location of the extracranial extent of leprous facial-nerve pathology may allow leprous facial palsy...

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INVITED COMMENTARY Location of the extracranial extent of leprous facial-nerve pathology may allow leprous facial palsy to be reanimated by free muscle transfer This paper investigates the position of lepromatous damage to the facial nerve between the brain and the muscle end plates. The temporozygomatic branch of the facial nerve is most commonly involved, leading to lagophthalmos, exposure keratitis and blindness. Should the buccal branch be involved, however, then the ability to show facial expression will be forfeited. Facial muscles paralysed for over 18 months are unlikely to recover and will need replacement. The author confirms that there is no damage to the proximal facial nerve in the skull, certainly as far as the middle ear, and that involvement within the stylomastoid canal is subclinical. He shows in biopsies of the facial nerve prior to its bifur- cation that myelinated and unmyelinated fibres are pre- sent in sufficient numbers to innervate a muscle graft. The presence of unmyelinated fibres is, nevertheless, a concern, and the suggestion is that their presence relates to probable oedema and compression within the canal, causing some axonotmesis. The latter can also be sup- ported by the quite common development of synkinesis on the contralateral unparalysed side. Axon counting of both myelinated and unmyelinated fibres under the elec- tron microscope would have been of interest at the point of nerve division and subsequent repair to the nerve – muscle graft. Having argued that the facial nerve is only minimally damaged in its proximal stump, the author quite correctly proceeds to the transfer of a muscle. The argument would have been convincingly proved if the muscle graft had worked, but unfortunately only static hold is achieved after 4 years and we are consequently left uncertain. Despite every test, be it electromyography or Doppler, one cannot be sure whether the failure of activity in the muscle is due to circulatory mishap or poor axonal migration. If the author is convinced of his argument then the muscle graft could be repeated quite satisfactorily. A more substantial series would further improve the balance of proof, and one does wonder why more were not attempted. Too much is made of ‘intelligent’ and ‘stupid’ muscles. Following a substantial number of various muscle transfers to achieve facial animation, there is no discernible difference in quality, and certainly it is not relevant to a spontaneous (responsive to emotion) smile. The author is to be congratulated on taking a problem, defining its pathology and devising a treatment plan; more needs to be attempted to follow in the path he has demonstrated. DOUGLAS HARRISON MBBS, FRCS 14 Queen Anne Street, London W1M 9LD, UK 20 British Journal of Plastic Surgery (2003), 56, 20 q 2003 The British Association of Plastics Surgeons. Published by Elsevier Science Ltd. All rights reserved. doi:10.1016/S0007-1226(03)00007-9

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Page 1: Location of the extracranial extent of leprous facial-nerve pathology may allow leprous facial palsy to be reanimated by free muscle transfer

INVITED COMMENTARY

Location of the extracranial extent of leprous facial-nerve pathology may allowleprous facial palsy to be reanimated by free muscle transfer

This paper investigates the position of lepromatousdamage to the facial nerve between the brain and themuscle end plates. The temporozygomatic branch of thefacial nerve is most commonly involved, leading tolagophthalmos, exposure keratitis and blindness. Shouldthe buccal branch be involved, however, then the abilityto show facial expression will be forfeited. Facialmuscles paralysed for over 18 months are unlikely torecover and will need replacement. The author confirmsthat there is no damage to the proximal facial nerve inthe skull, certainly as far as the middle ear, and thatinvolvement within the stylomastoid canal is subclinical.He shows in biopsies of the facial nerve prior to its bifur-cation that myelinated and unmyelinated fibres are pre-sent in sufficient numbers to innervate a muscle graft.The presence of unmyelinated fibres is, nevertheless, aconcern, and the suggestion is that their presence relatesto probable oedema and compression within the canal,causing some axonotmesis. The latter can also be sup-ported by the quite common development of synkinesison the contralateral unparalysed side. Axon counting ofboth myelinated and unmyelinated fibres under the elec-tron microscope would have been of interest at the pointof nerve division and subsequent repair to the nerve–muscle graft.

Having argued that the facial nerve is only minimallydamaged in its proximal stump, the author quite correctly

proceeds to the transfer of a muscle. The argumentwould have been convincingly proved if the musclegraft had worked, but unfortunately only static hold isachieved after 4 years and we are consequently leftuncertain. Despite every test, be it electromyography orDoppler, one cannot be sure whether the failure ofactivity in the muscle is due to circulatory mishap orpoor axonal migration.

If the author is convinced of his argument then themuscle graft could be repeated quite satisfactorily.

A more substantial series would further improve thebalance of proof, and one does wonder why more werenot attempted.

Too much is made of ‘intelligent’ and ‘stupid’muscles. Following a substantial number of variousmuscle transfers to achieve facial animation, there is nodiscernible difference in quality, and certainly it is notrelevant to a spontaneous (responsive to emotion) smile.

The author is to be congratulated on taking a problem,defining its pathology and devising a treatment plan;more needs to be attempted to follow in the path he hasdemonstrated.

DOUGLAS HARRISON MBBS, FRCS14 Queen Anne Street, London W1M 9LD, UK

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British Journal of Plastic Surgery (2003), 56, 20q 2003 The British Association of Plastics Surgeons. Published by Elsevier Science Ltd. All rights reserved.doi:10.1016/S0007-1226(03)00007-9