HEMIFACIAL SPASNM by James N

HEMIFACIAL SPASNM BY James N. Greear, Jr., M.D.

HEN1MIFACIAL SPASAT is a condition of wvhiichi the most prominent objective evidence is irregtular, intermittent contractions of the Muscles suipplied by one of the facial nerves. Usually at the lheight of the attack all the muscles of one side of the face are eitlher in a clonic or sustained state of contraction. Irregularity in site, rhythm, and degree is the salient clharacteristic. Not onily is the disorder distressing to the patient; in its severe manifestations it can and muay le disabling. Except for the fact that only the motor division of the facial nerve is involved, many of the features of the affliction suggest that it is related to trigeimiinal neuiralgia. Hemifacial spasm lhas been recognized for centuries. Aretaeuis (i) described several different facial conditions, amnong whliicih vas palpebral spasm. Hall (2) was the first to give a detailed report of a case of hemifacial spasm; lhe pointed out that "It established a distinct diagnosis between a spasmodic condition, and a case, very similar in appearance, consisting of a paralysis of one side of the face. Ehni and WVoltman (3) have listed the followving clharacteristics as of iinportance in the recognition of primlary or cryptogenic lhemifacial spasnm: The spasms, whiclh occur only in adults, are of an intermittenit or twvitclhing natture, are usually unilateral, and, when bilateral, are not synchronous or e(qual in extent or severity. The eyelids on the lhomolateral side are almost alwvays involved. The patient feels no compuilsion to make the movement, is unable to stop it by exercise of the will, and cannot reproduce it volun- tarily. The spasms may persist in sleep. Psychiic tupsets of any sort, fatigue, and voluntary movements of the face exaggerate the spasms, which are limited to muscles innervated by the facial nerve. The condition does not resemble a tic, whliich is a hiabit spasm and usually involves muscles stipplied by several nerves. A tic 448 4Janes N. Greear, Jr. produces, in a perverted and exaggerated manner, a movement, or a group of movements, which has a useful basis in ordinary life. A tic may be partially or completely controlled by the will and ceases during sleep, whereas hemifacial spasm cannot be controlled and may persist during sleep. Hemifacial spasm may be the result of organic lesions of the central nervous system (4-7). It may follow recovery from facial paralysis. However, the great majority of cases are so-called "primary" or "cryptogenic hemifacial spasm." Differentiation between the postparalytic and cryptogenic forms may be difficult, and the history of a previous facial paralysis may be necessary to establish the diagnosis. Wartenberg (8), in his excellent work on the subject, has em- phasized the clinical similarity of the two. His conclusions are in agreement with those of Babinski, whom he quotes as follows: "I do not believe it is possible to establish a clear distinction between the primitive hemispasm and the hemispasm following facial paralysis." An approach to successful treatment of the disorder depends on knowledge of the neuroanatomy of the region and of the changes that occur in nerves undergoing degeneration and regeneration. The facial (seventh) nerve is mixed. The larger component is motor in function; the sensory and secretory fibers are in the smaller component. Chorobski and Penfield (9) have written: The autonomic efferent fibers so far described in the facial nerve leave the brain stem with the roots of that nerve to be distributed peripherally by two branches, the greater superficial petrosal and the chorda tympani nerve. In the chorda tympani, secretory fibers join the submaxillary, sublingual and certain accessory salivary glands of the tongue. The vasodilation fibers innervate the blood vessels of these glands and of the tongue. Secretory fibers enter the greater superficial petrosal nerve to supply the lacrimal gland. Vasodilation and secretory fibers pass through the nerve to supply the mucous membrane of the nose, upper pharynx, soft palate, roof of the mouth and upper lip. The facial nerve emerges from the lateral part of the caudal portion of the pons along with its sensory and secretory components (the nervus intermedius) and enters the internal acoustic meatus in company with the acoustic nerve. At the bottom of the meatus the nervus intermedius and the facial are incorporated and enter the facial canal. The sensory and secretory fibers enter the geniculate ganglion, from which some of Hemifacial Spasm 449 the fibers leave to form the greater superficial petrosal and others join the chorda tympani at a point above the stylomastoid foramen. Walsh (1o) has observed that intracranial involvement of the facial nerve is often associated with involvement of other nerves at the base, and such involvement is likely to be bilateral, while extracranial involvement of the facial nerve is likely to be unilateral. According to Ford and Woodhall (ii), it has been shown that after the severing of a peripheral fnerve the distal segment under- goes degenerative changes throughout its entire length. A few hours after section the distal ends of the axis cylinders of the proximal portion of the nerve begin to proliferate, and from three to six of these fine fibers may arise from each of the severed axons; these newly formed fibers follow the course of the degenerated distal portion of the nerve, even to its finest branches. They explain the mass movement, associated movements, and contractions of the face, which are invariably present in every case in which the facial nerve degenerates and subsequently regenerates, on the basis that nerve fibers which formerly supplied one muscle or a certain group of muscles may, in attempting to establish con- tinuity with the degenerated part of the nerve, enter other adjacent peripheral nerve trunks. As a result of multiplication of regenerating neurofibrils, a single axon may eventually supply two or more muscles. Therefore, the phenomena observed following recovery from facial paralysis which involved degeneration of the nerve would indicate misdirection of regenerating nerve fibers. As has been previously stated, there are no distinguishing features between primary or cryptogenic hemifacial spasm and postparalytic henmi- facial spasm. In the former, however, there is no possibility of regeneration of injured nerve fibers, while in the latter this possibility must be taken into account. In facial paralysis, in the postparalytic hemifacial spasm, and in primary or cryptogenic hemifacial spasm, only the motor component of the facial nerve is affected, usually completely, but sometimes partially. Therefore a lesion producing such changes in the function of the nerve must be assumed to be distal to the point at which the autonomic branches of the nerve leave the motor division. 450 james N. Greear, Jr. Gardner and Pinto (12) cite two articles by Granit, Leksell, and Skogland in vlhich it was showvn that an artificial synapse is produced in a mixed nerve by injury or pressure on the nerve. Thley found that this pressure mlay l)e so mild as not to produce interference vith normual nerve transmission; yet, due to loss of the instulating myelin slheath, a portion of the imnptulse may pass from an efferent to an afferent fiber. For instance, in catusalgia they believe that the efferent sympatlhetic imlpulse reaclhes a point of comupressioin of the nerve and juimps across to the naked axis cylinder of the pain fiber. Tlhus the efferent symlpatlhetic imptulse is converted into an afferent pain impulse. In 1952 Taarnlh0j (13) reported ten consectutive patients vith triaemiinal neuiralaia wvlio wvere treated by dividing the dtiral shleatl enclosing the sensory root of the Gasserian ganolion wvitlhout dividing the nerve itsell. This procedur-e afforded these patients relief fromn their tic dotulouLretux without resuiltant anesthesia of the face. lie wvas encoturaged to perform this operation becauise of the resuilt of removal of ani epiderm-loid from the cerebellopontine antgle o1 a thirty-one-year-old imaui, who was suifferino' fromll trigeminal neuiralgia. Follovinao the operation the patient wvas free from paim and retainedi normoal sensationi in the face. In considering the anatomy of the trigeminal root, Taarnll0j (13) decided that there was oine site wvhiere small changes in the tissuies couild give rise to compression of the root, i.e., in the part of the root that rtuns fromii thie ganlglion posteriorly, tlhrouiglh the narrow clhannel formiied by the dtira to the upper slharp mlargin of the petrouis bone. (Gar(dner and Pinto (i2) are of the opinion that tic douilotireuix can l)e explained by the cross-circtuitinc' of auito- nomn ic imnpuilses into somatic pain fibers. WVilliamiis, Lambert, anid \Voltmlan (14) disctussed the tvo lhy- potlheses that have been offered as to the cauise of hemnifacial spasmi of bothi the primary or cryptogenic and the postparalytic types. The first of these is that hem-ifacial spasmii is a central effect duLe eitlher to deo'eneration of cells in the Rolandic imotor cortex or to degeneration of cells in time facial nucleus in the medtulla. The seconid hypotlhesis offer-ed is that heinifacial spasm is a disorder of the lower imiotor neuiron. They reviewed the experimental wvork of Howve, Tower, and Dtuel, and concltuded that their experiments Hemifacial Spasm 451 would exclude central effects as the cause of the spasm or the synkinesis. However, these experimental data do not exclude the possibility that repeated discharge from the injured area of the nerve may be the cause of the spasm, or that fiber interaction in the injured area may account for synkinesis. On this basis one of them (Woltman) conjectured that the fundamental lesion in both hemifacial spasm and Bell's palsy might be a fibrous constriction of the sheath of the facial nerve somewvhere in its course through the temporal bone, but probably in close relationship to the stylomastoid foramen. Woltman, Williams, and Lambert (15) reported that they had observed edema, redness, and thickening of the nerve and sheath in the facial canal in so-called "refrigerative Bell's palsy" suffi- ciently often to justify the conclusion that this was the usual site of the lesion. They concluded that it was feasible to consider similar pathologic changes in cases of primary or cryptogenic hemifacial spasm. Therefore 9 patients were treated by surgical decompression of the facial nerve in its canal. One patient has remained free from hemifacial spasm. Another was free from symptoms for 21/4 years, and the remaining 7 had recurrence of symptoms at varying intervals after operation (16). They noted that following decompression of the facial nerve for relief of hemifacial spasm, the synkinesis or associated movements of the facial muscles disappeared. Such associated movements have been attributed to branching or misdirection of nerve fibers during regeneration, and thus it would appear that some other ex- planation for associated movements must be sought. The authors suggested that "crossfiring," or the excitation of fibers by impulses traveling over adjacent fibers, was a plausible deduction. The clinical experiences of Taarnh0j (13), and more recently of Gardner and associates (12), in tic douloureux lend support to this idea. Many of the earlier authors were of the opinion that the lesion producing hemifacial spasm was in the facial nucleus and the pons (17-21); others believed that it was a reflex phenomenotn (22, 23). More recently, however, the belief has been expressed that there is a fairly localized.lesion involving the motor division of the seventh nerve in the facial canal in the region of the stylomastoid foramen (14). 452 James N. Greear, Jr. Before Williams, Lambert, and Woltman (14) published their results, the only effective treatments were to produce either partial or complete paralysis of the facial nerve involved, or an anastomosis between another of the motor cranial nerves and the facial. Anas- tomosis between the spinal accessory and the facial was described by Abadie and Cuneo (24) in 1905. This method of treatment is still employed by some surgeons today. De Sp6ville (25) is said to have been the first to advise the treatment of blepharospasm by alcohol injections. Since his first report on this form of therapy, it has probably been more frequently employed in the treatment of hemifacial spasm than any other therapeutic measure. The sim- plicity and ease of carrying out this treatment make it a desirable office procedure, and it can be repeated as often as necessary to control the spasm of the facial muscles involved. In 1927 C. S. O'Brien (26) described a modification of the Van Lint procedure for producing temporary akinesia of the orbicularis oculi and accessory muscles of lid closure in ophthalmic surgery. The point of injection of the anesthetic agent was directly over the condyloid process of the mandible. By dissection it was found that this point was just anterior to the parotid plexus. If this injection is made about i cm. posterior to the area described by O'Brien it will include a good portion of the parotid plexus, which will embrace the branches of the facial nerve supplying all muscles from the frontals to the chin. The procedure which I have followed is to inject 1.5 c.c. of 2 percent procaine at this point and wait for five minutes, leaving the needle in place. If at the end of five minutes paralysis of the muscles of that side of the face has taken place, 1.5 to 2 C.C. of 95 percent alcohol is injected through the same needle. It is seldom necessary to repeat this procedure in order to produce paralysis of the muscles responsible for the most annoying symptoms-those near the corner of the mouth, the nasolabial fold, and the orbicularis oculi and frontals.

CASE REPORTS CASE 1. A seventy-year-old white man, whose general health had always been good, consulted me for examination of his eyes in January, 1945. He had no unusual symptoms but needed correction of refraction. Vision was essentially normal in both eyes, and his eyes were well co- Hemifacial Spasm 453 ordinated. In November, 1946, he complained that the left eyelids felt heavy and twitched on use, but no abnormalities were apparent at that time. On March 30, 1950, he reported that the left eye was twitching a great deal and scarcely could be kept open by the end of the day. He was unable to use his eyes continuously for more than 20 minutes because of the recurring attacks of spasm of all the facial muscles on the left side. The twitching and spasmodic contractions had begun in the left eyelid and during the course of several years had spread to involve most of that side of the face. He was not conscious that the spasm existed during sleep and had never been told, if it had been noted. He had consulted both ophthalmologists and neuro- surgeons, but none had offered any form of therapy for relief of his distressing symptoms. General physical examination at this time revealed no abnormality other than the hemifacial spasm. Intermittent irregular contractions of the left side of his face were more marked in the region of the left eye. The eyelids were almost completely closed during severe attacks, when the left nasolabial fold also was accentuated and the left corner of the mouth was retracted. On April 24, 1950, 0-5 c.c. of 2 percent novocain was injected in the region of the left parotid plexus and he was asked to sit and read for half an hour. He stated that he read with comfort for the first time in months. Later, an injection of alcohol given at the same point resulted in paralysis of most of the muscles supplying the face on the left side. This injection gave instant relief which lasted for eight months. With subsequent injections by one of my colleagues the relief became progressively shorter. In June, 1953, he was given an injection of alcohol into the facial nerve in the region of the stylomastoid foramen, and the spasm had not recurred in March, 1954. Following the alcohol injections a mild paralytic ectropion of the lower left lid developed-a complication which is more likely to occur in older people. CASE 2. A fifty-eight-year-old white woman consulted me on May 22, 1953, complaining of spasm of the right side of the face. A year before she had become aware of spasmodic twitching about the right eye and "her vision seemed to dance." After the symptoms had been present for six months she consulted a physician, who offered no relief. The spasms gradually became more severe, but hot packs applied to the right side of her face gave her transient relief. At the time that I first saw her she said that she was never free from the spasm, but that it did not interfere with sleep and that she slept well. It was always present in the morning, either on awakening or shortly thereafter. Such activity as reading made it worse. There had been no associated pain or interference with function, but because of her consciousness of the spasm she had tended to withdraw from social contact, Her history was otherwise essentially negative. A

u CASE 2 A. Near height of attack of spasm of right side of face. Note narrowing of palpebral fissure, retraction of right side of nose and corner of mouth, increase in nasolabial fold, and dimpling of cheek. B. Quiescent period between attacks. Note right nasolabial fold and dimpling of cheek. C. Appearance after injection of alcohol in region of parotid plexus. Hemifacial Spasm 455 The oIlyV abnormalities revealed on physical examination were the intermittent contractures of the facial muscles on the right, chiefly about the eye, aind( some twitching and retraction of the mouth to the right. Thesc maniifestations varied in intensity andl at times were absent for- several minuttes, but when attention wias drawn to them, either by examination or conversation, they were accentuated. There was no evi(lence of (lysfLunction of any of the other cranial nerves. At all times the pallpebral fissture on the right was slightly narrower than that on the left and( at the height of a severe attack the right fissure was completely close(l. The nasolabial fold oni the right was accentuatecd, especially (lutr-iing the attacks, whetn the right cornier of the mnouthl was drawni to the right ain(l the riglht platysma muscle was olviously cointracte(l (Fig. iA). Neurological examination was enitirely negaltive except for the (listtLirbalce in the right seventh cranial nerve. Vision was correcte(d to 2j0/20 in each eye, andlher eyes were well coordinatedl for both distant and near vision. Ophthalmoscopic examination did not reveal abnormalities of the fundus in either eye. Her periplheral fields of vision and intraocular pressure (Schiiitz) were normal. On July 1 1, 193, 2 c.c. of ninety-five l)ercent alcolhol were injected into the regioin ol the aanterior portion of the parotid l)lexus. A pre- ceding injection of i.- c.c. of 2 percent lprocaine had pro(luced cessa- tion of all spasmodic contractionis. She was last seen one week later and welcomed the freedom from the f'acial spasm, even though it involved an exclhanige for p)aralysis of the muscles of the right side of her face. Slhe was lhear-d from in Mlarchl, 1954, eight montlhs later, and she stated that lher con(litioni was unchanged sinice treatmeilt. While it is agreed that any procedture that prodtuces paralysis of the facial nerve is undesirable, the patient wvlho lhas suiffered fromi hemifacial spasm for any lengtlh of timne seems to consider the paralysis a far miore acceptable state than the severe spasms. A second disadvantage of alcolhol injection tlherapy is that it mtlst be repeated at intervals of fronm six to eighlt imontlhs, and, in somne instances, at progressively slhorter intervals. To obtain imiore permnanent relief, Colemian tried sectioning and immediate restuttiring of the uipper branclhes of the facial nerve, buit after reoeneration of the nerve fibers the spasms recurred. HIe wvas of the opinion that anastonmosis betwveen the spinal accessory and the facial, or thie hypoglossal and the facial, was the method of choice in severe cases. Recently Gordon (27) recom- miiended partial section and ligation of uipper branches of the facial nerve. Thiis procedure does not prodtuce complete paralysis, and it does relieve the spasm to a great extent. Spurling (28) has lhad 456 James N. Greear, Jr. some satisfactory results with a method that involves crushing the facial nerve just at its exit from the stylomastoid foramen. If the spasm recurs after the traumatized nerve regenerates, he performs a facial glossopharyngeal anastomosis. Decompression of the facial nerve in the lower portion of the facial canal, as outlined by Williams (14), has been used with success by Lathrop (29) in two cases. In resistant cases Schwartz (30) is of the opinion that at present partial section is the procedure of choice. Because in so many instances hemifacial spasm has recurred when the nerves regenerate after surgical procedures, alcohol injections, as long as they are effective, offer a simple method of giving relief to the patient. SUMMARY The two cases of primary or cryptogenic hemifacial spasm reported here were treated by injection of alcohol in the region of the parotid plexus. In reviewing the literature one is impressed with the present tendency to regard this malady as the result of a lesion of the seventh cranial nerve in the facial canal, most probably in the region of the stylomastoid foramen. The treatment of this distressing disorder is still not definitely established. Alcohol injection in the region of the parotid plexus, however, is a simple office procedure and can be repeated as often as necessary to relieve hemifacial spasms of more severe degree. Therefore I can see no objection to its being employed until a more permanent cure has been developed. Partial section of the upper branches of the facial nerve, followed by ligation of the sectioned portion to prevent regeneration, may prove to be a more permanent form of therapy. Alcohol injection, like the other methods of treatment currently in general use, makes no attempt to attack the problem at its source. The work of Woltman, Lam- bert, and Williams impresses one as being a definite step in the right direction. REFERENCES 1. Aretaeus (C.A.D. 200), cited in C. C. Mettler, History of Medicine. Philadelphia, Blakiston, 1947, p. 511. 2. Hall, M., A case of permanent spasmodic contraction of the muscles of one side of the face, Edinburgh M. & S. J., 13:63-64, 1817. 3. Ehni, G., and H. W. Woltman, Hemifacial spasm; review of io6 cases, Arch. Neurol. & Psychiat., 53:205-211, 1945. Hemifacial Spasm 457 4. Campbell, E. H., and C. Keedy, Hemifacial spasnm; etiology in 2 cases (basilar aneurysm), J. Neurosurg., 4:342-347, 1947. 5. Cushing, H., On convulsive spasm of the face produced by cerebellopontine tumors, J. Nerv. & Ment. Dis., 44:312-321, 19i6. 6. Laine, E., Hemispasme facial gu6ri par intervention sur la fosse post6rieure, Rev. Neurol., 80:38-40, 1948. 7. Sicard, J. A., and V. Bollack, L'hemispasme facial d'origine corticale cerebrale, Rev. Neurol., 24:742-743, 1912. 8. WVartenberg, R., Hemifacial Spasm: A Clinical and Pathophysiological Study. New York, Oxford University Press, 1952. 9. Chorobski, J., and W. Penfield, Cerebral vasodilator nerves and their pathway from medulla obloiigata, with observations on pial and intracerebral vascular plexus, Arch. Neurol. & Psychiat., 28:1257-1289, 1932. to. WValsh, F. B., Clinical Neuro-Ophthalmology. Baltimore, Williams and Wilkins, 1947. ii. Ford, F. R., and B. Woodhall, Phenomena due to misdirection of regeneration fibers of cranial, spinal and autonomic nerves: clinical observation, Arch. Surg., 36:480-496, 1938. 12. Gardner, W. J., and J. P. Pinto, The Taarnh0j operation: relief of trigeminal neuralgia without numbness, Cleveland Clinical Quarterly, 20:364-367, 1953. 13. Taarnh0j, Palle, Decompression of trigeminal root and the posterior part of ganglion as treatment in trigeminal neuralgia; preliminary communication, J. Neurosurg., 9:288-290, 1952. 14. Williams, H. L., E. H. Lambert, and H. W. Woltman, The problem of synkinesis and contracture in cases of hemifacial spasm and Bell's palsy, Ann. Otol., Rhin. & Laryng., 61:850-872, 1952. 15. Woltman, H. W., H. L. Williams, and E. H. Lambert, Attempt to relieve hemifacial spasm by neurolysis of facial nerves; report of two cases of hemifacial spasni with reflections on nature of the spasm, the contracture and mass movement, Proc. Staff. Meet., Mayo Clin., 26:236-240, 1951. i6. WVoltman, H. WV. (Mayo Clinic). Personal communication. 17. Buzzard, E. F., Varieties of facial spasm and their treatment, Practitioner, 91:745-754, 1913- i8. Babinski, J., Hemispasme facial peripherique, N. iconog. de la Salpetriere, Par., 18:419-423, 1905. 19. Wartenberg, R., Associated movements in the oculomotor and facial muscles, Arch. Neurol. & Psychiat., 55:439-488, 1946. 20. Dana, C. L., Textbook of Nervous Diseases. joth ed., New York, William Wood & Co., 1925, p. 119. 21. Russell, J. S. R., Facial spasm, in: C. Allbut and H. D. Rolleston, A System of Medicine, ed. 2., London, Macmillan & Co., 1919, v.8, p. 638. 22. Alajouanine, T., and R. Thuriel, Les spasmes de la face et leur traitement. Paris, Masson, 1936. 23. Urechia, C. I., and Mme. Retezeanu, Hemispasme facial apres tine plaie du nez, Rev. Neurol., 65:427-429, 1936. 24. Abadie, C., and Ctin6o, Traitement du blepharospasme grave par l'anastomose spino-faciale, Arch. d'opht., 25:201-215, 1905. 25. de Sp6ville, Deux cas de blepharospasme, gu6ris par deux proc6d6s differents, Clin. ophth., Paris, 12:131, 1906. 26. O'Brien, C. S., Local anesthesia in ophthalmic surgery, Tr. Am. M. Assn., Sect. Ophth., 1927, pp. 237-253. 27. Gordon, D. M., Hemifacial spasm; 2 cases, Arch. Ophth., 37:282-293, 1947. 28. Spurling, R. G. (Louisville, Ky.). Personal communication. 29. Lathrop, F. D. (Lahey Clinic, Boston, Mlass.). Personal communication. 458 4amnes N. Greear, Jr. 30. Schwartz, H. G. (WAV\shington University School of Medicine, St. Louis, Mo.). Personal commutnication. DISCUSSION DR. DONALD J LYL. 1\yM impression- is that hiemifacial spasm is an irritative lesion of the facial nerve; if the lesioni is more severe, B3ell's palsy or intranuclear facial paralysis is prodtuced. Hemifacial spasms are caused by a number of lesions of various types: inflammation, vascular disturbances, neoplasm, trauma, and, with regeneration, sometimes posttraumatic causes when axons are misdirected or miscarried. The regeneration is lpoorly distributted or aberrantly distributed. Oc- casionally tlhesc conditionis are found iIn syphilis and multiple sclerosis. These factors shouldI be investigated, as well as the possibility of fun11c- tional distturbainces, whiclh are usually bilateral, whereas the organic disturbance of hemifacial spasm is unilateral. Psychiatrists and neu- rologists are of the opinion that most of the cases are psychogenic, and they do not believe that there is a definite organic background. Brain stem and cerebral causes of hemifacial spasm are rare. Some- times they are founld in the apraxic types. The site of the lesion producinig hemifacial spasm, as Dr. Greear stated, appears to be leriplheral in by far the majority of cases. Dr. Greear's outlinie of treatmeint is, I am sure, the most advanced procedure at the preseint time. The patient miiust exchange spasm for paralysis, whicli he uistually is willinig to (1o. An irritative lesion is replaced by a paralytic on1e. Furtl-her knowledge of the catuse, type, and location of the lesion may result in iilproved treatment. I would like to mention two things: First, we have found ectropion very frequently is produced by spasnm of the orbicularis, and with it the eyelashes turn in and sometimes secondary infection is produced. This must be gtuarded against, so that in severc cases we do a tarsor- raphy, so that the cornea and vision are savedI. The second thing is: We are using cortisone when wc feel the facial nerve is swollen, and we have hadl some fairly good results in cases where the nerve is in- flamed. XVe have used cortisone systemically. We anticipate possibly injectiing cortisone into the stylomastoid canal. DR. WALTER F. DIJGGAN. I shlouldl like to menition one case of hemifacial spasm in a womnan in lher forties. I gave her several O'Brien injections at intervals and( tried to inject low (lown on the jaw. She also received quininc. Slhe was improved enough so that she refused to have any surgery. This was not a total cure by any means, but the spasms were less marked and less frequent, and she is leading a rela- tively comfortable life. I just wanted to mention that the O'Brien injections will lprodluce relief, thouglh not a total cure. I was delighted to hear Dr. Greear's presentationi, because this is an uncommon con- (lition, and it is a l)roblel1l as to wvhat to (1o to help these patients.