Facial pain

Oral medicine

Facial pain Arnold

P. Friedman,

DEPARTMENT

M.D., New York, N. 4’.

OF NEUROLOGY,

COLUMBIA

UNIVERSITY

HOSPITAL;

AND

PSYCHIATRY,

THE

COLLEGE

; THE HEADACHE

MONTEFIORE

OF PHYSICIANS

NEUROLOGICAL UNIT,

DIVISION

INSTITUTE,

AND

SURGEONS,

PRESBYTERIAN

OF NEUROLOGY

AND

HOSPITAL

F

acial pain is a symptom which may be associated with a variet.y of clinical conditions. The underlying disorder may be anatomic, physiologic, or psychologic. Although methods of affording relief have been found, the basic causes and mechanisms producing the pain, in most instances, remain unsolved. To the patient, such a symptom is disturbing not only because of the unpleasant quality of the sensation but because of possible unpleasant psychologic connotations. For the physician, precise diagnosis and treatment of facial pain is usually quite difficult because of the extremely complex cranial innervation, the intricate vascular supply, and the extent to which responses to a painful stimulus are modulated by the emotional state. For purposes of clinical management, we can group facial pain into three main categories : (1) typical neuralgias, primarily neurogenic; ( 2) atypical neuralgias, primarily vascular and psychogenic; and (3) facial pain secondary to other extracranial and intracranial causes. Such a classification has many defects, but it permits a rational approach to diagnosis and therapy. In the present discussion the main emphasis will be upon atypical neuralgias and their subdivisions. ATYPICAL

NEURALGIAS

Atypical neuralgias are characterized by attacks of pain in the head, face, and neck. This pain is not well localized, and it may occur in paroxysms or be continuous. There is considerable confusion regarding the nomenclature of this held

730

Presented at the monthly conference of the New York Institute of Clinical Oral at the New York Academy of Medicine on Feb. 25, 1963. Part of this article is reprinted from Archives of Neurology, January, 1960.

Pathology

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pain

731

group of neuralgias. The mechanism of the pain is not clearly understood, and, because of the diffuse localization, the pain may be classified either as headache or as facial neuralgia. In 1924 Frazier and Russell1 suggested the term atypical neuralgia. Before and since that time, essentially identical craniofacial pain syndromes have been described under a variety of names. On the basis of the clinical picture and mechanism, it is difficult to separate any of these various syndromes. History

Miillendorff, in 1867, described this symptom complex as red migraine, with hemicrania, homolateral redness of the face, injection of the eye, lacrimation, and dilatation of the temporal arteries. Bing* called it erythroprosopalgia and related it to the sympathalgies faciales of Alajouanine and Thure13 Sluder4 characterized it as sphenopalatine neuralgia, or lower half headache. There is no factual clinical or laboratory evidence that such condition as sphenopalatine neuralgia exists as an entity. It would appear that the disorder described in many of Sluder’s cases would now be considered as trigeminal neuralgia or atypical neuralgia. Pasteur Vallery-Radot5 and others published reports of such cases under the title “Syndrome of Hemicephalic Vasodilatation of Sympathetic Origin. ” Harris6 called the syndrome ciliary (migrainous) neuralgia. Later, in 1932, Vail7 referred to vidian neuralgia. Brickner and Riley* preferred to call it autonomic facial cephalalgia. Horton, MacLean, and Craig9 identified a new syndrome which they originally named erythromelalgia of the head but changed in 1941 to histamine cephalalgia. Gardner and co-workers1o described the same syndrome as petrosal neuralgia. Symonds,” in agreement with other authors, believed this to be a migraine variant. Among others who reported similar cases in the literature are Dandy, Taptas, Lenormant, Kunkle and associates, and White and Sweet. Symptoms

The pain of atypical neuralgia has the following characteristics: It may be paroxysmal, of several hours’ duration, or constant; it does not follow the anatomic course of the cranial nerves; it is not precipitated by stimulation of a trigger area ; it is usually described as a pressure or as a pulling, stabbing, or drawing sensation. It is associated with autonomic nervous system signs, such Table

I. Synonyms of craniofacial

Red migraine Sphenopalatine neuralgia Erythromelalgia of the head Sympathetic hemicrania Migrainous (diary) neuralgia Carotodynia Vi&an neuralgia Autonomic facial cephalalgia Histaminic cephalalgia Petrosal neuralgia (From .8rch. Newrol., January,

syndromes iWW&~dOdf

Bing Pasteur Vallery Harris JW Vail Riley Horton Gardner 1960.)

Radot

1867 1908 1910 1925 1926 1932 1932 1935 1941 1947

Table

II. Criberia

Distri~~utjon Character

of

neuralgias Does not. follow

pith

of pain

Duration

nervous

Precipitation

nerve

Hours

by external

or da>-s

Lacrimation, flushing, other symptoms

system sigus stimuli

Absent Younger

age group

Pharmacology Vaaoconstrictor drugs Vasodilator drugs Narcotics

Frequent No relief Frequent

relief

Relief by surgical or chemical of cranial nerve

relief

interruption Sane

Personality

Neurotic Arch. Nevrol.,

nasal congestion,

NO

zone

Age

(From

distribution

Effuse, deep-seated, poorly localized; described as pulbng, gripping, etc.

of pain

Autonomic

Trigger

of atypical

January,

traits

prominent

1960.)

as lacrimation, nasal congestion, or increased skin temperature. The pain is not relieved by surgical section of sensory nerve fibers, but it is frequently relieved by vasoconstrictors. Commonly the condition is associated with a personality problem. Pathogenesis

In spite of a great deal of study within recent years, much uncertainty remains regarding the cause and mechanisms of atypical neuralgias. Most of the theories seem to agree that in some cases periodic attacks of local dilatation of extracranial vessels occur in areas mainly supplied by the branches of the external carotid arteries. In support of the hypothesis of vasodilatation is the presence of a distended temporal artery in some cases, the injection of the eye, the congestion of the nose, the local increase in skin temperature, the occasional relief upon compression of the temporal or carotid artery, and the usual good response to vasoconstrictive agents. However, this alone does not explain the secretory phenomena and other associated manifestations from the autonomic nervous system and the photophobia that is sometimes encountered. The pathophysiological mechanisms that trigger the attacks are not well understood. Recent studies of headaches arising in the scalp arteries suggest that such pain depends partly on the release into the tissues about dilated vessels of a pain-threshold-lowering substance with properties similar to bradykinin and serotonin.‘z I found it convenient to subdivide the typical neuralgias into two main groups-cluster headache and atypical neuralgia variants. Frequently it is not possible to differentiate one type from the other on a descriptive basis. In these cases, the temporal relationship of attacks may change from periodic

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733

bouts with long periods of remission to several months of daily attacks of pain, or even continuous pain. CLUSTER HEADACHE

The clinical picture is one of periodic excruciating and agonizing unilateral pain involving the eye and/or temple, associated with injection and tearing of the ipsilateral eye and rhinorrhea or stuffiness of the nose. Such attacks frequently occur in showers or clusters; there may be increased surface temperature and also swelling of the temporal vessels of the involved side of the head. Pain is the outstanding complaint. It is constant, excruciating, burning, and boring. It may spread from the orbital region and temple to the neck and often to the face. The attacks are short, commencing and often terminating suddenly; they tend to awaken the patient at night 1 or 2 hours after he has gone to sleep. During the attack the patient tends to move about rather than be quiet. The attacks may occur as frequently as four or five times in a period of 24 hours. In the first stage of an attack, compression of the common carotid artery, and sometimes of the temporal artery, frequently gives prompt relief. (As previously noted, the pathogenesis of this head pain is primarily vascular.) It should be noted, however, that psychogenic factors can also be of significance. ATYPICAL

NEURALGIA

VARIANTS

The clinical picture in this group of conditions is not so distinct. The pain frequently is characterized as being deep-seated or poorly localized, and it is described as pulling or gripping. The attacks tend to be prolonged, and association with cranial autonomic symptoms and signs is less marked. In many instances the attacks of pain are periodic at first, but later the pain may become continuous. The headache occurs predominantly in female patients. Atypical neuralgia variants have multiple mechanisms which include vascular, muscular, and psychogenic components alone or in combination. In many inst.ances, the patients are suffering from psychoneurotic conversion or compulsion reactions, and there is frequently a hist.ory of the initial pain occurring at the time of a Table

Ill. Comparison

of cluster headaches and atypical Cluster

Family history

of headache

Sex

20%

Age at onset Location of pain

Predominantly 30-50 yr. Unilateral-orbital,

Character

Sharp, throbbing

of pain

Duration of pain Seasonal occurrence Cranial autonomic nervous system signs Pharmacologv Vasoconsthctors Analgesics Emotional problems (From

Arch. Newol.,

Minutes Spring,

headache male

to hours fall

facial

neuralgia

Atypical neuralgia variants 60% Predominantly 30-50 yr. Diffuse-unilateral bilateral Variable-pulling, etc. Hours to days None

Common

Uncommon

Relief Inadequate Prominent

Inadequate Frequent relief Predominant

January,

1960.)

variants

female and gripping,

significant event in the emotional life of the pat,ient. The diagnosis should not be made by exclusion but on evid~~ncc patented irk psychological cxamination of the patient. This type o-f patient often has undcrgonc many unnecessary surgical, dental, and medical proccdurc~s. ‘l’hc reactioil to drugs is lrcclucntly ephemeral and inconsistent with thrt known l~h:~rmacologic action of the t*hemicals taken. As previously noted, separation of t,hesc patients into t,wo groups is of some value to the clinician in understanding the mnnagemcnt of the problem, but it must be clearly understood t.hat many int~crmcdiate forms occur. PSYCHOLOGICAL

ASPECTS

Although these two groups differ with respect to the clinical description of the craniofacial pain, as well as to the timing and accompanying cranial vasomotor phenomena, they are linked to each other in that they are related to the patient’s emotional conflict in the handling of life’s stress In discussing psychological aspects of facial pain, it is important to understand that the response to a painful sensation is depondent not only on the strength of the stimulus but also on the individual patient’s reaction to pain. The latter is based upon the patient’s emotional state and behavior pattern. It should be clearly understood t,hat a person’s reaction to pain may be distinct from the sensation that he is experiencing. A mild pain stimulus may cause much suffering because of what it connotes to the patient, whereas the reaction to a strong stimulus may be well tolerated. In the evaluation of all painful states of the face, the psychological aspects of the problem must be given careful consideration. The personality pattern most commonly observed was that of an adult who overconscientious, and efficient, and who in was ambitious, perfectionistic, some instances had difficulty in sexual adjustment. It should be noted that a similar personality type is observed in patients who have classic migraine, hypertension, or asthma. Also, far more persons who have these personality traits adjust well to their environment and have no medical problems. The most frequent character structure of these patients could be described as masochistic. Face pain may either represent repressed, forbidden scxnal wishes or provide a warning as a punishment for attempts to gratify such impulses. In other instances, pain may be a symbolic representation of repressed rage and anger for which punishment is desired.“’ It was particularly interesting that many of these patients could not recognize that they were under greater stress or were more emotionally upset or fatigued prior to an attack than in tho preceding months or years. Furthermore, during their attacks they continued to work in spite of loss of sleep, pain, and increased stress. The attacks occur and continue, whether the patient is at work or on vacation; on land, ocean, or desert; in warm or cold, dry or wet climates. In some patients, however, the presenting complaint of facial pain may be a symptom of an anxiety state or a depression. In such patients investigation reveals an array of behavior disturbances and neurotic reactions forming an integral part of the presenting complaint of facial pain. The importance of

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735

psychological factors in patients with facial pain frequently presents a problem with reference to the type of therapy needed. It must be decided whether appropriate treatment requires exploration of the underlying cause or whether supportive psychological treatment with the use of proper chemical agents will give the patient adequate relief. FACIAL PAIN SECONDARY CAUSES

TO OTHER EXTRACRANIAL

AND INTRACRANIAL

Facial pain, often severe, may be caused by a wide variety of extracranial and intracranial conditions of diverse origin. This group would include pain of dental origin, tumors of the mandible and disorders of the temporomandibular joint, disorders of the nasal and paranasal structur& (such as sinusitis), tumors of the nasopharynx, temporal arteritis, postherpetic neuralgia, referred pain from cervical disc and coronary thrombosis, tumors of the cranial nerves (mainly five and eight), intracranial tumors with secondary nerve compression, aneurysms and anomalies of blood vessels, and numerous other conditions. Atypical facial pain must also be differentiated from typical neuralgias and migra,ine, classic or common. A discussion of the diagnosis and differential diagnosis of this group of disorders is beyond the scope of this article. An approach to such a multitude of clinical conditions in a localized area such as the face can be made with the realization that pain in these conditions is usually conducted by specific neuroanatomic pathways at various levels, starting peripherally and moving centrally in the nervous system. Thus, pain can be considered to arise at the specific nerve endings for pain in the skin by involvement of peripheral nerves, sensory root ganglia, posterior roots, and of pain pathways in the spinal cord and brain stem. Thalamic pain and modification of pain perception by cerebral lesions Table

IV. Differentiation

Distribution Character

of pain of pain

Duration of pain Autonomic nervous system signs Precipitation by external stimuli Trigger zone Age Pharmacologv Vasoconstr:lctor Vasodilator Narcotics Relief by surgical or chemical interruption of cranial nerve Personality (From

Arch.

Newel.,

of typical

and atypical

Typical Limited in the field of one of the cranial nerves Paroxysmal, sharp, localized

neuralgia

Yes

Atypical Does not follow nerve dist,ribution Diffuse, deep-seated, poorly localized; described as pulling, gripping, etc. Hours or days Lacrimation, flushing, nasal congestion, other symptoms No

Present Older age group

Absent Younger

No relief Inadequate Inadequate

Frequent relief No relief Frequent relief

Seconds to minutes None

relief relief

Relief Neurotic traits prominent January,

1960.)

not

age group

No relief Neurotic traits

prominent

TREATMENT

In the management of patients with atypical facial pain, we must recognize that we are dealing with a symptom and not a discasc. The object of treatment is twofold: (1) to relieve the underlying cause and prevent subsequent is attacks and (2) to alleviate the pain of an immediato attack. I’rcvcntion difficult, whereas control of an attack of pain is usually successful. Management of the patient should be considered from two aspects-prophylactic and symptomatic. REFERENCES 1. Frazier,

2. 3.

4. 5. 6. 7. 5. 9. 10. 11. 12. 13.

C. H., and Russell, E. C.: Neuralgia of the Face: An Analysis of 754 Cases With Relation to Pain and Other Sensory Phenomena Before and After Operation, Arch. Neurol. & Psychiat. 11: 557, 1924. hemiVallery-Radot, P., Wolfromm, R., and Barbizet, J.: Syndrome de vase-dilatation cephalique ou cephalee histaminique, Presse med. 59: 589, 1951. Bing, R., and Haymaker, W.: Textbook of Nervous Diseases, ed. 5, St. Louis, 1939, The C. V: M&by Company, p. 682. (or Mtskel’s Ganglion) in Nasal Headaches, Sluder, G. : The Role of the Sphenopalatine New York J. Med. 87: 989, 1908. h&nic6phalique d’oriVallery-Radot? P., and Blamoutier, P.: Syndrome de vasodilatation gine sympathique, Bull. et mem. Sot. med. hop. Paris 49: 1488, 1925. Harris. W.: Ciliarv (Migrainous) Neuraleia and Its Treatment, Brit. M. J. 1.: 457. 1936. Vail, H. H.: Vidi&‘Ne&algia, Ann. Oto?. Rhin. & Laryng. 41’: 837, 1932. ’ Brickner, R. M., and Riley, H. A.: Autonomic Facie-Cephalnlgia,., Bull. Neurol. Inst. New York 4: ‘422, 1935. _ Horton, B. T., MacLean, A. R., and Craig, W. MCI<.: New Syndrome of Vascular Head ache: Result of Treatment With Histamine; Preliminary Report, Proc. Staff Meet. Mayo Clin. 14: 257, 1939. Gardner, W. J., Stowell, A., and Dutlinger, R.: Resection of Greater Petroeal Nerve in Treatment of Unilateral Headache, J. Neurosurg. 4: 105! 194i. Symonds, C. P.: A Particular Variety of Headache, Brain 79: 217, 1956. Ostfeld, A. M., Chapman, L. F., Goodell, IT., and Wolff, H. G. : Studies in Headache: A Summary of Evidence Implicating a Locally Active Chemical Agent in Migraine, Tr. Am. Neural. A. 81: 35, 1956. Friedman, A. P.! and Merritt, H. H. : Headache : Diagnosis and Treatment, Philadelphia, 1959, F. iz. Davis Company, p. 282.