with the plantar aspect of the
foot. The pairs of tips were placed perpendicular to the skin and
applied with uniform manual pressure until skin blanching
occurred,
beginning
with
the
widest
separation
between
the
2
tips and sequentially decreasing tip separation with eachsuccessive application. Absence of 2-point discrimination was
noted when the patient reported that only 1 point was sensed, and
the
separation
(sensory
threshold
distance
[mm])
between
these
2
tips
was
recorded
as
the
endpoint
of
the
test.
All monofilament and 2-point discrimination tests were
performed by the same nurse examiner who had previous
experience
testing
over
500
consecutive
patients
with
the
same
testing
protocol
technique.
Testing
was
done
with
the
patient
in
a
quiet room and constant room temperature to prevent tempera-
ture-dependent variations in flexibility of the monofilaments and
2-point
discrimination
tester.
No
verbal
cues
were
given
during
the
examination.
Before
the
testing
procedure,
a
Harris
foot
mat
was
made to identify abnormalpressure areas such as callosities,which
were
avoided
to
decrease
the
potential
for
erroneous
grading
ofsensory
threshold.
Controls,
validity,
and
protocol
of
both
testing
techniques
were
validated
by
comparison
with
a
second
tester
at
random intervals (data not shown).
The preoperative sensory study was done at the initial
evaluation.
The
final
postoperative
sensory
study
was
performed
at
the
time
of
discharge
from
the
clinic
when
the
patient
had
reached maximum medical improvement and resumed usual and
customary activities. The time after surgery for thefinal evaluation
was
similar
for
diabetic
and
non-diabetic
patients
(Table
1).
2.3. Surgery
Surgical
treatment
for
tarsal
tunnel
syndrome
was
performed
as
previously
described
[18,19,23]. All
surgery
was
done
by
1
surgeon at the same medical center. A pneumatic tourniquet was
inflated briefly (maximum, 10 min) when it was needed to
facilitate exposure or hemostasis within the fibro-osseous tunnel.
Approximately 20% of the distal posterior tibial neurovascular
bundle located in the deep posterior compartment of the calf was
released, estimated by an intraoperative contrast study as
previously described [23]. The flexor retinaculum posterior to
the medial malleolus, and both the external and internal investing
fascia of the abductor hallucis muscle, were exposed and released;
the internal investing fascia of the abductor hallucismuscle spread
at least 6 mm following release. The abductorhallucismuscle belly
was preserved. The medial portion of the plantar fascia (approxi-
mately 25%) was released.
2.4. Data analysis
Data analysiswasperformed with statistical software (Predic-
tive Analytic Software [PASW] Statistics 17 [formerly SPSS
Statistics 17], SPSS Inc., Chicago, IL). The sample data collected
were scored at fixed intervals and the sample data were not
random because of the self selection of subjects participating in
this study. Furthermore, normal distribution of data could not be
assumed and parametric statistical methods could not be used
becauseof the small sample size; therefore, thesmall samplesizeprecluded a statistical comparison of non-diabetic and diabetic
feet. For comparison of preoperative and postoperative sensation,
theWilcoxon signed rank test (non-parametric)wasusedbecause
of the small sample size of patients and the rank ordering of the
monofilament and 2-point discrimination data [2426]. Preoper-
ative and postoperative data were compared for touch pressure
threshold and 2-point discrimination for the medial calcaneal,
medial plantar, and lateral plantar nerve regions in non-diabetic
and diabetic patients, and percent change from before to after
surgery was calculated (percent difference between the mean
preoperativeandpostoperativevalues,with preoperative valueas
denominator). Preoperative and postoperative data were com-
pared
fornerve
conduction
time
for
themedial plantar
and lateral
plantar nerves in non-diabetic patients. Significant differenceswere defined by P 0.05.
3.
Results
Symptoms ofpain and paresthesias were improvedafter surgery
in non-diabetic and diabetic patients (Tables 1 and 2). The motor
nerve
conduction
studies
for the
medial and
lateral
plantar
nerves
showed
that
the
average preoperative
severity
of
neuropathy
was
mild ormoderate; in thenon-diabetic patients, small butsignificant
improvement in conduction velocity was noted after surgery, but
postoperative
data
were
not
available
in
diabetic
patients
because
of
limitations
in
health
insurance
coverage
(Table
3).
Sensory evaluation at an average of 89 months after surgery
showed
marked,
significant
improvement
of
mean
touch
pressure(1-point)
threshold
with
monofilament
testing,
compared
with
preoperative
values,
for
medial
calcaneal,
medial
plantar,
and
lateral plantar nerves in both non-diabetic and diabetic patients
(Table 4).
There
was
a
significant
but
small
improvement
of
mean
sensory
density
(2-point
discrimination)
from
before
to
after
surgery
in
the
medial calcaneal nerve region in non-diabetic patients, but not in
diabetic patients. However, there was no change in mean sensory
density
from
preoperative
to
postoperative
values
in
the
medial
or
lateral
plantar
nerve
regions
in
both
non-diabetic
and
diabetic
patients (Table 5).
By the final postoperative follow-up evaluation, none of the
diabetic
neuropathic
patients
developed
any
foot
ulcer
or
Charcot
arthropathy.
W.H. Gondring et al./Foot and Ankle Surgery 18 (2012) 241246 243
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4.
Discussion
The abnormal preoperative monofilament and 2-point discrim-
ination findings in the present study (Tables 4 and 5) suggest that
late
nerve
entrapment
was
predominant
in
this
patient
population
[16,17].
Entrapment
neuropathy
frequently
is
unrecognized
in
diabetic
patients
who
have
a
plantar
sensory
deficit
[4]. The
1-
point,
monofilament
test
is
a
measure
of
sensory
touch
pressure
threshold and is used clinically to determine the presence or
absence of protective sensation. The postoperative improvement
in
mean
sensory
touch
pressure
(1-point)
threshold
in
the
diabetic
patients
(Table
4) supports
the
hypothesis
that
nerve
entrapment
Table
3
Relation between preoperative and postoperative nerve conduction latency in non-diabetic and diabetic patientswho had tarsal tunnel release for entrapment neuropathy.a
Patients Nerve region Number of feet Mean (range) latency (ms) Number of feet Mean (range) latency (ms) % change of mean P
Preoperative Postoperative
Non-diabeticc Medial plantar 24 7.2 (6.87.5) 8 6.8 (6.27.3) (6) 0.02
Lateral plantar 24 7.4 (7.08.1) 8 6.9 (6.47.6) (7) 0.02
Diabeticd Medial plantar 10 7.2 (6.57.8) 0 NAb NA
Lateral plantar 10 7.5 (7.17.9) 0 NA NA
a Preoperative nerve conduction studies were done in 24 feet of 22 non-diabetic patients and 10 feet of 8 diabetic patients. Postoperative nerve conduction studies weredone in 8 feet of 8 non-diabetic patients.
b NA,not available: postoperativenerve conduction studieswere not done in the diabetic patients because thiswas not covered by the health insurance for these patients.c In non-diabetic patients, preoperative neuropathy in the medial plantar nerve region was absent in 4 feet, mild in 13 feet, moderate in 6 feet, and severe in 1 foot;
preoperative neuropathy in the lateral plantar nerve region was absent in 2 feet, mild in 15 feet, moderate in 5 feet, and severe in 2 feet.d In diabetic patients, preoperative neuropathy in themedial plantar nerve region was absent in 2 feet,mild in 3 feet,moderate in 2 feet, and severe in 3 feet. Preoperative
neuropathy in the lateral plantar nerve region was mild in 3 feet, moderate in 4 feet, and severe in 3 feet.
Table
2
Relation between preoperative and postoperative pain in non-diabetic and diabetic patients who had tarsal tunnel release for entrapment neuropathy.a
Patients Nerve region Number of feet Number of feet with pain rated
none/mild/moderate/severe
Preoperative Postoperative
Non-diabetic Medial calcaneal 24 0/13/8/3 2/19/3/0
Medial plantar 24 0/12/6/6 2/19/3/0
Lateral plantar 24 0/18/5/1 0/21/3/0
Diabetic
Medial
calcaneal
10
0/2/4/4
6/2/2/0Medial plantar 10 0/1/5/4 5/4/1/0
Lateral plantar 10 0/2/3/5 5/3/2/0
a Pain measured with visual analog scale (VAS) (minimum, 0; maximum, 10): none, 0; mild, 13; moderate, 47; severe, 810.
Table 4
Relation betweenmeanpreoperative andpostoperativequantitativemonofilament touchpressure (1-point) sensory threshold innon-diabetic anddiabeticpatientswhohad
tarsal tunnel release for entrapment neuropathy.a
Patients Nerve region Number of feet Mean sensory threshold (g) P
Preoperative Postoperative % change
Non-diabetic Medial calcaneal 24 1.9 0.8 (59) 0.009
Medial plantarb 21 2.1 0.5 (77) 0.001
Lateral plantarb 21 8.5 0.3 (97) 0.001
Diabetic Medial calcaneal 10 65.6 0.8 (99) 0.003
Medial plantar 10 32.9 0.8 (98) 0.003
Lateral plantar 10 62.0 0.5 (99) 0.006
a Non-diabetic, 24 feet in 22 patients; diabetic, 10 feet in 8 patients.b For non-diabetic patients, monofilament sensory threshold was not done for the medial and lateral plantar nerves in 3 feet of 2 patients.
Table 5Relation between mean preoperative and postoperative quantitative 2-point discrimination sensory threshold in non-diabetic and diabetic patients who had tarsal tunnel
release for entrapment neuropathy.a
Patients Nerve region Number of feet Mean sensory density (mm) Pc
Preoperative Postoperative % change
Non-diabeticb Medial calcaneal 20 14.9 14.0 (6) 0.009
Medial plantar 17 14.1 14.0 (0) NS
Lateral plantar 17 14.3 14.1 (2) NS
Diabetic Medial calcaneal 10 15.0 14.9 (1) NS
Medial plantar 10 14.9 14.2 (5) NS
Lateral plantar 10 14.8 14.4 (3) NS
a Non-diabetic, 24 feet in 22 patients; diabetic, 10 feet in 8 patients.b For the 24 feet that had tarsal tunnel release in 22 non-diabetic patients, quantitative density (2-point discrimination) testing was not done for the medial calcaneal
region in 4 feet of 2 consecutive patients and for the medial and lateral plantar regions in 7 feet of 6 consecutive patients.c
NS,
not
significant
(P
>
0.05).
W.H. Gondring et al./Foot and Ankle Surgery 18 (2012) 241246244
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is an important component of diabetic peripheral neuropathy that
may be improved with tarsal tunnel decompression surgery. The
absence of improved mean sensory density (2-point discrimina-
tion) for the medial and lateral plantar nerve regions suggests that
sensory improvement after tarsal tunnel release in these patients
was specific to touch pressure sensation.
Previous studies of posterior tibial nerve decompression in
non-diabetic and diabetic patients had shown sensory improve-
ment after surgery, including 1-point and 2-point sensory
testing [1316,18]. In diabetic patients, tarsal tunnel release
may decrease the risk of developing a plantar ulcer or having an
amputation [16]. In a previous study of 36 patients who were
evaluated at a mean of 32 months after tarsal tunnel release for
symptomatic diabetic neuropathy, no new ulcers developed
even though subjective sensation was improved in only 50%
patients [13]. The risk of developing a neuropathic ulcer may
increase when the threshold of decreased protective sensation
(10 g force) is reached, which corresponds to 98% sensory loss
[27]. In the present study, the diabetic sensory impairment was
corrected to a touch pressure threshold between normal and
decreased light touch, with restoration of protective sensation,
which would be expected to decrease the risk of developing
diabetic foot ulcers [18].
The marked improvement of touch pressure sensation indiabetic patients (Table 4) suggests that compression neuropathy
was a primary mechanism of neuropathy in these patients.
However, other potential contributions to neuropathy, such as
metabolic, microvascular, immunologic and inflammatory, and
endocrinologic factors, may be influenced by compression of the
nerves and blood vessels in the tarsal tunnel or may be
independent of compression. Previous studies had shown that
increased pressure may contribute to neural dysfunction in
entrapmentneuropathy [2832] because of thedetrimental effects
of pressure on nerve conduction [29,3338], neural ischemia [39
42], axonalflow [4345],and localnervedemyelination [34,46,47].
Therefore, the observed improvement in touch pressure sensation
after
tarsal
tunnel
release
(Table
4) may
have
occurred,
in
part,
because of associated improvements in local nerve metabolism,microcirculation, and cellular physiology that may have been
affectedbypressure. Further studywouldbe required todetermine
the
molecular
and
cellular
aspects
of
nerve
function
that
may
be
improved
by
tarsal
tunnel
release
in
diabetic
patients.
Neverthe-
less, the present data confirm that nerve compression is a primary
mediator of diabetic neuropathy, and correction of nerve
compression
may
improve
most
of
the
impairment
of
touch
pressure,
but
not
sensory
density,
associated
with
neuropathy
(Tables 4 and 5).
The 2-point discrimination test has been used to evaluate
healing
of
axons
after
complete
or
incomplete
nerve
laceration
and
repair
in
the
hand
[48]
but
cannot
be
compared
directly
to
the
monofilament test because the 2 testsmeasure different aspects of
sensory
nerve
function:
touch
pressure
and
sensory
density
[49].The
2-point
discrimination
test
may
measure
different
properties
of
the
foot
than
other
tests
[50].
A
previous
study
of
upper
and
lower extremity nerve function in diabetic patients who were
younger (average age, 52 years) and were followed longer after
nerve
decompression
surgery
(average,
23
months)
than
the
present
patients,
showed
improvement
in
2-point
discrimination
in most patients after nerve decompression surgery [14]. In the
present study, absence of improvement of 2-point discrimination
at
an
average
of
89
months
after
surgery
(Table
5)
may
suggest
that
sensory
density
impairment
may
be
permanent
in
this
older
population or may improve more slowly, over a longer period than
the available follow-up time [14]. Although improvement in 2-
point
discrimination
after
nerve
decompression
has
been
reported
previously
[14,51], this
sensory
function
may
be
more
resistant
to
recovery because it may occur earlier, and may be more
longstanding, in the natural history of neuropathy [16,17].
Limitations of the present study include the small sample size
and limited duration of postoperative follow-up evaluation.
Computer-based methods are available to measure 2-point
discrimination [16], but the method used in the present study
may be more widely applicable and practical in the clinical
situation. Furthermore, postoperative nerve conduction studies
were not available in diabetic patients (Table 3). Nevertheless, the
study provides evidence that tarsal tunnel release may improve
touch pressure sensation in patients who have diabetic peripheral
sensory neuropathy, possibly preventing ulcers by restoring
protective sensation in the foot [16]. Nerve entrapment resulting
in diabetic sensory compressive neuropathy may be undiagnosed
and infrequently recognized as a precursor to diabetic foot ulcers,
and a high index of suspicion for nerve entrapmentmay be advised
to improve early recognition and treatment.
Conflict
of
interest
None.
Acknowledgments
The authors thank Melody Huss, LPN, RN, BSN for expert
sensory testing and Paul Giesenhagen, PT for nerve conduction
studies.
References
[1] Reiber GE. The epidemiology of diabetic foot problems. Diabet Med1996;13(Suppl. 1):S611.
[2] Trepman E, Nihal A, Pinzur MS. Current topics review: Charcot neuroarthro-pathy of the foot and ankle. Foot Ankle Int 2005;2:4663.
[3] Sharma KR, Cross J, Farronay O, Ayyar DR, Sherbert RT, Bradley WG. Demye-linating neuropathy in diabetes mellitus. Arch Neurol 2002;59:75865.
[4] Boulton AJ, Malik RA, Arezzo JC, Sosenko JM. Diabetic somatic neuropathies.Diabetes Care 2004;27:145886.
[5] Harris M, Eastman R, Cowie C. Symptoms of sensory neuropathy in adultswith
NIDDM
in
the
U.S.
population.
Diabetes
Care
1993;16:144652.[6] Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputation.
Basis for prevention. Diabetes Care 1990;13:51321.[7] Nishimura T,Hirata H, TsujiiM, Iida R,Hoki Y, Iino T, et al. Pathomechanism of
entrapment neuropathy in diabetic and nondiabetic rats reared in wire cages.Histol Histopathol 2008;23:15766.
[8] Dellon AL. Neurosurgical prevention of ulceration and amputation by decom-pression of lower extremity peripheral nerves in diabetic neuropathy: update2006. Acta Neurochir Suppl (Wien) 2007;100:14951.
[9] Dellon AL. Treatment of symptomatic diabetic neuropathy by surgical decom-pression of multiple peripheral nerves. Plast Reconstr Surg 1992;89:68999.
[10] Smith AG, Singleton JR. Diabetic neuropathy. In: Bromberg MB, Smith AG,editors. Handbook of peripheral neuropathy. Boca Raton: Taylor and Francis;2005. p. 1808.
[11] Trepman E, Kadel NJ, Chisholm K, Razzano L. Effect of foot and ankle positionon tarsal tunnel compartment pressure. Foot Ankle Int 1999;20:7216.
[12] Bracilovic A, Nihal A, Houston VL, Beattie AC, Rosenberg ZS, Trepman E. Effectof foot and ankle position on tarsal tunnel compartment volume. Foot AnkleInt 2006;27:4317.
[13] Caffee HH. Treatment of diabetic neuropathy by decompression of the poste-rior tibial nerve. Plast Reconstr Surg 2000;106:8135.
[14] Aszmann OC, Kress KM, Dellon AL. Results of decompression of peripheralnerves in diabetics: a prospective, blinded study. Plast Reconstr Surg 2000;106:81622.
[15] Ducic I, Taylor NS, Dellon AL. Relationship between peripheral nerve decom-pression and gain of pedal sensibility and balance in patients with peripheralneuropathy. Ann Plast Surg 2006;56:14550.
[16] Dellon AL. Preventing foot ulceration and amputation by decompressingperipheral nerves in patients with diabetic neuropathy. Ostomy WoundManage 2002;48:3645.
[17] Siemionow M, Zielinski M, Sari A. Comparison of clinical evaluation andneurosensory testing in the early diagnosis of superimposed entrapmentneuropathy in diabetic patients. Ann Plast Surg 2006;57:419.
[18] Gondring WH, Shields B. A touch pressure sensory assessment of the surgicaltreatment of the tarsal tunnel syndrome. Foot Ankle Surg 2011;17:2669.
[19] Gondring WH, Shields B, Wenger S. Tarsal tunnel syndrome: an outcomesanalysisof the surgical treatment of the tarsal tunnel syndrome.Foot Ankle Int
2003;24:54550.
W.H. Gondring et al./Foot and Ankle Surgery 18 (2012) 241246 245
8/11/2019 Touch pressure and sensory density after tarsal tunnel release in diabetic.pdf
6/6
[20] Bell-Krotoski JA, Fess EE, Figarola JH, Hiltz D. Threshold detection andSemmesWeinstein monofilaments. J Hand Ther 1995;8:15562.
[21] Bell-KrotoskiJ, Tomancik E. The repeatability of testing with SemmesWein-stein monofilaments. J Hand Surg 1987;12A:15561.
[22] Mackinnon SE, Dellon AL. Two-point discrimination tester. J Hand Surg1985;10A:9067.
[23] Gondring WH, Trepman E, Shields B. Tarsal tunnel syndrome: assessment oftreatment outcome with an anatomic pain intensity scale. Foot Ankle Surg2009;15:1338.
[24] McClave JT, Benson PG, Sincich T. Statistics for business and economics. UpperSaddle River, NJ: Prentice Hall; 2008.
[25]
Neter
J,
Kutner
MG, Nachtshein
CJ,
Wasserman
W. Applied
linear
statisticalmodels. Boston: McGraw-Hill; 1996.[26] Walpole RE, Meyers RH, Ye K. Probability and statistics for engineers and
scientists. Upper Saddle River, NJ: Prentice Hall; 2002.[27] Jeng C, Michelson J, Mizel M. Sensory thresholds of normal human feet. Foot
Ankle Int 2000;21:5014.[28] Gelberman RH, Hergenroeder PT, Hargens AR, Lundborg GN, Akeson WH.The
carpal tunnel syndrome. A study of carpal canal pressures. J Bone Joint Surg1981;63A:3803.
[29] Gelberman RH, Szabo RM, Williamson RV, Hargens AR, Yaru NC, Minteer-Convery MA. Tissue pressure threshold for peripheral nerve viability. ClinOrthop Relat Res 1983;178:28591.
[30] Gelberman RH, Yamaguchi K, Hollstien SB, Winn SS, HeidenreichJr FP, BindraRR, et al.Changes in interstitialpressure and cross-sectional area of the cubitaltunnel and of the ulnarnerve withflexion of the elbow. An experimental studyin human cadavera. J Bone Joint Surg 1998;80A:492501.
[31] Okutsu I, Ninomiya S, Hamanaka I, Kuroshima N, Inanami H. Measurement ofpressure in the carpal canal before and after endoscopic management of carpaltunnel syndrome. J Bone Joint Surg 1989;71A:67983.
[32]
Werner
CO,
Elmqvist
D,
Ohlin
P.
Pressure
and
nerve
lesion
in
the
carpal
tunnel.Acta Orthop Scand 1983;54:3126.
[33] Bentley FH, Schlapp W. The effects of pressure on conduction in peripheralnerve. J Physiol 1943;102:7282.
[34] Denny-Brown D, Brenner C. Paralysis of nerve induced by direct pressure andby tourniquet. Arch Neurol Psychiatr 1944;51:126.
[35] MacGregor RJ, Sharpless SK, Luttges MW. A pressure vessel model for nervecompression. J Neurol Sci 1975;24:299304.
[36] Marin EL, Vernick S, Friedmann LW. Carpal tunnel syndrome: median nervestress test. Arch Phys Med Rehabil 1983;64:2068.
[37] Matsen FA, Mayo KA, Krugmire RB, Sheridan GW,Kraft GH. A model compart-mental syndrome in man with particular reference to the quantification ofnerve function. J Bone Joint Surg 1977;59A:64853.
[38] Werner RA, Bir C, Armstrong TJ. Reverse Phalens maneuver as an aid indiagnosing carpal tunnel syndrome. Arch Phys Med Rehabil 1994;75:7836.
[39] Kirkeb A, Wisnes A. Regional tissue fluid pressure in rat calf muscle duringsustained contraction or stretch. Acta Physiol Scand 1982;114:5516.
[40] Lundborg G, Gelberman RH, Minteer-Convery M, Lee YF, Hargens AR. Mediannerve compression in the carpal tunnel functional response to experimen-tally induced controlled pressure. J Hand Surg 1982;7:2529.
[41]
Rydevik B,
Lundborg
G,
Bagge
U.
Effects
of
graded compression on
intra-neural blood flow. An in vivo study on rabbit tibial nerve. J Hand Surg1981;6:312.
[42] Sugimoto H, Miyaji N, Ohsawa T. Carpal tunnel syndrome: evaluation ofmedian nerve circulation with dynamic contrast-enhanced MR imaging.Radiology 1994;190:45966.
[43] Dahlin LB, McLean WG. Effects of graded experimental compression on slowand fast axonal transport in rabbit vagus nerve. J Neurol Sci 1986;72:1930.
[44] Dahlin LB,RydevikB,McLeanWG, Sjostrand J.Changes in fast axonal transportduring experimental nerve compression at low pressures. Exp Neurol1984;84:2936.
[45] Radius RL, Bade B. Pressure-induced optic nerve axonal transport interruptionin cat eyes. Arch Ophthalmol 1981;99:21635.
[46] Fullerton PM,Gilliatt RW. Pressure neuropathy in the hind foot of the guinea-pig. J Neurol Neurosurg Psychiatry 1967;30:1825.
[47] Hopkins AP, Morgan-Hughes JA. The effect of local pressure in diphtheriticneuropathy. J Neurol Neurosurg Psychiatry 1969;32:61423.
[48] Jerosch-Herold C. Should sensory function after median nerve injury andrepair be quantified using two-point discrimination as the critical measure?
Scand
J
Plast
Reconstr
Surg
Hand
Surg
2000;34:33943.[49] Gelberman RH, Szabo RM, Williamson RV, Dimick MP. Sensibility testing in
peripheral-nerve compression syndromes. An experimental study in humans.J Bone Joint Surg Am 1983;65A:6328.
[50] Periyasamy R,Manivannan M,Narayanamurthy VB. Correlation between two-point discrimination with other measures of sensory loss in diabetes mellituspatients. Int J Diabetes Dev Ctries 2008;28:718.
[51] SiemionowM,AlghoulM,Molski M,AgaogluG. Clinical outcome ofperipheralnerve decompression in diabetic and nondiabetic peripheral neuropathy. AnnPlast Surg 2006;57:38590.
W.H. Gondring et al./Foot and Ankle Surgery 18 (2012) 241246246