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, USA
b
Steven L. Craig School of Business, Missouri Western State University, St. Joseph, MO, USA
c
Department 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
diabetic patients die within 1 year of a lower extremity amputation
[1].
The pathogenesis of diabetic peripheral neuropathy and nerve
injury may be multifactorial, including (1) metabolic abnormalities
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
inammatory 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, inammatory 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 brosis. 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 lower extremities have shown that diabetic patients with 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 protective
sensation 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 and postoperative (average,
89 months) anatomic, quantitative sensory testing was done with touch pressure 1-point threshold
(SemmesWeinstein monolaments) and 2-point discrimination.
Results: There was marked, signicant postoperative improvement of mean touch pressure 1-point
threshold, compared with preoperative values, for medial 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: gondring@stjoelive.com (W.H. Gondring).
Contents lists available at SciVerse ScienceDirect
Foot and Ankle Surgery
j ou r nal h o mepage: w ww. el sevi er . co m/ l oc at e/ f as
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
the assessment of sensory threshold for protective sensation using
SemmesWeinstein monolaments (evaluating 1-point touch
pressure sensory threshold of large ber myelinated nerve
endings) and does not include 2-point discrimination testing for
sensory density of small ber unmyelinated nerve endings [4].
In non-diabetic and diabetic patients who have entrapment of
the posterior tibial nerve at the tarsal tunnel, tarsal tunnel release
may improve 1-point sensation, as measured with Semmes
Weinstein monolaments [18]. However, limited information is
available about the effect of tarsal tunnel release in diabetic
patients on clinical measurements of 2-point discrimination with
simple, inexpensive clinical tools. Previous studies with 2-point
discrimination had combined information about upper and lower
extremity entrapment [17], and no anatomic information is
available about the postoperative changes in sensation for the
medial calcaneal, medial plantar, and lateral plantar nerve regions
in diabetic patients.
The purpose of this study was to evaluate the effect of tarsal
tunnel release in diabetic patients on quantitative touch pressure
sensation (1-point sensation, determined with SemmesWein-
stein monolaments) and sensory density (2-point discrimination,
determined with a simple 2-point testing device) in the anatomic
distribution of the branches of the posterior tibial nerve. We
hypothesized that nerve entrapment is an important component of
diabetic peripheral neuropathy; the contribution of nerve entrap-
ment to neuropathy could be quantied with simple, non-invasive
tests; and tarsal tunnel decompression may improve sensory
impairment in diabetic neuropathic patients.
2. Materials and methods
This was a prospective non-blinded, non-randomized case
study of 10 feet in 8 consecutive diabetic patients, and 24 feet in 22
consecutive non-diabetic patients, who had tarsal tunnel release
and were followed clinically from 2005 to 2007 by 1 surgeon
(WHG) at St. Joseph Orthopedics and Heartland Regional Medical
Center (St. Joseph, MO, USA). Most patients were overweight or
obese (Table 1). All patients had plantar pain and numbness, and
pain was typically described as a burning sensation. In the diabetic
patients, the average preoperative ankle-brachial index was
normal, and average glycemic control was poor (Table 1). There
was no previous history of diabetic foot ulcer or Charcot
arthropathy in any of the patients.
Approval for the study was obtained from the Institutional
Review Board of Heartland Regional Medical Center. The patients
received an informed consent letter, gave written informed
consent to participate, and signed a Health Insurance Portability
and Accountability Act agreement.
2.1. Evaluation
All patients presented for surgical evaluation because of plantar
foot pain and/or numbness. Clinical evaluation of each patient by
the treating surgeon included a health history and physical
examination, including a description of symptoms of pain and
paresthesias in the feet. The preoperative duration of symptoms
(pain and paresthesias) was noted (Table 1); the severity of
symptoms was estimated on a visual analog scale (VAS) (mini-
mum, 0; maximum, 10) and recorded preoperatively and at the
time of discharge, when the patient reached maximum medical
improvement. Pain was rated based on the VAS: none, 0; mild, 13;
moderate, 47; and severe, 810. Patients were questioned, and
tested when clinically indicated, for causes of peripheral neuropa-
thy other than diabetes, including exposure to toxins (arsenic,
mercury, lead, drugs, pesticides, insecticides, or alcohol); vascular
insufciency; or medical conditions (autoimmune, endocrine,
infectious, or inammatory disorders). Self testing blood glucose
values were obtained from the patient both before surgery and at
the time of nal follow-up visit. Hemoglobin A
1c
values were
obtained from the referring physicians before surgery and at time
of discharge when the patient reached the maximum clinical
recovery.
Preoperative motor nerve conduction velocity was determined
by a single observer using the same electrodiagnostic apparatus for
all patients, as previously described [19]. Severity of neuropathy
was graded as absent (nerve conduction latency, 6.8 ms), mild
(6.97.3 ms), moderate (7.47.5 ms), or severe (7.6 ms). The
diagnosis of diabetes-associated tarsal tunnel syndrome (diabetic
sensory neuropathy) was made, and surgical decompression was
recommended, when the patient had all 5 criteria: (1) plantar
hindfoot, midfoot, and forefoot pain and/or numbness; (2) positive
Tinel sign at the posterior tibial nerve; (3) abnormal motor nerve
conduction velocity and latency in the distribution of the posterior
tibial nerve; (4) diagnosis of diabetes with abnormal blood glucose
and hemoglobin A
1c
values; and (5) failure of non-operative
treatment to improve the patients pain. Non-diabetic patients had
all except the fourth criterion. Patients were excluded from having
tarsal tunnel decompression surgery if they had chronic pulmo-
nary obstructive disease or depression. None of the patients had
any prior tarsal tunnel surgery.
Non-operative treatment included patient education, non-
steroidal anti-inammatory medication, topical capsaicin cream
(Zostrix, Rodlen Laboratories, Inc., Vernon Hills, IL; Capzasin,
Chattem, Inc., Chattanooga, TN), and a brace at night to immobilize
the foot and ankle in neutral position, as previously described [19].
The duration of non-operative treatment varied (average, 10 wks;
Table 1
Demographic and clinical features of non-diabetic and diabetic patients who had
tarsal tunnel release for entrapment neuropathy.
a
Non-diabetic Diabetic
Number of patients 22 8
Sex, female 16 (73) 4 (50)
Age (years) 58 (3181) 63 (5181)
Number of feet 24 10
Left only 10 3
Right only 10 3
Bilateral 2 2
Duration of diabetes (years) NA
b
9 (516)
Diabetes treatment
Oral drugs NA 6 (75)
Insulin NA 2 (25)
Body mass index (BMI)
c
Obese 11 (50) 5 (63)
Overweight 7 (32) 2 (25)
Normal 4 (18) 1 (12)
Ankle-brachial index 1.1 (0.91.49) 1.1 (0.921.34)
Fasting blood glucose (mg/dL)
d
Preoperative NA 211 (85277)
Postoperative NA 219 (98189)
Hemoglobin A
1c
(%)
e
Preoperative NA 17.2 (6.714.3)
Postoperative NA 17.4 (6.513.3)
Preoperative duration
of symptoms (mo)
25.8 (1.596) 31 (848)
Severity of symptoms
f
Preoperative 7.6 (210) 8.5 (510)
Postoperative 1.5 (06) 1.6 (04)
Final evaluation after surgery (months) 9 (120) 8 (336)
a
Data reported as number, number (percent), or average (range, minimum to
maximum).
b
NA, not applicable.
c
Obese (body mass index [BMI] 30 kg/m
2
), overweight (BMI, 2529.9 kg/m
2
),
and normal body weight (BMI < 25 kg/m
2
).
d
Fasting blood glucose: normal, 6099 mg/dL.
e
Hemoglobin A
1c
: normal, <6%.
f
Pain and paresthesias, visual analog scale (minimum, 0; maximum, 10).
W.H. Gondring et al. / Foot and Ankle Surgery 18 (2012) 241246 242
range, 420 wks), in part because of difcult 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-
laments (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 monolaments had been
calibrated by the manufacturer. The examiner applied the
monolaments 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
monolament to 908. The monolaments were applied sequen-
tially from the smallest (1.65 monolament; 0.008 g) to the largest
(6.65 monolament; 300 g) until the sensory threshold was
determined, dened as the force applied by the smallest
monolament that the patient could feel at the site tested. Data
recorded included the size of the smallest monolament 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-
Criminator
TM
, 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 each
successive 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 monolament 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 exibility of the monolaments 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 abnormal pressure areas such as callosities, which
were avoided to decrease the potential for erroneous grading of
sensory 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 nal 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 the nal 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
inated briey (maximum, 10 min) when it was needed to
facilitate exposure or hemostasis within the bro-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 exor 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 hallucis muscle spread
at least 6 mm following release. The abductor hallucis muscle belly
was preserved. The medial portion of the plantar fascia (approxi-
mately 25%) was released.
2.4. Data analysis
Data analysis was performed 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 xed 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
because of the small sample size; therefore, the small sample size
precluded a statistical comparison of non-diabetic and diabetic
feet. For comparison of preoperative and postoperative sensation,
the Wilcoxon signed rank test (non-parametric) was used because
of the small sample size of patients and the rank ordering of the
monolament 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
preoperative andpostoperative values, with preoperative value as
denominator). Preoperative and postoperative data were com-
pared for nerve conduction time for the medial plantar and lateral
plantar nerves in non-diabetic patients. Signicant differences
were dened by P 0.05.
3. Results
Symptoms of pain and paresthesias were improved after 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 or moderate; in the non-diabetic patients, small but signicant
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, signicant improvement of mean touch pressure
(1-point) threshold with monolament 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 signicant 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 nal 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
4. Discussion
The abnormal preoperative monolament and 2-point discrim-
ination ndings 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 decit [4]. The 1-
point, monolament 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 patients who 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-diabetic
c
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
Diabetic
d
Medial plantar 10 7.2 (6.57.8) 0 NA
b
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 were
done in 8 feet of 8 non-diabetic patients.
b
NA, not available: postoperative nerve conduction studies were not done in the diabetic patients because this was 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 the medial 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 6/2/2/0
Medial 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 between mean preoperative and postoperative quantitative monolament touch pressure (1-point) 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 threshold (g) P
Preoperative Postoperative % change
Non-diabetic Medial calcaneal 24 1.9 0.8 (59) 0.009
Medial plantar
b
21 2.1 0.5 (77) 0.001
Lateral plantar
b
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, monolament sensory threshold was not done for the medial and lateral plantar nerves in 3 feet of 2 patients.
Table 5
Relation 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) P
c
Preoperative Postoperative % change
Non-diabetic
b
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 signicant (P > 0.05).
W.H. Gondring et al. / Foot and Ankle Surgery 18 (2012) 241246 244
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 specic 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 in
diabetic 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 inammatory, and
endocrinologic factors, may be inuenced 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
entrapment neuropathy [2832] because of the detrimental effects
of pressure on nerve conduction [29,3338], neural ischemia [39
42], axonal ow [4345], and local nerve demyelination [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
affected by pressure. Further study would be required to determine
the molecular and cellular aspects of nerve function that may be
improved by tarsal tunnel release in diabetic patients. Neverthe-
less, the present data conrm 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
monolament test because the 2 tests measure 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 entrapment may be advised
to improve early recognition and treatment.
Conict of interest
None.
Acknowledgments
The authors thank Melody Huss, LPN, RN, BSN for expert
sensory testing and Paul Giesenhagen, PT for nerve conduction
studies.
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