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Trigeminal neuralgia
TRIGEMINAL TREATMENT
BP .2ND
NOVOCAIN A
NEURALGIA
INJECTION
DISCUSSION OF
W. K. LIVINGSTON, M.D.,
T
OF PAIN
THE
TRIGGER
Zoos,
SOURCES
PORTLAND,
ORE.
HE clinical picture of trigeminal neuralgia has been frequently described. Its surgical treatment is reasonably well standardized. It is known that a partial division of the posterior root of the fifth cranial nerve, properly done, will confer a permanent relief from pain. Differences of opinion among surgeons t,reating t,his syndrome exist as to t,he advisability and indications for alcohol injections of the peripheral divisions of this nerve, as a substitute for, or preliminary to, a sensory root se&ion. And there are differences of opinion as to the technique for carrying out the root, section. Dandy1 advocates a posterior approach in preference to the usual temporal approach to the sensory root, stating that he can thereby selectively divide the root close to the pons so as to abolish the pain and at the same time preserve much of the sensation of touch in the face. Stibbez has recently submitted evidence tending to support Dandy’s contention that the small fibers believed to conduct the pain are grouped together in the posterior portion of the root as it enters the pons. Smyth” has studied the relationship of fibers subserving different sensory functions in each part of the face, as they are distributed in the spinal trigeminal tract of the medulla, and SjiiyvisV has described a new operation involving a selective division of the trigeminal tracts within the brain which is designed to abolish pain without causin g an anesthesia in the cornea of the eye or loss of the sense of touch in the face. Walker” describes two cases treated by partial trigeminal tractotomy and his analysis of the changes in the sensory discrimination of these patients and two cases of thrombosis of the posterior inferior cerebellar artery, suggests that the spinal tract of the fifth nerve carries sensations of pain, heat, touch, deep pressure-pain, and to a slight degree touch. These are important and practical contributions which not only advance knowltrigeminal neuralgia but may be of assistance in settling edge regarding problems relating t,o other painful syndromes. But the problem of the origin of the pain in trigeminal neuralgia remains unxcttled. This problem is of fundamental importance to an understanding About this question of the etiology and treatment of this pain syndrome. hinges the principal controversy amon, 0~the clinical and research students of trigeminal neuralgia. I am inclined to favor a peripheral origin for the pain attacks and am of the opinion that an irritant focus at the periphery is capable a pathologic state of activity within the thalamus or other of inaugurating brain centers which assists in the creation of the complete clinical picture. This opinion is based on the observations reported in this paper. In four Cases which apparently represent idiopathic trigeminal neuralgia, the pain
l’rigewtinal
Neurulgia
571
attacks have been abolished by repeated injections of novocain into the trigger zones. The number of cases so treated is not sufficiently large to justify any final conclusions, but inasmuch as these observations may have some bearing on the problem of pain sources in this condition, it seems justifiable to present them. In addition it might be worth while t,o review briefly the onset and course of the pain syndrome, as well as the differential diagnosis, not in the orderly sequence necessary for establishing a textbook picture of this disease, but solely as they may relate to the question of the source of the pain. ONSET
AND
COURSE
Trigeminal neuralgia usually appears in middle life and afflicts males and females in about equal numbers. Its onset is of considerable interest and the detailed accounts of the onset and progress of the painful attacks by patients suffering from “idiopathic” trigeminal neuralgia suggest a peripheral origin for the pain. In the typical instance t,here is no antecedent history of illness or injury and no premonitory symptoms. The patient may be washing his fact when, with contact at a certain area in the face, there occurs a lancinating shock of pain, “as if an exposed nerve in a tooth had been touched.” The attack of pain is momentary and may not recur for a considerable interval. Close inspection of the face at the point from which the pain seemed to originate reveals nothing and the patient tends to forget about it. At a later date, and with equal suddenness, touching this same spot again precipitates the lancinating pain. As t,hc attacks tend to become more serere and frequent, the patient learns to associate this “trigger zone” with his pains and tries to avoid any form of contact, with this portion of his face. The commonest location of the trigger zone seerns to be in the distribut>ion of the maxillary division of the fifth nerve, often just lateral to the nasal ala, although it may occur anywhere on the face, and not infrequently as the syndrome progresses secondary trigger Remissions are known to occur, sometimes lasting for zones may develop. months or years, but, ordinarily the painful attacks become progressively worse and can occur in such rapid succession as to be almost continuous. The pain, which at first is confined to a small part of t,he face, perhaps one side of the upper lip, tends to spread over the distribution of one division of the fifth nerve and t,hen to involve one or both of the other divisions. It is unquestionably severe. It has been likened to an electric shock of great intensity, and no one seeing a patient during an attack and observing the facial grimace, the expression of frightened agony and almost breathless immobility, can doubt its severity. In the effort to avoid attacks many patients refuse to eat or talk, and withdraw from all activities and contacts that may bring on the pain. Others in a sort of desperation may deliberately precipitate a series of attacks so that in the short interval of freedom from pain that may follow, they are permitted to eat a few mouthfuls of food or talk with a degree of comfort. Many patients have submitted to one or more injections of alcohol into the peripheral divisions of the nerve, and it is of interest to note that the injection of alcohol into one division may confer relief from pain in the other This is particularly true when the injection divisions as well as the one injected.
572
W. K. Livingston
is made into the nerve division that was first involved in the painful attacks. As an example one might cite a case in which the maxillary division was first involved and later the pain had spread to the ophthalmic division. Because of the danger of cornea1 ulcer followin g an interruption of sensory impulses from the eye, the surgeon may be reluctant to inject alcohol into the ophthalmic division. But if a successful injection of the maxillary division is carried out all of the pain may disappear, not only that felt in the maxillary region, but in the ophthalmic area as well. A further point of interest relatin g to alcohol injections is the observation that following an injection, the relief of pain and the persistence of anesthesia in the face do not parallel one another. Immediately after an injection the zone of anesthesia may conform quite exactly to t,he known distribution of the injected division. Within a short time, often within two or three weeks, this zone becomes progressively smaller, and in some instances quite a normal sensation of touch and sensitivity to pain may return to the face, months or years before the painful attacks recur. It is quite apparent in instances of this kind that the nerve fibers have not been destroyed, but that the injection has merely interrupted for an interval their ability to conduct impulses from the periphery to the receiving centers. DTPFERESTIAL
DIAGNOSIS
In the medical literature dealing with trigeminal neuralgia considerable emphasis has been placed upon the necessity for distinguishing between “symptomatic” and “idiopathic” cases. Under the former term are grouped those eases in which a local focus of pathology is demonstrable, the removal of which may be followed by a disappearance of the painful attacks. The latter term does not deny the possibility of a peripheral origin for the pain, it merely indicates that the etiology is unknown. A careful search for local pathology is indicated in every case of facial pain, and this statement applies with equal force to the cases with typical paroxysmal trigeminal pain as to those with atypical attacks. Among the causes apparently responsible for the pain attacks, infection of the jaw or of the sinuses seems to be important. Harris6 points out the fact that the neuralgia usually begins in the maxillary or mandibular divisions, and believes that the syndrome is attributable to a “septic terminal neuritis in the terminal filaments in the jaws.” But other dental conditions in which infection is at least not obvious, may cause identical pains. A malocclusion, particularly the type in which the offending tooth is solidly fixed in dense rburnated bone, may give rise to paroxysmal pain, and its correction may be followed by a cure. It seems justifiable to say that these various local conditions can cause the syndrome because in many instances the removal of the irritant factor has been followed by a disappearance of the pain. Perhaps the most interesting of the local lesions giving rise to trigeminal pain is a ’ ’ myositis ’ ’ of the temporal or masseter muscles. Stookey’ observed twenty-two cases of this type in a five-year period. In this condition it may be possible to demonstrate a minute nodule in the muscle which is extremely sensitive to pressure. The muscle elsewhere may be stimulated without eliciting
Trigeminal
Neuralgia
573
a pain response, but if this discrete kernel is pressed upon, an excruciating pain is felt in the lip, in the temporal region, or over t,he distribution of one or more divisions of the fifth nerve. Although spontaneous pain attacks are less common in this affliction, paroxysmal pains may occur without any apparent local stimulation. In the severe cases due to a local area of myositis, the pains may be identical with those occurring in the idiopathic cases, even to the facial grimace. The tiny area of involved muscle may be difficult to find, particularly when it occurs in the anterior margin of the masseter muscle. But once identified, the condition may yield to appropriate treatment by baking and massage. The first few treatments may aggravate the pain, but in from two to six weeks the nodule disappears and simultaneously the pains leave and do not return. On the other hand, there are many surgeons who believe that the pain syndrome in the symptomatic cases is not identical with that of the “genuine” or idiopathic case. It is certainly true that one rarely encounters a case of trigeminal neuralgia of long standing in which teeth have not been sacrificed and sinuses repeatedly operated upon without being benefitted. Some observers insist that there is some essential difference in the type of pain, and therefore in the mechanism underlying the symptomatic and the idiopathic cases. Dandy1 believes that the source of irritation in major trigeminal neuralgia is always at the posterior root of the fifth nerve, and thinks that he can identify the cause in all of his cases as due to pressure from a tumor (5 per cent), an aneurysm of the basilar artery (5 per cent), or pressure from an artery (90 per cent). Concerning the pain he says, “A peripheral lesion along the sensory branch of Given a paroxysmal pain, it a nerve can never produce a paroxysmal pain. always means that the upper neuron that is between the ganglia of the nerve and the brain stem is affected, and it is only a lesion there that can do it.” I do not know what he means by the “upper neuron” in this quotation, nor do I believe that he is justified in making so flat an assertion regarding paroxysmal pain. Many instances of paroxysmal pain have been reported as cured by the elimination of a peripheral source of irritation. I am inclined to agree with Harris0 who says, in speaking of “symptomatic” types, “these cases differ in no respect from the so-called genuine or idiopathic paroxysmal trigeminal neuralgia, either in their type of pain, trigger zones, or results of treatment by alcohol injection or root section. ” A
“CENTRAL”
ORIGIN
FOR
PAIN
In spite of evidence that a peripheral lesion may cause paroxysmal attacks of pain indistinguishable from that of idiopathic trigeminal neuralgia, and the fact that an alcohol inject.ion of the primary divisions of the nerve can stop the pain, there is much to be said in favor of a central origin for the pain. Lewy and Grants have marshalled an impressive number of observations tending to support their contention that trigeminal neuralgia is a special form of the thalamic syndrome. The hyperpathia that develops in the classical type of the thalamic syndrome is attended by pain having a peculiarly unbearable quality (affective tone), it tends to radiate widely, has a high threshold and deficient localization
574
IV. K. Livingston
for stimuli, and is characterized by explosive reactions. The pain of trigeminal neuralgia has some of these same features, in particular the unbearable feeling tone and the tendency to explosive reaction. It seems to differ from thalamic pain in that stimuli are accurately localized and the pain confined to one or more divisions of the single nerve rather than radiating widely. However, Lewy and Grant were able to demonstrate that in 32 per cent of their cases the hyperpathia of trigeminal neuralgia was not confined to the face but extended over one side of the body. They were further able to show that in forty of their fifty cases there existed signs of pyramidal or extrapyramidal involvement. Their observations were interpreted as pointing toward a lesion in the region of the optic thalamus as a possible cause for trigeminal neuralgia. This assumption seemed to be confirmed by postmortem studies carried out on six cases. In all six the brain showed an atrophy of the ipsilateral hemisphere, a widening of the lateral ventricle, and foci of softening located either within the thalamic nuclei or in the thalamocortical tract. The pathology could be interpreted as accounting for a removal of the cortical inhibition, which, according to Head and Holmes,” acts to dampen the characteristic thalamic overresponse to pain sensation. This evidence would be more impressive if the brain pathology had been found on the side contralateral to the location of the pain. The fact that in five of their six cases in which the pain was unilateral the brain atrophy was most obvious on the ipsilateral side, suggests either that some unrecognized relationship exists between the thalamus and the face, or that the findings were incidental to the trigeminal neuralgia and not causal. “Why, if the pain is of central origin, should a blocking To the question, of peripheral portions of the nerve terminate the pain?” Lewy and Grant point out that the activity of the thalamus is dependent upon, or conditioned by, a constant influx of sensory impulses. With the cessation of such conditioning impulses the abnormal activity of the thalamus would no longer be apparent. Frazier, Lewy, and Rowe lo have reported a case which supports this interpretation. This woman suffered from intolerable pain over one side of the body and face, which was apparently due to a hemorrhage in the thalamic region. Her facial pain was relieved by blockin, 0 the fifth nerve and the hyperpathia of the side of the body was relieved by a chordotomy. But of all the arguments adduced by Lewy and Grant in favor of a central origin for the pain of trigeminal neuralgia, the one that impresses me most is t,he observation that the pain and sensory changes which they noted in their cases present features which can be explained only by implicating neurons in synaptic relation with one another. They say, ‘ ’ Summation and radiation, after-effect and hyperpathia, spat,ial and temporal amalgamation, and finally, complete transmutation of sensations characterize the physiopathologic pattern they imply that some of sensibility in trigeminal neuralgia. ’ ’ Furthermore, pathologic condition in the brain may cause a delay in discharge, so that with a recruitment of more pain impulses, there eventually occurs the augmented discharge so characteristic of the paroxysmal pain of trigeminal neuralgia and so similar to the “explosive pain reactions ” of the thalamic disease. Since all of these neurophysiologic activities are dependent upon an interaction between neurons in intimate synaptic relation with each other in some brain
l’rigentinnl
Neumlgin
center, Lewy and Grant conclude that the pain in t,rigeminal neuralgia must be of central origin. In actual fact, these observations merely imply that the internuncial activities in the brain center contribute to the pain picture in the fully developed case of trigeminal neuralgia. A peripherally situated irritative focus might initiate the abnormal activities developing in the thalamus or other central nervous system centers.” One other observation is frequently mentioned as supporting the view that the origin of the pain is central, i.e., the high incidence of trigeminal neuralgia in cases of disseminated sclerosis. Keith ROSS*~has reported fortyone cases in which the chronic spastic paraplegia was complicated by trigeminal tic. Harris6 has called attention to the fact that trigeminal neuralgia is bilateral in 17 per cent of the cases associated with multiple sclerosis and that it is bilateral in less than five per cent of other eases. This association between a disease characterized by obvious pathologic changes in the brain, and the pain syndrome of trigeminal neuralgia could be interpret,ed as favoring a brain lesion as the primary cause for the latter condition. On the other hand, it might be interpreted as Harris has done when he asserts that the sclerotic plaques merely heighten the irritability of the central neurons so that the pain syndrome would be more likely to develop secondary to some peripheral source for reiterated impulses of abnormal intensity. CASES
TREATED
BY
“TRIGGER
70NE" d
ISJECTIONS
CASE l.-Mrs. J. W., aged ‘78, had suffered for more than ten years with a trigeminal neuralgia involving the right side of her face. She recalled that the first sign of trouble was a sensitive spot above her right eye. When this was touched, a twinge of pain shot out over the distribution of the ophthalmic division of the fifth nerve. Later the maxillary division was involved and at times the pain was also felt in the lower jaw. The effect of t,he lancinating pain was sometimes so severe that she was unable to eat or talk. Examination showed that she had two trigger zones. The most sensitive one was located about three quarters of an inch to the right of the midline and an equal distance above the margin of the orbit. It was very accurately iodized and even light cottonwool stimulation precipitated pain attacks. She seeemed to tolerate light touch in this area less well than firm pressure. She had a second trigger zone in the region of the nasal ala, but this spot did not seem to be so accurately localized or so sensitive, although lancinating attacks of pain could be elicited by stimulation of this region. On Sept. 13, 1938, I infiltrated the trigger zone of her forehead with 2 per cent novocain. Following the injection I was unable to elicit pain by local pressure, but the supraorbital nerve just below this point seemed to be slightly sensitive to pressure. I, therefore, supplemented the injection by an infiltration of the nerve at the supraorbital notch. Peculiarly enough, these injections seemed to diminish the sensitiveness of the trigger zone near the nose, at least, I could not thereafter precipitate an attack of pain by stimulating it,. Four days later she reported that she had had a few mild attacks of pain in the ophthalmic distribution but none in the maxillary or mandibular divisions. Again I could not elicit pain by stimulation of the region of the nasal ala, but stimulation of the upper trigger zone on the forehead caused paroxysmal pain.
576
TV. K. Livingston
This area was again infiltrated with a few minims of 2 per cent novocain. This second injection was followed by nine days of complete relief and she said, “I feel like this is a different existence than I’ve had for the past ten years.” I could elicit slight complaint of tenderness by direct pressure over the supraorbital notch but could not precipitate an attack. She was given four injections, the last one on Oct. 18, 1938, after which she had no pain. for six months. In April, 1939, she experienced a few twinges of pain in the maxillary division, which seemed to originate just lateral to the nose and spread in shocklike vibrations over the check and upper jaw. There was no complaint of pain in the supraorbital region at that time. One injection was given at the secondary trigger zone near t,he nose, and at the t,ime of this writing, eleven months after t,he last injection there has been no recurrence of pain. CASE 2.-Mrs. L. L., aged 57, noted a sensitive spot “at the lower edge of the right cheek bone” about four years previously. She’ stated that touching this spot was “like hitting an exposed nerve.” For a time the pain was local but it gradually spread over the entire right side of the face. For a time (two years previously) the right upper eyelid was said to “droop” but this condition spontaneously disappeared. She dreaded to touch her face and claimed that touching the hairs of the trigger zone caused the worst pain. As t,hc paroxysmal pains increased in frequency and severity it became difficult for her to eat. I was able to locate two trigger zones, one just lateral to and above the crease formed by the nasal ala, and the other just lateral to the angle of the lips on the right. Both of these spots were injected on July 10, 1939, the injection being confined to the skin, During the injection she said, “Now you may not believe this, but sometimes when I touch the face and get a shock, I can feel it in one particular tooth; it isn’t always the same tooth, and yet I haven’t, Following the inj&ion neither she nor I had a tooth in my head for years.” could elicit an atta,ck of pain. The side of the inject,ions were locally tender for two days but she had no pain attacks for four days, then mild attacks recurred with contact, and on the sixth day severe shocks returned. She had two more injections, on July 17 and August 31, since which time there has been no recurrence. CASE 3.-Mrs. H. T., aged ‘78, presented typical major trigeminal neuralgia of ten years’ duration. Two trigger zones, one to the right of the base of the nose, the other at the former site of the right upper first molar (patient edentulous for years). She rarely wore her plates as the contact of the upper plate with the tender area precipitated paroxysmal pain. She lived largely on Novocain was injected in both trigger soft food that did not require chewing. zones on June 19, 1936, with marked relief persisting for several weeks. She had two other injections in 1936 and remained reasonably free from attacks until in March, 1938, at which time she was having frequent attacks which seemed to start at the base of the nose and spread to the eye and temple. At this time she had two injections, the second one being directly into the infraorbital nerve. In August, 1938, she reported that she had been having sharp attacks of increasing severity for several months. Two injections conferred only partial relief.
Trigenzinal
Neuralgia
In September, she had a herpes zoster involving the right flank and groin and at the same time developed an auricular fibrillation. She was confined to the hospital on Sept. 21, and died on Oct. 9, 1938. During her hospital stay she complained bitterly of her facial pain and of persistent pain in the groin. She was given two injections into each trigger zone, following which she complained much less of her face though she continued to complain of the postherpetic pain. She became increasingly disoriented and irrational so that it was impossible to evaluate the effect of these last injections, although it was noted that she no longer continued to grimace or put her hand to her face. CASE 4.-Dr. R. IL S., aged 63, suffered from a typical trigeminal neuralgia for several years. His pains involved the upper and middle divisions of the fifth nerve. In October, 1935, an alcohol injection of the maxillary division conferred relief from the pain in bot,h divisions for about eighteen months. In July, 1938, hc consulted Dr. Frank Kistnrr of the Portland Clinic seeking relief. Since his physical condition seemed to preclude operative treatment, novocain injections were carried out by Dr. Kistner, the last one being given on Aug. 17, 1938. About six months later he had a slight recurrence of pain in the form of transient twinges of pain which lasted for a few days and disappeared spontaneously. Otherwise, he has remained entirely free from attacks during a period of observation of seventeen months. COMMENT
AS a method of treatment for facial pain, the novocain injections have given results that are at least encouraging in a number of instances in my own experience and that of members of the Portland Clinic. I have been able to collect several cases so treated which have been called “trigeminal neuralgia,” but I have not included them in this report because on careful analysis of the story in each instance thcrc is found some feature which leads to doubt that the pain syndrome represents a “typical” trigeminal neuralgia. The four cases here reported represent the only typical cases encountered since this method of treatment was undertaken, But as I stated earlier in this paper, my primary purpose was not the advocacy of a method of treatment,, worthwhile though it may prove to be. My interest has been confined to the question of the origin for the pain. I have no way of knowing in what percentage of cases of major trigeminal neuralgia this method of novocain injection of the trigger points would be successful. In this sense the report of four cases has no significance. But, if, as I believe, these four represent the “idiopathic” type of trigeminal neuralgia, they may acquire a significance. Their relief by rcpcatcd novocain injection, coupled with the observat,ion that local pathology in the teeth, jaw, sinuses, or the muscles can cause pain indistinguishable from the idiopathic type, would suggest, that perhaps all cases of trigeminal neuralgia had a peripheral origin. It would suggest further that, the ability to identify and properly treat such peripheral sources of irritation might obviate the necessity for surgical operation in many instances. But the fact. that the origin of the syndrome may be found at the periph ery does not imply that activities within the thalamus or other brain cen-
tcrs do not contribute to the fully developed pain syndrome. There is considerable evidence to suggest that the irritant focus initiates a state of pathologic physiology within the brain centers. An interruption of the impulses tending to maintain this abnormal state may terminate the pain, or at least afford a period of relief that persists until the physiologic disturbance is again created by incoming impulses. It is only by invoking some such concept as this that I am able to account for such observations as that of Percival BailepLX3 who abolished the pain in one of his cases by a simple injection of novocain into one of t,he primary divisions of t,hc fifth nerve. His patient, il woman, suffered from typical attacks of tic douloureux of several years’ duration. She cntcred the hospital for an alcohol injection. Since her pain involved both the maxillary and the ophthalmic divisions, Dr. Bailey injected the maxillary division with novocain to det,crmine whether or not an injection of alcohol into this division would affect the pain in both divisions. The alcohol injection was never given because after the novocain injection her pains did not, recur, and during an observation period of two years, her clinical curt remained complete. ~2np attempt to explain how t,hc mechanism responsible for trigeminal neuralgia may function, is, of course, speculative, but I venture this interpretation. The peripheral lesion, whatever its nature, acts merely as an irritative focus from which the centers are continually bombarded by a&rent impulses. This bombardment eventually creates an abnormal internuncial activity within the thalamus, which discharges explosively whenever a particularly strong impulse or combinat,ion of impulses arrives at, the proper instant. In the fully developed syndrome of trigeminal neuralgia the slightest stimulation of the trigger point might be sufficient to detonate the pain paroxysm. But if the afferent impulses cease, either because of the removal of the source of irritation, or by repeated interruption of the messages, the abnormal activity within the thalamus tends to subside and the paroxysmal pain disappears. This concept is hypothetic, but it seems to be consistent with the following facts : 1. That patients with sympt,omatic trigeminal neuralgia, in whom the pains are, indistinguishable from the idiopathic type, have been cured bY removal of pathologic conditions of the teeth, jaws, or sinuses. 2. That myositis of facial muscles may cause typical tic douloureux, and the pain disappears when the mgositis is treated. 3. That alcohol injection of the main divisions of t,he fifth nerve, or evulsion of more peripheral portions, has resulted in a cure for variable periods of time. 4. That the pain at,tacks startin, 0 in the distribution of one division of the nerve tend to spread until it eventually involves one or both of the other divisions. 5. That the alcohol injection of the division first involved in the pain process may stop the pain in other divisions as well. 6. That repeated injections of novocain into trigger points may abolish the pain for variable periods of time. REFERENCES 1. lkmly, 2. Stihbe,
w. E. : J. Indiana E. P.: Lancet 1:
M. A. 31: 859.862 ant1
(X9-672, 918-931,
1938. 1949.
Trigeminal 3. 4. 5. 6. 7. 8. 9. 10. 11.
Neuralgia
Smyth, G. E.: Brain 62: 41-87, 1939. Sjijqvist, 0.: Acta Psychiat. et. Neurol. supp. 17: l-139, 1938. Walker, A. E.: J. Neurophysiol 2: 234248, 1939. Harris, W.: Lancet 1: 1114-1116, 1939. Trigeminal Neuralgra. Nelson’s Loose-Leaf Surgery, vol. 5, p. 550. Stookey, B.: Lewy, F. H., and Grant, F. C.: Arch. Neurol. & Psychiat. 40: 11X6-1134, 1938. Head, H., and Holmes, G.: Brain 34: 102-254, 1911. Frazier. C. H.. Lewv, F. H.. and Rolve. 8. N.: Brain 60: 44-51. 1937. Livingston, WI K.: -West. J. Surg. O&t. & Gynec. 46: 341-347 ‘and 426-434, 1935; Arch. Surg. 37: 353-370, 1935. 12. Ross, K.: Med. J. Australia 1: 587-588. 1937. 13. Bailey, P.: Personal communication.
579
also
BP .2ND
NOVOCAIN A
NEURALGIA
INJECTION
DISCUSSION OF
W. K. LIVINGSTON, M.D.,
T
OF PAIN
THE
TRIGGER
Zoos,
SOURCES
PORTLAND,
ORE.
HE clinical picture of trigeminal neuralgia has been frequently described. Its surgical treatment is reasonably well standardized. It is known that a partial division of the posterior root of the fifth cranial nerve, properly done, will confer a permanent relief from pain. Differences of opinion among surgeons t,reating t,his syndrome exist as to t,he advisability and indications for alcohol injections of the peripheral divisions of this nerve, as a substitute for, or preliminary to, a sensory root se&ion. And there are differences of opinion as to the technique for carrying out the root, section. Dandy1 advocates a posterior approach in preference to the usual temporal approach to the sensory root, stating that he can thereby selectively divide the root close to the pons so as to abolish the pain and at the same time preserve much of the sensation of touch in the face. Stibbez has recently submitted evidence tending to support Dandy’s contention that the small fibers believed to conduct the pain are grouped together in the posterior portion of the root as it enters the pons. Smyth” has studied the relationship of fibers subserving different sensory functions in each part of the face, as they are distributed in the spinal trigeminal tract of the medulla, and SjiiyvisV has described a new operation involving a selective division of the trigeminal tracts within the brain which is designed to abolish pain without causin g an anesthesia in the cornea of the eye or loss of the sense of touch in the face. Walker” describes two cases treated by partial trigeminal tractotomy and his analysis of the changes in the sensory discrimination of these patients and two cases of thrombosis of the posterior inferior cerebellar artery, suggests that the spinal tract of the fifth nerve carries sensations of pain, heat, touch, deep pressure-pain, and to a slight degree touch. These are important and practical contributions which not only advance knowltrigeminal neuralgia but may be of assistance in settling edge regarding problems relating t,o other painful syndromes. But the problem of the origin of the pain in trigeminal neuralgia remains unxcttled. This problem is of fundamental importance to an understanding About this question of the etiology and treatment of this pain syndrome. hinges the principal controversy amon, 0~the clinical and research students of trigeminal neuralgia. I am inclined to favor a peripheral origin for the pain attacks and am of the opinion that an irritant focus at the periphery is capable a pathologic state of activity within the thalamus or other of inaugurating brain centers which assists in the creation of the complete clinical picture. This opinion is based on the observations reported in this paper. In four Cases which apparently represent idiopathic trigeminal neuralgia, the pain
l’rigewtinal
Neurulgia
571
attacks have been abolished by repeated injections of novocain into the trigger zones. The number of cases so treated is not sufficiently large to justify any final conclusions, but inasmuch as these observations may have some bearing on the problem of pain sources in this condition, it seems justifiable to present them. In addition it might be worth while t,o review briefly the onset and course of the pain syndrome, as well as the differential diagnosis, not in the orderly sequence necessary for establishing a textbook picture of this disease, but solely as they may relate to the question of the source of the pain. ONSET
AND
COURSE
Trigeminal neuralgia usually appears in middle life and afflicts males and females in about equal numbers. Its onset is of considerable interest and the detailed accounts of the onset and progress of the painful attacks by patients suffering from “idiopathic” trigeminal neuralgia suggest a peripheral origin for the pain. In the typical instance t,here is no antecedent history of illness or injury and no premonitory symptoms. The patient may be washing his fact when, with contact at a certain area in the face, there occurs a lancinating shock of pain, “as if an exposed nerve in a tooth had been touched.” The attack of pain is momentary and may not recur for a considerable interval. Close inspection of the face at the point from which the pain seemed to originate reveals nothing and the patient tends to forget about it. At a later date, and with equal suddenness, touching this same spot again precipitates the lancinating pain. As t,hc attacks tend to become more serere and frequent, the patient learns to associate this “trigger zone” with his pains and tries to avoid any form of contact, with this portion of his face. The commonest location of the trigger zone seerns to be in the distribut>ion of the maxillary division of the fifth nerve, often just lateral to the nasal ala, although it may occur anywhere on the face, and not infrequently as the syndrome progresses secondary trigger Remissions are known to occur, sometimes lasting for zones may develop. months or years, but, ordinarily the painful attacks become progressively worse and can occur in such rapid succession as to be almost continuous. The pain, which at first is confined to a small part of t,he face, perhaps one side of the upper lip, tends to spread over the distribution of one division of the fifth nerve and t,hen to involve one or both of the other divisions. It is unquestionably severe. It has been likened to an electric shock of great intensity, and no one seeing a patient during an attack and observing the facial grimace, the expression of frightened agony and almost breathless immobility, can doubt its severity. In the effort to avoid attacks many patients refuse to eat or talk, and withdraw from all activities and contacts that may bring on the pain. Others in a sort of desperation may deliberately precipitate a series of attacks so that in the short interval of freedom from pain that may follow, they are permitted to eat a few mouthfuls of food or talk with a degree of comfort. Many patients have submitted to one or more injections of alcohol into the peripheral divisions of the nerve, and it is of interest to note that the injection of alcohol into one division may confer relief from pain in the other This is particularly true when the injection divisions as well as the one injected.
572
W. K. Livingston
is made into the nerve division that was first involved in the painful attacks. As an example one might cite a case in which the maxillary division was first involved and later the pain had spread to the ophthalmic division. Because of the danger of cornea1 ulcer followin g an interruption of sensory impulses from the eye, the surgeon may be reluctant to inject alcohol into the ophthalmic division. But if a successful injection of the maxillary division is carried out all of the pain may disappear, not only that felt in the maxillary region, but in the ophthalmic area as well. A further point of interest relatin g to alcohol injections is the observation that following an injection, the relief of pain and the persistence of anesthesia in the face do not parallel one another. Immediately after an injection the zone of anesthesia may conform quite exactly to t,he known distribution of the injected division. Within a short time, often within two or three weeks, this zone becomes progressively smaller, and in some instances quite a normal sensation of touch and sensitivity to pain may return to the face, months or years before the painful attacks recur. It is quite apparent in instances of this kind that the nerve fibers have not been destroyed, but that the injection has merely interrupted for an interval their ability to conduct impulses from the periphery to the receiving centers. DTPFERESTIAL
DIAGNOSIS
In the medical literature dealing with trigeminal neuralgia considerable emphasis has been placed upon the necessity for distinguishing between “symptomatic” and “idiopathic” cases. Under the former term are grouped those eases in which a local focus of pathology is demonstrable, the removal of which may be followed by a disappearance of the painful attacks. The latter term does not deny the possibility of a peripheral origin for the pain, it merely indicates that the etiology is unknown. A careful search for local pathology is indicated in every case of facial pain, and this statement applies with equal force to the cases with typical paroxysmal trigeminal pain as to those with atypical attacks. Among the causes apparently responsible for the pain attacks, infection of the jaw or of the sinuses seems to be important. Harris6 points out the fact that the neuralgia usually begins in the maxillary or mandibular divisions, and believes that the syndrome is attributable to a “septic terminal neuritis in the terminal filaments in the jaws.” But other dental conditions in which infection is at least not obvious, may cause identical pains. A malocclusion, particularly the type in which the offending tooth is solidly fixed in dense rburnated bone, may give rise to paroxysmal pain, and its correction may be followed by a cure. It seems justifiable to say that these various local conditions can cause the syndrome because in many instances the removal of the irritant factor has been followed by a disappearance of the pain. Perhaps the most interesting of the local lesions giving rise to trigeminal pain is a ’ ’ myositis ’ ’ of the temporal or masseter muscles. Stookey’ observed twenty-two cases of this type in a five-year period. In this condition it may be possible to demonstrate a minute nodule in the muscle which is extremely sensitive to pressure. The muscle elsewhere may be stimulated without eliciting
Trigeminal
Neuralgia
573
a pain response, but if this discrete kernel is pressed upon, an excruciating pain is felt in the lip, in the temporal region, or over t,he distribution of one or more divisions of the fifth nerve. Although spontaneous pain attacks are less common in this affliction, paroxysmal pains may occur without any apparent local stimulation. In the severe cases due to a local area of myositis, the pains may be identical with those occurring in the idiopathic cases, even to the facial grimace. The tiny area of involved muscle may be difficult to find, particularly when it occurs in the anterior margin of the masseter muscle. But once identified, the condition may yield to appropriate treatment by baking and massage. The first few treatments may aggravate the pain, but in from two to six weeks the nodule disappears and simultaneously the pains leave and do not return. On the other hand, there are many surgeons who believe that the pain syndrome in the symptomatic cases is not identical with that of the “genuine” or idiopathic case. It is certainly true that one rarely encounters a case of trigeminal neuralgia of long standing in which teeth have not been sacrificed and sinuses repeatedly operated upon without being benefitted. Some observers insist that there is some essential difference in the type of pain, and therefore in the mechanism underlying the symptomatic and the idiopathic cases. Dandy1 believes that the source of irritation in major trigeminal neuralgia is always at the posterior root of the fifth nerve, and thinks that he can identify the cause in all of his cases as due to pressure from a tumor (5 per cent), an aneurysm of the basilar artery (5 per cent), or pressure from an artery (90 per cent). Concerning the pain he says, “A peripheral lesion along the sensory branch of Given a paroxysmal pain, it a nerve can never produce a paroxysmal pain. always means that the upper neuron that is between the ganglia of the nerve and the brain stem is affected, and it is only a lesion there that can do it.” I do not know what he means by the “upper neuron” in this quotation, nor do I believe that he is justified in making so flat an assertion regarding paroxysmal pain. Many instances of paroxysmal pain have been reported as cured by the elimination of a peripheral source of irritation. I am inclined to agree with Harris0 who says, in speaking of “symptomatic” types, “these cases differ in no respect from the so-called genuine or idiopathic paroxysmal trigeminal neuralgia, either in their type of pain, trigger zones, or results of treatment by alcohol injection or root section. ” A
“CENTRAL”
ORIGIN
FOR
PAIN
In spite of evidence that a peripheral lesion may cause paroxysmal attacks of pain indistinguishable from that of idiopathic trigeminal neuralgia, and the fact that an alcohol inject.ion of the primary divisions of the nerve can stop the pain, there is much to be said in favor of a central origin for the pain. Lewy and Grants have marshalled an impressive number of observations tending to support their contention that trigeminal neuralgia is a special form of the thalamic syndrome. The hyperpathia that develops in the classical type of the thalamic syndrome is attended by pain having a peculiarly unbearable quality (affective tone), it tends to radiate widely, has a high threshold and deficient localization
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for stimuli, and is characterized by explosive reactions. The pain of trigeminal neuralgia has some of these same features, in particular the unbearable feeling tone and the tendency to explosive reaction. It seems to differ from thalamic pain in that stimuli are accurately localized and the pain confined to one or more divisions of the single nerve rather than radiating widely. However, Lewy and Grant were able to demonstrate that in 32 per cent of their cases the hyperpathia of trigeminal neuralgia was not confined to the face but extended over one side of the body. They were further able to show that in forty of their fifty cases there existed signs of pyramidal or extrapyramidal involvement. Their observations were interpreted as pointing toward a lesion in the region of the optic thalamus as a possible cause for trigeminal neuralgia. This assumption seemed to be confirmed by postmortem studies carried out on six cases. In all six the brain showed an atrophy of the ipsilateral hemisphere, a widening of the lateral ventricle, and foci of softening located either within the thalamic nuclei or in the thalamocortical tract. The pathology could be interpreted as accounting for a removal of the cortical inhibition, which, according to Head and Holmes,” acts to dampen the characteristic thalamic overresponse to pain sensation. This evidence would be more impressive if the brain pathology had been found on the side contralateral to the location of the pain. The fact that in five of their six cases in which the pain was unilateral the brain atrophy was most obvious on the ipsilateral side, suggests either that some unrecognized relationship exists between the thalamus and the face, or that the findings were incidental to the trigeminal neuralgia and not causal. “Why, if the pain is of central origin, should a blocking To the question, of peripheral portions of the nerve terminate the pain?” Lewy and Grant point out that the activity of the thalamus is dependent upon, or conditioned by, a constant influx of sensory impulses. With the cessation of such conditioning impulses the abnormal activity of the thalamus would no longer be apparent. Frazier, Lewy, and Rowe lo have reported a case which supports this interpretation. This woman suffered from intolerable pain over one side of the body and face, which was apparently due to a hemorrhage in the thalamic region. Her facial pain was relieved by blockin, 0 the fifth nerve and the hyperpathia of the side of the body was relieved by a chordotomy. But of all the arguments adduced by Lewy and Grant in favor of a central origin for the pain of trigeminal neuralgia, the one that impresses me most is t,he observation that the pain and sensory changes which they noted in their cases present features which can be explained only by implicating neurons in synaptic relation with one another. They say, ‘ ’ Summation and radiation, after-effect and hyperpathia, spat,ial and temporal amalgamation, and finally, complete transmutation of sensations characterize the physiopathologic pattern they imply that some of sensibility in trigeminal neuralgia. ’ ’ Furthermore, pathologic condition in the brain may cause a delay in discharge, so that with a recruitment of more pain impulses, there eventually occurs the augmented discharge so characteristic of the paroxysmal pain of trigeminal neuralgia and so similar to the “explosive pain reactions ” of the thalamic disease. Since all of these neurophysiologic activities are dependent upon an interaction between neurons in intimate synaptic relation with each other in some brain
l’rigentinnl
Neumlgin
center, Lewy and Grant conclude that the pain in t,rigeminal neuralgia must be of central origin. In actual fact, these observations merely imply that the internuncial activities in the brain center contribute to the pain picture in the fully developed case of trigeminal neuralgia. A peripherally situated irritative focus might initiate the abnormal activities developing in the thalamus or other central nervous system centers.” One other observation is frequently mentioned as supporting the view that the origin of the pain is central, i.e., the high incidence of trigeminal neuralgia in cases of disseminated sclerosis. Keith ROSS*~has reported fortyone cases in which the chronic spastic paraplegia was complicated by trigeminal tic. Harris6 has called attention to the fact that trigeminal neuralgia is bilateral in 17 per cent of the cases associated with multiple sclerosis and that it is bilateral in less than five per cent of other eases. This association between a disease characterized by obvious pathologic changes in the brain, and the pain syndrome of trigeminal neuralgia could be interpret,ed as favoring a brain lesion as the primary cause for the latter condition. On the other hand, it might be interpreted as Harris has done when he asserts that the sclerotic plaques merely heighten the irritability of the central neurons so that the pain syndrome would be more likely to develop secondary to some peripheral source for reiterated impulses of abnormal intensity. CASES
TREATED
BY
“TRIGGER
70NE" d
ISJECTIONS
CASE l.-Mrs. J. W., aged ‘78, had suffered for more than ten years with a trigeminal neuralgia involving the right side of her face. She recalled that the first sign of trouble was a sensitive spot above her right eye. When this was touched, a twinge of pain shot out over the distribution of the ophthalmic division of the fifth nerve. Later the maxillary division was involved and at times the pain was also felt in the lower jaw. The effect of t,he lancinating pain was sometimes so severe that she was unable to eat or talk. Examination showed that she had two trigger zones. The most sensitive one was located about three quarters of an inch to the right of the midline and an equal distance above the margin of the orbit. It was very accurately iodized and even light cottonwool stimulation precipitated pain attacks. She seeemed to tolerate light touch in this area less well than firm pressure. She had a second trigger zone in the region of the nasal ala, but this spot did not seem to be so accurately localized or so sensitive, although lancinating attacks of pain could be elicited by stimulation of this region. On Sept. 13, 1938, I infiltrated the trigger zone of her forehead with 2 per cent novocain. Following the injection I was unable to elicit pain by local pressure, but the supraorbital nerve just below this point seemed to be slightly sensitive to pressure. I, therefore, supplemented the injection by an infiltration of the nerve at the supraorbital notch. Peculiarly enough, these injections seemed to diminish the sensitiveness of the trigger zone near the nose, at least, I could not thereafter precipitate an attack of pain by stimulating it,. Four days later she reported that she had had a few mild attacks of pain in the ophthalmic distribution but none in the maxillary or mandibular divisions. Again I could not elicit pain by stimulation of the region of the nasal ala, but stimulation of the upper trigger zone on the forehead caused paroxysmal pain.
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This area was again infiltrated with a few minims of 2 per cent novocain. This second injection was followed by nine days of complete relief and she said, “I feel like this is a different existence than I’ve had for the past ten years.” I could elicit slight complaint of tenderness by direct pressure over the supraorbital notch but could not precipitate an attack. She was given four injections, the last one on Oct. 18, 1938, after which she had no pain. for six months. In April, 1939, she experienced a few twinges of pain in the maxillary division, which seemed to originate just lateral to the nose and spread in shocklike vibrations over the check and upper jaw. There was no complaint of pain in the supraorbital region at that time. One injection was given at the secondary trigger zone near t,he nose, and at the t,ime of this writing, eleven months after t,he last injection there has been no recurrence of pain. CASE 2.-Mrs. L. L., aged 57, noted a sensitive spot “at the lower edge of the right cheek bone” about four years previously. She’ stated that touching this spot was “like hitting an exposed nerve.” For a time the pain was local but it gradually spread over the entire right side of the face. For a time (two years previously) the right upper eyelid was said to “droop” but this condition spontaneously disappeared. She dreaded to touch her face and claimed that touching the hairs of the trigger zone caused the worst pain. As t,hc paroxysmal pains increased in frequency and severity it became difficult for her to eat. I was able to locate two trigger zones, one just lateral to and above the crease formed by the nasal ala, and the other just lateral to the angle of the lips on the right. Both of these spots were injected on July 10, 1939, the injection being confined to the skin, During the injection she said, “Now you may not believe this, but sometimes when I touch the face and get a shock, I can feel it in one particular tooth; it isn’t always the same tooth, and yet I haven’t, Following the inj&ion neither she nor I had a tooth in my head for years.” could elicit an atta,ck of pain. The side of the inject,ions were locally tender for two days but she had no pain attacks for four days, then mild attacks recurred with contact, and on the sixth day severe shocks returned. She had two more injections, on July 17 and August 31, since which time there has been no recurrence. CASE 3.-Mrs. H. T., aged ‘78, presented typical major trigeminal neuralgia of ten years’ duration. Two trigger zones, one to the right of the base of the nose, the other at the former site of the right upper first molar (patient edentulous for years). She rarely wore her plates as the contact of the upper plate with the tender area precipitated paroxysmal pain. She lived largely on Novocain was injected in both trigger soft food that did not require chewing. zones on June 19, 1936, with marked relief persisting for several weeks. She had two other injections in 1936 and remained reasonably free from attacks until in March, 1938, at which time she was having frequent attacks which seemed to start at the base of the nose and spread to the eye and temple. At this time she had two injections, the second one being directly into the infraorbital nerve. In August, 1938, she reported that she had been having sharp attacks of increasing severity for several months. Two injections conferred only partial relief.
Trigenzinal
Neuralgia
In September, she had a herpes zoster involving the right flank and groin and at the same time developed an auricular fibrillation. She was confined to the hospital on Sept. 21, and died on Oct. 9, 1938. During her hospital stay she complained bitterly of her facial pain and of persistent pain in the groin. She was given two injections into each trigger zone, following which she complained much less of her face though she continued to complain of the postherpetic pain. She became increasingly disoriented and irrational so that it was impossible to evaluate the effect of these last injections, although it was noted that she no longer continued to grimace or put her hand to her face. CASE 4.-Dr. R. IL S., aged 63, suffered from a typical trigeminal neuralgia for several years. His pains involved the upper and middle divisions of the fifth nerve. In October, 1935, an alcohol injection of the maxillary division conferred relief from the pain in bot,h divisions for about eighteen months. In July, 1938, hc consulted Dr. Frank Kistnrr of the Portland Clinic seeking relief. Since his physical condition seemed to preclude operative treatment, novocain injections were carried out by Dr. Kistner, the last one being given on Aug. 17, 1938. About six months later he had a slight recurrence of pain in the form of transient twinges of pain which lasted for a few days and disappeared spontaneously. Otherwise, he has remained entirely free from attacks during a period of observation of seventeen months. COMMENT
AS a method of treatment for facial pain, the novocain injections have given results that are at least encouraging in a number of instances in my own experience and that of members of the Portland Clinic. I have been able to collect several cases so treated which have been called “trigeminal neuralgia,” but I have not included them in this report because on careful analysis of the story in each instance thcrc is found some feature which leads to doubt that the pain syndrome represents a “typical” trigeminal neuralgia. The four cases here reported represent the only typical cases encountered since this method of treatment was undertaken, But as I stated earlier in this paper, my primary purpose was not the advocacy of a method of treatment,, worthwhile though it may prove to be. My interest has been confined to the question of the origin for the pain. I have no way of knowing in what percentage of cases of major trigeminal neuralgia this method of novocain injection of the trigger points would be successful. In this sense the report of four cases has no significance. But, if, as I believe, these four represent the “idiopathic” type of trigeminal neuralgia, they may acquire a significance. Their relief by rcpcatcd novocain injection, coupled with the observat,ion that local pathology in the teeth, jaw, sinuses, or the muscles can cause pain indistinguishable from the idiopathic type, would suggest, that perhaps all cases of trigeminal neuralgia had a peripheral origin. It would suggest further that, the ability to identify and properly treat such peripheral sources of irritation might obviate the necessity for surgical operation in many instances. But the fact. that the origin of the syndrome may be found at the periph ery does not imply that activities within the thalamus or other brain cen-
tcrs do not contribute to the fully developed pain syndrome. There is considerable evidence to suggest that the irritant focus initiates a state of pathologic physiology within the brain centers. An interruption of the impulses tending to maintain this abnormal state may terminate the pain, or at least afford a period of relief that persists until the physiologic disturbance is again created by incoming impulses. It is only by invoking some such concept as this that I am able to account for such observations as that of Percival BailepLX3 who abolished the pain in one of his cases by a simple injection of novocain into one of t,he primary divisions of t,hc fifth nerve. His patient, il woman, suffered from typical attacks of tic douloureux of several years’ duration. She cntcred the hospital for an alcohol injection. Since her pain involved both the maxillary and the ophthalmic divisions, Dr. Bailey injected the maxillary division with novocain to det,crmine whether or not an injection of alcohol into this division would affect the pain in both divisions. The alcohol injection was never given because after the novocain injection her pains did not, recur, and during an observation period of two years, her clinical curt remained complete. ~2np attempt to explain how t,hc mechanism responsible for trigeminal neuralgia may function, is, of course, speculative, but I venture this interpretation. The peripheral lesion, whatever its nature, acts merely as an irritative focus from which the centers are continually bombarded by a&rent impulses. This bombardment eventually creates an abnormal internuncial activity within the thalamus, which discharges explosively whenever a particularly strong impulse or combinat,ion of impulses arrives at, the proper instant. In the fully developed syndrome of trigeminal neuralgia the slightest stimulation of the trigger point might be sufficient to detonate the pain paroxysm. But if the afferent impulses cease, either because of the removal of the source of irritation, or by repeated interruption of the messages, the abnormal activity within the thalamus tends to subside and the paroxysmal pain disappears. This concept is hypothetic, but it seems to be consistent with the following facts : 1. That patients with sympt,omatic trigeminal neuralgia, in whom the pains are, indistinguishable from the idiopathic type, have been cured bY removal of pathologic conditions of the teeth, jaws, or sinuses. 2. That myositis of facial muscles may cause typical tic douloureux, and the pain disappears when the mgositis is treated. 3. That alcohol injection of the main divisions of t,he fifth nerve, or evulsion of more peripheral portions, has resulted in a cure for variable periods of time. 4. That the pain at,tacks startin, 0 in the distribution of one division of the nerve tend to spread until it eventually involves one or both of the other divisions. 5. That the alcohol injection of the division first involved in the pain process may stop the pain in other divisions as well. 6. That repeated injections of novocain into trigger points may abolish the pain for variable periods of time. REFERENCES 1. lkmly, 2. Stihbe,
w. E. : J. Indiana E. P.: Lancet 1:
M. A. 31: 859.862 ant1
(X9-672, 918-931,
1938. 1949.
Trigeminal 3. 4. 5. 6. 7. 8. 9. 10. 11.
Neuralgia
Smyth, G. E.: Brain 62: 41-87, 1939. Sjijqvist, 0.: Acta Psychiat. et. Neurol. supp. 17: l-139, 1938. Walker, A. E.: J. Neurophysiol 2: 234248, 1939. Harris, W.: Lancet 1: 1114-1116, 1939. Trigeminal Neuralgra. Nelson’s Loose-Leaf Surgery, vol. 5, p. 550. Stookey, B.: Lewy, F. H., and Grant, F. C.: Arch. Neurol. & Psychiat. 40: 11X6-1134, 1938. Head, H., and Holmes, G.: Brain 34: 102-254, 1911. Frazier. C. H.. Lewv, F. H.. and Rolve. 8. N.: Brain 60: 44-51. 1937. Livingston, WI K.: -West. J. Surg. O&t. & Gynec. 46: 341-347 ‘and 426-434, 1935; Arch. Surg. 37: 353-370, 1935. 12. Ross, K.: Med. J. Australia 1: 587-588. 1937. 13. Bailey, P.: Personal communication.
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also