Journal ofNeurology, Neurosurgery, andPsychiatry, 1978, 41, 829-833

Hemifacial spasm: treatment by posterior fossasurgery

G. C. A. FABINYI AND C. B. T. ADAMS

From the Department of Neurosurgery, Radcliffe Infirmary, Oxford

S U M MARY Nine cases of hemifacial spasm have been treated by posterior fossa explorationwithout mortality or significant morbidity. In only three was definite pathology found, but thehemifacial spasm was abolished in eight patients and markedly diminished in the remainingpatient. The condition has recurred in one patient. Microsurgical techniques make the operationsafe and accurate. We suggest that this procedure is the best approach for hemifacial spasmrequiring treatment. Where no definite pathology is found, the effectiveness of the procedure isprobably due to fibrosis and hence mild trauma to the facial nerve induced by the spongewrapped around the nerve.

Hemifacial spasm is a distressing, common, andwell-defined condition which is difficult to treat.It is an involuntary unilateral spasm of the musclessupplied by the facial nerve and is intermittent andusually worsened by fatigue or emotional upsets.It most often occurs in middle-aged women andtends to be gradually progressive in both intensityand frequency of attacks, although in some casesremissions of varying times may be seen. With thisprogression there is an associated mild weakness ofthe facial muscles, but the condition itself is rarelyassociated with other neurological disorders. Itmay be seen with trigeminal neuralgia (Campbelland Keedy, 1947), and the combination of tri-geminal neuralgia and facial hemispasm is some-times called tic convulsif (Cushing, 1920). Hemi-facial spasm should be differentiated from facialmyokymia (Matthews, 1966) and other nervoustics or abnormal facial movements which havebeen described and classified (Harrison, 1976) butdo not resemble true hemifacial spasm, which isquite characteristic.The difficulty in treating hemifacial spasm is

reflected in the many surgical approaches (Scoville,1969b; Potter, 1972; Harrison, 1976) described todeal with it. As yet no simple operation or medi-cation has been devised that will relieve the dis-tressing spasm without the penalty of facial weak-ness or possible return of the spasm after a varyinglength of time.Address for reprint requests: Mr C. B. T. Adams, Department ofNeurosurgery, Radcliffe Infirmary, Oxford OX2 6HE.Accepted 30 March 1978

Patients and methods

In the last two years we have treated nine patients,seven females and two males. The ages rangedfrom 40-76 years with a mean of 54 years. In eachcase the diagnosis has been made on clinicalgrounds. Tomography of the petrous bones wasperformed in the first six patients but no caseshowed any abnormality. In one case a computertomograph scan was performed in a patient withboth trigeminal neuralgia and hemifacial spasmwho was shown to have a meningioma of thepetrous bone (Fig. 1). We have not used electro-myography in the diagnosis or assessment of thesepatients. In four cases previous surgery on theperipheral facial nerve had been performed. Thiswas with success of varying duration, but in eachcase the spasm returned to its initial severity. Twopatients had had snaring of the facial nerve bywire at the stylomastoid foramen while two hadhad partial extracranial division of this nerve.

OPERATIVE TECHNIQUEThe operative approach was via a small suboc-cipital craniectomy through a curved retromastoidskin incision. Bony removal was extended to theangle between the sigmoid and transverse sinuses.The dura mater was opened in a cruciate fashion,the cerebellum exposed to reveal the subarachnoidcistern which was opened, and CSF sucked out.The cerebellum was gently retracted, although inolder patients it hardly required any retraction.The eighth nerve was identified passing to the

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(causing an obvious groove in the nerve when theartery was separated from the nerve) or splittingthe nerve.Where there was no evidence of any pathology

the seventh nerve was dissected free and a smalltriangular piece of nonabsorbable (Ivalon) spongewas introduced between the eighth and seventhnerves and then wrapped around the seventhnerve. After haemostasis a tight dural closurewas performed and the wound closed with multiplelayers of silk.A possible cause was found in three cases. In

one case a small branch of the anterior inferiorcerebellar artery was found splitting the facialnerve into two unequal parts. This was treated bydivision of the smaller bundle of nerve fibres andseparation of the artery away from the remainingnerve (Fig. 2). The patient with trigeminal neur-algia and hemifacial spasm, caused by a menin-gioma arising from the apex of the petrous bone,was treated by removal of the tumour alone. Aprominent vertebral artery impinged on the nervein the third case and a piece of sponge was inter-posed between the nerve and vessel. The averageoperating time has been one to two hours and ineach case has been performed under generalanaesthesia. We consider the operative microscopean essential adjunct to the safe and accurate per-formance of this procedure.

Results (Table)

Fig. 1 CT scan to show meningioma arising from theright cerebellopontine angle.

internal acoustic meatus. The arachnoid mater was

cut around this, and the seventh nerve and nervous

intermedius exposed by gently retracting theeighth nerve. The flocculus of cerebellum was re-

tracted to reveal the choroid plexus of the foramenof Luschka and the vein of the lateral recesspassing immediately behind the eighth nerve as

it entered the brainstem. Note was taken of thearteries in relation to the seventh and eighthnerves. These were very variable but were usuallythe anterior inferior cerebellar artery and itsbranches but occasionally the vertebral arteryitself or the posterior inferior cerebellar arterylooped against these nerves. Vessels-arteries or

veins-frequently lay against the seventh nerve butwere not considered pathological unless indenting

Most patients left hospital by the tenth post-operative day. There was no mortality. Morbiditywas due to damage of the seventh and eighthnerves except in the patient with a petrous menin-gioma (age 76 years) who had transient postopera-tive confusion. Partial deafness was seen in fivepatients. In one patient the deafness alreadyexisted and was unchanged after operation. Innone of the other four was it of clinical signifi-cance. A temporary conductive deafness occurredin three of these four, probably because of smallamounts of blood entering the middle ear viamastoid air cells. A nerve deafness and vertigowas a transient problem in one patient, and an-other patient had postoperative vomiting for fivedays. There has been no episode of CSF leakagevia the wound or middle ear. Facial weakness waspresent in two patients before operation and in theone with severe preoperative weakness it wasworse afterwards. Temporary mild weaknessoccurred after operation in one other patient.

Follow-up of these patients has extended fromthree to 22 months. In each case there has beendiminution of the hemifacial spasm. On two oc-

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Hemifacial spasm: treatment by posterior fossa surgery

Table Summary of findings in nine cases of hemifacial spasm treated by posterior fossa exploration

Patient Unit Age Sex Date of Operativefindings Complications Resultnumber number (yr) operation

1 39078 57 F 11/2/76 Prominent vertebral artery Temporary vertigo and No spasmcompressing facial nerve minimal facial weakness

2 39143 76 F 29/3/76 No apparent abnormality Increased pre-existing No spasmfacial weakness, mildnerve deafness (temporary)

3 37476 55 F 12/4/76 No apparent abnormality None Immediate relief-mild asymptomaticspasm returned after18 months

4 37943 38 M 14/9/76 Artery found splitting None Spasm ceasedfacial nerve completely after

several weeks-hasnot recurred

5 39976 41 F 30/11/76 No apparent abnormality Temporary mild No spasmconductive deafness

6 38339 40 F 12/5/76 No apparent abnormality Temporary mild Spasm ceased afterconductive deafness several weeks

7 40815 42 F 1/8/77 No apparent abnormality Temporary nausea and mild Occasional spasm-conductive deafness "80% improvement"

8 36685 59 F 8/8/77 No apparent abnormality None No spasm9 40859 76 M 11/8/77 Meningioma of petrous Temporary confusion. Both spasm and

temporal compressing Preoperative partial trigeminaltrigeminal and facial nerves nerve deafness unchanged neuralgia relieved

casions the spasm has taken up to four weeks afteroperation to disappear but in four patients therelief was immediate and complete. In one casethere has been recurrence of occasional twitchingsome 18 months after operation but this is notparticularly worrisome to the patient. Anotherpatient still experiences mild twitching threemonths after operation but is no longer embar-rassed by it. There has been no difference in theresults between those patients with pathologyand those in whom there were no apparentabnormalities.

Discussion

The cause of hemifacial spasm is disputed. Rarecauses such as facial neurinomas, cerebello-pontine angle tumours, basilar impression, andvarious vascular lesions, such as a basilar arteryaneurysm or redundant arterial loops, have beendescribed in association with hemifacial spasm(Ehni and Woltman 1945). It is probable that thebenign nature of this condition has discouragedmany clinicians from extensive or invasive neuro-radiological procedures. The treatment is alsoproblematical. Until recently the treatment hasbeen deliberately to traumatise the peripheral partof the facial nerve. Alcohol injection, partial nervesection, or facio-hypoglossal or facio-accessoryanastomoses have all been recommended (Harri-son, 1976). These procedures all produce a pro-found, if temporary, facial weakness. As the facialweakness recovers, usually after 12-24 months,the spasm often recurs. Our experience with partial

nerve section at the stylomastoid foramen has beenextremely unsatisfactory for these reasons, andmade us consider exploration of the posteriorfossa.Whether this nonlethal and, to some, trivial

condition should be treated at all is a matter forjudgment. Only the patient can say if the social orprofessional embarrassment of the conditionwarrants surgical intervention, although the fre-quent eye closure during car driving may be animportant factor in deciding whether or not to askfor treatment. Clearly the effectiveness, safety, andside effects of any treatment need to be consideredwhen making a decision.The first series of cases treated by posterior

fossa exploration was described by Gardner andSava (1962) who found 14 of 19 patients hadcompression of the facial nerve by either anarteriovenous malformation, a cirsoid aneurysmof the basilar artery, or a redundant anterior in-ferior cerebellar artery or internal auditory artery.Others have shown that when the facial nerve isexplored in its intracranial part, compressing vas-cular structures appeared in a consistently highpercentage of patients, (Neagoy and Dohn, 1974;Janetta et al., 1977; Petty and Southby, 1977).Janetta (1976) considers that compression distor-tion of the facial nerve at the brainstem, at thepoint where the myelin changes from oligoden-droglia to Schwann cells, is the cause of hemifacialspasm. What exactly constitutes a pathologicallyplaced vessel is open to varying interpretations(Morley, 1976).

Various complications have been reported after

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G. C. A. Fabinyi and C. B. T. Adams

Fig. 2 Lighth nerve retracted by the sucker to show the facial nerve split into two bythe anterior inferior cerebellar artery.

this operation (Scoville, 1969a; Janetta, 1976). Inparticular deafness of a varying degree is common,and it should certainly be explained to the patientbefore operation that such a complication is poss-ible. Contralateral deafness may be a contraindica-tion to this procedure.The results of the posterior fossa approach with

decompression of the facial nerve (usually byinterposing sponge or gelatin foam between it and

the offending vessel) have so far appeared excel-lent. Janetta reports excellent to good results in40 of 45 patients so treated, with follow-up extend-ing up to seven years (Janetta et al., 1977). It isknown that this condition has a tendency to recureven several years after nerve division or othersurgery. For this reason long-term studies will beneeded to ascertain definitively the place ofposterior fossa exploration. Previous authors have

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Hemifacial spasm: treatment by posterior fossa surgery

suggested that the good effect of the operation isdue to the separation of the compressing vesselfrom the nerve by interposing a prosthesis ofsponge or gelatin foam. However, in most of our

cases, although we could see vessels near the facialnerve, we could not convince ourselves that theywere pathological. In such cases the operation was

just as effective, and we suggest that where com-pression is of doubtful significance, the relief ofspasm is brought about by a mild degree of traumato the nerve at its exit from the brainstem by thefibrosis induced by the nonabsorbable sponge. Thedelay in complete abolition of the spasm forseveral weeks, which was noted in two patients,supports the concept that it is the fibrosis aroundthe nerve that produces the cessation of spasm.

We thank various neurological colleagues for en-

trusting their patients to us.

References

Campbell, E., and Keedy, C. (1947). Hemifacial spasm:

a note on the aetiology in two cases. Journal ofNeurosurgery, 4, 342-347.

Cushing, H. (1920). The major trigeminal neuralgiasand their surgical treatment based on experienceswith three hundred and thirty-two gasserian opera-

tions. A merican Journal of Medical Science, 160,157-184.

Ehni, G., and Woltman, H. W. (1945). Hemifacialspasm. Review of one hundred and six cases.

Archives of Neurology and Psychiatry, 53, 205-211.Gardner, W. J., and Sava, G. A. (1962). Hemifacialspasm-a reversible pathophysiologic state. Journalof Neurosurgery, 19, 240-247.

Harrison, M. S. (1976). The facial tics. Journal ofLaryngology and Otology, 90, 561-570.

Janetta, P. J. (1976). Vascular compression of thefacial nerve at the brainstem in hemifacial spasm:treatment by microsurgical decompression. InCurrent Controversies in Neurosurgery. Edited byT. P. Morley. W. B. Saunders: Philadelphia.

Janetta, P. J., Abbasy, M., Maroon, J. C., Ramos,F. M., and Albir, M. S. (1977). Aetiology anddefinitive microsurgical treatment of hemifacialspasm. Journal of Neurosurgery, 47, 321-328.

Matthews, W. B. (1966). Facial myokymia. Journalof Neurology, Neurosurgery, and Psychiatry, 29,35-39.

Morley, T. P. (1976). Introduction to article byJanetta, P. J. In Current Controversies in Neuro-surgery. Edited by T. P. Morley. W. B. Saunders,:Philadelphia.

Neagoy, D. R., and Dohn, D. F. (1974). Hemifacialspasm secondary to vascular compression of thefacial nerve. Cleveland Clinic Quarterly, 41, 205-214.

Petty, P. G., and Southby, R. (1977). Vascular com-pression of lower cranial nerves: observationsusing microsurgery, with particular reference totrigeminal neuralgia. Australian and New ZealandJournal of Surgery, 47, 314-320.

Potter, J. (1972). The surgical treatment of hemifacialspasm. Journal of Laryngology and Otology, 86,889-892.

Scoville, W. B. (1969a). Hearing loss following ex-ploration of the cerebello-pontine angle in thetreatment of hemifacial spasm. Journal of Neuro-surgery, 31, 47-49.

Scoville, W. B. (1969b). Partial extracranial section ofthe seventh nerve for hemifacial spasm. Journal ofNeurosurgery, 31, 106-108.

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