Journal ol'the Neurological Sciences, 1976, 28: 217 223 JC~ Elsevier Scientific Publishing Company, Amsterdam - Printed in The Netherlands

217

THE NEUROPATHIC FACTOR IN THE AETIOLOGY OF DIABETIC FOOT ULCERS

M. J. G. HARRISON and !. B. FARIS

Departme~It o1" Neurological Studies, The Middlesex Hospital, Mortimer Street, London (Great Britain) (Received 3 October, 1975)

SUMMARY

The nature and severity of changes due to peripheral neuropathy has been assessed clinically and electrophysiologically in 39 diabetic patients, 23 of whom had penetrating ulcers on the sole of the foot. Patients suffering from diabetic foot ulcers were found to have sensory loss to pin prick in the feet more frequently than "controls". The electrophysiological measurements confirmed the severity of the neuropathy with absent sural nerve action potentials in 95 ~ of the ulcer patients and inexcitability of small foot muscles in 40~. Weakness of small foot muscles due to neuropathy is thought to underlie the foot deformity that leads to maldistribution of weight bearing, and subsequent pressure necrosis of analgesic skin.

INTRODUCTION

Ulceration of the foot represents one of the most serious complications of diabetes mellitus, contributes significantly to the morbidity of the disease, and is a frequent cause for admission to hospital of diabetic patients. Septic, neuropathic, ischaemic and combined aetiologies have been proposed (Oakley, Catterall and Martin 1956). There has been increasing awareness of the importance of the neuropathic role (Kelly and Coventry 1958; Catterall 1973). Sensory loss in the feet due to diabetic neuropathy has been considered a critical factor (Ellenberg 1968), together with deformity of the architecture of the foot (Kelly and Coventry 1958). The latter change with a splayed metatarsus, hammer toes, hallux valgus, and prominent metatarsal heads is well-recognised clinically. Recently the maldistribution of weight bearing of such feet, and the importance of pressure points have been demonstrated quantitatively by Stokes, Faris and Hutton (1975). The role of diabetic neuropathy in producing foot deformity and in predis-

218 TABLE I AGE OF PATIENTS A N D D U R A T I O N OF DIABETES Age (years)

Footlesion (n 23) Controls (n : 16)

25 34

35 44

45 54

55 64

0

3

5

8

I

0

2

5

65 74

7~, and above

Duration (years)

F o o t lesion (n 23) Controls

0 10

11 2(J

21 30

31 or more

7

9

5

2

7

7

2

(n .... 16)

posing to foot ulcers has been further studied in a group of diabetic patients, some of whom were the subject of the parallel study by Stokes et al. (1975). The special feature of the electrophysiological study has been the attempt to measure the severity of the neuropathy affecting the feet. METHODS

Twenty-three patients had foot ulcers. It was considered impossible to identify a rigorously-matched control group that would take account of all the variables (age, sex, duration and severity of diabetes, types of treatment and quality of control, presence of other complications, etc.). Instead, patients were chosen from the diabetic clinic or when in the ward to fill gaps in the study programme. An attempt was made to choose patients whose age and duration of diabetes was not too dissimilar from that of the ulcer group (Table 1), but other characteristics were not matched. There were 16 men and 7 women with ulcers, and 6 men and t0 women without:_ A clinical examination noted any evidence of peripheral neuropathy. Pain loss was assessed by the appreciation of pin prick. Electromyographic (EMG) studies included attempts to measure median nerve (index to wrist) sensory action potentials (Gilliatt and Sears 1958), sural nerve action potentials (Burke, Skuse and Lethlean 1974), and median and lateral popliteal motor nerve conduction velocity (Thomas, Sears and Gilliatt 1959). In addition the amplitude of the muscle action potential that could be evoked by stimulation of the peripheral nerves in 2 small foot muscles was recorded. Surface electrodes were positioned over the extensor digitorum brevis and over the abductor hallucis brevis during stimulation of the lateral and medial popliteal nerves at the knee and ankle. The electrode placement was varied tO produce the maximum response with supramaximal stimulation. When no response was

219 TABLE 2 CLINICAL EVIDENCE OF NEUROPATHY Grading 0

I

11

I11

Foot lesions (n 23) Controls (n : 16)

0

9

9

5

2

7

4

3

Grade Grade Grade Grade

n o r m a l clinical examination. absent ankle jerks ± sensory change. weakness o f toe m o v e m e n t s . weakness o f foot a n d toe movement.

0: h I1: I11 :

obtained the maximal stimulus used was a square wave pulse of 0.5 msec at 200 V. The absence of a recordable muscle action potential was often due to visible and palpable wasting of the small foot muscles. However, in some cases a high threshold in the peripheral nerve may have contributed to a failure to produce a response. RESU LI-S

Clinical evidence of neuropathy There was evidence of peripheral neuropathy in all ulcer patients. Two of the control patients had no signs of neuropathy. The patients were placed in one of 3 categories according to the severity of the neuropathy as defined in Table 2. There is a tendency for the ulcer patients to show a more extensive neuropathy with more of the ulcer patients having detectable weakness (14/23, 61 ~ cf. 7/16, 44~/o) though the difference is not statistically significant. The sensory examination appeared to show a real difference, however. All but one of the ulcer patients had a demonstrable disturbance of appreciation of pin prick (Table 3), and this was more extensive than in the control group. In each case the sensory disturbance was in a distal stocking distribution. The single exception was a patient who had evidence TABLE 3 LOSS O F P A I N S E N S I B I L I T Y N o loss F o o t lesions (n 23) Controls (n : 16)

Toes

Foot

Below shin

Below knee

I

5

5

2

9

I0

2

1

1

1

Pain loss in 22/23 foot lesion patients, and 6/16 controls; Z'~

13.0, P < 0.001.

Below thigh

220 TABLE 4 EMG FINDINGS

Foot lesion patients Controls

Z"P

No response from No response from extensor digitorum abductor hallucis brevis brevis

No sural nerve action potential

Median nerve sensor3action potentia! small

18:41 (44 %) 5"29 (I 7 %} 4.8 0.05

36.38 (95 "i0 t I,,25 (44 "

The neuropathic factor in the aetiology of diabetic foot ulcers.

The nature and severity of changes due to peripheral neuropathy has been assessed clinically and electrophysiologically in 39 diabetic patients, 23 of...
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