586 THE JOURNAL OF BONE AND JOINT SURGERY

MORTON’S METATARSALGIA

CLINICAL, ELECTROPHYSIOLOGICAL AND HISTOLOGICAL OBSERVATIONS

R. J. GUILOFF, J. W. SCADDING, L. KLENERMAN

From the Westminster Hospital, the National Hospitalfor Nervous Diseases, London

and Northwick Park Hospital, Harrow

In an attempt to improve the accuracy of diagnosis, 16 patients suffering from Morton’s metatarsalgiawere investigated clinically and electrophysiologically. The histological findings were related to these

observations. The precise aetiology of Morton’s metatarsalgia remains obscure, but the findings arecompatible with an entrapment syndrome. Nerve conduction studies have a place in the investigation ofpatients with atypical presentation ofpain in the foot. Further refinement ofthe electrophysiological techniqueshould be possible.

Morton’s neuralgia (Morton 1876) is diagnosed clinically,but this may sometimes be difficult and patients may

endure the discomfort of a digital neunoma for manyyears before definitive treatment is carried out. The

aetiology of the condition is not clear. It has beensuggested by Nissen (1948) that the nerve lesion isischaemic in origin, but others, including Kopell andThompson (1963), Lassmann, Lassmann and Stockinger

(1976), Ochoa (1976) and Gauthier (1979) have suggestedthat it is an entrapment neuropathy. Most orthopaedic

surgeons use the term Morton’s metatarsalgia and thisname will be used throughout the text.

The purpose of this investigation was to attempt toobtain objective criteria for diagnosis before operationby the use of digital sensory nerve conduction tests, andto correlate the clinical, electrophysiological and histo-logical features. On the basis of these observations and

of relevant data in the literature, possible mechanisms of

pain production will be briefly discussed.

MATERIALS AND METHODS

Sixteen consecutive patients with a clinical diagnosis of

Morton’s metatarsalgia were studied. Their ages rangedfrom 24 to 78 years (mean 46.3 years). Fourteen werefemale (mean age 46.2 years, range 24 to 78 years) andtwo were male (aged 41 and 53 years). All were first

R. J. Guiloff, MD, MRCP, Consultant NeurologistWestminster Hospital, Dean Ryle Street, London SW1P 2AP, England.

J. W. Scadding, MD, MRCP, Consultant NeurologistNational Hospital for Nervous Diseases, Queen Square, LondonWCIN 3BG, England.

L. Klenerman, ChM, FRCS, Consultant Orthopaedic SurgeonNorthwick Park Hospital and Clinical Research Centre, WatfordRoad, Harrow, Middlesex HAl 3UJ, England.Requests for reprints should be sent to Mr L. Klenerman.

© 1984 British Editorial Society of Bone and Joint Surgery030l-620X/84/4084 $2.00

examined clinically by an orthopaedic surgeon and thenreferred to a neurologist for detailed study, includingelectrophysiological tests, before being offered operation.

One patient declined operation after electrical testing.The decision to operate and the digital cleft to be

explored were based on the history and clinical exami-

nation. All operations were carried out through plantarincisions. The electrophysiological studies were then

correlated with the operative findings.Fifteen patients had measurements of motor con-

duction in their posterior tibial nerves with surface

electrodes over both abductor digiti quinti and abductorhallucis (Mayer 1963 ; Goodgold, Kopell and Spielholz1965; Kaeser 1965; Johnson and Ortiz 1966). Sunal

sensory nerve action potential was recorded in fourpatients (DiBenedetto 1970, 1972; Burke, Skuse andLethlean 1974; Guiloff and Sherratt 1977). In all 16patients sensory conduction in the posterior tibial nervewas measured orthodromically with averaging tech-niques, using recording surface electrodes at the anklebelow the medial malleolus. Stimulation was deliveredthrough ring electrodes encircling the appropriate toes.Full details ofthe technique used for recording the medialplantar sensory nerve action potential (SAP), from thegreat toe (Toe I) to the ankle, have been published by

Guiloffand Sherratt (1977).The technique used in this present study was similar,

except that the stimulating electrodes were standardMedelec ring electrodes and these were used on the lessertoes. Sometimes two toes were stimulated simultaneously

(Ishibashi et a!. 1977). Normal values for the medialplantar SAP from Toe I have been published (Guiloffand Sherratt 1977). For the other toes, the unaffected

digits of the opposite foot were used as controls. Thetemperature of the skin of the dorsum of the foot was

between 28#{176}and 33#{176}Cwhen measured towards the endofthe procedure.

MORTON’S METATARSALGIA 587

VOL. 66-B, No. 4, AUGUST 1984

Table I. Clinical and electrophysiological findings in 16 patients. Siteof pain(*) is correlated with digital SAPs, recorded as amplitude inmicrovolts and latency to peak in milliseconds

TOES I-V

Right LeftPain site

Age SAP Latency SAP LatencyCase Sex (years) (p V) (msec) R L (p V) (msec)

6.41 F 25 1.5001.2 4.9

#{149}

�

IIIIIIIVandV

2.81.50.7

4.86.16.1

2 F 35 1.00.8

7.17.0

IIIIandIV

1.31.0

7.08.0

3t F 78 0a

IIII and IV

0

4 F 32 1.01.51.31.4

6.56.76.47.0

I 1.1II 0III #{149}0IIIandIV � 0

6.1

5 F 24 2.51.51.0

5.86.56.1

IIIIIV

3.01.01.0

5.86.85.8

6 M 53 1.21.21.01.1

6.57.06.76.6

1 0.7II � 0.8III � 0IVandV #{149}0

7.37.5

7

8t

F 25

“

F\67�

3.01.01.3

0

6.37.78.6

S

I 4.0II 2.5IIIandIV 0

I 0IIIandIV

6.22.0

9 F 55 000

I 2IIIandIV � 0.8IVandV 4

6.07.25.5

10 F 75 3.52.01.8

4.64.64.0

I 3.5II #{149}1.8IV #{149}1.5

4.24.54.0

11 F 55 00

I 0IIIandIV 0

12 F 54 1.00

6.6 I 1.5III and IV 0.9

6.67.0

13 F 45 0

0

a

‘

III

IIIandIV

0

0.9 5.8

14 F 48 1.0

06.5

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I 1.0Ilandill #{149}0

6.4

15 M 41 1.50.9

6.87.6

I 1.5III and IV 0

8.0

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7.4

6.7

#{149}#{149}

I 2.7II � 0III #{149}0IVandV 1.3

7.7

6.6

*only the toes marked with an asterisk were painful

tIn Cases 3 and 8 the age of the patient and the absence of recordable

SAP on stimulating the great toe precluded any further useful testing

Sections of all excised digital nerves were examinedby light microscopy after being fixed in formalin and

embedded in paraffin. Three nerves were studied byelectron microscopy ; these were fixed in 2% glutaralde-hyde in a cacodylate buffer (Karnovsky 1965), post-fixed

in osmium tetroxide and embedded in Araldite. Sections1 �tm thick were cut for light microscopy and stainedwith thionine and acnidine orange. Ultra-thin sectionswere stained with unanyl acetate and lead citrate.

RESULTS

Clinical findings (Table I). The mean length of history ofpain was 2.7 years (range 2 months to 19 years). Pain

affected the right foot in six patients, the left in seven

and both feet in three. In nine cases it was localised t#{248}

the cleft which showed a neunoma at operation, in seven

of them between the third and fourth toes and in twobetween the second and third toes. Five patients withneunoma in the cleft between the third and fourth toes

(3-4 cleft) localised the pain differently : one to the fourthtoe ; one to the second and fourth toes ; one to the third,

fourth and fifth toes; one to the second, third and fourthtoes ; and one to all toes. Another patient with evidenceof a neuroma in the 3-4 cleft had pain in these toes but,after operation, residual pain in the same area wasrelieved by excision of a further neuroma from the 2-3cleft. One patient with a neuroma at the 3-4 cleftcomplained of pain in the 2-3 cleft.

Pain was intermittent in eight patients, constant infive and of both types in three. Intermittent pain was

described in various ways, such as : stabbing, shooting,pricking, like needles, an electric shock on knives.

Constant pain was described as : a dull ache, gripping,throbbing, twisting on squeezing ; or like a bar in the foot,which might feel piercing or hot.

Pain was triggered by walking in all the patients.Seven related it to the wearing of shoes. Warm weatherwas given as a triggering factor by one patient andsqueezing of the foot by another. In five patients the paincame on at rest ; in three of this group it was intermittent

(stabbing, shooting, or like knives), in two it was aconstant dull ache.

Pain was relieved by rest in 12 patients (by takingthe shoes off in seven), by walking in one and sponta-

neously in three patients. Rest pain was relieved bywalking in one patient, freeing the foot from thebedclothes in one, and spontaneously in three patients.Pain was elicited by pressure in the appropriate inter-

metatarsal space in eight patients. One patient, who hadhad a previous operation for Morton’s metatansalgia, hadsensory loss in the appropriate toes, but no other patienthad significant sensory signs before operation.

Three patients had bilateral hallux valgus, one hadpronated flat feet and one had previously had a fractureinvolving the foot.Nerve conduction studies (Table I). All the variables ofmotor conduction in the posterior tibial nerve were

within normal limits in the 15 patients examined. Theseincluded distal motor latency, compound motor actionpotentials and motor conduction velocity with surfaceelectrodes over abductor hallucis and abductor digitiminimi.

R L

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1/1/1/

588 R. J. GUILOFF, J. W. SCADDING, L. KLENERMAN

THE JOURNAL OF BONE AND JOINT SURGERY

Digital SAPs obtained in 16 patients by stimulatingthe appropriate toes were absent on the affected side ineight patients (Cases 1, 4, 6, 7, 13, 14, 15 and 16 in

Table I). Figure 1 illustrates the findings in this group.SAPs were absent in both the affected and unaffectedsides in three patients (Cases 3, 8 and 1 1 in Table I).SAPs were normal on both sides in three patients (Cases2, 5 and 10 in Table I), and an example of this is shownin Figure 2. In two patients they were absent on thenormal side but present on the affected side (Cases 9 and

12 in Table I, and Fig. 3). In summary, SAPs were absentin 13 (affected side 8, both sides 3, normal side only 2)�nd normal on both sides in 3.

Recordings of sensory action potential (SAPs) at the ankle onstimulating toes numbered I to V. R and L-right and left foot.Calibration signal 5 �tV. Time scale : staircase 1 msec, step 0. 1 msec.Figure 1-Case 16. Woman aged 30 with pain R and L, II and III.Note absence of SAP from these toes, while present from I, IV and V.Bilateral neuromata at the 2-3 cleft found at operation. Figure 2-Case5. Woman aged 24 with pain in R IV. Note similar SAPs both sides inall toes tested. Neuroma excised R 3-4 cleft. Figure 3-Case 9. Womanaged 55 with pain L III, IV and V. Note absent SAPs on R, but presenton L. Neuroma excised from L 3-4 cleft, histology showed some

preserved myelinated fibres (see Figs 4, 5 and 6).

Operative findings. In 14 of the 15 patients subjected tooperation, typical neuromata were found. There was

marked local thickening of the affected nerve, which wasusually adherent to the underlying intermetatarsal bursa.

One patient who had bilateral symptoms had the nervesto both the appropriate interspaces resected. No obvious

neuromata were visible at operation but changes similarto those found in Morton’s metatarsalgia were confirmedhistologically, and her symptoms had been successfullyrelieved when she was seen for follow-up 18 months later.Pathological findings. Figures 4, 5 and 6 show the mainhistological features. The epineunium of most nervefascicles was thickened, with fibrosis of epineural bloodvessels. There was variable loss of myelinated fibres ; in

severe lesions no myelinated fibres were present, though

unmyelinated fibres were seen by electron microscopy.

In some fascicles the loss ofmyelinated fibres was diffuse,but in a single digital nerve the fascicles comprising the

nerve sometimes contained myelinated fibres in markedlydifferent states of preservation. Renaut bodies (Dyck1975) were a common finding. Endoneunial collagen was

increased, particularly in areas of myelinated fibredestruction. Unmyelinated fibres usually appeared to benormal, but in some axons degenerative changes wereseen, consisting of axonal swelling, a pale flocculent,amorphous axoplasm and surrounding overlappingSchwann cell processes (Dyck and Hopkins 1972;Thomas and King 1974). Some single unmyelinated

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axons with normal structures were abnormally large(more than 2.5 �.tm diameter), suggesting that these wereeither demyelinated fibres, or possibly as yet unmyeli-nated sprouts of myelinated fibres. Myelinated fibres

with thin myelin sheaths in relation to total fibre diameterwere occasionally seen ; these may have been remyelinat-ing preserved fibres or myelinated fibre sprouts.

DISCUSSION

The clinical features of our patients do not differsubstantially from those in previous published series

(Morton 1876 ; Betts 1940 ; Bickel and Dockerty 1947;Kopell and Thompson 1963 ; Nora and Ghislandi 1965;Morris 1977 ; Lassmann 1979). Usually the paroxysmal

pain is triggered by walking and relieved by removing

..

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MORTON’S METATARSALGIA 589

VOL. 66-B, No. 4, AUGUST 1984

the shoes and by various manipulations of the foot, butpain may occur at night or without apparent precipitating

factors. This has been described before (Morton 1876;

Bickel and Dockerty 1947), but is easily overlooked orneglected in taking a history.

The sensory action potential (SAP) was absent in

the affected foot in 8 of the 16 cases. In one of themhistology showed complete absence of myelinated fibres(Case 1). Two of the three patients with absent SAPs inboth feet were over 60 years of age, and it is known thatthe technique used here is not reliable over the age of 60.In the third case the specimen showed complete absence

ofmyelinated fibres (Case 1 1).

In five cases the digital SAP was present on theaffected side. In two of them no SAP could be recorded

from the non-affected side (false positives in 12.5%). Inone of these last two (Case 9), histology of the specimenshowed relative preservation of myelinated fibres.Another possible explanation for the preservation of theSAP in the affected side could be that ring electrodes

stimulate nerves unrelated to the neuroma-at, say, the3-4 cleft, to the undamaged medial digital nerve of ToeIII and lateral digital nerve of Toe IV-which maycontribute in a greaten on lesser degree to the potentialrecorded at the ankle.

There was, then, no good correlation between painand the presence or absence of digital SAP. Lack of

correlation between amplitude of the median nerve SAPand sensory signs has been noted before (Gilliatt andSears 1958). However, there was a relation betweenpresence and absence of digital SAPs and the presence

and absence of myelinated fibres in three patients, as hasbeen shown in other neuropathies in the sural nerve(Lambert and Dyck 1975). Patients with and withoutmyelinated fibres in the specimens and false-positive

cases on electrophysiological study support the idea thatmyelinated fibre loss does not of itself play a major role inthe pathogenesis of the pain characteristic of this condi-tion.

,�

N’;

0

- �1 ‘!.w� � � �

. � � . � �

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Fig. 6

Case 9. Histology of part of plantar neuroma. Figure 4-Lightphotomicrograph. Three fascicles are shown, with myelinated fibreswell preserved in some areas and depleted in others. Towards one sideof the largest fascicle is a pale-staining Renaut body (thionine andacridine orange, x 140). Figure 5-Electron micrograph. In the areashown, only small myelinated fibres are present, and one of these hasan inappropriately thin myelin sheath. The unmyelinated fibres appearnormal. There is an increase in endoneurial collagen (uranyl acetateand lead citrate, x 2700). Figure 6-Higher power electron micrographof a myelinated fibre, showing an inappropriately thin myelin sheath

( x 4650).

The method used in this work for recording digitalSAPs allows potentials of not less than 0.7 �tV to bediscriminated and reliably recorded. By increasing thenumber ofsweeps averaged and by recording with needleelectrodes, it may be possible to increase the resolution(Behse and Buchthal 1971 ; Buchthal and Rosenfalck1971). Inaddition, themethodused here does not stimulate

only the fibres in a single interdigital nerve. This could bedone by stimulating the digital nerves on the adjacentsides of two toes using suitably adapted surface on needleelectrodes. This work is currently in progress.

The electrophysiological findings do not lead us to

590 R. J. GUILOFF, J. W. SCADDING, L. KLENERMAN

THE JOURNAL OF BONE AND JOINT SURGERY

advise this method for routine testing of patients withMorton’s metatarsalgia, and it cannot replace clinical

assessment. It may help in young patients with atypicalfeatures, provided that the findings are interpreted in the

light of the clinical picture.The light and electron microscopic appearances of

the resected digital nerves were similar to those reportedby others (Nissen 1948 ; Ringertz and Unander-Schanin1950; Meachim and Abbenton 1971 ; Lassmann et a!.

1976; Ochoa and Noordenbos 1979). There is nowgeneral agreement that the pain of Morton’s metatarsal-gia is due to the observed neural changes. These consistof variable myelinated fibre loss with relative pneserva-tion ofunmyelinated fibres, excessive collagen depositionin the endoneurium, and fibrosis of endoneunial bloodvessels, which has been designated an endantenitis by

some authors. There is less agreement about the patho-genesis of these changes, some favouring an ischaemicbasis (Nissen 1948 ; Scotti 1957), and others arguing thatpressure effects alone are responsible (Ringertz and

Unander-Scharin 1950 ; Ochoa 1976 ; Ochoa and Noon-denbos 1979). The observations of Ringertz andUnander-Schanin (1950) that blood vessel changes wereas severe in their control material, and of Ochoa andNoordenbos (1979) of the similarity of the changes to

those of chronic entrapment lesions, are convincingevidence in favour of pressure effects. The presence ofRenaut bodies also suggests a compressive pathology(Jefferson, Neary and Eames 1981). This underlines thedifficulty that few studies have been able to reportdetailed examination of control material. From the

evidence available, it is clean that many of the neural

changes are also seen in painless plantar nerves, but areusually less severe (Ringertz and Unanden-Schanin 1950;Meachim and Abberton 1971). Our limited observationsdo not contribute to the elucidation of pathogenesis.

The digital “neuroma” found in Morton’s metatar-

salgia is quite unlike the typical neuromatous outgrowthswhich develop on injured nerves in other sites (Morris,

Hudson and Weddell 1972). Since endoneurial tubes areclearly disrupted in many Morton’s lesions, it is likelythat an intraneural neuroma forms (Sutherland 1968).Repeated pressure may prevent neuroma formation in

the region of maximum compression, but it seemspossible that this occurs proximally. The changes inplantar nerves immediately proximal to the site ofcompression between the metatarsal heads are poorly

described in the literature and are currently the subject

of further study.The mechanisms of pain in Morton’s metatansalgia

remain unclear. Although a differential fibre loss is

commonly found, with preservation of C fibres, thisseems unlikely to be the cause, since similar changes

have been found in control nerves. Chronic abnormalimpulse generation occurs in damaged peripheral nerve

axons of all classes, both as spontaneous activity and asmechanical sensitivity (Wall and Gutnick 1974; Govnin-

Lippman and Devor 1978 ; Scadding 1981). It is suggestedthat these properties are more likely to account for thecharacteristic pain on walking and for the spontaneous

pain reported by a number of our patients. Successfulrelief of symptoms in the great majority of patients by

excision of the appropriate nerve supports the idea that

a local initiation of impulses generates pain.

We wish to thank Professor P. K. Thomas for providing facilities at The Royal Free Hospital, and Miss Jane Workman for technical help. DrR. G. Willison kindly provided electrophysiological facilities at The National Hospital for Nervous Diseases, Queen Square, and Dr N. M. F.Murray helped with some of the recordings.

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