INTERNATIONAL JOURNAL 01. LEPROSY^

Volume 65, Number 2Printed in the U.S.A.

(ISSN 01-3S-916X)

Cervical Branch of the Facial Nerve in Leprosy'Bruce M. Richard and Peter R. Corry'

The pathogenesis of leprosy is poorly un-derstood. The present understanding is thatleprosy bacilli gain entrance to nerves (bymethods unknown) and are phagocytosedby Schwalm cells. A pattern of nerve in-volvement is recognized, with certain "sitesof predilection" being rendered preferen-tially nonfunctional leading to recognizedimpairment patterns. There is considerabledebate as to whether the nerve is primarilydamaged at these sites of predilection orwhether the nerve is involved more distallyand/or proximally, but because of the me-chanical problems of the sites of predilec-tion any long-term compression will lead toirreversible nerve damage at these sites.

Also, the involved nerves are often asso-ciated with a nearby skin patch. Whetherthe bacteria gain access to the nerve by theblood stream, as evidenced by its segmentaland longitudinal fascicular nature, or by alocal skin lesion, as evidenced by the asso-ciation with skin patches, is not known ( 21 ).

The prevalence of facial nerve involve-ment is 4%—l0% of all cases of leprosy(4. 14, 15, 19, 22) The facial nerve differs fromthe other nerves involved in leprosy be-cause it is a pure motor nerve (in its extracranial portion). Motor loss from a facialnerve lesion is usually restricted to tem-poro-zygomatic branches where they crossthe zygomatic arch, leading to orbicularisoculi paralysis. That the zygomatico-tem-pond branches are more frequently in-volved than other branches is attributed tothe double fascia entrapment overlying thezygomatic arch ( 7 ' 5) and to their superficiallocation. Possibly other secondary factors,such as the colder temperature, increased

' Received for publication on 23 August 1996.Accepted for publication in revised form on 13January 1997.

= B. M. Richard, F.R.C.S., Green Pastures Hospital,Pokhara, Nepal. P. R. Corry, B.A., B.M., B.Ch., SHOAnesthetics, Royal Liverpool University Hospital,Liverpool, U.K.

Reprint requests to B. Richard, Reconstructive Sur-geon, Western Regional Hospital, do InternationalNepal Fellowship, P. 0. Box 5, Pokhara, Nepal.

stretch and the increased likelihood of traumaat this site, are relevant.

However, this has been challenged byDastur, et al. ( 2 . 8) with their study compar-ing facial nerve involvement with trigemi-nal nerve malar skin patches and suggestingthat there is retrograde motor branch infec-tion with the leprosy bacilli and, thus, facialpalsy. That the upper part of the face ismore commonly involved than the lower isnoted, (1, 4, 7, S. 14, 15, Is, 19, 22, 25) but notIR it proven.That the nerve is involved more distallythan proximally is not proven but assumed,in that palsies are more frequent in the zy-gomatic region. The recorded incidence offacial nerve involvement is based on screen-ing examinations for weakness of eye clo-sure because of the sequelae of lagophthal-mos and possible loss of vision. In mostleprosy clinics there is no routine testing ofall of the facial nerve's branches.

You might expect the cervical branch ofthe facial nerve to be involved frequentlysince it innervates a panniculus carnosusmuscle, with its muscle fibers inserted su-perficially into the dermis. It is also sur-rounded by sensory cutaneous neck nerveswhich are frequently involved. However,most leprologists do not regularly examinethe action of the platysma since any func-tional deficit would be of little clinical rele-vance. Some believe the cervical branchnever to be involved (6) while we at GreenPastures Hospital (GPH) have noticed it tobe occasionally involved in those with a fa-cial nerve palsy.

The classical understanding remains un-proven and challenged by several issues.Leprosy nerve pathology is segmental andhas an uneven involvement of fascicles. Re-cent intra-operative electrodiagnostics tofind the most proximal lesion in the medianand ulnar nerves has demonstrated lesionsfar more proximal than the naked eye canperceive ( 2( "). The phenomenon of mis-reinnervation of the facial musculature(synkinesis) ( 18 ) also suggests that thepathology is often more proximal than justa named terminal nerve branch; perhaps as

170

65, 2^Richard and Carry: Cervical 13ranch of Facial Nerve^171

far as the division of the main facial nervetrunk, allowing regenerating axons to heable to misreinnervate a nerve fascicle.Most patients with sonic degree of facialmuscle weakness also have evidence ofmis-reinnervation, the commonest being el-evation of the upper lip on gentle eye clo-sure. The platysma is an extremely superfi-cial muscle, and the cervical branch of thefacial nerve is known to have anastomoticconnections with the transverse cutaneouscervical nerve ( 2 '). For these reasons wemight expect it to be involved more fre-quently. However, the cervical branch ofthe facial nerve is deep to the platysmamuscle, and because of its anatomical sitewould be protected from secondary factors.

We wanted to know whether or not thecervical branch of the facial nerve was in-volved in leprosy. And if involved, whatwas the relationship with any pre-existingfacial nerve lesion or enlarged cervical sen-sory nerves?

SUBJECTS AND METHODSOne-hundred-two consecutive leprosy

patients attending Green Pastures Hospitalover a period of 3 months were examinedaccording to the protocol. Seven patientsrequesting reconstruction of a facial defor-mity caused by a near total facial nervepalsy also were examined.

For each patient, their name, age, sex,type of leprosy, treatment nature, and stagewas recorded. A note was made of any re-action, and whether the patient was takingcorticosteroids at the time. The patient wasasked if there had been any ear discharge inthe last 12 months (which would indicate apossibility of middle ear disease, providingan alternative explanation for a facial nervelesion). Consenting patients then had a fur-ther clinical examination of the facialnerve's five main peripheral branches byasking, for the voluntary contraction of eachmuscle group. In viva facial nerve anatomyis not stylized to the five branches describedin anatomy textbooks but, rather, has sev-eral interfascicular interconnections, and noone named branch is responsible for one fa-cial expression.

We tested as follows: temporal branch byelevation of the frontalis muscle, zygomaticbranch by eyelid closure, buccal branch byholding air in the buccal pouch against re-

sistance and by the ability to elevate the an-gle of the mouth, and the cervical branch bycontracting the platysma. The mandibularbranch, with its connection to the infra-or-bital buccal plexus was tested by the "buc-cal" branch tests and not formally by anydepressor actions of the orbicularis mus-cles. Each action was recorded as beingnormal or weak. In order to examine the fa-cial nerve it is usual to teach patients tocarry out movements on instruction, or tomimic actions. Such as, "smile," "close youreyes," "blow out your cheeks" and "frown."The platysma, however, is more difficult be-cause previously we did not examine for itsfunction and because there is no commandto initiate it, so it has to he a mimicked ac-tion. We were unsure whether patientswould correctly mimic the platysma action,leaving us with a result where a nonfunc-tioning platysma might mean that there wasno cervical branch activity or simply a fail-ure in the patient's comprehension.

To overcome this and to compare anynonfunctioning platysma with branches ofthe facial nerve that we know we can exam-ine clinically, we decided to test the fron-talis, buccal and platysma muscles usingelectrical stimulation delivered by an eu-trophic (" ") muscle stimulator (DynamicMedical Instruments). Current was deliv-ered via 2 cm' carbon rubber electrodeswith the active electrode being placed onthe motor point of the relevant muscle. Thestimulator delivers 80 microsecond com-pensated rectangular pulses at between 0and 18 volts. Each was recorded as beingpositive or negative, depending on whethera contraction could be stimulated before themaximum output was reached or not, or be-fore it became too painful.

Also, because some patients may havehad a platysma palsy which was partial orrecent, the function of the cervical branchof the facial nerve was recorded electro-physiologically using strength-duration ( 12 )curves in all patients. These indicate thestrength of impulses of various durationsrequired to produce visible contraction inthe muscle. A Myodyne stimulator (Elec-tro-Medical Supplies) of the constant volt-age type was used to supply rectangular im-pulses of different durations varying from300 ms to 1 ms via a 2 cm 2 carbon rubberelectrode and a button electrode.

172^ International Journal of Leprosy^ 1997

TABLE^Patients seen in .vurgical assessment clinic with severe lagophthalmos or fa-cial nerve palsy requesting a reconstructive procedure.

Patient Age Sex Leprosytype

UM/Bilateral.'

Facial branches involved

Frontal^Zygomatic^Buccal^Mandibular^Cervical

I 67 Male Rt64 Male 131. Lt +

3 17 dale 131, RtI a

4 60 Male Ill .t5 50 Male LL Rt

Lt6 55 Male 13137 9 Female id Lt +

Normal facial nerves are not included.

The patient was seated comfortably ingood light, and the skin resistance was re-duced by cleansing with an alcohol swab.The indifferent electrode (anode) was ap-plied to the anterior aspect of the neck inthe inidline, and the active electrode (cath-ode) was applied to the motor point withcare being taken to keep it over the samepoint throughout the test. Current was ap-plied using the longest stimulus first (300ms), and the voltage was increased until theminimum observable contraction was ob-tained. The strength-duration curve was plot-ted, and each patient was classified as inner-vated, denervated or partially innervated onthe basis of the shape of the graph ('').

Corneal and maxillary sensation weretested using cotton wisps. and a skin patchwas looked for on the face. If a recent his-tory of ear discharge was elicited, the drumswere checked and recorded as intact or per-forated.

RESULTSOf the 102 patients examined, 96 had a

complete record for computerized statisticalanalysis. Patients were generally middleaged (median age 44 years, range 11-77),76 were male (79%) and 20 female (21%).The patients had been classified as 46%borderline tuberculoid (BT), 28% border-line lepromatous (BL), 15% lepromatous(LL), 6% borderline (BB), 3.3% pureneural ( PN) and I % tuberculoid (TT). Ofthe 96 patients, 52 (54%) had completedmultidrug therapy, 44 (46%) were on ther-apy, and no patient was new. As regardsleprosy reactions in the previous 12

months, 69 (73%) of the patients had hadnone, 20 (21%) had had a type I or reversalreaction and 6 (6%) had had a type 2 or ery-thema nodosum leprosum (ENL) reaction.Nineteen patients (20%) were on cortico-steroids.

For each patient there are two records offacial nerve examination, one for each side,right and left. Of 192 nerves (96 patients)only one platysma was found to be para-lyzed. This was a right-sided palsy and wasassociated with a near total palsy in theother branches of the facial nerve. No pa-tient was found to have an isolated cervicalbranch nerve palsy on voluntary contractionor eutrophic stimulation. No patient had adenervated or partially denervated cervicalbranch of the facial nerve by strength-dura-tion curves.

The strength-duration curves were vali-dated for denervation for one of our patients(PS), in that 2 weeks after surgery to exciseher facial nerve and reconstruct her right fa-cial palsy, she had a denervated curve onthe right and a normal one on the left. Nopatient was unable voluntarily to contracttheir platysma. Twenty-five patients hadsome form of facial nerve palsy; 9 wereunilateral and 16 bilateral.

Statistical analysis of the data did not es-tablish a relationship between loss of max-illary sensation, enlargement of cutaneousneck nerves, or the presence of face patcheswith any pattern of facial nerve palsy.Twenty-six of the patients had had a reac-tion in the previous 12 months, and 19 wereon corticosteroids but only 4 had any facialnerve involvement. The study questionnaireonly inquired if there had been a reaction in

65, 2^Richard and Cor': Cervical Branch of Facial Nerve^173

TABLE 2. Frequencies ()1 . different tspesoljacial nerve palsies.

Type of facial nerve palsy No. nerves

Lagophthalmos only 19Lagophthalmos and buccinator weakness I3Lagophthalmos and frontalis weakness 5All branches excluding platysma 3All branches including platysma 5Frontalis only weakBuccinator only weak 3

the past 12 months and, thus, any relation-ship between a previous reaction and facialnerve palsy was not possible to establishfrom these data. Two patients had an eardischarge, one with no facial nerve lesionand one with a bilateral lagophthalmos but noother facial nerve involvement. There was noevidence to suggest that a facial nerve palsywas associated with middle ear disease.

Patients referred to the surgical assess-ment clinic for facial nerve problems re-quiring more than simple tarsorrhaphy werealso examined for platysma function. Theirclinical details are summarized in Table I.Most of these patients had a sumical proce-dure to help relieve their impairment and, atthe same time, a biopsy of portions of theirnonfunctioning facial nerve. A biopsy ofthe cervical branch of the facial nerve wasalso done regardless of whether there was aplatysma palsy or not. (The results of thiswork will be the subject of another paper).

Combining all of the patients with any de-gree of facial palsy, i.e., 25 from the consec-utive examinations and 7 from the surgicalassessment clinic, a total of 32 patients with50 involved facial nerves were available foranalysis. The frequency of named nervebranches involved alone, or in associationwith other involved facial nerve branches,making up the different patterns of facialnerve palsies can be seen in Table 2.

DISCUSSIONThis study demonstrates that the platys-

ma is occasionally palsied in leprosy, andthat in our sample this only occurred whenthe facial nerve already had some otherpalsy. This is the first study which has actu-ally examined the status of the platysma,and it certainly refutes the claim that it isnever involved ("). There was no case of anisolated platysma palsy, confirming that

there needs to be a facial palsy before therecan be a platysma palsy. To prove this state-ment, however, would need the screeningof a very large number of patients (1000perhaps). Patients without lagophthalmosor any degree of eye weakness would needto be examined for facial nerve involve-ment, and this is now a possibility since weknow from this study that all patients re-gardless of age or other factors can easilymimic this platysma contraction. This obvi-ates the need for electrical testing to exam-ine for a platysma palsy. It also means thata nonfunctioning platysma on clinical ex-amination is, in fact, a palsied platysma.While lagophthalmos is regularly examinedfor, and an obvious facial paresis would benoticed, less severe forms of facial muscleparesis will only be found if formally ex-amined for.

The facial nerve once it has comethrough the mastoid foramen has only mo-tor branches. Some of these are deep, suchas the posterior auricular nerve which be-comes the auricular branch to the intrinsicmuscles of the external ear, and the occipi-tal branch, which supplies the occipitalbelly of the occipitofrontalis. There is also adigastric branch for the posterior belly ofthe digastric, and stylohyoid branch for themiddle part of the stylohyoid muscle. Noneof these muscles are easy to examine for apalsy, and we are not aware of any reportedoccurrences. It is of interest that patient no.3, who had a bilateral platysma palsy, didhave one small muscle belly (on the rightonly) that contracted under the chin in a su-perior-inferior direction when voluntarilytrying to contract his platysma. This couldbe a cervical branch innervated strap mus-cle, suggesting mis-reinnervation of the cer-vical nerve, or it is his stylohyoid musclewhich is innervated by the stylohyoidbranch of the facial nerve.

The more well-known branches of the fa-cial nerve (frontal, temporal, zygomatic,buccal, marginal mandibular, and cervical)all run deep to the superficial lobe of theparotid gland and superficial muscular andaponeurotic system (SMAS) before enter-ing, their respective muscles on their deepsurface ( 29 ).

The problem with any facial nerve palsyis to determine the site of the nerve lesion.If it is a lower motor neuron type, then

I 74^ haeraational Journal of 1.epro.sy^ I997

where anatomically is it damaged and bywhat'? In leprosy we have alwaysthat the nerve damage is distal and at thesites of predilection. We believe that themycobacterium is in the nerve at the levelof the lesion and that the ensuing pathologyis a direct result of the destructive nature ofthis local infection and any local and sys-temic immunological reaction. The distri-bution of the disease to certain portions ofperipheral nerves is attributed to: a) theanatomical position permitting a relativesuperficiality and, therefore, coolness forwhich the mycobacteria are said to have anaffinity CI, and b) the anatomical positioncausing the nerve to pass through a fibro-osseus tunnel at these sites, making it un-able to avoid compression when it becomesswollen in an inflammatory reaction. Whichof these two reasons is the more importantis not known. Is the relative coolness due tosuperficiality the primary cause for M. lep-rae infection in that portion of the nerve'?Or is the leprosy bacterium's affinity fornerves more generalized than we think, andmuch more of a peripheral nerve trunk is in-fected but only the swollen portion at the"site of predilection" undergoes compres-sion and presents the clinical picture of neu-ritis that is recognized by the clinician'?

There is now evidence to suggest thatnerve involvement in the peripheral nervetrunks, can he more proximal. Turkof, et a!.have demonstrated electrophysiologicallyother involvements in the peripheral nervetrunks at levels much higher than 'previ-ously noticed macroscopically. These arenot at sites of compression, and after neu-rolysis there was some functional improve-ment ( 26 . 27). A post-mortem study on threelepromatous patients has found some im-munohistochemical evidence of facialnerve involvement within the internal audi-tory meatal and tympanic portions of thetemporal bone, but no nerve damage wasobserved (').

There is also considerable debate as towhether the infection begins in the dermisand spreads centripetally, ascending alongthe nerve, or whether it is a systemic dis-ease due to hematogenous infection. Theresulting lesions of a systemic disease couldbe the result of disseminated infective ma-terial or immunological reactions to the in-fective agent's antigens. To support the as-

cending infection theory, there is kliko,a/. 's anatomical and pathological study ofamputated limbs from leprosy patients ( '').They serially examined the nerves fromproximal nerve trunks down to distal der-mal nerve endings, and demonstrated in-creasing nerve destruction the more distallythe nerve was examined, culminating in to-tal destruction of dermal nerves and sensorynerve endings. A recent report of armadil-los infected intravenously with M. lepraeshowed extensive involvement of the pe-ripheral nerves, increasing in intensity asthe nerve was followed distally in those an-imals that had developed disseminated dis-ease ( 2 `). In support of a systemic diseasetheory there is: a) the production of skinpatches typical of nonleprom►tous leprosyin an inbred strain of guinea pig as the re-sult of an autoin►nnune response to an in-jected sensory nerve antigen (`.(' 25 ); b)the pure neural (PN) classification of lep-rosy where patients have the typical neuritisbut are never shown to have a skin lesion;c) patients in reversal reaction frequentlyget a worsening neuritis at the sites ofpredilection but not associated with anearby skin patch in reaction whereas facialnerve palsy often has a history of a type Ireaction in a nearby malar skin patch at thesame time as the development of the palsy.

Dastur, et a!. were the first to suggest aretrograde infection of the zygomaticbranches of the facial nerve from a con-comitant trigeminal facial skin patch infec-tion. There is a known interconnection fromthe zygomaticofacial branch of the maxil-lary division of the trigeminal nerve withthe zygomatic branches of the facial nerve.Based on a study of I 1 cases, Dastur, et al.hypothesized that the leprous infection en-ters the malar skin through sensory nerveterminals of the trigeminal nerve and pro-gresses in such a way as to involve the mo-tor fibers of the facial nerve in this area, ei-ther because of the close proximity to, orthe actual anastomotic connections betweenthe palpebral branches of the maxillary di-vision of the trigeminal nerve and the zygo-matic branches of the facial nerve C). Otherstudies also have supported the idea that thefacial skin patch was causative for the sub-sequent facial nerve palsy (".'"). Hogeweg,et al. showed that a malar skin patch in typeI reaction was a precondition for facial

65, ')^

Richard and Corry: Cervical Brunch of Facial Nerve^175

nerve damage on the same side ("). Patientswith I agophthalmos often have hypopig-mewed anesthetic malar patches ( 2 '').

Secondary factors operating on the nervebranches in the zygoinatic region are alsothought to be important. Dastur, et al. wereimpressed by the close apposition of thesebranches against the zygoma and consid-ered compression against unyielding fibro-osseous tissues at this site a "mechanicalpredisposition. - Their study also showedthat the nerves are not thickened (S). Lub-bers, et al. looked at 57 patients with lag-ophthalmus to assess the degree of paralysisof facial muscles and found that most(SI%) had involvement of at least one othermuscle group. Upper and lower facial mus-cles were found to be affected in the sameproportion and so they found little supportfor the statement that the superficial courseof the facial nerve above the zygomaticbone is decisive for exclusive paralysis ofthe zygomatic branch (").

However, many other facial nerve motorbranches have similar anastomotic connec-tions with cutaneous sensory nerves, in-cluding the postauricular and the cervical.The facial nerve also has an ill-defined areaof sensory innervation of the external ear( 21, and perhaps the facial nerve lesion isdirect bacterial invasion from this skinsource into the facial nerve's cutaneous sen-sory branch. Cutaneous nerves in the neckare one of the most commonly enlargednerves to he found in leprosy, yet our studyhas not found the platysma to be as com-monly paralyzed. In fact, it is only involvedwhen part of a more serious facial nerve le-sion. This observation, together with thephenomenon of mis-reinnervation, suggeststhat cervical branch involvement only oc-curs as facial nerve pathology progressesmore proximally from its zygomatic posi-tion toward the trunk. Or it could be that thetrunk is always involved and we only seethe lagophthalmos problem more com-monly than other branch involvement be-cause of all the secondary factors of com-pression at the zygoma (SMAS and deepinvesting cervical fascia fixed to the perios-teum over the zygoma), cooler temperatureand exposure to trauma. Another superficialmotor nerve in the neck is the accessorynerve supplying the trapezius muscle.There is no report of this muscle being

weak or paralyzed in leprosy, even thoughit is situated superficially just under the skinin the posterior triangle of the neck, and of-ten surrounded by many enlarged cutaneoussensory nerves. Evidence of its superficial-ity is the frequency of inadvertent damagein nonleprosy patients having a biopsy of alesion in the posterior triangle of the neck

and the patient presenting later with acomplaint of muscle weakness.

Of the facial nerve innervated facial mus-cles, the orbicularis oculi is the musclemost frequently involved alone by leprosy(Table 2). Then an orbicularis oculi weak-ness together with the buccinator or, lessfrequently, with the frontalis, is the nextmost likely finding. The low frequency of apalsy of all branches excluding the cervical,and then including the cervical, implies aworsening nerve scenario progressing prox-imally along the facial nerve trunk ratherthan increasing frequencies of skin acquirednerve involvement.

SUMMARYThis study demonstrates that the pla-

tysma is occasionally palsied in leprosy andthat this only occurs when the facial nervealready has some other palsy. That thereneeds to be a facial palsy before there canhe a platysma palsy is strongly suggested,in that there was no case of an isolatedplatysma palsy. Patients, regardless of ageor other factors, could mimic a platysmacontraction. This obviates the need for elec-trical testing to examine for a platysmapalsy. It also means that a nonfunctioningplatysma on clinical examination is, in fact,a palsied platysma. While lagophthalmos isregularly examined for, and any obvious fa-cial paresis would be noticed, less severeforms of facial muscle paresis will only befound if formally examined for.

The mechanism whereby the facial nerveis involved in leprosy is not clarified, butour findings suggest that proximal spread ofa lesion that began in the zygomatico-tem-poral branches and reaches to the facialnerve trunk is more likely than new lesionsdeveloping de novo in other peripheral fa-cial nerve branches. That the primary lesionis within the facial nerve trunk in all casesbut we only see the frequent zygomaticsequelae due to secondary factors is notexcluded.

I76^ International Journal of Leprosy^ 1997

RESUMENEste estudiii deinuestra que los imisculos de Ia

platisma en los pacicntes con lepra puede') ocasional-mettle sufrir paralisis y que est() solo ocurre cuando elnervio facial ticne ya alguna writ parillisis. La idea deque se requicre de una paralisis facial preexistente paraque ocurra parillisis en Ia platisma derives del hecho deque no se ha reportado un solo caso (le paralisis aislada(le lit platisma. Los pacientes, independientemente deLt edad 0 de otros factores, pueden inducirse a contraerla platisma. Esto obvia la necesidad de las pruebaselectricas pant examinar una posible paralisis de Iaplatisma. Una platisma no funcional al examen clinic()es, de hecho, una platisma paralizada. Mientras queregularmente se hace el examen para lagoltalmos ycualquier paresis facial obvia es facilmente notada, lasformes nienos several de las paresias faciales sal()pueden distinguirse si el examen se hacc en forma di-rigida. El mecanismo poi - el cud] se afecta el nervio fa-cial en Ia lepra no estit Nen aclarado per() nuestros re-sultados stigieren (Inc la dispersiOn proximal de unalesiOn que council/a en his ranizts zigomtitico-temporaly alcanza el tronco ncrvioso del nervio facial, es etasprobable que la apariciiiii de novo de lesiones en otrasritinas perifericas del nervio facial. No se exluye Iaposibilidad de que la lesiOn primaria este dentro deltronco del nervio facial en todos los cases y que soloveamos las secuelas sigoinitticas debido a otros fac-tures secundarios.

RESUNIECette etude demontre que le platysma est parfois

paralyse dans Ia leprc, et que ceci survient quand lenerf facial a deja tine inure paralysie. Qu'il y ait hesoind'avoir one paralysie faciale avant qu'il puisse y avoirone paralysie platysma est fOrtement suggere par lefait qu'il n'y avail aucttn cas de paralysie isolec duplatysma. Des patients, quel que suit leur age ou d'autresfacteurs, pouvaient inviter tine contraction du platysma.Ceci montre le besoin d'un test electriquc pour re-chcrcher une paralysie du platysma. Ceci signifieegalement qu'un platysma non fonctionnel a l'examenclinique est, en fait, un platysma paralyse. Alors qu'onrecherche regulierement l'existence d'un lagophtal-mos, et que des paralysies faciales evidentes seront[tutees, des formes monis severes de paresie du musclefacial seront trouvees seulement si on les rechercheformellement.

Fe mecanisme par lequel le nerf facial est impliquedans la lepre West pas clarifie, mais nos observationssuggerent que la dissemination de proche en prochedune lesion qui a commence dans les branches zygo-matico-temporelles et atteint le tronc du nerf facialest plus vraisemhlahle que des nouvelles lesions sedeveloppant de novo dans d'autres branches Ile-ripheriques du nerf facial. II nest pas exclu que Ia le-sion primaire ne soil dans toils les cas dans le tronc dunerf facial, mais que 110(15 ne voyions les sequelles zy-gonizttiques frequentes que suite a des facteurs sec-ondaires.

Acknowledgment. We thank Dr. Alison Ander-son (statistician) for her hours of help in getting thedata onto a computer program (Epi-Info 6.1). We alsothank Dr. Franke Woepel for allowing us to use the fa-cilities of Green Pastures I lospital, and we thank allthe patients for their quiet endurance of us and our ex-amination of them.

REFERENCESI. At.Nor, J. L., AnoutAuvuit, J. and OfittRi.iN, C.

Traumatic lesions of the spinal accessory nerve. II.Clinical study and results of a series of 25 cases.Rev. Chir. Orthop. Reparatrice Appar. Mot. 80( 1994) 297-304.

2. ANTIA, N. II.. DIVEKAR, S. C. and DAsTuR, D. K.The facial nerve in leprosy. I. Clinical and opera-tive aspects. Int. J. Lepr. 34 (1966) 103-117.

3. CHAco, J., MmioRA, A., ZAUBERNIAN, II. and LAN-

DAU, Y. An electromyographic study of lagoph-thalmos in leprosy. Int. J. Lepr. 36 (1968)288-295.

4. CounRiGirr, P. I). Defining the magnitude of oc-ular complications from leprosy: problems ofmethodology. Int. J. Lepr. 56 (1988) 566-573.

5. CRAWFORD, C. E., EvAsis, D. H. L. and EVANS, E.M. Experimental neuritis induced by sensorynerve myelin may provide a model for non-lepro-matous leprosy. Nature 251 (1974) 223-225.

6. CRAwFoRD, C. L. and Mims, M. J. Why is thecervical branch of the facial nerve not enlarged inleprosy'? J. Anat. 184 (1994) 188.

7. DASTUR, D. K. Pathology and pathogenesis ofpredilective sites of nerve damage in leprous neu-ritis. Neurosurg. Rev. 6 (1983) 139-152.

8. DAsTuR, I). K., ANTIA, N. II. and DivEKAR, S. C.The facial nerve in leprosy. 2. Pathology, patho-genesis, electromyography and clinical correla-tions. Int. J. Lepr. 34 (1966) 118-138.

9. DoNNrk, T. R. and KLINE, I). G. Extracranialspinal accessory nerve injury. Neurosurgery 32(1993) 907-910.

10. FARRAGIINR, D. Trophic electrical stimulation forhuman muscle in chronic traumatic facial paraly-sis. Clin. Rehab. 1 (1987) 366-370.FARRAGIIER, 1)., KIDD, G. L. and TALLis, R. Eu-trophic electrical stimulation for Bell's palsy. Clin.Rehab. 1 (1987) 265-271.

12. FORSTER, A. and PALASTANGA, N. Clayton Hee-

trotherapy. 8th edn. London: Bailliere Tindall,1981, pp. 70-76.

13. liotittwEG, M., UDAYA KIRAN, K. and SUNEETHA,

S. The significance of facial patches and type Ireaction for the development of facial nerve dam-age in leprosy; a retrospective study among 1226paucihacillary leprosy patients. Lepr. Rev. 62(1991) 143-149.

14. LUBBERS, W. J., SC:HIPPER, A., FloGEwat, M. andD0 Soi.DENHo00, R. Paralysis of facial muscles inleprosy patients with lagophthalmos. Int. J. Lepr.62 (1994) 220-224.

65, 2^Richard and Cor': Cervical Branch of Facial Nerve^177

15. LuitnEks, W. J., SciiiiTER, A., I lociEwEG, M. andto Sot.DENuotT, R. Eye disease in newly diag-nosed leprosy patients in eastern Nepal. Lepr. Rev.65 (1994) 231-238.

16. MAI -sums:, S., Slum, T., OtivAmx, M., SAKANrro,K. and •stikunixku, H. Inummohistochemicalstudy on temporal hone of autopsy cases with My-cobacterium leprae infection. Nippon JibiinokokaGakkai Kalil() 98 (1995) 1881-1886.

17. Mitxo, T. L., LiAlArrio:, C. and KINFt I, Y. Damageand regeneration of peripheral nerves in advancedtreated leprosy. Lancet 342 (1993) 521-525.

18. RANNLY, D. A. The prevalence and consequencesof mis-reinnervation in facial neuritis. Int. J. Lepr.42 (1974) 316-322.

19. Roclumr, R A., SinsuwAN, S. and Mrrxii, D. Le-sions of the facial and trigeminal nerve in leprosy-an evaluation of 43 cases. Int. J. Oral Stag. II(1982) 14-20.

20. SABIN, T. D., IlAcKETT, E. R. and BRAND, P. W.Temperatures along the course of certain nervesoften affected in lepromatous leprosy. Int. J. Lepr.42 (1974) 38-42.

21. SARIN, T. D. and Swill', T. R. Diseases of the Pe-ripheral Nervous System. 2nd edn. Philadelphia:W. 13. Saunders Co., 1994, pp. 1955-1987.

22. SCIIIPPER, A., Ltlinwits, W. J., HociEwtiG, M. andOn SOLDENIIDIT, R. Disabilities of hands, feet andeyes in newly diagnosed leprosy patients in east-ern Nepal. Lepr. Rev. 65 (1994) 239-247.

23. Scoo.ARD, I). M., LATtiRoP, G. W. and TRUMAN,R. W. Infection of distal peripheral nerves by Al./eprae in infected armadillos: an experimentalmodel of nerve involvement in leprosy. Int. J.Lepr. 64 (1996) 146-151.

24. SIIFTTY, V. P., ANTIA, N. H. and JA(otts, J. M.The pathology of early leprous neuropathy. J.Neurol. Sci. 88 (1988) 115-131.

25. SIIETTY, V. P., Mts -ritv, N. F. and ANTIA, N. II.Serum demyelinating factors and adjuvant like ac-tivity of M. /epnie; possible causes of early nervedamage in leprosy. Lepr. Rev. 57 (1985) 221-227.

26. TiutKor, E., "FANIRWEKAR, S., MANSUKIIANI, K.,Nlio.Fsl, H. and MAYR, N. Intraoperative spinalroot stimulation to detect most proximal site ofleprous ulnar neuritis. Lancet 343 (1994)1604-1605.

27. TuttKor, E., Txxinwo:AR, S., MANSUKHANI, K.,Mit.t.Esi, II. and MAytz, N. Intraoperativetroneurodiagnostics to detect a second granulomain the cuhital area of the median nerves affectedby leprosy: a new approach to prevent incompletesurgery. Int. J. Lepr. 63 (1995) 409-416.

28. UDAYA KIRAN, K., 110GEwtiG, M. and SUNEFTIIA,S. Treatment of recent facial nerve damage withlagoplithalmos, using a semistandard steroid regi-men. Lepr. Rev. 62 (1991) 150-154.

29. WILLIAM, P. L. Gray's Anatomy. 38th edn. Edin-burgh: Churchill Livingstone, 1995, pp.1243-1248.