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The neuralgias and vascular algias of the face
Oral THE
NEURALGIAS
ORION
Medicine
AND VASCULAR
ALGIAS
OF THE FACE
H. STUTIWILLE,
.D.D.S., M.D., F’.A.C.S., CHICAGO, ILL., AND -JACQUES TAx+NA(~, I).I>.S., Ml)., P.IRIS, FHASCE
UR profession is often confronted with patients suffering from undefined facial pain. After eliminating the possibilities of underlying pathology, most of these are diagnosed as cases of trigeminal neuralgia, and this diagnosis is usually correct. We should remember, however, that facial sensibility is not entirely under the dependence of the trigeminal nerve; sometimes it is an atypical neuralgia. Most of the facial neuralgias are relieved by section of the sensory root of the fifth cranial nerve, which should prove their origin. In certain cases, however, retrogasserian neurotomy failed to bring the expected result. The situation is still rather confused. Besides cases where there is a possibility of central pain, and those of psychogenic origin, there is a complex group of conditions which have been described under various names such as sphenopalatine ganglion neurosis, Vidian neuralgia, geniculate neuralgia, pseudotrigeminal neuralgia, and sympathalgias of the face. More recently, similar cases have been reported under the headings of migraine, paroxysmal vascular headaches, and erythromelalgia of the head. Despite the differences between these conditions, t,hey still have some points in common and should be considered as clinical varieties of a larger group. It is difficult to find a proper name for the group; atypical neuralgia is not entirely satisfactory. The terminology itself, “sphenopalatine ganglion, of the sensory Vidian nerve, geniculate ganglion,” suggests an involvement portion of the facial nerve. On the other hand, do not the terms “sympathalgias, vascular headaches, erythromelalgia” express the participation of the sympathetic and vascular sensibility? There are two main lines of thought regarding atypical neuralgia: Is the neuralgia related to t,he seventh nerve, or is it due to sympathetic disturbances and the exacerbation of the vascukr sensibility? These questions do not imply, however, that the fifth nerve can be eliminated from the picture entirely.
0
A Clinical
Picture
The patient, middle-aged, male or female, is pale, anxious and nervous, suffering from a burning, nagging, or quivering type of pain, difficult to deFrom the Department of Maxillafacial Surgery, the Chica o College of Dental Surgery and the Stritch Chicago, 81.
1413
Cook County Hospital, Chicago, 111.. School of Medicine, Loyola University,
scribe. The pain is deep in the face. OIL one sitle, fell mostly in the r(JOt of the nose, the temple, or around and behind t.he orbit. \vith no definite limit>s. It, radiates to the ears, ,ja\t~? and treth, c~hanging in int,cnsity, distribution, and characteristics. In association with the pain, there are intense ~wso~tt~tor reactions. The patient experiences a flush, and warmth on one side of the face. with watering of the eyes and nose. Examination reveals a congestiolt of the nasal mu~osa, mostly 011one side. and injected conjunct,i\,a of the eve aild strong pulsations of the temporal artery. Sensory disturbances have also been observe& including hyperesthesia of the skin on the affected side, temporary cloudiness of vision, a transitory Claude-Bernard-Horner syndrome. deafness, and tinnitus. Sometimes there are motor disturbances as expressed by myoclonia in the territory of t,he seventh nerve. Sluder. in 1910. described the sphcnopalatine sytltlromr as it “comples symptom partly neuralgic (painful 1, mot,or. sensory and gustatory.” with a wide radiation of pain to the ear, being severest at a point 5 cm. back of the mastoid and extending t,o the occiput, neck, shoulders, breast, arm, forearm, hands, and fingers. Sometimes the throat on t>he affected side feels sore. and on rare occasions there is itching of the skin, taste dist,urbances, scotoma, and a sense of stiffness and muscle weakness in the upper extremity. Usually the pain is constant, but in certain cases the pain I~:I;V stop and then reappear as a migraine, or stop anal reappear with a. stabbing sharpness, as a tic. In 1933. Alajoua,nine and Thnrel described “Iles sympathalgies faciales.” These authors insistetl on the inll)ortallc(a oI’ the vasonlotor reactions which accompany the neuralgia, stating they dicl not consider the nervousness of the patient an ordinary reaction to thr pain. hut rat,her an inherent characteristic of t,he pain itself. After a study of 200 cases, (:lwser and Beerman in 19.18 mentioned the tenderness of the cer\-ical sympathetic ganglion and of the cerrical artery in atypical neuralgia. They also insisted on the presence of vasornot,or phenomena.
The Seventh Nerve:
Review of the Literature
The theory that, at.?-pica1 neuralgias are oi’ ix seventh nerve origin was instigated by the disco\,ery of the sensory function of the facial nerve. and the difficulty in explaining certain types of facial pain which could not, be related to the fift,h nerve alone. As early as 1874. Bernhardt, while studying facial palsy cases. reported a slight hyperesthesia in the area of the chorda t,ympani. In 1895, Strong, by observing the anatomy of the tadpole and frog, found that not only the internal mandibular, but also the palatine branch of the seventh nerve in these animals, supplies taste fibers. Dixon, in 1898, studied the sensory distribution of the seventh nerve in man, and stressed the analogy between this nerve in man and in the lower animals. In its distribution, it would be a “typical branchial nerve.”
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In 1906 Spiller drew attention to the preservation of the deep sensibility of the face after removal of the Gasserian ganglion. Cushing also indicated the preservation of a crude form of sensibility after operation on the Gasserian ganglion in the anterior two-thirds of the tongue, probably because of the seventh nerve. J. Ramsay Hunt, in 1910, basing his conclusions on cases of herpes zoster affecting the geniculate ganglion, put “an opening wedge in the discovery of a the sensory system of the seventh small but important system of sensibility,” nerve. More recently, this author proposed an explanation of atypical neuralgia. “In a case of complete geniculate neuralgia, one would expect pain in the ear, and in the deeper structures of the face and the posterior orbitonasal regions. These cases of deep prosopalgia are, I believe, scattered in various groups of painful disorders of the face which are described under such headings as atypical neuralgia, sympathalgia, and a type referred to by Gushing as pa.inful convulsive tic.” Rhinehart, in 1919, made a study of serial sections of the head of the albino mouse, describing a ramus cutaneous facialis which emerges after the facial nerve is crossed by the auricular branch of the tenth nerve. They become intermingled, some of the fibers of each distribution passing out with the fibers of the other. In 1931, Baudoin pointed out the sensory unity that the neryus intermedius, geniculate ganglion, and chorda tympani constitute, comparing this unity to that in the posterior root of the spinal nerve. Gerard, in an experimental study in 1923, concluded that deep pain sensations from the muscles of the face are carried by the seventh nerve. In his experiments, aft,er severing the nerve, he observed painful responses to the electric stimuli in the deep structures of the face. In the same year, Davis made a study of deep facial sensibility with the following conclusions : “The pressure pain sensibility of the face is retained following trigeminal neurectorny although all superficial cutaneous sensibility is lost.” The facial nerve in man, therefore, is a mixed nerve and contains a general visceral-sensory compound. -Davis and Pollock in 1932 studied the roll of the sympathetic system in the production of pains in the head, and brought forth further evidence of the sensory role of the seventh nerve. On the basis of their experiments, they wrote that ordinary sensations of pain, touch, and temperature are conducted through the peripheral and central pathways of the trigeminal nerve and that deep pressure pain sensibility is transmitted through the seventh nerve. There are no afferent sympathetic fibers in the cervical sympathetic. In 1925, in a contribution to the study of the sphenopalatine ganglion and facial nerve, Ruskin underlines the many connections which this nerve has. “In the light of such wide connections, one begins to see how an irritation of the nerve can produce disturbances ranging from neuralgia of the face to that of the neck.”
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In this author’s opinion, the connection with the otic and the ciliaI*\. ganglion would explain the dist.urb;rnces in the eye and ill the mantlibular region. The connection with t,he vagus nerve would explain the relief of the laryngeal pain by anesthetization of the ganglion. The connections with the lesser occipital and cutaneous cervicaal branches probably account for the l)ains of the neck. “The tlif?ic*ult,y in the situat,ion lies, however, in explaining the causes of a reflex passing by such distant branches.” The author caonsiders the sphenopalatine neuralgia as being a c*ombinatio~l of four tlifferent factors : 1. 2. :I. 1.
A A A A
Irigeniinal maxillary syntlr~onie. sensory facial nerve syndroirle. sympathetic syndrome. local sphenopalatine ganglion syndrome.
In 1928, 5ung$, Tagantl, and Phavanne demonstrated t,hat the IIIUCOUS glands of the nose and palate receive their postganglionic fibers from the ganglion. The great superficial petrosal nerve is the pathway of the preganglionic secretory fibers. This suggests that the ganglion was also J,al,asyiupathetic. Zachary Blier, in his study of the ganglion in 1930, noticetl that the posterior nasal nerves and the Vidian nerve are capable of protlucing extremel, powerful reflexes. Stimulations of these nerves produce reflex efFects npolt anal heart. In the case of the Vidian the head, neck, tongue, respiration. nerve, the afferent fibers run in the greater superficial petrosal and not the sympathetic because se&on of the sym],athetic? does not; abolish t!:e reflexes. In 1938, Olaf Tlarsell esperimentctl on the rabbit and obserrrci the effect of stimulation of the nasal mucosa on the behavior of the blootl T-essei.+in the ear. The maxillary nerve was first sectioned proximal to the sphenopalatine branches and lat,er the nasal II~LKYXI in the sphenopalat,ine region was stimulated by a weak faratlic current,. Photographs under low magnification of t,he blood vessels of the ear show marked vasoconstriction where the electric stimulus was applied. After sectioning the cord between \-ertebrae (1 7 and C 6. vasoconstriction did not take place. On the basis of this experiment, Larsell offers an explanation for 1)asa.l heatlache : (‘onstriction of t,he blood vessels vwsal headache IIe presents produces ischemia. and ischemiw produces pain. as a reflex arc. which seems in good accord with what we know of the physiologic anatomy of certain reflexes, such as the pupillary dilatation reflex. Chorobski and Penfield presented a different view in 1932. They insistetl on the seventh nerve as a parasympathetic compownd. They observed that stimulation of the facial nerve produces vasodilatation of certain pial arteries. Section of the greater superficial I)etrosal nerve put an entl to the reaction. Stimulation of the peripheral portion of t,he clivided greater superficial petrosal Stimulation of the peripheral portion of ner\Te put ill1 end to the reaction. the divided greater sul)erfic*ial petrosai nerve produces energetic dilatation of The)- pointetl alit the significance of ill1 anastomosis bethe same arteries. tween the great superficial petrosa nerve anti the carotid nerve. 011 one hand, fibers from the former enter the carotid nerve and pass both centrally and peripherally to it. On the other hand, fibers flaom the internal carotid
nerve enter the great superficial petrosal nerve in its proximal portion. The authors consider these last fibers as afferent from the pial vessels. The facial nerve would thus be a nerve of vascular sensibility. Undoubtedly the seventh nerve plays an important role in atypical neuralgia because of its various functions and because of its peripheral and central connections, especially with the fifth, ninth, and tenth nerves. Recognition of another factor is essential: the vascular mechanism commanded by the autonom ic system. Opinion is divided regarding the sensory function of the seventh nerve : A. According to some authors, the sensory part of the seventh nerve transmits stimuli to the nervous centers. From there a sympathetic response is initiated which is characterized by rasoconstrictions of the facial vessels, and a corresponding ischemia. The pain experienced is clue to ischemia and related chemical changes acting upon the nepre endings of the fifth and seventh nerves. R. According to other authors, the stimulation of the seventh nerve provokes a parasympathetic response characterized by vasodilatation of the pial vessels. The sensory portion of the seventh nerve would be t,hen responsible for the pain experienced. The question now is, “Can these two concepts be reconciled?” There is a similarity in the function of the seventh, ninth, and tenth nerves. Each contains motor, vasodilator, and sensory fibers, and many peripheral and close central connections. Opinions vary as to the innervation and pathway of the nerves to the vascular system. The hypothesis that the sympathetic nervous system innervates the blood vessels is difficult to sustain; however, it is plausible that some afferent axons pass through sympathetic branches and ganglia of the head and neck regions as well as through the abdominal region. A second hypothesis is that sensory fibers running beside the blood vessels of the neck and face are branches of the upper thoracic spinal nerves and the ragus. The seventh nerve then would carry vascular sensibility from the pial vessels in the cranium. The fifth nerve (ophthalmic division) also has an important role in the ini.racranial vascular sensibility. Any one of these nerves could be affected by vasomotor reactions whether they were spastic contractions of the smooth muscle of the vessel wall or sudden distention of the vessel wall. It is probable that more than one nerve c~ulcl be affected, thus supporting the concept of polyneuralgia.
The Sympathetic System Tn the vascular diseases such as arteritis obliterans, many cases of angina pectoris, Raynaud’s disease, deep venous thrombosis, causalgia, posttraumatic syndromes, and phantom limb, the vasomotor phenomena are closely associated with pain. There may or may not be, an organic lesion. In certain cases of Raynaud’s disease, for instance, just a hyperexcitability of the sympathetic system occurs. In other cases, contact of the cervical rib or the pressure of a
contracting scalenus is enough to pt,ovoke vascular spasm and pain. Today wt: know the importance of t,he vasomotor reactions and of the autonomic system in the genesis 01’ pain, and j\‘e hare discovered a remarkable weapon I’or t,he treatment of many painful conditions. This type of pain which is associated with vasontotor disturbances and trophic changes is relieved by blocking or suppressing t,he corresponding sympathetic centers. C’ervical sympathectomy for the treatment of at,ypical neuralgia has been tried, with varying results. Some obtained relief of t,he pain while others did not. E’r;riicois-E’1,~tllk iI1 1896 c~stal.)lishecl the idea of thr (+etltrip(+il flutctioll of the sympathetic nerrous system, and demonstrated the part it played in physiology. About the same time, Jaboulay was suggesting cervical sympathectomies for the treat,ment of facial neuralgias that were accompanied by obvious vasomotor attacks. Chalier, who investigated Jaboulay’s cases some years after surgery had been performed, reported a considerable proportion of good results. Langley’s opinion on the sensory function of the sympathetic nervous system was: “All that seems to be possible is to consider as afferent aut,onomic, those impulses which gi\-e rise to reflexes in autonomic tissues and which are incapable of giving rise to sensation (Erectly, and to consider all other afferent fibers as somatic.” (:uidrtl I)?- thr> \vork o 1’ I.‘1.ali~ois-l.‘1,;lllk. llcriche c~onsidt~t8e(l\~asomotor clisturbances as being the essential factor of many painful conditions. He insisted on pain being due to ischemia, but did not overlook vasodilatation as a possible factor, nor, in a more general way, vasomotor disturbances. In conjunction with Fontaine, he observed that when the sympathetic chain is exposed and one pinches the superior cervical ganglion, or the two first rami communicans, or the trunk itself. one causes a sharp pain in the teeth of the lower jaw, in the bone itself, and in t,he angle of the jaw, or in the region of the temporomandibular joint. Novocainization prevents this. Leriche also reportetl that if the adventitia of the carotid bifurcation or of the common carotid is seized with a forceps, the same pain is observed with less intensity. If one pinches t,he special capsule of the thyroid gland in front, or the pedicle of t,he inferior parathyroid, the same pain appears. Tf the primary branches of the crrvical nerve and the great occipital nerve of Arnold are pinched wit,h forceps, sometimes the same pain is evoked. The explanation of these nerves sets up vasomotor phenomena in offered is that “stimulation the trigeminal sphere and that in this way pain in the face may he brought about,, although the trigeminal is not directly affected.” The treat,rnent proposed by this author is surgical removal of the superior cervical ganglion. This type of’ syrrlpnthrctomy has provet snccaessful in ;I few cases. In others, no improvement and no lasting results were noted. In 1932, Harry Hrlsoll studied the facial sensibility after a radical operation of the fifth nerve. and concluded that facial sensibility depends chiefly upon the fifth nerve. hut “as soon as t,he face is deprived of this source, some
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other nerve-either the VII, the sympathetic, or both take over-or it may be through anastomosis with the branches of the cervical plexus. The zero of cutaneous sensibility can be reached not merely through resection of the peripheral nerve supply, but requires deletion of the sympathetic supply as well.” Lewis writes that the direct cause of the pain is not oxygen lack, but the stimulation of the sensory nerves by the metabolic products of muscular activity. Ordinarily these products are removed through oxidation, but where the blood supply is inadequate they accumulate in excess. In 1928 Frazier treated cases of atypical neuralgia by removal of the superior cervical ganglion, or sometimes the middle cervical ganglion, with The pain, however, was not relieved. stripping of the periarterial plexus. M. Peet had a different idea. He agreed that atypical neuralgia pain can he of sympathetic origin, due to vasospasm, but he was not sure that the cervical sympathetic would differ so much from the sympathetic system in other parts of the body. From the results of his experiments, he assumed that there are sensory fibers from the vagus which pass through the superior cervical ganglion on their way to the head. For all these authors, the sympathetic system was responsible for the pain, the common idea being that vasoconstriction provokes ischemia, and ischemia provokes pain.
Is Pain Due to the Exacerbation of Vascular Sensibility? In 1932 Temple Fay conducted some highly interest,ing experiments. He noticed that stimulation by faradic current about the bifurcation of the carotid is extremely painful to the patient. The sheath of the carotid is also extremely sensitive. The pain may be referred to the tongue, the upper and lower jaws, the face about the orbit, the temporal region in the occipital area, deep in the eye and the head, and to the throat by appropriate selection of Connecting the pain with its origin! he points about the arterial bifurcation. wrote : “This type of pain probably finds its port of entry to the brain and consciousness through branches given off by the vagus nerve, which associate themselves with the large cranial vessels and travel with the sympathetic Fibers from the Lower cervical and branches to their field of distribution. upper thoracic cord, by way of the carotid sheath, are important pathways for this type of pain.” Penfield first studied on a physiologic basis, during surgical intervention, the sensibility of the intracra.nial part, which could be involved in craniofacial neuralgias (migraine), pointing out the elective sensibility of the dura mater and of the venous sinuses. Referred pain, caused by stimulation of the lateral wall of the superior sagittal sinus in its anterior part, is felt in the forehead, over the temple, the ear, neck, or at the top of the cranium. Stimulation of the same sinus more anteriorly brings pain over the eyebrow and in the nose, felt as a more or less violent headache. Nausea may he experienced, with eventual vomiting. In migraine, pain which may be felt, in the head or the face comes from dilated intracranial vessels, and most especially from the middle meningeal
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artery, the venous sinuses. ant1 the pial vessels. The ophthalmic division o I the fifth nerve is the sensory pat,h\tr;lv though the se\renth nervt may also 1~ involved. Kuntz believes that vascular sensihilit,y is involved in another way. ln 1943 he wrote: “Hypertension or spastic contract,ion of the smooth muscle in vessel walls is known to be a major effect in the production of pain referable to blood vessels, either 1)s its direct effect on sensory receptors or the consequent ischemia of t,he adjacent territory.” According to a paper presented by Tine1 in 19:%$ pain is due t,o an esa(‘rrhation of vascular sensibility. This type of sensibility ~~ultl usually be a latent, one, its role being in the regulation of vegetative reflexes, but in cases of pathologic exacerbation. it would become a conscious one. His theory is opposite 10 that of liuntz for he invokes the distention of the vessel wall. either arterial ()I’ venous. as opposecl to the theory that the spastic (#ontraction of the smooth muscle of the vessel wall is the main cause of pain. In causalgia. we obser\-e an extreme \-nsodilatation of small arteries which sheets the resistanc*c oi’ c~otlstrictetl c~apillarirs. 111~‘ases of Iierichc’s syndromes which follow trauma to bones or art,iculations. and in acromelalgia of old cases are less painful. people, t,he same thing is true. The erythromelalgia for the rise in arterial pressure is not, so high, due to all intense vasodilatation. Tn Raynaud’s disease, the rather moderated pain of ischemia is f’ollowed by the much more severe pain of secolltlary vasodilatation. In conclusion, discordance in peripheral circulation of a reflex origin. sudden rises in hloo;l pressure a,nd distended vessels with exacerbation of VRSeular sensibility are the conditions front which pain will arise. Iiorton, Xlacl,can. al~tl (‘raig reportetl a ” tww s~-r~lr~n~t~0r mscular Ireaclache” in 1939. They noticed tenderness oreta the branches of the external carotid arteries, and that many paCents obtained relief by pressure over the eye or temporal vessels. A few discovrretl that digital compression of the common carotid on the side of the pain brought relief. These authors insisted upon the coincidence of \-asodilata.tion with the onset of pait). The most interesting part of their findings is the allergic factor. TheJ demonstrated that subcutaneous injection of 0.3 to 0.5 mg. of histamine could provoke headache. This headache was associated with ~.asoclilatation which On the l)asis of their expericould be stopped wit,h injection of epinephrinr. ments, they recommended tlesensitiza,tion. A paroxysmal temporal headache similar to an atypical facial neuralgia was described by Newman in 1945. The pain was relieved by infiltration OF the great, occipital nerve. Tn 194’7, Gardner, Stowell and Dutlinger proposed resection of the greater superficial pet,rosal nerve in the treatment of unila.teral headache. They insisted upon the importance of the parasympathetic discharges. VasodilataCon would provoke the pain, the sensory pathway involved being the seventh nerve. Thus vascular sensibility, reflex action, and the facial sensory system are the basis of this explana,tion of atypical neuralgia.
1)e Seze and Vermeil, in 1948, l~roposcd, as a surgical treatment for migraine, the retrogasserian neurotomy of the ophthalmic contingent in the sensory root of the fifth nerve, and the electrocoagulation of the middle meningeal artery. They recall that, resection ot’ a segment of the temporal artery or even the simple infiltration of Kovocain around the artery may bring relief from the pain. As a medical treatment, vasodilatation should be provoked preventively either by phenolization of the sphenopalatine ganglion, the stel1at.e ganglion block, or by administration of vasodilator drugs (histamine diphosphate, nicotinic acid, or sodium nicotinate) . In 1950, Marcussen and Wolff wrote a report of various headaches. They recall that in an attack of migraine, the pain is known to arise from dilatecl The preheadache phenomena are rearteries inside or outside the cranium. lated to rasoconstriction, which was confirmed by electroencephalographic tracings which showed changes similar to those noticed during periods of cerebral anoxemia. The pain is associated with vasodilatation, but they demonstrate that vasodilatation alone cannot provoke pain. Referring to Pickering’s suggestion, they believe that in addition to the stretching of the vessel wall, there may be another factor, such as sensitization of the pain nerve ending with a chemical agent. Rudolph Jaeger recently wrote : “There are many so-called atypical head and face pains regarded as separate clinical ent.ities that are probably nothing else but migraine. These include the sphenopalatine neuralgias, the erythromelalgias, the post-traumatic headaches, and numerous other ill-defined pains of the face and cranium.” In his opinion, t,he sensation would pass down the nerves of the blood vessels to enter the brain ultimately by the usual afferent pathways. Discussion 1. It seems to be an undeniable fact that the autonomic system is involved in the pain-producing mechanism of atypical neuralgias, but there is a divergence of opinion as to how. 2. Would it be that the sympathetic system has a sensory function proper? Although some experiments seem to prove, while others disprove this theory, it would be the general tendency to deny the cervical sympathetic system any sensory function. 3. What seems more probable and even certain is that pain may be provoked by a reflex action from the autonomic system. We have seen how vasoconstriction and the consecutive ischemia may generate pain by action on the afferent nerves. A %icious circle” may be organized; the pain will persist, diffuse, and aggravate. In atypical neuralgia, however, we observe that the maximum of pain conincides with marked and even intense vasodilatation phenomena. This fact opposes the theory of pain produced by ischemia, and rather favors the concept of pain produced by distention of the arterial wall. 4. This is the concept of an exacerbated vascular sensibility as the main The idea that blood vessels which supply the nerves are intimately factor.
3. The ~r~ost.Iwcbtlt \vUt.ks point out t,he al~logy which exists I,et\veetr migraine and atyl)ic;d ll?11Yi11&$& In migraine, the two recognized phases 01’ vasotlilatatiw with l~rehra&che pheuomena ard the second phase of vasotlilatat,ion with paill we111 to oppose the unique phase of atypical neuralgia. But, do they really oppose it! (.‘oulcl not t,he hackground of a diffuse and persistent paiu with paresthesia wrtwpuntl t.o vasoconstriction and ischemia I The paroxysmicd episotlc, lvith \-asotlilatat,ion phenomena and int,ense p:zill, w~ould t,hen correspoml to the secotltl l)hase oi’ migraine. References Triyemiilal Neuralgia, Suggested Basis of Treatment W. E., and Rlobinsotl, iv.: (Use of Vasodilators, Nicotinic Acitl and Amy1 Nitrate), Lancet 2: 555556. Alajouanine, T., and Thurel, R.: Les sympathalgies faeiales, J. m6d. franp. 22: 188-194, 1933. IZaudouin: 1,~ systemo scnhitif &I nerd I’a~l.iuI, gazette des Hospitaux 23: 301-X4, 19X1. Hernhardt, M. : (~‘ollected Papers on D&cases of Nervous System, vol. 5, 18i4. Billingsley, P. R., and Hanson, S. LV.: I:ranches of the Superior (:er\-ical Sympathetic Gmlglion, .I. Camp. Neural. 29: ::5!)-::lj(i, 19 1s. Iilier, Z.: Physiology of the Sphenoyalatine Ganglion, Am. J. Physiol. 93: 398, 1930. Hroch, 0. J., and 1 trehq 0.: Temporal Arteritis, Sord. med. 30: 1:‘51-1%X, 1946. Temporal -Irt.eritis-3 New Cases, Nord. med. 34: 111 lBroth, 0. J., and I-trchus, 0.: 1115, 1947. of Myelinatetl Afferent Fibers in the Branches of the Cat ‘Y Brueseh, S. R.: Distribution h’acial Nerve. J. Coma. Seurol. 81: 169-191. 1944. Chorobski, J., and f’enlield, %‘.: Cerebral Vasodilator Xerves and Their Pathway From the Medulla Obloncata, Arch. Ncuroi & Psychiat. 28: X57-1287, 1932. Major Trigeminal Neuralgias, (_‘ushing, H.: Am. i. ill. SC. 160: 157, liJ20. L>andy, tV. E.: Am. J. Rurg. 24: 667, 19;:ti. Dandy, W. E.: Treatment of Hemicrani;L (-\ligraine) by Removal of Inferior Cervical and First ‘l’horacic Sympathetic Ganglion, Bull. Johns Hopkins Hosp. 48: Xi-361j Adams,
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,J. A. 11. .2. 131: 126.5, 1946. Dantes, 1). A.: Temporal .Alteritis, I)avis. Loyal: The Deco Sensibilitv of the Face. Arch. Seurol. $ Psvchiat. 9: 263. 1923. Davis: L.,” and Pollock, i,. J.: Th: Rble of the’Hympathetie Nervo& System in the Production of Pain in the Head. Arch. Neurol. & Psvchiat. 27: 282. 1932. Davis, I,., and Pollock, 1,. J.: The RRle of Autonomic Nervous System ‘in the Production of Pain, J. A. X. A. 106: 350, 193fi Zona de 1 ‘ol~c~ill(~ avcc par:tlyric~ f:lvi:rle, Sov. tie Svurologirs. DrjcrinrA, J. J., and Tincl, J.: Rev. neural. 23: 4liti. 191%. tie Seze, H.. Guillaume. .I.$ Hil-~a~l(~~~I-l)u~l~:~~, C’.? ant1 I
Grra.rd, Glaser,
Afferent Impulses of the ‘l’rigeminal Nerve, the Intramedullary Course of X. W.: the Painful, Thermal and Tactile Impulses, Arch. Neurol. & Psychiat 9: 306, 1923. M. A., and Beerman: Atypical Facial Neuralgias, Arch. Int. Med. 61: 172, 1938.
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Physiopathology of Spasmodic Coryza; Study of Procaine O., and Cloetens, W.: Infiltration of the Temporal Artery and Venous Pressure, Acta oto-rhino.-laryng. belg. 1: 3-53, 1947. leur individualite; leur traitement Guillaume, J.: Les neurolgies meningees localisees; chirurgical, Presse med. 54: 31-32, 1946. Guillaume, J., and de Seze, 8.: Rev. neurol. 79: 140, 1947. Harris, W.: Ciliary (Migrainous) Neuralgia and Its Treatment, Brit. M. J. 1: 457, 1936. System in Sensory Conduction and Certain NeuHarris, W.: The Role of the Sympathetic ralgias, Brit. M. J. 2: 112-115, 1936. of Intractable Unilateral Cephalalgia, J. A. M. A. Hayes, Walter G.: Surgical Treatment 136: 538541, 1948. Helson, H. : The Part Played by the Sympathetic System as an Afferent Mechanism in the Region of the Fifth Nerve, Brain 55: 114-121, 1932. Henriques, J. A. de Campos: Cases, Rev. expan. oto-neuro-oftal. y neurocir. 5: 432-438, 1946. Horton, B. T.: A New Syndrome of Vascular Headache, Proc. Staff Meet., Mayo Clin. 14: 257-260, 1938. Temporal Arteritis, 39 Cases, Proc. Central Sot. Clin. Research 19: 78-79, Horton, B. T.: 1946. Horton, B. T., MacLean, A. R., and Craig, TV. M.: New Syndrome of Vascular Headache, Proe. Staff’. Meet.. Mavo Clin. 14: 257.1939. Humb, J. R.: Geniculate’NeuGalgia, Arch. Neural. & Psychiat. 37: 253-258, 1937. du goitre extirpe dans la maladie de Basedow et la Jaboulay, M. : La regeneration section du sympathique cervical dans cette maladie, Lyon m6d. 31: 389. 1896. Jaeger, Rudolph: Headache, J. Internat. Coil. Surgeons 13: 57-63, 1950. cervico, thoraciaque, Paris, 1928, Masson k Cie. Jonnesco. D.: Le sympathique Jung, P.,’ Tagand, I&and Chava.nne, F.: Sur ie role trdphique des nerfs secretoires de la muquense nasale, Compt. rend. Sot. de biol. 99: 515, 1928. Jung, L., Tagand, R., and Chavanne, F.: Etude expbrimentale du role secr&oire et du role trophique des elements nerveux du carrefour sphenopalatin, Sonete Franqaise du O.R.L. 2: 1926. - 301. ---I ----ICuntz, A.: Nerve Fibers of Spinal and Vagus Origin Associated With the Cephalic Sympathetic Nerve, Ann. Otol., Rhin. & Laryng. 43: 50-67, 1936. Kuntz, A.: Recent Advances in Some Aspects of Visceral Neurology, Confinia neurol. 5: 78-112, 1942. Nervous System, Brain 26: l-26,1903. Langley, J. N.: The Autonomic Lanalev, J. N.: ‘The Vascular Dilatation Caused bv the Svmnathetic and the Course of Vasomotor Nerves, J. Physiol. 58: 70-73, 1923: ” c Larsell, Olaf: The Sympathetics of the Head, West. J. Surg. 46: 633, 1938. Larsell, O., and Burns, E. M.: Some Aspects of Some of the Cranial Nerves, Ann. Otol., Rhin. & Laryng. 40: 661, 1931. Larsell, O., and Fenton, R. A.: The Embryology and Neurohistology of the Sphenopalatine Ganglion Connections. A Contribution to the Study of Otalgia, Laryngoscope 37: 371, 1928. Leriche, R., and Fontaine, R.: Rev. neurol., m6m. de 1’Acad. de chir. 62: 877, 1936. Quelques indications nouvelles de l’ablation du ganglion cervical superior, Leriche, R.: Ste. de Chirurgie de Paris 15: 12, 1920. Leriche, R.: The Surgery of Pain (translated by Young), 1939. Rev. de chir. 60: 553, 1922. Leriche, R.: Sensory Effect of Resection of the Sympathetic, l,eriche, R., and Kunlin, J.: Traitement des phlebites post-operatoires par l’infiltration novoeainique de sympathique lombaire, Presse m8d. 42: 1481-1482, 1932. Lewis. T.: Pain. New York. 1942. The Macmillan Comuanv. Lindgren, Inga,’ and Give&ran& Herbert: Surgical T”reatment of Angina Pectoris, J. Neurosurg. 4: 19-30, 1947. Livingstone, W. K.: Phantom Limb Pain-Report of 10 Cases, Arch. Surg. 37: 352-353, 1938. Lopes, P. Mata: Variety of Oc,ular Sympathalgia, Arch. de oftal. hispano-am. 5: 371-377, 1945. Love, J. G., and Adson, A. W.: Effect of Cervicothoracic Sympathectomy on Headaches, Arch. Neurol. & Psychiat. 35: 1203-1207, 1936. MacCallan: Communication Between the Facial and the Glossopharyngeal Nerve, J. Anat. and Physiol. 19: 28-30, 1895. Marcussen, R. M., and Wolff, H. G.: Studies on Headache, Arch. Neurol. & Psychiat. 63: 42-51, 1950. Facial Neuralgia, Arch. Otolaryng. 35: 735-739, 1942. Martin, R. C.: Atypical Nadler, S. B.: Paroxysmal Temporal Headache, J. A. M. A. 129: 335, 1945. Newman, D. A.: Paroxysmal Temporal Headache, J. A. M. A. 129: 1045, 1945. The Role of the Sympathetic in Painful Diseases of the Face, Arch. Neural. & Peet, M.: Psychiat. 22: 313, 1929.
Godin,
Y
“,
Penfield,
W.: Operative ‘l’rwtmrut of Aligraiue and Observations on the Mechanism of Vascular Pain, ‘1’~. Am. Acad. Ophth. 37: 50.66, 19X?. I’rntield, W.: Proc. -1m. Rc\-. Serv. & Meut. Dis. 15: X9, 1935; Arch. Seurol. & PsJchial. 36: 75, 19X; Arch. Jeurol. 6 I’sychiat. 44: -1-r),1940. l’ickc~ring, (+. \V.: I~~speril~~ental Obwrvatiow 011 Headac~he. Hrit. M. .I. 1: !IOi, IX!!. l’icbrrr, .I. R.: 1x3 troubles III, Ii8 sensibility ~lalls les paralysies du uerf facial, I’lesse mC!tl. 30: “4?“44 l’w’. Rhinehat,t: I>. A:: ‘l’t;ti :Yvr, our I.‘aci:tlin ill the Albino Jlouse, .J. Camp. Neural. 30: Sl. 1919. RicarI! A.: ‘I’emporal .\rterilis, Ke*ectiou of Superticial ‘J‘emporal Artery ill Facial Syrll pathalgia, I,you chir. 42: Z50-2,52! l!r-Ji. Roger et Binet: Le syndrome g6uicult: 1x1 Roger. Traite tie physiologie uormalt~ et patho logiyue, Paris, i9:;6, Alasson C (‘ie, vol. 10, p. 42T. Coutribntion to the Study of the Sphenopalatine Ganglion, Laryngowope Ruskin, S. I,.: l!)2.5. 35: Si-IOS, Scwall, 1,:. C.: Surgical Krmo\.al of the Spheuopalatine Ganglion, Ann, Otol., Hhio. tk I,arYflg. 40: i!l. ICI:\;. Sham-, R. C.! Sympathc~tic System aud Pain Phenomena, Arch. Surg. 27: 1072, 193::. Prognosis aud ‘l’reatment of C+angllon Palatine Sluder, (+reeulieltl: j:tiology, Diagnosis, Neuralgia, .I. A1. 1\[. A., pp. 1201.1205, Sept. 27, 191X Anatomical :rr;tl (‘liuical Relation to the Hphenoid Sinus, to the (‘a\-erw Nuder, (Jreenficld: 0u.s Sinus : and I 11thTIT, 11’. \-: VT and Vidian Serves, Tr. Am. Laryng. Assoc.. l!)L!. Sludrr, Grernliel~l: S~III~I.OIII~~ 11f S1-)trrllol):tlatillr (+anglion Neurosis, Aul. .J. 11. SC.. I)rceutwr, 101t1. Sluder: Greenlirltl: J~‘urther ( ‘liuical C)bsrr\-at,ious ou the Sphenopalatine C&ngliou ( Motor, selrsor~ and (:ustatol~,i~), Sew 1.ark M. .J. 91: 850-851, 1910. Souques: %OII:I cer\-ival et paralysie facialr, Rev. neural. 27: 625-628, 1914. Suille:. w. G.: l)eeJ) I’wssure Sensibility of the \TI Nerve, .T. Nerv. & Merit. I)is. 33:
ix,
l!)(IH.
XV. C:.: Preservation of Deep Sellsi bility After Section of the Trigeminal Xerve. .J. Morphol. 10: 121, IY’E. <*t Strong. I). s.: (‘ranial Srrveb of Anlphibia, ‘I’errarol. .J.: Dispuostic Interest of Referwcl Pain in the Territory of the Cranial Serves. ‘Rev. oto-;~euro-oftal. 10: 246 II):??. :-lrch. iutcarnat. (lr neural. 57: 1. -\ug.; 1, Sept.; 1: Oct.. ‘[‘i ntll, .I. : Les algies nympathiques, 19:w. ‘l?nel, .J.: T,e systitimcl IIPI’~BUS \,CgGtatif, Paris, 19X7, Massou & Cie. \‘ail, H. 13.: Reflex Pain in \‘idian Seuralgia, Arch. Otolaryng. 21: 277-296, 1937. Algivi favialrs. algies c~rauit~nnw, algiw nteningies. Seniairrr (1. hC,p. Paris 24: Vermeil: 1%.174, 194s. Yen Htorch, 1’. .J. t:.: l\[igrainci, Am. Pratt. 1: 631~639! lCJ4i. B’inblad. I).: ‘l’ernp~~ral Arteritis, Nerd rtlell. 32: 2X2X-2859, 194ti. Wolff, H. C+.: Mechanisms of Headache. Arch. Keurol. & Psyehiat. 50: 224-X12, 194.). Sl,iller,
NEURALGIAS
ORION
Medicine
AND VASCULAR
ALGIAS
OF THE FACE
H. STUTIWILLE,
.D.D.S., M.D., F’.A.C.S., CHICAGO, ILL., AND -JACQUES TAx+NA(~, I).I>.S., Ml)., P.IRIS, FHASCE
UR profession is often confronted with patients suffering from undefined facial pain. After eliminating the possibilities of underlying pathology, most of these are diagnosed as cases of trigeminal neuralgia, and this diagnosis is usually correct. We should remember, however, that facial sensibility is not entirely under the dependence of the trigeminal nerve; sometimes it is an atypical neuralgia. Most of the facial neuralgias are relieved by section of the sensory root of the fifth cranial nerve, which should prove their origin. In certain cases, however, retrogasserian neurotomy failed to bring the expected result. The situation is still rather confused. Besides cases where there is a possibility of central pain, and those of psychogenic origin, there is a complex group of conditions which have been described under various names such as sphenopalatine ganglion neurosis, Vidian neuralgia, geniculate neuralgia, pseudotrigeminal neuralgia, and sympathalgias of the face. More recently, similar cases have been reported under the headings of migraine, paroxysmal vascular headaches, and erythromelalgia of the head. Despite the differences between these conditions, t,hey still have some points in common and should be considered as clinical varieties of a larger group. It is difficult to find a proper name for the group; atypical neuralgia is not entirely satisfactory. The terminology itself, “sphenopalatine ganglion, of the sensory Vidian nerve, geniculate ganglion,” suggests an involvement portion of the facial nerve. On the other hand, do not the terms “sympathalgias, vascular headaches, erythromelalgia” express the participation of the sympathetic and vascular sensibility? There are two main lines of thought regarding atypical neuralgia: Is the neuralgia related to t,he seventh nerve, or is it due to sympathetic disturbances and the exacerbation of the vascukr sensibility? These questions do not imply, however, that the fifth nerve can be eliminated from the picture entirely.
0
A Clinical
Picture
The patient, middle-aged, male or female, is pale, anxious and nervous, suffering from a burning, nagging, or quivering type of pain, difficult to deFrom the Department of Maxillafacial Surgery, the Chica o College of Dental Surgery and the Stritch Chicago, 81.
1413
Cook County Hospital, Chicago, 111.. School of Medicine, Loyola University,
scribe. The pain is deep in the face. OIL one sitle, fell mostly in the r(JOt of the nose, the temple, or around and behind t.he orbit. \vith no definite limit>s. It, radiates to the ears, ,ja\t~? and treth, c~hanging in int,cnsity, distribution, and characteristics. In association with the pain, there are intense ~wso~tt~tor reactions. The patient experiences a flush, and warmth on one side of the face. with watering of the eyes and nose. Examination reveals a congestiolt of the nasal mu~osa, mostly 011one side. and injected conjunct,i\,a of the eve aild strong pulsations of the temporal artery. Sensory disturbances have also been observe& including hyperesthesia of the skin on the affected side, temporary cloudiness of vision, a transitory Claude-Bernard-Horner syndrome. deafness, and tinnitus. Sometimes there are motor disturbances as expressed by myoclonia in the territory of t,he seventh nerve. Sluder. in 1910. described the sphcnopalatine sytltlromr as it “comples symptom partly neuralgic (painful 1, mot,or. sensory and gustatory.” with a wide radiation of pain to the ear, being severest at a point 5 cm. back of the mastoid and extending t,o the occiput, neck, shoulders, breast, arm, forearm, hands, and fingers. Sometimes the throat on t>he affected side feels sore. and on rare occasions there is itching of the skin, taste dist,urbances, scotoma, and a sense of stiffness and muscle weakness in the upper extremity. Usually the pain is constant, but in certain cases the pain I~:I;V stop and then reappear as a migraine, or stop anal reappear with a. stabbing sharpness, as a tic. In 1933. Alajoua,nine and Thnrel described “Iles sympathalgies faciales.” These authors insistetl on the inll)ortallc(a oI’ the vasonlotor reactions which accompany the neuralgia, stating they dicl not consider the nervousness of the patient an ordinary reaction to thr pain. hut rat,her an inherent characteristic of t,he pain itself. After a study of 200 cases, (:lwser and Beerman in 19.18 mentioned the tenderness of the cer\-ical sympathetic ganglion and of the cerrical artery in atypical neuralgia. They also insisted on the presence of vasornot,or phenomena.
The Seventh Nerve:
Review of the Literature
The theory that, at.?-pica1 neuralgias are oi’ ix seventh nerve origin was instigated by the disco\,ery of the sensory function of the facial nerve. and the difficulty in explaining certain types of facial pain which could not, be related to the fift,h nerve alone. As early as 1874. Bernhardt, while studying facial palsy cases. reported a slight hyperesthesia in the area of the chorda t,ympani. In 1895, Strong, by observing the anatomy of the tadpole and frog, found that not only the internal mandibular, but also the palatine branch of the seventh nerve in these animals, supplies taste fibers. Dixon, in 1898, studied the sensory distribution of the seventh nerve in man, and stressed the analogy between this nerve in man and in the lower animals. In its distribution, it would be a “typical branchial nerve.”
NEURALGIAS
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In 1906 Spiller drew attention to the preservation of the deep sensibility of the face after removal of the Gasserian ganglion. Cushing also indicated the preservation of a crude form of sensibility after operation on the Gasserian ganglion in the anterior two-thirds of the tongue, probably because of the seventh nerve. J. Ramsay Hunt, in 1910, basing his conclusions on cases of herpes zoster affecting the geniculate ganglion, put “an opening wedge in the discovery of a the sensory system of the seventh small but important system of sensibility,” nerve. More recently, this author proposed an explanation of atypical neuralgia. “In a case of complete geniculate neuralgia, one would expect pain in the ear, and in the deeper structures of the face and the posterior orbitonasal regions. These cases of deep prosopalgia are, I believe, scattered in various groups of painful disorders of the face which are described under such headings as atypical neuralgia, sympathalgia, and a type referred to by Gushing as pa.inful convulsive tic.” Rhinehart, in 1919, made a study of serial sections of the head of the albino mouse, describing a ramus cutaneous facialis which emerges after the facial nerve is crossed by the auricular branch of the tenth nerve. They become intermingled, some of the fibers of each distribution passing out with the fibers of the other. In 1931, Baudoin pointed out the sensory unity that the neryus intermedius, geniculate ganglion, and chorda tympani constitute, comparing this unity to that in the posterior root of the spinal nerve. Gerard, in an experimental study in 1923, concluded that deep pain sensations from the muscles of the face are carried by the seventh nerve. In his experiments, aft,er severing the nerve, he observed painful responses to the electric stimuli in the deep structures of the face. In the same year, Davis made a study of deep facial sensibility with the following conclusions : “The pressure pain sensibility of the face is retained following trigeminal neurectorny although all superficial cutaneous sensibility is lost.” The facial nerve in man, therefore, is a mixed nerve and contains a general visceral-sensory compound. -Davis and Pollock in 1932 studied the roll of the sympathetic system in the production of pains in the head, and brought forth further evidence of the sensory role of the seventh nerve. On the basis of their experiments, they wrote that ordinary sensations of pain, touch, and temperature are conducted through the peripheral and central pathways of the trigeminal nerve and that deep pressure pain sensibility is transmitted through the seventh nerve. There are no afferent sympathetic fibers in the cervical sympathetic. In 1925, in a contribution to the study of the sphenopalatine ganglion and facial nerve, Ruskin underlines the many connections which this nerve has. “In the light of such wide connections, one begins to see how an irritation of the nerve can produce disturbances ranging from neuralgia of the face to that of the neck.”
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In this author’s opinion, the connection with the otic and the ciliaI*\. ganglion would explain the dist.urb;rnces in the eye and ill the mantlibular region. The connection with t,he vagus nerve would explain the relief of the laryngeal pain by anesthetization of the ganglion. The connections with the lesser occipital and cutaneous cervicaal branches probably account for the l)ains of the neck. “The tlif?ic*ult,y in the situat,ion lies, however, in explaining the causes of a reflex passing by such distant branches.” The author caonsiders the sphenopalatine neuralgia as being a c*ombinatio~l of four tlifferent factors : 1. 2. :I. 1.
A A A A
Irigeniinal maxillary syntlr~onie. sensory facial nerve syndroirle. sympathetic syndrome. local sphenopalatine ganglion syndrome.
In 1928, 5ung$, Tagantl, and Phavanne demonstrated t,hat the IIIUCOUS glands of the nose and palate receive their postganglionic fibers from the ganglion. The great superficial petrosal nerve is the pathway of the preganglionic secretory fibers. This suggests that the ganglion was also J,al,asyiupathetic. Zachary Blier, in his study of the ganglion in 1930, noticetl that the posterior nasal nerves and the Vidian nerve are capable of protlucing extremel, powerful reflexes. Stimulations of these nerves produce reflex efFects npolt anal heart. In the case of the Vidian the head, neck, tongue, respiration. nerve, the afferent fibers run in the greater superficial petrosal and not the sympathetic because se&on of the sym],athetic? does not; abolish t!:e reflexes. In 1938, Olaf Tlarsell esperimentctl on the rabbit and obserrrci the effect of stimulation of the nasal mucosa on the behavior of the blootl T-essei.+in the ear. The maxillary nerve was first sectioned proximal to the sphenopalatine branches and lat,er the nasal II~LKYXI in the sphenopalat,ine region was stimulated by a weak faratlic current,. Photographs under low magnification of t,he blood vessels of the ear show marked vasoconstriction where the electric stimulus was applied. After sectioning the cord between \-ertebrae (1 7 and C 6. vasoconstriction did not take place. On the basis of this experiment, Larsell offers an explanation for 1)asa.l heatlache : (‘onstriction of t,he blood vessels vwsal headache IIe presents produces ischemia. and ischemiw produces pain. as a reflex arc. which seems in good accord with what we know of the physiologic anatomy of certain reflexes, such as the pupillary dilatation reflex. Chorobski and Penfield presented a different view in 1932. They insistetl on the seventh nerve as a parasympathetic compownd. They observed that stimulation of the facial nerve produces vasodilatation of certain pial arteries. Section of the greater superficial I)etrosal nerve put an entl to the reaction. Stimulation of the peripheral portion of t,he clivided greater superficial petrosal Stimulation of the peripheral portion of ner\Te put ill1 end to the reaction. the divided greater sul)erfic*ial petrosai nerve produces energetic dilatation of The)- pointetl alit the significance of ill1 anastomosis bethe same arteries. tween the great superficial petrosa nerve anti the carotid nerve. 011 one hand, fibers from the former enter the carotid nerve and pass both centrally and peripherally to it. On the other hand, fibers flaom the internal carotid
nerve enter the great superficial petrosal nerve in its proximal portion. The authors consider these last fibers as afferent from the pial vessels. The facial nerve would thus be a nerve of vascular sensibility. Undoubtedly the seventh nerve plays an important role in atypical neuralgia because of its various functions and because of its peripheral and central connections, especially with the fifth, ninth, and tenth nerves. Recognition of another factor is essential: the vascular mechanism commanded by the autonom ic system. Opinion is divided regarding the sensory function of the seventh nerve : A. According to some authors, the sensory part of the seventh nerve transmits stimuli to the nervous centers. From there a sympathetic response is initiated which is characterized by rasoconstrictions of the facial vessels, and a corresponding ischemia. The pain experienced is clue to ischemia and related chemical changes acting upon the nepre endings of the fifth and seventh nerves. R. According to other authors, the stimulation of the seventh nerve provokes a parasympathetic response characterized by vasodilatation of the pial vessels. The sensory portion of the seventh nerve would be t,hen responsible for the pain experienced. The question now is, “Can these two concepts be reconciled?” There is a similarity in the function of the seventh, ninth, and tenth nerves. Each contains motor, vasodilator, and sensory fibers, and many peripheral and close central connections. Opinions vary as to the innervation and pathway of the nerves to the vascular system. The hypothesis that the sympathetic nervous system innervates the blood vessels is difficult to sustain; however, it is plausible that some afferent axons pass through sympathetic branches and ganglia of the head and neck regions as well as through the abdominal region. A second hypothesis is that sensory fibers running beside the blood vessels of the neck and face are branches of the upper thoracic spinal nerves and the ragus. The seventh nerve then would carry vascular sensibility from the pial vessels in the cranium. The fifth nerve (ophthalmic division) also has an important role in the ini.racranial vascular sensibility. Any one of these nerves could be affected by vasomotor reactions whether they were spastic contractions of the smooth muscle of the vessel wall or sudden distention of the vessel wall. It is probable that more than one nerve c~ulcl be affected, thus supporting the concept of polyneuralgia.
The Sympathetic System Tn the vascular diseases such as arteritis obliterans, many cases of angina pectoris, Raynaud’s disease, deep venous thrombosis, causalgia, posttraumatic syndromes, and phantom limb, the vasomotor phenomena are closely associated with pain. There may or may not be, an organic lesion. In certain cases of Raynaud’s disease, for instance, just a hyperexcitability of the sympathetic system occurs. In other cases, contact of the cervical rib or the pressure of a
contracting scalenus is enough to pt,ovoke vascular spasm and pain. Today wt: know the importance of t,he vasomotor reactions and of the autonomic system in the genesis 01’ pain, and j\‘e hare discovered a remarkable weapon I’or t,he treatment of many painful conditions. This type of pain which is associated with vasontotor disturbances and trophic changes is relieved by blocking or suppressing t,he corresponding sympathetic centers. C’ervical sympathectomy for the treatment of at,ypical neuralgia has been tried, with varying results. Some obtained relief of t,he pain while others did not. E’r;riicois-E’1,~tllk iI1 1896 c~stal.)lishecl the idea of thr (+etltrip(+il flutctioll of the sympathetic nerrous system, and demonstrated the part it played in physiology. About the same time, Jaboulay was suggesting cervical sympathectomies for the treat,ment of facial neuralgias that were accompanied by obvious vasomotor attacks. Chalier, who investigated Jaboulay’s cases some years after surgery had been performed, reported a considerable proportion of good results. Langley’s opinion on the sensory function of the sympathetic nervous system was: “All that seems to be possible is to consider as afferent aut,onomic, those impulses which gi\-e rise to reflexes in autonomic tissues and which are incapable of giving rise to sensation (Erectly, and to consider all other afferent fibers as somatic.” (:uidrtl I)?- thr> \vork o 1’ I.‘1.ali~ois-l.‘1,;lllk. llcriche c~onsidt~t8e(l\~asomotor clisturbances as being the essential factor of many painful conditions. He insisted on pain being due to ischemia, but did not overlook vasodilatation as a possible factor, nor, in a more general way, vasomotor disturbances. In conjunction with Fontaine, he observed that when the sympathetic chain is exposed and one pinches the superior cervical ganglion, or the two first rami communicans, or the trunk itself. one causes a sharp pain in the teeth of the lower jaw, in the bone itself, and in t,he angle of the jaw, or in the region of the temporomandibular joint. Novocainization prevents this. Leriche also reportetl that if the adventitia of the carotid bifurcation or of the common carotid is seized with a forceps, the same pain is observed with less intensity. If one pinches t,he special capsule of the thyroid gland in front, or the pedicle of t,he inferior parathyroid, the same pain appears. Tf the primary branches of the crrvical nerve and the great occipital nerve of Arnold are pinched wit,h forceps, sometimes the same pain is evoked. The explanation of these nerves sets up vasomotor phenomena in offered is that “stimulation the trigeminal sphere and that in this way pain in the face may he brought about,, although the trigeminal is not directly affected.” The treat,rnent proposed by this author is surgical removal of the superior cervical ganglion. This type of’ syrrlpnthrctomy has provet snccaessful in ;I few cases. In others, no improvement and no lasting results were noted. In 1932, Harry Hrlsoll studied the facial sensibility after a radical operation of the fifth nerve. and concluded that facial sensibility depends chiefly upon the fifth nerve. hut “as soon as t,he face is deprived of this source, some
h-EURALGIAS
ASD
VASCUIAR
ALGIBS
OF FACE
1419
other nerve-either the VII, the sympathetic, or both take over-or it may be through anastomosis with the branches of the cervical plexus. The zero of cutaneous sensibility can be reached not merely through resection of the peripheral nerve supply, but requires deletion of the sympathetic supply as well.” Lewis writes that the direct cause of the pain is not oxygen lack, but the stimulation of the sensory nerves by the metabolic products of muscular activity. Ordinarily these products are removed through oxidation, but where the blood supply is inadequate they accumulate in excess. In 1928 Frazier treated cases of atypical neuralgia by removal of the superior cervical ganglion, or sometimes the middle cervical ganglion, with The pain, however, was not relieved. stripping of the periarterial plexus. M. Peet had a different idea. He agreed that atypical neuralgia pain can he of sympathetic origin, due to vasospasm, but he was not sure that the cervical sympathetic would differ so much from the sympathetic system in other parts of the body. From the results of his experiments, he assumed that there are sensory fibers from the vagus which pass through the superior cervical ganglion on their way to the head. For all these authors, the sympathetic system was responsible for the pain, the common idea being that vasoconstriction provokes ischemia, and ischemia provokes pain.
Is Pain Due to the Exacerbation of Vascular Sensibility? In 1932 Temple Fay conducted some highly interest,ing experiments. He noticed that stimulation by faradic current about the bifurcation of the carotid is extremely painful to the patient. The sheath of the carotid is also extremely sensitive. The pain may be referred to the tongue, the upper and lower jaws, the face about the orbit, the temporal region in the occipital area, deep in the eye and the head, and to the throat by appropriate selection of Connecting the pain with its origin! he points about the arterial bifurcation. wrote : “This type of pain probably finds its port of entry to the brain and consciousness through branches given off by the vagus nerve, which associate themselves with the large cranial vessels and travel with the sympathetic Fibers from the Lower cervical and branches to their field of distribution. upper thoracic cord, by way of the carotid sheath, are important pathways for this type of pain.” Penfield first studied on a physiologic basis, during surgical intervention, the sensibility of the intracra.nial part, which could be involved in craniofacial neuralgias (migraine), pointing out the elective sensibility of the dura mater and of the venous sinuses. Referred pain, caused by stimulation of the lateral wall of the superior sagittal sinus in its anterior part, is felt in the forehead, over the temple, the ear, neck, or at the top of the cranium. Stimulation of the same sinus more anteriorly brings pain over the eyebrow and in the nose, felt as a more or less violent headache. Nausea may he experienced, with eventual vomiting. In migraine, pain which may be felt, in the head or the face comes from dilated intracranial vessels, and most especially from the middle meningeal
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artery, the venous sinuses. ant1 the pial vessels. The ophthalmic division o I the fifth nerve is the sensory pat,h\tr;lv though the se\renth nervt may also 1~ involved. Kuntz believes that vascular sensihilit,y is involved in another way. ln 1943 he wrote: “Hypertension or spastic contract,ion of the smooth muscle in vessel walls is known to be a major effect in the production of pain referable to blood vessels, either 1)s its direct effect on sensory receptors or the consequent ischemia of t,he adjacent territory.” According to a paper presented by Tine1 in 19:%$ pain is due t,o an esa(‘rrhation of vascular sensibility. This type of sensibility ~~ultl usually be a latent, one, its role being in the regulation of vegetative reflexes, but in cases of pathologic exacerbation. it would become a conscious one. His theory is opposite 10 that of liuntz for he invokes the distention of the vessel wall. either arterial ()I’ venous. as opposecl to the theory that the spastic (#ontraction of the smooth muscle of the vessel wall is the main cause of pain. In causalgia. we obser\-e an extreme \-nsodilatation of small arteries which sheets the resistanc*c oi’ c~otlstrictetl c~apillarirs. 111~‘ases of Iierichc’s syndromes which follow trauma to bones or art,iculations. and in acromelalgia of old cases are less painful. people, t,he same thing is true. The erythromelalgia for the rise in arterial pressure is not, so high, due to all intense vasodilatation. Tn Raynaud’s disease, the rather moderated pain of ischemia is f’ollowed by the much more severe pain of secolltlary vasodilatation. In conclusion, discordance in peripheral circulation of a reflex origin. sudden rises in hloo;l pressure a,nd distended vessels with exacerbation of VRSeular sensibility are the conditions front which pain will arise. Iiorton, Xlacl,can. al~tl (‘raig reportetl a ” tww s~-r~lr~n~t~0r mscular Ireaclache” in 1939. They noticed tenderness oreta the branches of the external carotid arteries, and that many paCents obtained relief by pressure over the eye or temporal vessels. A few discovrretl that digital compression of the common carotid on the side of the pain brought relief. These authors insisted upon the coincidence of \-asodilata.tion with the onset of pait). The most interesting part of their findings is the allergic factor. TheJ demonstrated that subcutaneous injection of 0.3 to 0.5 mg. of histamine could provoke headache. This headache was associated with ~.asoclilatation which On the l)asis of their expericould be stopped wit,h injection of epinephrinr. ments, they recommended tlesensitiza,tion. A paroxysmal temporal headache similar to an atypical facial neuralgia was described by Newman in 1945. The pain was relieved by infiltration OF the great, occipital nerve. Tn 194’7, Gardner, Stowell and Dutlinger proposed resection of the greater superficial pet,rosal nerve in the treatment of unila.teral headache. They insisted upon the importance of the parasympathetic discharges. VasodilataCon would provoke the pain, the sensory pathway involved being the seventh nerve. Thus vascular sensibility, reflex action, and the facial sensory system are the basis of this explana,tion of atypical neuralgia.
1)e Seze and Vermeil, in 1948, l~roposcd, as a surgical treatment for migraine, the retrogasserian neurotomy of the ophthalmic contingent in the sensory root of the fifth nerve, and the electrocoagulation of the middle meningeal artery. They recall that, resection ot’ a segment of the temporal artery or even the simple infiltration of Kovocain around the artery may bring relief from the pain. As a medical treatment, vasodilatation should be provoked preventively either by phenolization of the sphenopalatine ganglion, the stel1at.e ganglion block, or by administration of vasodilator drugs (histamine diphosphate, nicotinic acid, or sodium nicotinate) . In 1950, Marcussen and Wolff wrote a report of various headaches. They recall that in an attack of migraine, the pain is known to arise from dilatecl The preheadache phenomena are rearteries inside or outside the cranium. lated to rasoconstriction, which was confirmed by electroencephalographic tracings which showed changes similar to those noticed during periods of cerebral anoxemia. The pain is associated with vasodilatation, but they demonstrate that vasodilatation alone cannot provoke pain. Referring to Pickering’s suggestion, they believe that in addition to the stretching of the vessel wall, there may be another factor, such as sensitization of the pain nerve ending with a chemical agent. Rudolph Jaeger recently wrote : “There are many so-called atypical head and face pains regarded as separate clinical ent.ities that are probably nothing else but migraine. These include the sphenopalatine neuralgias, the erythromelalgias, the post-traumatic headaches, and numerous other ill-defined pains of the face and cranium.” In his opinion, t,he sensation would pass down the nerves of the blood vessels to enter the brain ultimately by the usual afferent pathways. Discussion 1. It seems to be an undeniable fact that the autonomic system is involved in the pain-producing mechanism of atypical neuralgias, but there is a divergence of opinion as to how. 2. Would it be that the sympathetic system has a sensory function proper? Although some experiments seem to prove, while others disprove this theory, it would be the general tendency to deny the cervical sympathetic system any sensory function. 3. What seems more probable and even certain is that pain may be provoked by a reflex action from the autonomic system. We have seen how vasoconstriction and the consecutive ischemia may generate pain by action on the afferent nerves. A %icious circle” may be organized; the pain will persist, diffuse, and aggravate. In atypical neuralgia, however, we observe that the maximum of pain conincides with marked and even intense vasodilatation phenomena. This fact opposes the theory of pain produced by ischemia, and rather favors the concept of pain produced by distention of the arterial wall. 4. This is the concept of an exacerbated vascular sensibility as the main The idea that blood vessels which supply the nerves are intimately factor.
3. The ~r~ost.Iwcbtlt \vUt.ks point out t,he al~logy which exists I,et\veetr migraine and atyl)ic;d ll?11Yi11&$& In migraine, the two recognized phases 01’ vasotlilatatiw with l~rehra&che pheuomena ard the second phase of vasotlilatat,ion with paill we111 to oppose the unique phase of atypical neuralgia. But, do they really oppose it! (.‘oulcl not t,he hackground of a diffuse and persistent paiu with paresthesia wrtwpuntl t.o vasoconstriction and ischemia I The paroxysmicd episotlc, lvith \-asotlilatat,ion phenomena and int,ense p:zill, w~ould t,hen correspoml to the secotltl l)hase oi’ migraine. References Triyemiilal Neuralgia, Suggested Basis of Treatment W. E., and Rlobinsotl, iv.: (Use of Vasodilators, Nicotinic Acitl and Amy1 Nitrate), Lancet 2: 555556. Alajouanine, T., and Thurel, R.: Les sympathalgies faeiales, J. m6d. franp. 22: 188-194, 1933. IZaudouin: 1,~ systemo scnhitif &I nerd I’a~l.iuI, gazette des Hospitaux 23: 301-X4, 19X1. Hernhardt, M. : (~‘ollected Papers on D&cases of Nervous System, vol. 5, 18i4. Billingsley, P. R., and Hanson, S. LV.: I:ranches of the Superior (:er\-ical Sympathetic Gmlglion, .I. Camp. Neural. 29: ::5!)-::lj(i, 19 1s. Iilier, Z.: Physiology of the Sphenoyalatine Ganglion, Am. J. Physiol. 93: 398, 1930. Hroch, 0. J., and 1 trehq 0.: Temporal Arteritis, Sord. med. 30: 1:‘51-1%X, 1946. Temporal -Irt.eritis-3 New Cases, Nord. med. 34: 111 lBroth, 0. J., and I-trchus, 0.: 1115, 1947. of Myelinatetl Afferent Fibers in the Branches of the Cat ‘Y Brueseh, S. R.: Distribution h’acial Nerve. J. Coma. Seurol. 81: 169-191. 1944. Chorobski, J., and f’enlield, %‘.: Cerebral Vasodilator Xerves and Their Pathway From the Medulla Obloncata, Arch. Ncuroi & Psychiat. 28: X57-1287, 1932. Major Trigeminal Neuralgias, (_‘ushing, H.: Am. i. ill. SC. 160: 157, liJ20. L>andy, tV. E.: Am. J. Rurg. 24: 667, 19;:ti. Dandy, W. E.: Treatment of Hemicrani;L (-\ligraine) by Removal of Inferior Cervical and First ‘l’horacic Sympathetic Ganglion, Bull. Johns Hopkins Hosp. 48: Xi-361j Adams,
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