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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 "pri- mary" 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 regenerat- ing 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 possi- bility must be taken into account. In facial paralysis, in the postparalytic hemifacial spasm, and in primary or cryptogenic hemifacial spasm, only the motor com- ponent 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 pro- duced 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 inter- ference 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 trigemi- nal 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.
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