Prevention of Denervation in Bell's Palsy

Prevention of Delayed Traumatic Facial Palsy

“…Neither the severity of the head injury, as judged by the length of posttraumatic amnesia, nor that of the associated injuries seems to have altered the expected incidence of this complication. These findings are in keeping with those of Taverner et al (1966) that, whereas cortisone had no influence on the course of Bell's palsy, corticotrophin significantly reduced the incidence of total denervation. Despite this demonstration of the effectiveness of corticotrophin in reducing the incidence of delayed posttraumatic facial weakness, we are not convinced that such prophylactic treatment need always be adopted as routine practice; for it is not entirely innocuous.…”

“…When Taverner et al (1966) succeeded in reducing the incidence of denervation and increasing the recovery from Bell's palsy by treatment with corticotrophin, we were stimulated to examine the possibility that this form of treatment might also be of value in preventing delayed posttraumatic facial weakness. Indeed, the incidence of this complication in susceptible patients has been reduced from 38-5 to 8%, and there seems to be no doubt therefore that the eight-day course of corticotrophin which we describe does offer considerable protection against delayed traumatic facial palsy.…”

Comparison of Corticotrophin and Prednisolone in Treatment of Idiopathic Facial Paralysis (Bell's Palsy)

“…Evidence has previously been presented that daily injections of corticotrophin significantly reduce the overall incidence both of denervation and of severe degrees of denervation carrying permanent disability in Bell's palsy (Taverner et al, 1966). It has sometimes been claimed that corticotrophin is more effective than oral steroid therapy in the treatment of inflammatory neurological disorders (Jonsson et al, 1951;Ross et al, 1958;Miller et al, 1961) but firm supporting evidence is lacking.…”

Facial paralysis.

“…Some such enthusiasm may of course be a spontaneous manifestation of that innate physical energy and joie de vivre that so often distinguishes the surgeon from his more debilitated medical colleagues. On the other hand, I do not find it easy to dissociate the repeated and urgent pleas that reverberate through the American literature describing Bell Russell (1960) and Brodie Hughes (1964) Dr. Taverner has been a pioneer in this field (Taverner, 1959 ;Langworth and Taverner, 1963 Recalling similarly graphic descriptions of the operative appearances of the sciatic nerve in syndromes which we now know to have had their origin at a much higher level from disc prolapse, the physician may be pardoned an unworthy suspicion that the surgeon who describes the swollen and congested facial nerve observed at operation for decompression is less likely to be familiar with the appearance of the entirely normal nerve under similar circumstances. He may even have some reservations about statements that the histopathological findings encountered in the very rare cases that have come to necropsy favour an ischaemic rather than an inflammatory pathogenesis, or that swelling of the nerve within its sheath is more significant than compression by the bony canal.…”