Touch pressure and sensory density after tarsal tunnel release in diabetic.pdf

8/11/2019 Touch pressure and sensory density after tarsal tunnel release in diabetic.pdf

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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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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.

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