Herbert C. Miller, D.O., FAAO
Reprinted with permission of the American Osteopathic Association.
Pain has been defined in many ways, as the sensation “resulting from the stimulation of specialized nerve endings,”‘ or, more poetically, as a punishment or penalty, as for crime. Other definitions include acute discomfort of body or mind, bodily or mental suffering or distress; a distressing sensation, as in a particular part of the body, and trouble experienced in doing something. (2) One's concept of pain may be colored by diverse circumstances or, in scientific language, feedback. Head pain is usually interpreted by the clinician from the therapeutic point of view, that is, in terms of measures that may stop in, rather than in pathophysiologic terms.
When analyzing head pain, the physician often prefers to look at it as a phenomenon or as the result of stimulation of specialized nerve endings. In reality, pain may be an interpretation of bodily or mental distress. Boshes and Arieff (3) stated:
Certain aspects of pain are predicated exclusively on a neural substrate. Here the basis is an event or an alteration in the nervous system per se, as contrasted to pain caused by malignant disease, infected tissue, fractures or the like. Various divisions of the nervous system may be implicated and a description of the disability or the manner of posture and movement is often sufficient to enable the trained observer to gain an impression as to whether the pain is genuine or functional. Such involvement may be at the receptive, the conductive, the perceptive or the apperceptive level, or combinations thereof.
This would appear to be a generally accepted concept, and yet head pain often is described and interpreted on the basis of a symptom complex rather than in terms of the anatomic and physiologic organization of the central nervous system. It is the purpose of this paper to attempt to describe some of the mechanisms involved in head pain and to provide these mechanisms with an osteopathic orientation.
Most of the sensory nerve distribution to the head and face occurs through the trigeminal nerve (Cr V) and fibers of cervical nerves C1, C2, and C3 (Fig. 1.). Smith (4) stated:
The trigeminal fibers subserving pain have their neurons in the trigeminal or semilunar ganglion which lies in a cave of the aura mater in the middle cranial fossa just anterior to the apex of the petrous temporal bone. The peripheral branches of the trigeminal nerve, . . . the ophthalmic, maxillary, and mandibular nerves . . . supply a fairly well defined cutaneous area and broadly speaking, the deep structures underlying it. There is little overlap with the adjoining cutaneous fields of the cervical nerves….
The glossopharyugeal nerve supplies common sensibility to the posterior third of the tongue, the pharynx, soft palate, tonsils and fauces, the auditory tube, the tympanic cavity and mastoid air cells, and the inner lining of the eardrum. The vagus nerve . . . supplies the general somatic afferent fibers to the posterior portion of the external auditory canal, part of the eardrum, and the skin of the cranial surface of the auricle adjoining the scalp.
The pain and temperature fibers of the glossopharyngeal and vagus nerves relay to the nucleus of the descending trigeminal tract.
The cutaneous distribution of C I is not consistent. Larsell (5) said:
Occasionally it gives a cutaneous branch to the skin of the upper part of the back of the neck and the lower part of the scalp.
The second cervical nerve chiefly supplies the area of the head and neck adjoining the trigeminal territory, to which the third cervical nerve contributes fibers. (4)
Kimmel (5) stated:
The nerve fibers supplying the cranial aura mater are derived from the trigeminal nerve, the upper three cervical nerves, and the sympathetic trunk. Nerve branches from the upper three cervical nerves and the superior cervical ganglion supply the aura mater of the posterior cranial fossa. The aural nerves derived from the three divisions of the trigeminal nerve and from the sympathetic plexuses on the internal carotid and middle meningeal arteries supply the remainder of the cranial aura mater.
The first division of the trigeminal nerve supplies the aura mater in the anterior cranial fossa, the diaphragm sellae, nearly all of the cerebral falx, the tentorium cerebelli, part of the superior sagittal sinus, the straight sinus, the superior wall of the transverse sinus, and the terminal parts of the cerebral veins entering these sinuses.
The maxillary division of the trigeminal nerve supplies the aura mater, covering the anterior part of the middle cranial fossa. Branches of the third, or mandibular, division of the trigeminal nerve supply the aura mater in the posterior and lateral parts of the middle cranial fossa and the aura mater lining most of the calvaria. (6)
Perhaps the more important aspect of pain is that it is not a single identifiable entity. It may be represented by vastly complicated and intricate processes or by the mere experiencing of the touch of a sharp object. The integration of actual pain reception and perception represents an area of widely diverse opinion. On the basis of the observation that successive surgical interruptions of peripheral nerves, posterior roots, spinal cord, and thalamus, and ablations of portions of the cerebral hemispheres, may all fail to give permanent relief from pain, Gooddy (7) concluded that “any nervous pathways are potential ‘pain pathways.' ”
Pain stimuli (or at least somatesthetic stimuli interpreted as pain) arising from the spinal cord (C1, C2, and C3) pass principally to the cuneate nucleus (homolateral), synapse, cross at this level, and ascend to the ventrolateral nucleus of the thalamus.(8)
Finneson (9) stated:
The function of the thalamus is to pass impulses on to the cerebralcortex, and it is presumed that these impulses are integrated by the association nuclei in the thalamus before being relayed. The portion of the thalamus that projects impulses to a specific cortical area receives in return corticothalamic projection fibers from that area, forming a circuit between thalamus and cortex.
Smith (4) said that pain fibers of the great auricular nerve synapse in the substantia gelatinosa Rolandi, from which second order neurons ascend in the lateral spinothalamic tract to the posteroventral nucleus of the thalamus. He added:
Pain fibers from the trigeminal nerve have their cell bodies in the semilunar ganglion…. Their central processes descend, as the spinal tract of the trigeminal nerve, in the lateral brain stem from the upper pons to the C-2 level of the cord or even somewhat lower, to terminate in the associated spinal trigeminal nucleus which lies adjacent and deep to the tract. The spinal tract and the spinal nucleus correspond to and are continuous with the dorsolateral fasciculus of the cord and the substantia gelatinosa respectively.
Pain afferents from the face, arriving via the trigeminal, glossopharyngeal, and vagal routes, relay to the portion of the spinal nucleus lying below the inferior limit of the fourth ventricle….
Second order neurons from the spinal trigeminal nucleus cross the midline . . . at the ventral secondary tract to ascend on the medial aspect of the lateral spinothalamic tract to gain the thalamus. There is doubt as to the thalamic termination of these fibers. The classic view is that the trigeminal lemniscus (combining the ventral and dorsal secondary trigeminal tracts) projects to the medial portion (arcuate nucleus) of the posteroventral nucleus of the thalamus…. From the posteroventral nucleus of the thalamus, third order neurons pass in the sensory radiation via the posterior limb of the internal capsule to the somatic sensory area of the cortex in the lowest portion of the postcentral areas (Brodmann's areas 3. 1. 2) just above the fissure of Sylvius. There is evidence of the face being represented bilaterally in the thalamus and cortex…. It is likely that the thalamus is responsible for the recognition of pain but that the perception of pain as a mental event requires cortical participation-probably diffuse and generalized cortical participation….
There is also evidence that pain pathways from both cord and medulla relay bilaterally in the reticular formation of the brain stem and ascend by slow, multisynaptic routes to the medial thalamic nuclei and become part of the diffuse thalamic system. The latter system, which is thought to control the general level and direction of attention. May also be responsible for the affective coloring of pain.
The sensitiveness of the vascular elements has been discussed by Wolff (11). His investigation showed consistent sensitiveness to compression, stretching, and faradic stimulation in the arterial system. The great venous sinuses were less sensitive than the arteries to these stimuli, and the lesser sinuses and veins lost sensitiveness in proportion to their distance from the greater sinuses.
Crosby and associates (11) stated:
The blood vessels of the head receive their preganglionic sympathetic innervation from T-1 to T-2, but C-8 and T-3 and even T-4 may also contribute. The axons pass out into the sympathetic chain and ascend to synapse in the stellate and the superior cervical sympathetic ganglia. The postganglionic fibers distribute from the superior cervical sympathetic ganglion with the external and internal carotid arteries to the head. The intracranial postganglionics follow along the internal carotid artery to the circle of Willis and along branches of the external carotid and distribute to the adventitia and the smooth muscle of intracranial vessels, including arterioles of the pie mater, but not to the blood vessels in the brain substance. Postganglionic fibers also distribute to the middle meningeal artery. The plexuses along the common carotid and the internal carotid are not continuous with those on the external carotid, so that stripping the plexuses from the common and internal carotids will not destroy the sympathetic supply to the blood vessels of the face and the head. Postganglionic fibers from the stellate ganglion ascend along the vertebral arteries and the basilar artery….
A parasympathetic innervation to some of the blood vessels of the head likewise has been demonstrated. Preganglionic parasympathetic fibers of the facial nerve turn off in the region of the geniculate ganglion to run in the great superficial petrosal nerve to the plexus on the internal carotid artery. Postganglionic fibers from small clusters of ganglion cells on the blood vessels distribute as vasodilators of the vessels.
The vascular tone (sympathetic-parasympathetic influence) appears to be mediated through the forebrain with connections in the hypothalamic nuclei. Crosby and associates (11) wrote:
The pathways by which these impulses are discharged to hypothalamic and midbrain segmental areas . . . constitute the various cortico-hypo-thalamic . . . systems and the cortico-thalamo-hypothalamic tracts by way of the dorsomedial thalarnic nucleus.
It seems probable, as others have suggested, that the cortical paths are regulatory over the hypothalamic systems…. The pathways in general provide for emotional accompaniments to cortically initiated motor responses carried over pyramidal and extrapyramidal systems. . . . Evidence has been forthcoming that pyramidal as well as extrapyramidal systems carry corticofugal fibers for autonomic centers of the spinal cord.
Before proceeding to a discussion of the types of stimuli that may be interpreted as pain, the character of nerve endings present in the meninges and associated structures of the head and neck should be considered in order to clarify the types of stimuli that may give rise to pain. Crosby and associates (11) wrote:
The sensory terminations in the aura have been studied by various observers…. The nerve endings at the base of the skull are less numerous than on the convexity. They are in the form of end-branches knob- or club-shaped terminations, or are like balls of twine.
They reported that Meissner corpuscles are associated with the finest tactile sensation. The Golgi-Mazzoni receptor is said to be a pressure receptor, of similar function to the Pacini corpuscle. The Krause corpuscle has been associated with discrimination of low temperatures. It has been suggested (11) that it may function to distinguish cool rather than cold. Ruffini end organs appear to serve in more than one type of receptor. The larger Ruffini endings serve as pressure endings, while smaller endings of this type are present in the subcutaneous connective tissue and are regarded as receptors of warmth. (11) Golgi, Meissner, and Pacini corpuscles have been described as receptors of discrimination in joint motion. They are credited with reporting motion characteristics in regard to rate of position change, direction of motion, and force required to produce position change. (12)
Now that the involved circuitry has been described, pain itself may be considered. Pain may result directly from factors originating outside the body (a sharp object or excessive heat), from pathophysiologic changes within the body (sustained muscle tension or a tumor) or from abnormally mediated psychologic factor~ through autonomic response. Pain may result from mechanical or psychologic stimulation or a combination of these. It may be described, then, as a response to stimuli that threaten tissue integrity or organizational integrity of the body unit.
Various authors have classified pain according to the particular portion of the nervous system immediate!! Responsible for the transmission of the stimulus to the central nervous system. As Boshes and Arieff (3) said pain may be classified as being at the receptive, the conductive, the perceptive, or the apperceptive level, at a combination of these.
Pain must be discerned as a local, projected, or referred phenomenon. Localized pain is restricted to the immediate area of reception, as in pain in a toot from an apical abscess. Projected pain in the head may be exemplified by trigeminal neuralgia, which Magoun (13) stated is . . .
apparently due to restriction in the aural investiture of the root as passes over the petrous ridge, in Meckel's cave housing the ganglia or in the sleeves around the three branches as they exist from the skull.
ain is projected at times over the entire hemiface served by the nerve. Referred pain may be exemplified by reference to the face of thrombosis of the posterior inferior cerebellar artery. (4)
Although these classifications of pain overlap to some degree, the use of a combination of classification helps to explain various phenomena of pain production. The Patient waiting for the attention of the dentist or surgeon may suppress pain mentally and say, “It doesn't hurt as it did yesterday,” until the approach of the time for local anesthetic preparation. Then a touch by any object may produce a unique response in the area of attention. The apperceptive mechanisms, mediated through the nuclei of the thalamus and modified through the cortifugal control systems of the cerebellum, (14-17) plus the pituitary-adrenal hyperfunction due to fear, cause pain uniquely individualized by the patient's level of apprehension. The cortifugal controls exerted through the cerebellum modify the intensity of activity occurring both on a motor level and through the thalamic nuclei. It appears that damage to or suppression of the control system may be responsible for the rigidity, hyperactivity, dysmetria, ataxia, and epileptiform activity exhibited by patients with brain damage or trauma.(15)
Sutherland (18) described his observations and conclusions in reference to stress mechanisms involving the aura mater and cranial sutures. The observations of the various types of nerve endings in the leptomeninges make the information supplied by stress on the aura mater and pie mater available to the centers of perception, apperception, and motor activity. It has been demonstrated (19) that the recurrent meningeal nerves in the spinal area (especially the branches that enter through the foremen magnum along with the internal carotid artery) are derived from the sympathetic trunk and supply the aura mater lining the posterior cranial fossa. This distribution makes available to this area information from the outer layers of the cranial aura mater, which forms the periosteum of the cranium, and the inner layer, which forms the investing aura of the brain (the tentorium cerebelli, falx cerebri, and falx cerebelli), and from the spinal cord meninges and supporting ligaments.
Ray and Wolff (20) in 1940 studied the probable causes of headache or head pain in relation to the aura mater from observations made on 30 patients during surgical procedures on the head; they concluded that the pains result primarily from inflammation, traction, displacement, and distention of pain-sensitive structures, of which cranial vascular structures are most frequent and widely distributed. Unfortunately, they failed to mention until Wolff's later work (10) that the actual pain sensitive nerve endings are located in the aura mater, the arachnoid, and the pie mater supporting the vascular structures. These factors cast new light on the observations of Sutherland, especially since the aura mater on the internal surface of the cranium is continuous with the periosteum of the head.
No studies have been published to support the possibility of a strain gauge type of reporting across the sutures, but the observation of the sensory distribution to the internal and external surfaces of the cranial vault would appear to make such an arrangement feasible. (4, 6)
The information available indicates that essentially the same types of stimuli elicit painful reactions whether they arise inside or outside the cranium. Psychologic modification, through mechanisms mentioned, is most likely to affect those areas of reception most easily observed through the special senses, such as sight and hearing.
Since involvement of the special senses introduces the possibility of modification of afferent stimuli by the limbic system, Aird (21) stated:
Neurophysiologic evidence has suggested that this portion of the nervous system is concerned with smell, taste, and other special senses, the gastrointestinal system and other autonomic functions, and behavioral reactions.
This brings pain into the area of psychoneurophysiologic processes of reception, conduction, and perception to the stage of apperception or total integration of the process of interpreting pain, and a possible introduction of the subject of pain threshold (which is beyond the scope of this paper).
It should be mentioned that there are definite interrelations between the cortifugal system, mentioned earlier, and the limbic system, which as yet are not clearly defined.
The foregoing discussion has described the circuitry necessary for the identification and response to head pain. Feedback mechanisms necessary to establish a cybernetic model have been outlined. On the basis of this description it should not be difficult for the knowledgeable physician to apply therapeutic measures. The knowledgeable osteopathic physician possesses the palpatory skills to intervene directly in the pathophysiologic process. Pain in the head, through the mechanism described, produces palpable reflex area or tissue response, in the superficial tissues such as the skin, the muscle, and deep connective tissues. By discriminatory palpation he can determine the relative duration or stage of chronicity of the condition and apply therapy.
Hoover (22-25) has written extensively and descriptively in regard to application of technique to the various ages or stages of the process involved in stress. He described a functional technique as opposed to structural technique. By this technique the physician may affect the established cybernetic system by entering the system as an aid in diminishing the stress system established. In this mode of treatment enough force is exerted, through the various planes of motion of accommodation of the tissue or articulation, to bring the structures involved to a point of what Hoover called “dynamic reciprocal balance.” (25) In this way the physician establishes a servocybernetic system which allows the tissue or articulation to establish a new state of equilibrium within the limits of its ability to accommodate physiologically. Hoover (24) stated:
Treatment by functional technic depends upon and is directed by the reaction of a part of the patient to demands for activity made upon that part.
By the recruitment of the demonstrable changes in tissue and its activity, it is possible for the palpating hand to discern the cybernetic mechanisms involved in the origin of head pain.
Harvey (25) stated:
A basic cybernetic mechanism is “feedback.” This is the process of transferring energy or information from the output of a circuit to its input and is a generally accepted control mechanism in all types of self-regulating systems that use closed-loop, negative feedback networks.
I have not found active and passive joint motion palpation to be sufficiently discriminating in the analysis of such cybernetic mechanisms to allow me to enter into a servocybernetic relation with the patient on a therapeutic level. After observation of several highly skilled osteopathic physicians in their approaches to palpation and treatment of a wide variety of pathophysiologic processes and syndromes, a method of diagnostic palpation became apparent. As the newly found method was used, its applications and uses began to reveal themselves, and this continues. Articles (27, 28) have been published by two of the highly skilled physicians whose work has been observed. The use of the principles presented by these physicians allows one to determine the area or areas of stress and the character of the assault involved and to counteract their deleterious effects.
The previous discussion of mechanisms in the central nervous system covered what is presently known of the circuitry involved in feedback mechanisms of the human body in relation to head pain. After the physician has determined the areas of stress and the character of the assault, he bases his treatment on the counterbalancing of the stress forces, that is, changing the characteristics of the input and feedback, so as to create a servocybernetic system. Establishing controlled input alters the level of control influence exerted by the negative feedback network.
The completion of treatment for any particular time is signaled by improved physiologic reaction of the tissues involved, that is, an increase in activity in hyperactive tissue, and a synchronous motion (internal or external rotation; flexion or extension) with the basal respiratory cycle or primary respiratory mechanism, as defined by Magoun. (13) This allows the patient to establish a new level of homeostasis compatible with his or her ability at any particular time to recover from the original assault.
Stress patterns of considerable duration complicated by numerous overlying injuries have responded in a surprising manner to treatment applied in this manner.
A 44-year-old white woman was admitted to the hospital with a chief complaint of severe headaches, which occurred in the left occipital area and radiated to the left temporal bone and vertex of the skull. The headaches were associated with nausea and vomiting. Their onset was associated with an automobile accident that had occurred six years before this admission. Following the accident hemianesthesia involving the left arm, leg, and side of the face developed. At that time the patient had been hospitalized for 22 days. Her condition improved with bed rest, but she had not been freed of pain, and paresthesia of the left arm, leg, and side of the face remained. She was unable to turn from a supine position to a left lateral recumbent position. It was not clear whether this was due to weakness, loss of proprioception, or loss of motor control. The patient had spent a total of 66 days in the hospital over the next two years for paresthesia of the left side of the body and headache (hemicephalgia on the left). The patient said that she had not been unconscious at the time of or after the accident. There was no familial history of neurologic disease or headache.
During the six years after the accident the patient had received nearly every know type of therapy for cephalgia and migraine, including administration of narcotics and adrenocorticoids and trigger-point injections.
The patient's surgical history included appendectomy, cesarean section, and total hysterectomy. Neurological examination did not demonstrate any abnormality, and the cellular structure of the cerebrospinal fluid and the chemical contents were not remarkable. The pressure of cerebrospinal fluid was in the middle of the normal range, and the Queckenstedt test did not show abnormality. Laboratory tests, including complete blood count, measurement of fasting blood sugar an creatinine, urinalysis, and the VDRL test for syphilis at the time of admission and discharge showed no abnormality. X-ray examination at the time of admission showed what appeared to be an articulation between the posterior tubercle of the posterior arch of the atlas an the occiput, and a decrease of the normal lordotic curvature of the cervical spine, that is, a reversal the normal cervical curve.
After a week's hospitalization, I was called in consultation, and my examination elicited the following additional findings: decrease in backward bending the cervical spine, decrease in mobility in all direction through the occipito-atlanto-axial articulation flattening of the cervical lordotic curvature, bilateral compression through the sacroiliac articulation sphenobasilar compression of the cranial mechanic, with vertical strain (spheroid high), side bending rotation, with convexity to the left, and slight torsion on the right. The entire paravertebral mass from occiput to sacrum was under extreme tension.
The findings were compatible with the following diagnosis: Spinal ligamentous strain and sprat (spheroid high), left side bending rotation, and right torsion of the cranial mechanism. Treatment was directed at relieving the stress on the meninges an vascular channel throughout the cranial sacral mechanism to reduce edema, muscle tensions and spasm and to reduce the level of afferent CNS input to establish a more physiologic level of function.
Both cranial treatment and fascial release technique were directed to the sphenobasilar vertical strain suboccipital area, and sacrum because of the hyperirritability of these tissues and their inability to react. The patient was not treated again for 48 hours because of other demands on the physician's time. At the second treatment the tissue reaction was much improved, an the patient could withstand deeper treatment to the involved area without excessive pain or tissue reaction After this treatment the patient's cervical spine was reexamined roentgenologically, and the films showed that the posterior arch of the atlas was no longer in contact with the occiput and that there was improvement in the cervical anteroposterior curvature. The patient's pain decreased over the next 24 hours, and she was released from the hospital to be seen at my office within 48 hours. The patient was seen twice a week for the next three weeks. At the end of this time the patient had been free of pain for approximately 10 days, end that length of time between treatments was extended to, a week.
As the patient's tissue response improved, the interval between treatments was lenghtened correspondingly, without recurrence of severe headaches until her daughter, who had a congenital cardiac valvular lesion, told her parents she was pregnant. Headaches recurred, but responded well to treatment. They recurred frequently but were terminated on the arrival for a normal healthy granddaughter. At the time of this report the patient still was seen on occasion for maintenance and preventive treatment
The treatment of this patient was carried out according to the principles already described.
After routine physical examination a thorough palpatory examination was carried out. Palpation began at the sacral area. With the patient in the supine position, her sacrum was cupped in the examiner's left hand, with the first finger extending over the right sacroiliac articulation to make contact with the right iliolumbar ligament (lower portion). The little finger was placed at the left sacroiliac articulation and the second and third fingertips placed just lateral to the tip of the spinous process of the fifth lumbar segment of the spine. Light palpation demonstrated relatively little activity of the tissues. When palpation was deepened it demonstrated a rigidity of the ligamentous structures supporting the sacroiliac articulations both anteriorly and posteriorly and extreme tension through the iliolumbar ligaments bilaterally.
The examining procedure is as follows: Light palpation is carried out with light contact with skin. The depth of palpation is increased by establishing a fulcrum and gently increasing the tension or pressure distal to the fulcrum so that the palpating hand may remain relaxed and be used as a palpating instrument rather than attempting to constantly monitor its own proprioceptive phenomena. The pressure is gently increased until reaction is stimulated in the layer of tissue the examiner wishes to palpate. The resulting tissue reaction will demonstrate to the examiner the resultant force (the summation of the various forces exerted at the time of injury) that elicited the protective reaction of the tissues under examination.
The transition from examination to treatment is a matter of following the resultant force to the point of dynamic reciprocal balance and maintaining this balance until the tissues complete their accommodation. This accommodation is accompanied with increased tissue relaxation, a feeling of increased tissue vitality, and a longitudinal to-and-fro motion corresponding to the primary respiratory cycle.
If continued force is applied to the injured tissues after the immediate response, the ensuing fatigue may result in an adverse or excessive reaction of the treated tissues, which appears to create a type of kinesthetic shock (a dissociation of the proprioceptive motor feedback mechanism resulting in a loss of coordinated, previously programmed or learned motion patterns with an increase in sensitiveness and possibly pain in the particular ligaments and connective tissues. This causes gait or motion aberration that is not typical of the individual. This usually occurs in a single member or limb or segment of such member or limb.
Each area found to be involved in the total stress mechanism is treated in a similar manner, the only differences being in the method of application of the testing or treating forces to accommodate the peculiarities of anatomic structure, of the region under study and treatment. In the cervical area palpation is performed along the lateral margin of the paravertebral mass that is located over the articular pillar. This permits palpation of the paravertebral mass, the periarticular ligaments, and the reaction of the musculature attached to the anterior aspects of these vertebral segments. In palpation of the cranium, the index finger approximates the lateral aspect of the great wing of the spheroid; the second finger is placed posterior to the sphenosquamal articulation; the third finger is placed at the parietotemporo-occipital articulation (asterion), and the little finger is placed on the occiput.
This contact is often altered to suit unusual injury patterns, but in any case the application of treatment follows the same basic principles. The fulcrum is usually established by crossing the thumbs. The flexor pollicis longus muscle of each thumb is utilized to maintain good contact and allow the hands to remain as relaxed as possible. Thus the hands may be free to move within the demonstrated force mechanisms and establish the dynamic reciprocal tension necessary to allow the tissues to overcome injury force mechanisms. The mastering of this type of therapeutic and diagnostic approach is not difficult but requires studious concentration to avoid hindering the activity of the tissues, so that they may reveal the stress patterns to which they have been subjected. The physician must remain relaxed and observant so he may participate in assisting the tissues to reach and maintain the point of dynamic reciprocal tension.
The studies reviewed here demonstrated the possibility that pain may arise from the neck and possibly lower levels. In many cases the involvement of arthrodial articulations may require more stringent or forceful modes of treatment than those described here. Hoover (22) described the use of high velocity manipulation to accomplish a “popping” of the joint so that the involved levels of discrimination must rearrange their synaptic organization in response to shock produced by the forceful articulatory motion. By this method a new level or at least a different degree of function is established.
The little understood mechanisms of the central nervous system are slowly revealing their intricacies through the devoted efforts of many dedicated and curious researchers. These workers can divulge their observations, but it becomes the responsibility of the physician to be aware of their discoveries, analyze the information, and apply it discreetly in clinical situations. The information presented here may give the osteopathic physician a slightly different view and increase the effectiveness of his application of osteopathic manipulative therapy to his patient.
The neuroanatomy and physiology involved in head pain have been discussed. Various types of input that may be characterized as pain have been mentioned, and mechanisms involved in the apperception as pain have been demonstrated. An attempt has been made to correlate the wide varieties of osteopathic manipulative approach to the particular situation in which pain is expressed in the head. A case history exemplifying my approach to such problems has been presented and the principles of treatment described.
Dorland's illustrated medical dictionary. Ed. 24. W.B. Saunders Co., Philadelphia, 1965
1. Emery, H.G., and Brewster, K.G., editors: New century dictionary of the English language. Appleton-Century-Crofts, Inc., New York, 1959
2. Boshes, B., and Arieff, A.J.: Clinical experience in the neurologic substance of pain. Med Clin North Am 52:111-21, Jan 68
3. Smith, B.H.: Anatomy of facial pain. Headache 9:7-13, Apr 69
4. Larsell, O.: The nervous system. In Human anatomy. By H. Morris. Ed. 11, edited by J.P. Schaeffer. Blakiston Co., New York, 1953
5. Kimmel, D.L.: The nerves of the cranial aura mater and their significance in aural headache and referred pain. Chicago Med Sch Quart 22:16-26, Fall 61
6. Gooddy, W.: On the nature of pain. Brain 80:11831, 1957
7. Netter, F.H.: Nervous system. Vol. 1. Ciba collection of medical illustrations. Ciba Pharmaceutical Co., Summit, N.J., 1953
8. Finneson, B.E.: Diagnosis and management of pain syndromes. Ed. 2. W.B. Saunders Co., Philadelphia, 1969
9. Wolff, H.G.: Headache and other headpain. Ed.2. Oxford University Press, New York, 1963
10. Crosby, E.C., Humphrey, T., and Lauer, E.W.: Correlative anatomy of the nervous system. Macmillan Co., New York, 1962
11. Korr, I.M., and Buzzell, K.A.: Personal communication to the author
12. Magoun, H.I.: Osteopathy in the cranial field. Ed.2. Journal Printing Co., Kirksville, Mo., 1966
13. Steriade, M.: The cerebello-thalamo-cortical pathway. Ascending (specific and unspecific) and corticofugal controls. Int J Neurol 7:177-200,1970
14. Gerstenbrand, F., et al.: Cerebellar symptoms as sequelae of traumatic lesions of upper brain stem and cerebellum. Int J Neurol 7:271-82, 1970
15. Snider, R.S., Mitra, J., and Sudilovsky, A.: Cerebellar effects on the cerebrum. A microelectrical analysis of somatosensory cortex. Int J Neurol 7:141-51, 1970
16. Ito, M.: Neurophysiological aspects of the cerebellar motor control system. Int J Neurol 7:162-76, 1970