Clinical review

Tibialis posterior dysfunction: a common and treatablecause of adult acquired flatfootJulie Kohls-Gatzoulis, John C Angel, Dishan Singh, Fares Haddad, Julian Livingstone, Greg Berry

Adults with an acquired flatfoot deformity may presentnot with foot deformity but almost uniformly withmedial foot pain and decreased function of theaffected foot (for a list of causes of an acquired flatfootdeformity in adults, see box 1).1 Patients whoseacquired flatfoot is associated with a more generalisedmedical problem tend to receive their diagnosis andare referred appropriately. However, in patients whoseadult acquired flatfoot deformity is a result ofdamage to the structures supporting the medial longi-tudinal arch, the diagnosis is often not made early.2

These patients are often otherwise healthier and tendto be relatively more affected by the loss of functionresulting from an acquired flatfoot deformity. The mostcommon cause of an acquired flatfoot deformity in anotherwise healthy adult is dysfunction of the tibialisposterior tendon, and this review provides an outlineto its diagnosis and treatment.

Sources and selection criteriaWe seached PubMed for publications by using the key-words flatfoot and tibialis posterior dysfunction.

Tibialis posterior dysfunction: a common conditionTibialis posterior dysfunction is well recognised byorthopaedic surgeons specialising in foot and anklesurgery and by podiatrists. However, greater generalawareness of this condition is required,2 as mostpatients presenting to a general practitioner receive adiagnosis of ankle sprain or arthritis. By the time mostpatients present to a specialist foot and ankle clinicthey have had the condition for several years and haveconsulted numerous doctors.3 Even general ortho-paedic surgeons and physiotherapists often miss thediagnosis.3 However, tibialis posterior dysfunction neednot remain a specialist diagnosis as it is usually diag-nosed without any investigations, from a history andphysical examination.2 Many patients benefit fromrelatively simple treatment, such as orthotic devices.4

Population based studies to identify the prevalence oftibialis posterior dysfunction are under way. In elderlypeople the condition may reach a prevalence of 10% inwomen5 and it is often seen in general practice(unpublished data).

Tibialis posterior tendon: the key dynamic supportof the medial longitudinal arch of the footUnderstanding the importance of the tibialis posteriortendon for the normal foot clarifies the role that the

dysfunctional tibialis posterior has in the developmentof an acquired flatfoot. This tendon courses just poste-rior to the medial malleolus inserting into the navicu-lar tuberosity (on the medial aspect of the foot) and themid-part of the plantar aspect of the tarsus. The tibialisposterior tendon is the primary dynamic stabiliser ofthe medial longitudinal arch,6 and its contractionresults in inversion and plantar flexion of the foot andserves to elevate the medial longitudinal arch, whichlocks the mid-tarsal bones, making the hindfoot andmidfoot rigid.7 This later action allows the gastro-cnemius muscle to act with much greater efficiencyduring gait. Without the tibialis posterior, the otherligaments and joint capsules gradually become weak,

Summary points

Dysfunction of the tibialis posterior tendon is acommon condition and a common cause ofacquired flatfoot deformity in adults

Women older than 40 are most at risk

Patients present with pain and swelling of themedial hindfoot. Patients may also report achange in the shape of the foot or flattening ofthe foot

The foot develops a valgus heel (the heel rotateslaterally when observed from behind), a flattenedlongitudinal arch, and an abducted forefoot

Conservative treatment includes non-steroidalanti-inflammatory drugs, rest, and immobilisationfor acute inflammation; and orthoses to controlthe more chronic symptoms

Surgical treatment in the early stages is hindfootosteotomy combined with tendon transfer

Arthrodesis of the hindfoot, and occasionally theankle, is required in the surgical treatment of thelater stages of tibialis posterior dysfunction

A film showing left sided tibialis posterior dysfunction is onbmj.com. Please note that the file is very large, so you willprobably need broadband to watch this film

Royal NationalOrthopaedicHospital, StanmoreHA7 4LPJulieKohls-Gatzoulisspecialist registrarorthopaedic andtrauma surgeryJohn C Angelconsultantorthopaedic surgeonDishan Singhconsultantorthopaedic surgeon

Middlesex Hospital,London W1N 8AAFares Haddadconsultantorthopaedic surgeon

Barnet GeneralHospital, BarnetEN5 3DJJulian Livingstonepodiatrist

McGill UniversityHealth Centre,Hpital Gnral deMontral 1650,Avenue Cedar,Montreal, CanadaH3G 1A4Greg Berryconsultantorthopaedic surgeon

Correspondence to:J Kohls-Gatzoulisgatzoulis@ntlworld.com

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and thus flatfoot develops. Furthermore, without thetibialis posterior the gastrocnemius is unable to actefficiently, and therefore gait and balance are seriouslyaffected.

PathogenesisHistological examination has shown that, rather thantendinitis (tendon inflammation), the process is one oftendinosis (tendon degeneration), and the tibialis pos-terior tendon becomes fibrotic through a process ofrepeated microtrauma.8 Some controversy remainsabout the underlying aetiology of this tendinosis.915 Apoor blood supply to the tendon has been identified asit courses posterior to the medial malleolus.9 Mechani-cal factors must be at play that predispose the tendonto progressive fibrosis.10 A growing body of researchproposes that abnormal forces arise from even mildflatfootedness, resulting in lifelong greater mechanicaldemands on the tibialis posterior than in a normalfoot.1114 Another possible mechanical aetiology isoverpull of the opposing peroneus brevis muscle.15

Rarely, rupture of the tibialis posterior tendon has alsobeen associated with a traumatic event such as anklefracture,16 ankle sprain,17 or a direct blow to thetendon.18 It is important to point out that, although thetibialis posterior tendon may rupture, this is not neces-sary for tibialis posterior dysfunction to develop.10

Likewise, iatrogenic loss of the tibialis posterior tendondoes not always lead to an acquired flatfootdeformity.14 15

Risk factorsMiddle aged women are most commonly affected, andthe prevalence is known to increase with age.19 20 Pesplanus (flatfoot),1114 hypertension,19 diabetes mellitus,19

steroid injection around the tendon,7 and seronegativearthropathies7 21 have all been identified as risk factorsin patients with insufficiency of the tibialis posteriortendon.

ClassificationJohnson and Stroms classification describes theprogression of tibialis posterior dysfunction, and alsoserves as a guide to management.22 In stage I dysfunc-tion, the tendon is still intact and to some degree func-tioning, but it is inflamed. In stage II dysfunction, thetendon has become dysfunctional and the foot hasdeveloped acquired flatfoot, but the deformity ispassively correctable. In stage III dysfunction, the footdeformity has become fixed, and degenerative changesare seen in the subtalar joint. Stage IV was notdescribed by Johnson and Strom but has been addedsubsequently by Myerson.7 Stage IV dysfunction occurswhen degenerative changes are also present in theankle joint.

Diagnosing tibialis posterior dysfunctionHistoryIn stage I, patients typically present with an insidiousonset of vague pain in the medial foot and swellingbehind the medial malleolus along the course of thetendon (fig 1).2 5 Patients usually have no history ofacute trauma. As the condition progresses to stage II,patients have more complaints related to loss of func-tion and change in the shape of the foot. They reporteither a unilateral worsening of a pre-existing bilateralflatfoot or a newly acquired flatfoot deformity.22 Wetested survey questions and found that medial pain orswelling behind the medial malleolus together with achange in foot shape picked up 100% of patients withtibialis posterior dysfunction and had a specificity of98% (box 2).5 Also the patient may have a feeling ofinstability, a limp, a restricted walking distance, and aninability to walk on uneven surfaces. This also leads toan increased awareness of other foot pathologies, suchas bunions, hallux rigidus, and metatarsalgia, whichmay be the reason why the patient seeks medical atten-

Box 1: Causes of an adult acquired flatfoot Neuropathic foot (Charcot foot) secondary to:

Diabetes mellitusLeprosyProfound peripheral neuritis of any cause

Degenerative changes in the ankle, talonavicular ortarsometatarsal joints, or both, secondary to:

Inflammatory arthropathyOsteoarthropathyFractures

Acquired flatfoot resulting from loss of thesupporting structures of the medial longitudinal arch:

Dysfunction of the tibialis posterior tendonTear of the spring (calcaneoanvicular) ligament(rare)Tibialis anterior rupture (rare)

Painful flatfoot can have other causes, such as tarsalcoalition, but as such a patient will not present with achange in the shape of the foot these are not includedhere.

Box 2: Symptoms suggesting tibialis posteriordysfunction Pain and/or swelling behind the medial malleolusand along the instep Change in foot shape Decrease in walking ability and balance Ache on walking long distances

Fig 1 Arrows indicate swelling along the tibialis posterior tendon

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tion. In the later stages, as the flatfoot deformity wors-ens, patients have less medial pain and swelling andmay even have lateral hindfoot pain secondary toimpingement of the fibula on the sinus tarsi.20

ExaminationIn stage I tibialis posterior dysfunction the signs are ofswelling and tenderness behind and below the medialmalleolus (along the course of the tendon), and someweakness or pain with inversion of the foot (fig 2).2 Thepatient may have some difficulty rising on one heelonly, or weakness after multiple heel rises.7 20

In the later stages the patient may have less swellingand pain but will have developed an acquired flatfootdeformity.2 Looking at the standing patient from theback best shows the asymmetry of a unilateral acquiredflatfoot deformity (fig 2). The affected heel is in a valgusposition (box 3), and flattening of the medial longitudi-nal arch and forefoot abduction are visible. This leadsto the commonly quoted too many toes sign wheremore than the normal (one and a half to two) toes areseen along the lateral border of the foot.2 In later stagesthe tendon may not be palpable at its insertion site (thenavicular tuberosity)1; this is best assessed with thepatient attempting to invert and point the footdownwards. The most commonly applied functionaltest is the single heel rise (fig 3)2: patients with tibialisposterior dysfunction are unable to perform an ipsilat-eral unsupported single heel rise (to go from aflatfooted stance to standing on only the toes of theiraffected foot).

Someone with a normal foot can perform a singleheel rise eight to 10 times, but by stage II patients areunable (or barely able) to perform a single unsup-ported heel rise. Even if the patient is supported tofacilitate the attempted heel rise, the heel will not invertas it normally does (fig 3).16 In stages III and IV, in addi-tion to the findings in stage II, the flatfoot deformityhas become fixed. This is examined by grasping theheel and attempting to correct the valgus of the hind-foot (box 4).

ImagingThe diagnosis of tibialis posterior dysfunction is essen-tially clinical. However, plain radiographs of the footand ankle are useful for assessing the degree ofdeformity and to confirm the presence or absence ofdegenerative changes in the subtalar and ankle articu-lations. The radiographs are also useful to excludeother causes of an acquired flatfoot deformity.1 The

Fig 2 Left tibialis posterior dysfunction deformity is easily visible.The medial longitudinal arch is flattened. The left heel is in valgus.Also visible is the too many toes sign, which results fromabduction of the left forefoot

Box 3: Definitions

Valgus: Angulation of an extremity at a joint orfracture site such that the distal part deviates awayfrom the midline

Varus: Angulation of an extremity at a joint such thatthe distal part deviates toward the midline

Fig 3 (top) Unsupported single heel rise on patients good (right)side. (bottom) Attempt to perform a single heel rise on the affectedleft side. The patient was unable to do so unsupported but for thepurpose of this photo was allowed to lean forward and supportherself on the counter in front of her. The heel of the left foot hasnot inverted into varus

Box 4: How to examine for tibialis posteriordysfunction

(1) Both of patients legs visible from knee down

(2) Observe heel alignment with patient standing withfeet shoulder width apart, feet parallel. (Heel becomesvalgus, arch collapses, and forefoot adducts in cases oftibialis posterior dysfunction)

(3) Inspect for swelling behind medial malleolus

(4) Ask patient to stand on tiptoes. Normally the heelshould bend inwards. A patient with tibialis posteriordysfunction will have great difficulty standing ontiptoes, and the heel will not bend inwards

(5) Ask the patient to perform 10 unsupported heelrises on each leg. A patient with tibialis posteriordysfunction will not be able to do this

(6) Palpate along the tibialis posterior tendon fortenderness

(7) Test tibialis posterior tendon for power. Ask thepatient to bring foot into an inverted and plantarflexed position from an everted and dorsiflexedposition against your resistance

(8) Examine for hindfoot movement. In stages I and II,the foot is supple and the flatfoot deformity can becorrected by rotating the heel inwards (the arch of thefoot will be reconstituted). In stage III and IV subtalararthritis is present, and movement of the subtalar jointwill be lessened and painful. Additionally in stage IV,ankle arthritis has set in and the ankle becomes stiffand painful

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most useful radiographs are bilateral anteroposteriorand lateral radiographs of the foot and a mortise (trueanteroposterior) view of the ankle. All radiographsshould be done with the patient standing (figs 4, 5).20 Inmost cases we see no role for magnetic resonanceimaging or ultrasonography, as the diagnosis can bemade clinically.

TreatmentConservative treatmentConservative treatment is indicated for nearly allpatients initially before surgical management isconsidered.4 The key factors in determining appropri-ate treatment are whether acute inflammation andwhether the foot deformity is flexible or fixed.However, the ultimate treatment is often determined

by the patients, most of whom are women aged 40 orolder. Compliance can be a problem, especially instages I and II. It helps to emphasise to the patients thattibialis posterior dysfunction is a progressive andchronic condition and that several fittings and a trial ofseveral different orthoses or treatments are oftenneeded before a tolerable treatment is found.

Stages I and II: the flexible footAny acute inflammation surrounding the sheath of thetibialis posterior tendon should be dealt with beforethe chronic aspect of the condition is treated. A periodof four to eight weeks of immobilisation in a plastercast below the knee or a removable boot (such as thosemade by Aircast) may be required to control accompa-nying inflammation.7 20 23 In conjunction, RICE (rest,ice, compression, and elevation) and anti-

Stages of tibialis posterior dysfunction and treatment options

Stage Description Conservative treatment Surgical treatment

Stage I Tendon inflamedNo change in foot shape

Acute: 4-8 weeks immobilisation; rest, ice,compression, and elevation (RICE); non-steroidalanti-inflammatory drugs (NSAIDs)Chronic lace-up, flat footwear and correctiveorthosis (off the shelf, University of CaliforniaBiomechanics Laboratory (UCBL) or ankle footorthosis (AFO))

Tendon debridement combined with correctiveosteotomy

Stage II Tendon elongatedAcquired flatfoot deformity

Acute: 4-8 weeks immobilisation, RICE, NSAIDSChronic: lace-up, flat footwear andcorrective orthosis (UCBL or AFO)

Tendon transfer and corrective osteotomy

Stage III Fixed deformityDegenerative changes at subtalar joint

Lace-up, semirigid shoes or customised footwearand accommodative orthosis (AFO)

Triple arthrodesis (subtalar, calcaneo-cuboid. andtalonavicular articulations)

Stage IV Fixed deformityDegenerative changes at subtalar and ankle joints

Lace-up, semirigid shoes or customised footwearand accommodative orthosis (AFO)

Pantalar arthrodesis (subtalar, calcaneo-cuboid,talonavicular, and ankle articulations)

Fig 4 Before surgery (top) and five years after surgery ( bottom) fora patient with stage II tibialis posterior dysfunction. The surgicalreconstruction included a Cobb split tibialis anterior tendon transferand a Rose varus calcaneal osteotomy

Fig 5 Stage III tibialis posterior dysfunction before and after surgery(a triple arthrodesis). (top) Preoperative film shows a plantar flexedtalus (arrows point to head of talus) and loss of arch contour andheight. (bottom) Postoperative film shows union and reconstitutionof the arch

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inflammatories can be used, but steroid injection iscontraindicated.7

Footwear has an important role, and patientsshould be encouraged to wear flat lace-up shoes, oreven lace-up boots, which accommodate orthoses.Stage I patients may be able to manage with an off theshelf orthosis (such as an Orthaheel or Formthotics).They can try a laced canvas ankle brace before movingto a casted orthosis. The various casted, semirigidorthoses support the medial longitudinal arch of thefoot and either hold the heel in a neutral alignment(stage I) or correct the outward bent heel to a neutralalignment (stage II). This approach is meant to serveseveral functions: to alleviate stress on the tibialis pos-terior; to make gait more efficient by holding the hind-foot fixed; and thirdly, to prevent progression ofdeformity.23 Devices available to do this are the orthosisof the University of California Biomechanics Labora-tory, an ankle foot orthosis, or a removable boot. Whenthis approach has been used, two thirds of patientshave good to excellent results.4

Stage III and IV: the rigid flatfootOverall, inflammation tends to be a less commonfeature of presentation with the rigid acquired flatfoot.Treatment revolves around accommodating the

deformity (rather than attempting to correct it) withcustomised moulded rigid orthoses, used in conjunc-tion with appropriate footwear (often custom made), asthe foot deformity worsens.

Surgical treatmentGood to excellent results for more than 80% ofpatients have been reported at five years follow up forthe surgical interventions recommended below.7 20

However, the postoperative recovery is a lengthy proc-ess, and most surgical procedures require patients towear a plaster cast for two to three months. Althoughmany patients report that their function is wellimproved by six months, in our experience a year isrequired to recover truly and gain full functionalimprovement after the surgery. Clearly, some patientsare not candidates for such major reconstructivesurgery.

Stage IIn individuals with notable flatfoot whosesymptoms do not resolve with conservative measures, acalcaneal osteotomy may be considered. This aims tocorrect the underlying foot deformity, to attempt topreserve the foots function,7 in conjunction with eithersurgical debridement of the tendon24 or tendontransfer.

Stage IIConsensus is growing that surgicaltreatment should entail tendon transfer in combina-tion with corrective osteotomy.7 22 The rationale behindthis approach is that the osteotomy is required to cor-rect the bony architecture of the foot in order to opti-mise the biomechanics of the reconstructed tibialisposterior tendon. Various osteotomies of the calcaneuscan correct the bony alignment7 22 25 and may beaugmented with a lengthening of the lateral column.The tendons used to reconstruct tibialis posterior areeither a split tibialis anterior tendon (fig 4) or flexordigitorum longus.

Stage IIIThe goal of surgical treatment is tocorrect the deformity and alleviate pain through a tri-ple arthrodesis of the subtalar, calcaneocuboid, andtalonavicular articulations (fig 5).

Stage IVThis has been reached when additionaldegenerative changes are present in the ankle joint.The salvage treatment at this stage is usually a pantalararthrodesis (ankle, subtalar, calcaneocuboid, andtalonavicular articulations).

ConclusionsThe tibialis posterior muscle is the key dynamicsupport of the medial longitudinal arch of the foot.When it fails progressively, the arch slowly collapses,the heel drifts into valgus, and the forefoot graduallyabducts, resulting in painful acquired flatfoot. Tibialisposterior dysfunction is often misdiagnosed as achronic ankle sprain, osteoarthritis, or collapsed archas a result of ageing or obesity, and it leaves the patientdebilitated. Prompt diagnosis prevents frustration forthe patient and allows treatment to be started at anearlier, more easily managed stage (fig 6). The diagno-sis of tibialis posterior tendon dysfunction is largely aclinical one. An increased awareness of the existence oftibialis posterior should serve to help patients with ear-lier referral and treatment and by limiting the amountof disability they experience.

Management of tibialis posterior dysfunction

Early Ache on walking long distance Medial pain or swelling Able to perform a single heel rise with difficulty

Intermediate Limited walking ability Pain medial or lateral Development of acquired flatfoot deformity Unable to perform single heel rise

Late Limited walking ability Rigid, fixed hindfoot in valgus

Non-steroidal anti-inflammatory drugs, rest

Refer (to podiatrist ororthopaedic surgeon)

for orthoses

Refer for appropriate orthosesor orthopaedic referral

If conservative treatmentfails: Surgery to

reconstruct tendon andcalcaneal osteotomy

Trial of appropriate orthosesor orthopaedic referral

If conservative treatmentfails: Triple arthrodesis(if ankle also arthritic:pantalar arthrodesis)

Fig 6 Treating tibialis posterior dysfunction

Resources for patients and doctors

www.footcaremd.comDesigned for patients and runand maintained by the American Orthopaedic Footand Ankle Society. The information about tibialisposterior dysfunction can be found under the headingprogressive flat foot

www.bofss.org.ukDesigned for both patients anddoctors and is run by the British Orthopaedic FootSurgery Society and gives good general advice aboutfoot care

www.orthoteers.co.ukA good site for doctors. Clickon flatfeet (in the paediatrics section) and then ontibialis posterior insufficiency

www.rcsed.ac.uk/fellows/jbarrie/hyperbookThewebsite for the Blackburn Foot and Ankle Hyperbook.Clicking on elective foot and ankle problems andthen on tibialis posterior insufficiency links you to acomprehensive list of causes, complaints,examinations, and stages

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Contributors: JK-G wrote the paper. JL gave podiatric advice.FH and GB are involved in collaborative research on tibialisposterior dysfunction and have worked with senior authors JCAand DS. DS is guarantor.Funding: None.Competing interests: None declared.

1 Mann RA. Acquired flatfoot in adults. Clin Orthop Rel Res 1983;181:46-51.

2 Johnson KA. Tibialis posterior tendon rupture. Clin Orthop Rel Res1983;177:140-7.

3 Haddad FS, Berry G, Singh D, Angel J. Tibialis posterior tendonitis: theforgotten epidemic. Presented at the British Orthopaedic Association,September 1999. J Bone Joint Surg 2000;82B(suppl 1):80.

4 Chao W, Wapner KL, Lee TH, Adams J, Hecht PJ. Non-operativetreatment of posterior tibial tendon dysfunction. Foot Ankle Internat1996;17:736-41.

5 Kohls-Gatzoulis JA, Singh D. Tibialis posterior dysfunction as a cause offlatfeet in elderly patients. Foot 2004;14:207-9.

6 Basmajian JV, Stecko G. The role of muscles in arch support of the foot.J Bone Joint Surg 1963;45A:1184-90.

7 Myerson MS. Adult acquired flat foot deformity. J Bone Joint Surg1996;78A:780-92.

8 Mosier SM, Lucas DR, Pomeroy G, Manoli A II. Pathology of theposterior tibial tendon in posterior tibial tendon insufficiency. Foot AnkleInt 1998;19:520-4.

9 Frey C, Shereff M,Greenidge N. Vascularity of the posterior tibial tendon.J Bone Joint Surg 1990;72A:884-8.

10 Mosier SM, Pomeroy G, Manoli A II. Pathoanatomy and aetiology of pos-terior tibial tendon dysfunction. Clin Orthop Rel Res 1999;365:12-22.

11 Dyal CM, Feder J, Deland JT, Thompson FM. Pes planus in patients withposterior tibial tendon insufficiency: asymptomatic versus symptomaticfoot. Foot Ankle Int 1997;18: 85-8.

12 Kohls-Gatzoulis JA, Singh D, Angel JC. Tibialis posterior insufficiencyoccurring in a patient without peronei: a mechanical aetiology. Foot AnkleInt 2001;22:950-2.

13 Mann RA, Thompson FM. Rupture of the posterior tibial tendon causingflat foot. J Bone Joint Surg 1985;67A:556-61.

14 Yeap JS, Singh D, Birch R. Tibialis posterior tendon dysfunction: aprimary or secondary problem? Foot Ankle Int 2001;22:51-5.

15 Mizel MS, Temple HT, Scranton PE II, Gellman RE,Hecht PJ,Horton GA,et al. Role of the peroneal tendons in the production of the deformedfoot with posterior tibial tendon deficiency. Foot Ankle Int 1999;20:285-9.

16 Monto RR, Moorman CT III, Mallon WJ, Nunley JA II. Rupture of theposterior tibial tendon associated with closed ankle fracture. Foot Ankle1991;11:400-3.

17 Borton DC, Saxby TS. Tear of the plantar calcaneonavicular (spring) liga-ment causing flatfoot. A case report. J Bone Joint Surg 1997;79B:641-3.

18 Beals TC, Manoli A II. An unusual cause of posterior tibial tendondegeneration. Foot Ankle Int 1998;19:177-9.

19 Holmes GB II, Mann RA. Possible epidemiological factors associatedwith rupture of the posterior tibial tendon. Foot Ankle 1992;13:70-9.

20 Pomeroy GC, Pike RH, Beals TC, Manoli A II. Current concepts review.Acquired flatfoot in adults due to dysfunction of the posterior tibial ten-don. J Bone Joint Surg 1999;81A:1173-82.

21 Myerson M, Solomon G, Shereff M. Posterior tibial tendon dysfunction:its association with seronegative disease. Foot Ankle 1989;9:219-25.

22 Johnson KA, Strom DE. Tibialis posterior tendon dysfunction. ClinOrthop Rel Res 1989;239:196-206.

23 Wapner KL, Chao W. Nonoperative treatment of posterior tibial tendondysfunction. Clin Orthop Rel Res 1999;365:39-45.

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25 Wacker JT, Hennessy MS, Saxby TS. Calcaneal osteotomy and transfer ofthe tendon of flexor digitorum longus for stage-II dysfunction of tibialisposterior. Three- to five-year results. J Bone Joint Surg 2002;84B:54-8.

(Accepted 14 September 2004)

Lesson of the weekClomipramine induced neuroleptic malignant syndromeand pyrexia of unknown originAlison M Haddow, Dawn Harris, Martin Wilson, Hannah Logie

Neuroleptic malignant syndrome is uncommon. Itsmajor characteristicsclassically, fever, muscular rigid-ity, and raised serum creatinine kinase concentrationoccur unpredictably and often in association withdopamine blocking drugs (box).1 We present a case ofneuroleptic malignant syndrome occurring in associa-tion with clomipramine, a drug not noted fordopamine blockade. Greater awareness of the possibil-ity of this potentially life threatening syndrome occur-ring in patients treated with antidepressants may beuseful given the continued increase in the prescribingof antidepressants of all classes.

Case reportA 57 year old mana long term inpatient with frontallobe dementia in an old age psychiatry wardwasadmitted to an acute medical assessment unit in Janu-ary 2003. He presented with sweating, pyrexia, musclerigidity, decreased responsiveness, and urinary incon-tinence (table). At the time of admission he was takingclomipramine and promazine, both started in 2001.He was empirically diagnosed as having urinary tractinfection and was prescribed intravenous and thenoral antibiotics. He improved and returned to his longstay ward. Urine and blood cultures showed no growthduring this admission. In May 2003, his conditiondeteriorated again with all previous symptoms andsigns recurring. At this stage, promazine was stopped

and further medical assessment was requested andagain he was diagnosed as having urinary tract infec-tion, and a course of antibiotics was prescribed. Inaddition to routine investigation, a liver ultrasoundwas done which showed no abnormality. Once againurine and blood cultures showed no growth. His con-dition improved, and he was transferred back to hisbase ward. Later the same month the mans sweating,pyrexia, muscular rigidity, and decreased responsive-ness returned. At this stage, an opinion was soughtfrom the department of medicine for the elderly. Dueto the length of his history and the lack of a positivemicrobiological culture, a drug reaction was suspectedand his current medication, ciprofloxacin andclomipramine, was stopped. Within 48 hours allsymptoms had resolved, and he was provisionallydiagnosed as having neuroleptic malignant syndrome.In June 2003 there was a trial reintroduction of clomi-pramine. After only three doses, however, thepreviously noted symptoms rapidly recurred again,resolving on withdrawal of the drug. A report was sentto the Committee on Safety of Medicines and thesupplier of clomipramine.

DiscussionPyrexia related to clomipramine has been reported ononly four occasions to the Committee on Safety ofMedicines, therefore some care was need in labelling

Clinical review

Neurolepticmalignantsyndrome canbe precipitatedby clomipramineand possiblyotherantidepressants

Royal CornhillHospital, AberdeenAB25 2ZHAlison M Haddowacting consultant inold age psychiatryDawn Harrismedical officer

Woodend Hospital,AberdeenMartin Wilsonspecialist registrar inmedicine for theelderlyHannah Logiesenior house officer inmedicine for theelderly

Correspondence to:A M Haddowalison.haddow@gpct.grampian.scot.nhs.uk

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