PERIPHERAL NERVE CONDUCTION IN DIABETIC

J. Neurol. Neurosurg. Psychiat., 1962, 25, 11.

PERIPHERAL NERVE CONDUCTION IN DIABETIC NEUROPATHYI

R. W. GILLIATT and R. G. WILLISON2

From the Institute of Clinical Research, the Middlesex Hospital Medical School, and the Departmentof Applied Electrophysiology, the National Hospital, Queen Square, London

The estimation of motor nerve conduction velocityand the direct recording of nerve action potentialsare now well established electrodiagnostic pro-cedures, and this paper is concerned with theirapplication to patients with diabetic neuropathy.

It is already known that in these patients motorconduction velocity may become slow (Ferrari-Forcade, Temesio, and Gomensoro, 1960; Mulder,Lambert, Bastron, and Sprague, 1961; Skillman,Johnson, Hamwi, and Driskill, 1961) and that nerveaction potentials may be lost (Gilliatt, Goodman,and Willison, 1961), these changes being similar tothose found in other forms of peripheral neuropathy.For the present paper we have selected a smallnumber of diabetic patients who have been exten-sively investigated, with the object of relating theelectrical findings to the particular clinical features ofindividual cases.

METHODS

The methods used for estimating motor conductionvelocity and for recording nerve action potentials havebeen fully described in previous publications (Gilliattand Sears, 1958; Thomas, Sears, and Gilliatt, 1959;Gilliatt et al., 1961). For the measurement of the latency ofthe knee jerk a special patellar hammer was constructedcontaining a micro-switch to trigger the oscilloscope; theelectrical response of the quadriceps muscle was thenrecorded through surface electrodes as described byMalcolm (1951) and by Bergamini and Sibour (1960).

RESULTS

SENSORY NEUROPATHY AFFECTING THE LOWER LIMBS

It is generally accepted that the most common formof diabetic neuropathy is that in which sensory dis-turbances occur in the lower limbs without muscularwasting or weakness but with depression or loss oftendon reflexes. In such cases the sensory distur-bance is often mainly subjective, pain and paraes-thesiae being present without conspicuous sensoryloss on clinical testing. We have examined five such

'Based on a paper read to the Association of British Neurologists inApril 19612Clinical research fellow, M.R.C.

patients, in all of whom the presenting complaintwas of pain in the legs or feet. None of the patientsshowed significant muscular wasting or weakness inthe lower limbs but reflex and sensory changes werepresent in all of them. Clinical details are sum-marized in Table I, from which it can be seen that the

TABLE ICLINICAL. FINDINGS IN PATIENTS WITH SENSORY NEUROPATHYCase Age KJ AJ Vibration Light Touch Pin Prick

Shin Foot Shin Foot Shin Foot

1 72 + + ± 0 + ±2 54 + ± ± 0 + +3 47 + ± + 0 ± i4 53 0 0 ± 0 + ±5 36 ± 0 ± 0 + ±

-P = normal

+ +± +

+ ±±

± == depresseJ 0 = absent

most constant feature was loss of vibration sen-sation in the feet. Other forms of sensation wereless uniformly affected and depression of tendonreflexes was also variable.As an illustrative example, Case 3 is described in

detail.Case 3. Mr. G. S. (M.H. K31441), a building contrac-

tor aged 47, was admitted to the Middlesex Hospitalunder the care of Dr. J. D. N. Nabarro in March 1958.Diabetes had been discovered two years previously andhad been treated by diet and tolbutamide. For a yearbefore admission the patient had suffered increasinglyfrom burning pain in the feet which became sufficientlysevere to prevent him working and to interfere with sleep.Neurological examination revealed no muscular wastingor weakness, and the deep reflexes were generally brisk,with the exception of the ankle jerks which were reduced.The plantar responses were flexor. There was somesubjective change in the sensations aroused by touch andpin prick over the feet and lower shins, touches producinga tingling sensation and pin prick having a peculiarlyunpleasant quality. A tuning fork (128 c/s) was appreciatedon the shins but not on the feet or toes. Joint sensationin the toes was normal.

In all five patients a standard procedure was usedfor the examination of nerve conduction. Velocitywas estimated in the motor nerve fibres to theextensor digitorum brevis by stimulation at the

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ankle and at the head of the fibula, muscle actionpotentials being recorded with a concentric needleelectrode. For the examination of nerve actionpotentials the anterior tibial nerve was stimulatedat the ankle with recording needles inserted closeto the lateral popliteal nerve at the head of the fibula.The results of these procedures in the five patientsare shown in Table II, from which it can be seen that

TABLE II

Case

CONDUCTION IN LATERAL POPLITEAL NERVE IN

PATIENTS WITH SENSORY NEUROPATHY

Motor Nerve Action PotentialVelocity(m./sec.) Velocity Amplitude

2

34SNormal range

to Peak(m./sec.)

33-0 Absent390 33

approximately34-0 Absent18-5 Absent15-2 Absent35 6-63 5' 33-8-51 82

(,t V)

Absent1I0

AbsentAbsentAbsent2-15-52

'From Thomas et al. (1959)"From Gilliatt et al. (1961)

the most frequent finding was loss of the nerveaction potential. A very small potential was presentin Case 2; in the remaining four patients the nerveaction potential was absent. Motor velocity was lessconstantly affected. There was one result within thenormal range and two just below the lower limit ofnormal; in only two out of the five patients wasmotor velocity substantially decreased. In these lasttwo patients the number of motor units in the exten-sor digitorum brevis which could be activated volun-tarily was also reduced, although no definite weaknessof dorsiflexion of the toes was demonstrated onclinical testing. This illustrates the difficulty ofdemonstrating weakness of the extensor digitorumbrevis by ordinary clinical examination when power isfully preserved in the long extensors of the toes.

In this group of patients it is clear that the exami-nation of nerve action potentials was a much moresensitive test of deranged function than the estima-tion of motor conduction velocity. While this maybe partly explained on the basis of a predominantlysensory clinical picture, it must be remembered thatin the estimation of motor velocity the figureobtained must necessarily apply to the fastest con-ducting fibres present; even if the majority of thenerve fibres are affected by a partial lesion, slowingwill not be detected if a few normal fibres survive.On the other hand the nerve action potentialdepends upon the passage of a synchronous volleyof impulses under the recording electrodes so thatit is highly sensitive to temporal dispersion of

impulses in different fibres. This probably explainsthe complete loss of the nerve action potential inCases 1 and 3 in spite of motor conduction velocitiesclose to the lower limit of the normal range.

MIXED MOTOR AND SENSORY NEUROPATHY We haveinvestigated two patients with widespread muscularweakness and wasting in addition to sensory dis-turbance. In this context we hesitate to use the word'polyneuropathy' as the term is usually taken toimply a symmetrical and peripheral disturbance,whereas in our two patients asymmetry and involve-ment of proximal muscles were conspicuous features.The relation of this group to the diabetic amyo-trophy described by Garland (1955) will be discussedin a subsequent section.

Case 6. Mrs. F. K. (M.H. J 1931 1) was first recognizedto have diabetes in 1952 at the age of 54. She was placedon a small daily dose of insulin. In 1955 she developeda right radial nerve palsy which recovered spontaneouslywithin a few weeks, and in 1957 she was seen again withthe complaint of pain and tingling in both hands, thepatient's description being suggestive of the carpal tunnelsyndrome. These symptoms also improved spontaneouslyafter a few months, but during the following year thepatient gradually developed generalized weakness of botharms and legs affecting proximal as well as distal muscles,so that she noticed difficulty in getting up from the sittingor kneeling position. The weakness was accompanied bynumbness and tingling in the hands and feet. In January1959 she was admitted to the Middlesex Hospital under

a

1mv

b

._ _~~~~~~~~

20msec

FiG. 1. Case 6. Action potentials recordedfrom the ex-tensor digitorum brevis with stimulation of (a) the anteriortibial nerve at the ankle, and (b) the lateral popliteal nerveat the neck of the fibula. Stimulus at mark in each trace.Conduction velocity between knee and ankle, 11J4 m./sec.

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Peripheral nerve conduction in diabetic neuropathy

the care of Dr. M. Kremer. In the upper limbs examinationrevealed wasting of the muscles of the shoulder girdles andof the small muscles of the hands; weakness was general-ized and bilateral but was more marked on the right sidethan the left. In the lower limbs there was wasting andsevere weakness of the quadriceps on both sides, with lesssevere weakness of other muscle groups; as in the arms thechanges were more marked on the right side than the left.The tendon reflexes were depressed or absent. The plantarresponses were flexor. Sensation was not severely affectedbut was subjectively altered over the right foot and overboth hands. Joint sensation was also mildly impaired inthe fingers and toes, and vibration sense lost in thelegs. Lumbar puncture revealed a protein level of110 mg./100 ml. in the cerebrospinal fluid.

Electrical testing was carried out shortly after heradmission to hospital and conduction velocity was foundto be markedly reduced in the motor fibres to the smallmuscles of the hands and feet. A figure of 10-6 m./sec. wasobtained for the right median nerve in the forearm and afigure of II 4 m.fsec. for the lateral popliteal nerve betweenknee and ankle. Illustrative tracings are shown in Fig. 1.

Case 7. Mr. B. C. (M.H. K75540), a business manageraged 62, first noticed weakness of the left leg in May 1960.The left knee would give way so that the patient fell,and later he became unable to straighten the left leg at all.Soon after the onset of weakness the patient noticednumbness of the soles of both feet and of the left leg belowthe knee. In August 1960 he was found to have glycosuria,and a provisional diagnosis of diabetic neuropathy wasmade.The patient was admitted to the Middlesex Hospital

under the care of Dr. Kremer in October 1960. Exam-ination at that time revealed mild diabetic retinopathy butno other abnormality in the cranial nerves. There wasslight weakness of the muscles of the shoulder girdles onboth sides but no weakness in the arms or hands. Thetendon reflexes in the arms were present but depressed.In the lower limbs weakness of hip flexion was present onboth sides but was more marked on the left. The quad-riceps muscle was severely wasted on the left, weaknessbeing such that the patient was unable to straighten theleft knee against gravity; muscle bulk and power weremildly reduced in the right quadriceps. The glutei andhamstrings were slightly affected on the left but not onthe right. Although there was little wasting below theknee, the anterior tibial and peroneal muscles were weakon both sides, particularly on the left, with sparing of thecalf muscles. The right knee jerk was depressed; the leftknee jerk and both ankle jerks were absent. The plantarresponses were flexor. Sensation was normal in the upperlimbs. In the lower limbs there was subjective impairmentof appreciation of both pin prick and cotton wool belowthe knee on the left and below the ankle on the right; therewere occasional errors in appreciation of passive move-ments of the toes. Vibration sense was present in the legsbut absent in the feet.

After the patient's admission to hospital the diagnosisof diabetes was confirmed by blood sugar estimation.Lumbar puncture revealed a protein level of 75 mg./100ml. in the cerebrospinal fluid.

0K

_ e c~~seFIG. 2. Electrical response of quadriceps to patellar tap(a) in Case 7, and (b) in a healthy subject. Mechanicalstimulus at mark and onset of reflex response at arrow ineach case. Calibration 1 mV. Five traces superimposed.

Several electrical examinations were carried out whilethe patient was in hospital. Motor conduction velocity inthe lateral popliteal nerve was 25 m./sec. on the left and33 m./sec. on the right. No action potential could berecorded from the lateral popliteal nerve at the headof the fibula on stimulation of the anterior tibial nerveat the ankle. In contrast to these findings, conductionvelocity in the motor fibres of the median nerve supplyingthe abductor pollicis brevis was normal (51 m./sec.).

In the left leg the knee jerk was absent but on the righta reflex response could just be obtained with reinforce-ment. Accordingly the latency of the right knee jerk wasrecorded using a special reflex hammer to trigger theoscilloscope (see Methods); the reflex response wasrecorded through a pair of surface electrodes 4 cm. apart,placed over the belly of the rectus femoris at the junctionof its upper and middle thirds. Only a small electricalresponse was obtained (Fig. 2a), its latency being markedlyincreased (39 msec.). For comparison, records obtainedin the same way from a healthy subject are shown in Fig.2b, the latency of the normal reflex response being 19-5msec.

In the first of these patients (Case 6) the smallmuscles of the hand were clinically affected andconduction in the motor fibres of the median nervewas markedly slowed. In the second patient powerin the hands was fully preserved and motor con-duction was normal. In both patients there waswidespread weakness in the legs and conductionvelocity in the lateral popliteal nerve was substanti-ally reduced. Wasting and weakness were mostmarked in the proximal muscles of the lower limbs,and in Case 7 it was possible to demonstrate that thelatency of the knee jerk was increased to nearlytwice the normal figure although this was recordedon the less affected side.

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14 R. W. Gilliatt and R. G. Willison

TABLE IIIELECTRICAL FINDINGS IN PATIENTS WITH ISOLATED NERVE LESIONS

Case Clinical Diagnosis Electrical Findings

8 Right ulnar nerve lesion

9 Left ulnar nerve lesion

10 Right lateral popliteal nervelesion

11 Right median nerve lesion

12 Right median nerve lesion

Affected Nerve

MCV slightly reducedNAP absentNormal MCVNAP of normal latency but reducedamplitudeNormal MCVNAP much reduced in amplitude,latency slightly increasedMotor conduction slowed distal to thewristSmall delayed NAP recorded at wristwhen index finger stimulatedMotor conduction severely sloweddistal to the wrist

Unaffected Nerves

Normal NAPs recorded from right and leftmedian and left ulnar nerveNormal MCV in right median and ulnar nervesNormal NAPs recorded from right and leftmedian and right ulnar nerveNormal MCV and NAP recorded from leftlateral popliteal nerve

Normal MCV in right ulnar nerveNormal NAP recorded from wrist when fifthfinger stimulated

Normal MCV in right ulnar nerveNormal MCV and NAP recorded fromright lateral popliteal nerve

Right ulnarRight ulnarRight ulnarRight medianRight ulnarRight medianUlnar'UlnarlMedian2

NAP = nerve action potential

ISOLATED PERIPHERAL NERVE LESIONS IN DIABETICPATIENTS In diabetic patients with apparentlyisolated peripheral nerve lesions it may be askedwhether the electrical abnormalities are also likelyto be restricted to the clinically affected nerve, orwhether more widespread changes may be found.We have investigated five such patients, two of thempresenting with ulnar nerve lesions, two with mediannerve lesions, and one with a lateral popliteal nervelesion. While we did not attempt to study conductionin every accessible nerve ofeach patient, observationswere made on 10 unaffected nerves, motor conductionbeing examined in six nerves and nerve actionpotentials in nine nerves. For all the unaffectednerves studied, results fell within the normal range(Table III).

In the large series of diabetic patients examined byMulder et al. (1961) mean velocities for clinicallyunaffected nerves were significantly below the nor-mal means. In our own patients the values forunaffected nerves also fell in the lower part of thenormal range but the number of patients studiedwas too small for this to be statistically significant.

TABLE

Case

8

12

Normal range

In the case of the clinically affected nerves, however,abnormalities of either motor velocity or of nerveaction potentials were present in every case. Motorconduction was clearly abnormal in two, slightlyabnormal in one, and normal in two. Nerve actionpotentials were reduced or absent in all four casesin which they were examined (Table III).The relation between clinical and electrical find-

ings is illustrated by the following case history:-

Case 8. Mr. M. L. (N.H. 87855), a storekeeper, wasdiscovered to have diabetes in 1956 at the age of 51; hiscondition appeared to be satisfactorily controlled by dietalone. In June 1958 the patient fell on the outstretchedright hand and four weeks later noticed that the hand wasweak. This weakness gradually increased and at the timeof the electrical examination in October 1959 severewasting and weakness were present in the ulnar-suppliedintrinsic muscles, without sensory loss. The clinicalexamination was complicated by the fact that the patient'sright little finger had been amputated many years before,so that power in the hypothenar muscles could not betested. However, in view of the presence of normalpower in the forearm muscles and the absence of sensory

Abductor digiti minimiFirst dorsal interosseousAbductor digiti minimiAbductor pollicis brevisAbductor digiti minimiAbductor pollicis brevisAbductor digiti minimiFirst dorsal interosseousAbductor pollicis brevis

4-46-52-98-32-725-62-0-3-73 0-5-02-9-5-0

43 037-549-242 554.740049 0-65 646-2-66-248-3-67-9

'From Gilliatt and Thomas (1960)'From Thomas (1960)

MCV -motor conduction velocity

MOTOR LATENCY AND CONDUCTION VELOCITY IN PATIENTS WITH ISOLATED PERIPHERAL NERVE LESIONS

Nerve Muscle Latency Conduction VelocityWrist to Muscle (msec.) Elbow to Wrist (m./sec.)



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Median

a

]0j

d

b P

... 2msecFIG. 4

FIG. 3. Case 8. Tracings recorded from (a) the median nerve and (b) the ulnar nerve above the elbow with stim-ulation at the wrist. Stimulus at mark in each tracefollowed by nerve action potential in (a) but not in (b).FIG. 4. Case 11. Records from the abductor pollicis brevis (a, b) and the abductor digiti miniimi (c, d) taken at highamplification to show initial deflection of muscle action potentials with stimulation of median and ulnar nerves justabove the wrist (a, c) and elbow (b, d). Stimulus at mark in each case.

loss, a local lesion of the ulnar nerve in the hand wassuspected and ascribed to the patient's fall in June 1958.The right ulnar nerve was stimulated just above the

wrist and elbow, and muscle action potentials were recor-ded from the abductor digiti minimi and the first dorsalinterosseous muscle; slight but uniform slowing ofconduction was present throughout the length of nerveexamined, values for the motor fibres to both musclesbeing just outside the normal range (Table IV). When theulnar nerve was stimulated at the wrist no action poten-tial was recorded from the nerve above the elbow (Fig. 3).For comparison the normal action potential recordedfrom the right median nerve at the elbow with stimul-ation at the wrist is also shown in Fig. 3. Nerve actionpotentials from the left median and ulnar nerves were alsoexamined and were normal.

In this patient the median and ulnar nerves onboth sides were examined and the conduction defectwas confined to the right ulnar nerve. The electricalabnormality extended at least as high as the elbowand it is clear that it could not be explained by alocal lesion in the hand as had originally been sug-gested on clinical grounds.

It is interesting that in all five patients withisolated lesions the nerves involved were those whichare most commonly affected in non-diabetic subjects,and that in some of our patients a history of localtrauma was obtained. For example, our patient witha lateral popliteal palsy (Case 10) had been crouch-ing on the floor with the affected leg tucked underhim, laying tiles in his house, during the weekbefore he developed foot-drop. This type of historymust raise the possibility that these were mechanical

compressive lesions occurring in diabetic subjectswho may or may not have had some predisposingabnormality of their peripheral nerves.

In the two patients with median neuropathy therewas marked slowing of conduction in the segment ofthe median nerve distal to the wrist, velocity in thesame fibres in the forearm being relatively normal.This combination of findings is most frequentlyencountered in the carpal tunnel syndrome (Simpson,1956; Thomas, 1960), and for this reason bothpatients were treated by surgical division of theflexor retinaculum.

Case 11. Mrs. S. M. (M.H. K48246), a 52-year-oldhousewife, was admitted to the Middlesex Hospital inMarch 1959. For 15 years the patient had suffered fromdiabetes for which she took a small daily dose of insulin.In 1955 she began to experience attacks of painfultingling in the right hand which would wake her at nightand which were relieved by hanging the arm out of bed.Subsequently, paraesthesiae also occurred during theday, and in the year before admission the patient alsonoticed wasting of the thenar muscles with difficulty inusing the hand. Similar but less severe symptoms werepresent on the left.Examination in March 1959 revealed severe wasting

and weakness of the median-supplied thenar muscles onthe right and mild wasting and weakness on the left. Therewas no evidence of abnormality outside the medianterritory. Sensation was normal except for a subjectivechange over the index, middle, and ring fingers of the righthand. Radiographs of the wrists were normal.Motor conduction was examined in the right median

0

$P I~~~~ JMm 00

Ulnar

iF. -3

FIG. 3

2msec

15

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and ulnar nerves. The results are shown in Table IV andillustrative tracings are shown in Fig. 4. It will be seen thatthere was marked slowing of conduction in the mediannerve distal to the wrist, latency from wrist to musclebeing 8-3 msec. (normal range 2-9-5 0 msec.). Con-duction velocity in the median nerve in the forearm wasonly slightly reduced, and conduction in the ulnar nervewas normal. Nerve action potentials were also recordedat the wrist with stimulation of digital fibres in the fingers,as described by Gilliatt and Sears (1958). The potentialrecorded from the median nerve when the index finger wasstimulated showed a small amplitude and an increasedlatency, whereas a normal potential was recorded fromthe ulnar nerve when the fifth finger was stimulated.The electrical findings appeared to confirm the presence

of a carpal tunnel syndrome and at operation on 19 March1959 the flexor retinaculum on the right was divided underdirect vision by Mr. R. D. Weeks. At the time of oper-ation a sharply defined area of abnormal vascularity ofthe nerve, approximately 07 cm. in length, was seen at thelevel of the distal margin of the retinaculum.

In spite of an apparently successful operation thepatient continued to complain ofweakness and discomfortin the hand. At a follow-up examination in June 1959 theright median nerve at the wrist was found to be electricallyinexcitable. Although there was no response to nervestimulation at the wrist, a few motor unit potentials in theabductor pollicis brevis were seen which were still undervoluntary control, but by the time of the next follow-upexamination in September 1959 even these were absent, themuscle showing the clinical and electrical appearances ofcomplete denervation. There was also some increase inmedian sensory disturbance but otherwise the patient'sclinical condition appeared to be unchanged.

Case 12. Mrs. R. F. (M.H. K52360), a 64-year-oldhousewife, was admitted to the Middlesex Hospital inJily 1959. Diabetes had been discovered in 1942; it wasfirst controlled by insulin and later by tolbutamide. In1943 the patient had sustained a right Colles fracture. In1957 she began to suffer attacks of numbness and tinglingin the fingers of the right hand with a sensation of tight-ness of the hand on rising in the morning. In the followingyear wasting of the thenar muscles was noticed, togetherwith difficulty in using the hand.

Examination in July 1959 revealed severe wasting andweakness of the right thenar muscles with subjectiveimpairment of superficial sensation affecting the thumband the index, middle, and ring fingers. There was noevidence of abnormality outside the median territory.Radiographs of the right wrist showed a mild deformityof the lower end of the radius attributable to her old Collesfracture, with secondary arthritic changes in the radio-carpal joint.Motor conduction was studied in the right median and

ulnar nerves. Results are shown in Table IV, from whichit will be seen that there was marked slowing ofconductionin the median nerve distal to the wrist (conduction time25-6 msec.) with only slight slowing in the forearm(conduction velocity 400 m./sec.). Conduction in theulnar nerve was normal. At operation on 28 July 1959 theright flexor retinaculum was divided by Mr. Valentine

20

15

3 10

Ea)

z-ilwJ5

-J

Mrs R.EOperat ion - Rt.w rist

28-7- 59

Normal range -

0. 20TIME (weeks)

40 60

FIG. 5. Case 12. Latencies of muscle action potentialsrecordedfrom the abductor pollicis brevis with stimulationof the median nerve just above the wrist, before and aftersurgical division of the flexor retinaculum, to show post-operative recovery ofnormal latency.

Logue who observed that the median nerve was consider-ably swollen under the upper part of the ligament.

After operation median nerve conduction was re-examined at three-monthly intervals; the results are shownin Fig. 5, in which conduction time from wrist to muscle isplotted against the post-operative period in weeks. Itcan be seen that conduction time decreased progressivelyafter operation and returned to the normal range at theend of one year.

Although mechanical factors may have deter-mined the site of the lesion in Case I1, the responseto surgery was quite unlike that seen in non-diabeticpatients with the carpal tunnel syndrome, and thecontinued deterioration of median nerve functionafter operation must be attributed to her diabetes.This result cannot be attributed to inadequatesurgery as an open operation was performed inwhich the flexor retinaculum was divided underdirect vision. In Case 12 post-operative recovery wasexcellent and did not differ from that observed innon-diabetic patients after surgical decompressionof the median nerve (Goodman and Gilliatt, 1961).Thus it appears that the lesion in this latter case waslargely or wholly due to mechanical compressionand that recovery was not impeded by the patient'sdiabetes.

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DISCUSSION

In our patients with sensory syndromes affecting thelower limbs an interesting parallel may be drawnbetween the changes in vibration sense and in nerveaction potentials. On clinical examination loss ofvibration sense in the feet was the only finding whichwas common to all five patients, and on electricalexamination diminution or complete loss of thelateral popliteal nerve action potential was alsopresent in every case. The appreciation of a tuningfork presumably depends upon synchronous con-duction in a large number of fibres, so that impulseswhich start together at the periphery arrive simul-taneously at the spinal cord. It may be suggested thatvibration sense is lost when there is slowing and dis-persion of impulses in individual fibres, so that burstsof activity in some fibres arrive at the spinal cord ata time when others are inactive, thus smoothing outthe rhythmic pattern for the nerve trunk as a whole.The presence of a recordable nerve action potentialalso requires synchronous conduction in a numberof fibres, and it is known that any slowing of con-duction causes temporal dispersion of the potential(Gilliatt et al., 1961). This could occur withoutcomplete loss of conduction in any single fibre andwould explain the reduction in vibration sense andin the size of the nerve action potential in one of ourpatients (Case2) who showed no other sensory change.

In our two patients with mixed motor and sensoryneuropathy, asymmetrical muscle wasting and weak-ness were the most conspicuous features and proxi-mal muscles were severely involved. The clinicalpicture thus resembled the diabetic amyotrophydescribed by Garland (1955), and one of our patients(Case 7) was subsequently examined by Dr. Garland,who accepted this diagnosis. The marked slowing ofmotor nerve conduction found in both patients istherefore of particular interest. Slowing of thisdegree is characteristic of peripheral neuropathy anddoes not occur in patients with muscle wasting dueto spinal cord disease (Henriksen, 1956). Theincreased latency of the knee jerk in Case 7 is alsocharacteristic of neuropathy, and comparableincreases in latency have not been found in patientswith wasting of the quadriceps due to anterior horncell lesions such as anterior poliomyelitis or motorneurone disease (Gilliatt, Lange, and Willison,unpublished observations). It therefore seems reason-able to suggest that the amyotrophy of Garland is infact a motor neuropathy with a particular tendencyto affect proximal muscles. It should be remembered,however, that extensor plantar responses were pre-sent in some of Garland's patients, and in view ofthis finding a combination of spinal and peripheralchanges must be postulated.

In our patients with isolated peripheral nervelesions the correlation between clinical and electricalabnormalities was closer than in other publishedseries. This difference may be related to the method ofstudy. Mulder et al. (1961) and Skillman et al. (1961)examined large numbers of unselected diabeticpatients whereas we have carried out a more detailedinvestigation of a small group. Furthermore, we havebeen able to examine nerve action potentials whereasthe other series are concerned only with motorconduction velocity. In relation to our findings intwo patients with the carpal tunnel syndrome it isinteresting that Mulder et al. found delayed con-duction in the median nerve distal to the wrist innine out of a total of 103 unselected diabetic patients,which suggests that there may be an increasedincidence of the carpal tunnel syndrome in diabetes.From their results and from our own it is clear thatmechanical factors are of considerable importance inthe aetiology of isolated peripheral nerve lesionsoccurring in diabetic patients.When considering changes in nerve conduction of

the type described in this paper it must be emphasizedthat only large myelinated fibres have been examined.Until new techniques have been evolved for the studyof small myelinated and non-myelinated fibres, ourpicture of peripheral nerve function is necessarilyincomplete. From what is already known of auto-nomic disturbances in diabetes (Martin, 1953;Sharpey-Schafer and Taylor, 1960) it is clear thatthe study of conduction in small fibres represents animportant field for investigation in the future.

SUMMARY

Peripheral nerve conduction has been studied in 12patients with diabetic neuropathy. In five patientswith predominantly sensory neuropathy affectingthe lower limbs, diminution or loss of lateralpopliteal nerve action potentials was the mostconstant finding. In two patients with mixed motorand sensory neuropathy marked slowing of motornerve conduction velocity was found, and in one ofthem the latency of the knee jerk was substantiallyincreased. When five patients with isolated peripheralnerve lesions were studied, electrical abnormalitieswere found only in the clinically affected nerves.

We wish to thank members of the staff of the MiddlesexHospital and of the National Hospital who have referredpatients for investigation. We are grateful to Dr. HughGarland for his help with Case 7.Grants towards the cost of the apparatus were made by

the Medical Research Council and the Mary KinrossCharitable Trust, and we also gratefully acknowledge theprovision of facilities by the Clinical Research Committeeof the Middlesex Hospital.

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REFERENCES

Bergamini, V., and Sibour, F. (1960). Riv. Patol. nerv. ment., 81, 415.Ferrari-Forcade, A., Temesio, P., and Gomensoro, J. B. (1960). Acta

neurol lat.-amer., 6, 43.Garland, H. (1955). Brit. med. J., 2, 1287.Gilliatt, R. W., Goodman, H. V., and Willison, R. G. (1961). J.

Neurol. Neurosurg. Psychiat., 24, 305.-, and Sears, T. A. (1958). Ibid., 21, 109.-, and Thomas, P. K. (1960). Ibid., 23, 312.Goodman, H. V., and Gilliatt, R. W. (1961). Ann. phys. Med., 6, 137.

Henriksen, J. D. (1956). M.S. Thesis. University of Minnesota.Malcolm, D. S. (1951). J. Neurol. Neurosurg. Psychiat., 14, 15.

Martin, M. M. (1953). Lancet, 1, 560.Mulder, D. W., Lambert, E. H., Bastron, J. A., and Sprague, R. G.

(1961). Neurology, 11, 275.Sharpey-Schafer, E. P., and Taylor, P. J. (1960). Lancet, 1, 559.Simpson, J. A. (1956). J. Neurol. Neurosurg. Psychiat., 19, 275.Skillman, T. G., Johnson, E. W., Hamwi, G. J., and Driskill, H. J.

(1961). Diabetes, 10, 46.Thomas, P. K. (1960). Neurology, 10, 1045.-, Sears, T. A., and Gilliatt, R. W. (1959). J. Neurol. Neurosurg.

Psychiat., 22, 175.

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PERIPHERAL NERVE CONDUCTION IN DIABETIC