[Facial nerve injury in neurosurgery: a rehabilitation potential of botulinum therapy]. / Porazhenie litsevogo nerva pri neirokhirurgicheskikh operatsiiakh: reabilitatsionnyi potentsial botulinoterapii.

Surgical treatment of posterior cranial fossa and cerebellopontine angle tumors is associated with a risk of facial nerve dysfunction. The causes for facial muscle paresis include nerve compression by the tumor, destruction of the nerve structure by the tumor growing from nerve fibers, nerve injury during surgical removal of the tumor, etc. The first 3 months after facial nerve injury are a potential therapeutic window for the use of botulinum toxin type A (BTA). During this period, the drug is introduced both in the healthy side to improve the facial symmetry at rest and during mimetic movements and in the affected side to induce drug-induced ptosis. Post-paralytic syndrome develops 4-6 months after facial nerve injury. At this stage, administration of BTA is also an effective procedure; in this case, drug injections are performed on the affected side at small doses and symmetrically on the healthy side at doses doubling those for the affected side. BTA injections are mandatory in complex treatment of facial muscle paralysis.

[Botulotoxin type A (lantox) for inducing temporal ptosis in neurosurgical patients].

The aim of our study was to assess the effectiveness of the ptosis induced by injection of Lantox (botulotoxin type A) into levator muscle projection in neurosurgical patients with lagophthalmos and trophic keratitis. The study included 66 patients at the age from 11 to 67 years. Lantox dose used was 10-25 U. Ptosis appeared after 1-7 days. Complete induced ptosis developed in 1-17 days and remained within 6-150 days. Full induced eyelid ptosis developed in 44 patients. Incomplete ptosis was observed in 19 patients. Drug resistance was seen in 3 patients. Our study results demonsrated effectiveness of the induced ptosis: complete recourse of trophic keratitis at development was seen in patients with complete drug-induced ptosis and significant decrease of trophic keratitis was observed in patients with semi-ptosis.