870 lines
43 KiB
XML
870 lines
43 KiB
XML
import Article from "@/components/Article";
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import { Metadata } from "next";
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export const metadata: Metadata = {
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title: "Article - Head Pain | Dr. Feely",
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authors: [{ name: "Herbert C. Miller, D.O., FAAO" }],
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description: `Pain has been defined in many ways, as the sensation “resulting
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from the stimulation of specialized nerve endings,”‘ or, more poetically, as a
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punishment or penalty, as for crime. Other definitions include acute
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discomfort of body or mind, bodily or mental suffering or distress; a
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distressing sensation, as in a particular part of the body, and trouble
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experienced in doing something. (2) One's concept of pain may be colored by
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diverse circumstances or, in scientific language, feedback. Head pain is
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usually interpreted by the clinician from the therapeutic point of view, that
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is, in terms of measures that may stop in, rather than in pathophysiologic
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terms.`,
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};
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const ArticleOsteopathicHeadPain = () => {
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return (
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<Article title="Head Pain" author="Herbert C. Miller, D.O., FAAO">
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<p>Reprinted with permission of the American Osteopathic Association.</p>
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<p>
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Pain has been defined in many ways, as the sensation “resulting from the
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stimulation of specialized nerve endings,”‘ or, more poetically, as a
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punishment or penalty, as for crime. Other definitions include acute
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discomfort of body or mind, bodily or mental suffering or distress; a
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distressing sensation, as in a particular part of the body, and trouble
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experienced in doing something. (2) One's concept of pain may be colored
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by diverse circumstances or, in scientific language, feedback. Head pain
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is usually interpreted by the clinician from the therapeutic point of
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view, that is, in terms of measures that may stop in, rather than in
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pathophysiologic terms.
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</p>
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<p>
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When analyzing head pain, the physician often prefers to look at it as a
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phenomenon or as the result of stimulation of specialized nerve endings.
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In reality, pain may be an interpretation of bodily or mental distress.
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Boshes and Arieff (3) stated:
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</p>
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<p>
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Certain aspects of pain are predicated exclusively on a neural
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substrate. Here the basis is an event or an alteration in the nervous
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system per se, as contrasted to pain caused by malignant disease,
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infected tissue, fractures or the like. Various divisions of the nervous
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system may be implicated and a description of the disability or the
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manner of posture and movement is often sufficient to enable the trained
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observer to gain an impression as to whether the pain is genuine or
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functional. Such involvement may be at the receptive, the conductive,
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the perceptive or the apperceptive level, or combinations thereof.
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</p>
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<p>
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This would appear to be a generally accepted concept, and yet head pain
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often is described and interpreted on the basis of a symptom complex
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rather than in terms of the anatomic and physiologic organization of the
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central nervous system. It is the purpose of this paper to attempt to
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describe some of the mechanisms involved in head pain and to provide
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these mechanisms with an osteopathic orientation.
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</p>
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<h2>Neural Pathways</h2>
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<p>
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Most of the sensory nerve distribution to the head and face occurs
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through the trigeminal nerve (Cr V) and fibers of cervical nerves C1,
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C2, and C3 (Fig. 1.). Smith (4) stated:
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</p>
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<p>
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The trigeminal fibers subserving pain have their neurons in the
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trigeminal or semilunar ganglion which lies in a cave of the aura mater
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in the middle cranial fossa just anterior to the apex of the petrous
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temporal bone. The peripheral branches of the trigeminal nerve, . . .
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the ophthalmic, maxillary, and mandibular nerves . . . supply a fairly
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well defined cutaneous area and broadly speaking, the deep structures
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underlying it. There is little overlap with the adjoining cutaneous
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fields of the cervical nerves….
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</p>
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<p>
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The glossopharyugeal nerve supplies common sensibility to the posterior
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third of the tongue, the pharynx, soft palate, tonsils and fauces, the
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auditory tube, the tympanic cavity and mastoid air cells, and the inner
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lining of the eardrum. The vagus nerve . . . supplies the general
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somatic afferent fibers to the posterior portion of the external
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auditory canal, part of the eardrum, and the skin of the cranial surface
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of the auricle adjoining the scalp.
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</p>
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<p>
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The pain and temperature fibers of the glossopharyngeal and vagus nerves
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relay to the nucleus of the descending trigeminal tract.
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</p>
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<p>
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The cutaneous distribution of C I is not consistent. Larsell (5) said:
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</p>
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<p>
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Occasionally it gives a cutaneous branch to the skin of the upper part
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of the back of the neck and the lower part of the scalp.
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</p>
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<p>
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The second cervical nerve chiefly supplies the area of the head and neck
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adjoining the trigeminal territory, to which the third cervical nerve
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contributes fibers. (4)
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</p>
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<p>Kimmel (5) stated:</p>
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<p>
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The nerve fibers supplying the cranial aura mater are derived from the
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trigeminal nerve, the upper three cervical nerves, and the sympathetic
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trunk. Nerve branches from the upper three cervical nerves and the
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superior cervical ganglion supply the aura mater of the posterior
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cranial fossa. The aural nerves derived from the three divisions of the
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trigeminal nerve and from the sympathetic plexuses on the internal
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carotid and middle meningeal arteries supply the remainder of the
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cranial aura mater.
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</p>
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<p>
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The first division of the trigeminal nerve supplies the aura mater in
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the anterior cranial fossa, the diaphragm sellae, nearly all of the
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cerebral falx, the tentorium cerebelli, part of the superior sagittal
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sinus, the straight sinus, the superior wall of the transverse sinus,
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and the terminal parts of the cerebral veins entering these sinuses.
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</p>
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<p>
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The maxillary division of the trigeminal nerve supplies the aura mater,
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covering the anterior part of the middle cranial fossa. Branches of the
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third, or mandibular, division of the trigeminal nerve supply the aura
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mater in the posterior and lateral parts of the middle cranial fossa and
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the aura mater lining most of the calvaria. (6)
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</p>
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<p>
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Perhaps the more important aspect of pain is that it is not a single
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identifiable entity. It may be represented by vastly complicated and
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intricate processes or by the mere experiencing of the touch of a sharp
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object. The integration of actual pain reception and perception
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represents an area of widely diverse opinion. On the basis of the
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observation that successive surgical interruptions of peripheral nerves,
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posterior roots, spinal cord, and thalamus, and ablations of portions of
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the cerebral hemispheres, may all fail to give permanent relief from
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pain, Gooddy (7) concluded that “any nervous pathways are potential
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‘pain pathways.' ”
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</p>
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<p>
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Pain stimuli (or at least somatesthetic stimuli interpreted as pain)
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arising from the spinal cord (C1, C2, and C3) pass principally to the
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cuneate nucleus (homolateral), synapse, cross at this level, and ascend
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to the ventrolateral nucleus of the thalamus.(8)
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</p>
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<p>Finneson (9) stated:</p>
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<p>
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The function of the thalamus is to pass impulses on to the
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cerebralcortex, and it is presumed that these impulses are integrated by
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the association nuclei in the thalamus before being relayed. The portion
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of the thalamus that projects impulses to a specific cortical area
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receives in return corticothalamic projection fibers from that area,
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forming a circuit between thalamus and cortex.
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</p>
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<p>
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Smith (4) said that pain fibers of the great auricular nerve synapse in
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the substantia gelatinosa Rolandi, from which second order neurons
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ascend in the lateral spinothalamic tract to the posteroventral nucleus
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of the thalamus. He added:
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</p>
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<p>
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Pain fibers from the trigeminal nerve have their cell bodies in the
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semilunar ganglion…. Their central processes descend, as the spinal
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tract of the trigeminal nerve, in the lateral brain stem from the upper
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pons to the C-2 level of the cord or even somewhat lower, to terminate
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in the associated spinal trigeminal nucleus which lies adjacent and deep
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to the tract. The spinal tract and the spinal nucleus correspond to and
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are continuous with the dorsolateral fasciculus of the cord and the
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substantia gelatinosa respectively.
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</p>
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<p>
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Pain afferents from the face, arriving via the trigeminal,
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glossopharyngeal, and vagal routes, relay to the portion of the spinal
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nucleus lying below the inferior limit of the fourth ventricle….
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</p>
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<p>
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Second order neurons from the spinal trigeminal nucleus cross the
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midline . . . at the ventral secondary tract to ascend on the medial
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aspect of the lateral spinothalamic tract to gain the thalamus. There is
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doubt as to the thalamic termination of these fibers. The classic view
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is that the trigeminal lemniscus (combining the ventral and dorsal
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secondary trigeminal tracts) projects to the medial portion (arcuate
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nucleus) of the posteroventral nucleus of the thalamus…. From the
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posteroventral nucleus of the thalamus, third order neurons pass in the
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sensory radiation via the posterior limb of the internal capsule to the
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somatic sensory area of the cortex in the lowest portion of the
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postcentral areas (Brodmann's areas 3. 1. 2) just above the fissure of
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Sylvius. There is evidence of the face being represented bilaterally in
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the thalamus and cortex…. It is likely that the thalamus is responsible
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for the recognition of pain but that the perception of pain as a mental
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event requires cortical participation-probably diffuse and generalized
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cortical participation….
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</p>
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<p>
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There is also evidence that pain pathways from both cord and medulla
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relay bilaterally in the reticular formation of the brain stem and
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ascend by slow, multisynaptic routes to the medial thalamic nuclei and
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become part of the diffuse thalamic system. The latter system, which is
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thought to control the general level and direction of attention. May
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also be responsible for the affective coloring of pain.
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</p>
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<h2>Vascular Elements</h2>
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<p>
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The sensitiveness of the vascular elements has been discussed by Wolff
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(11). His investigation showed consistent sensitiveness to compression,
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stretching, and faradic stimulation in the arterial system. The great
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venous sinuses were less sensitive than the arteries to these stimuli,
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and the lesser sinuses and veins lost sensitiveness in proportion to
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their distance from the greater sinuses.
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</p>
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<p>Crosby and associates (11) stated:</p>
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<p>
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The blood vessels of the head receive their preganglionic sympathetic
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innervation from T-1 to T-2, but C-8 and T-3 and even T-4 may also
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contribute. The axons pass out into the sympathetic chain and ascend to
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synapse in the stellate and the superior cervical sympathetic ganglia.
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The postganglionic fibers distribute from the superior cervical
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sympathetic ganglion with the external and internal carotid arteries to
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the head. The intracranial postganglionics follow along the internal
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carotid artery to the circle of Willis and along branches of the
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external carotid and distribute to the adventitia and the smooth muscle
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of intracranial vessels, including arterioles of the pie mater, but not
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to the blood vessels in the brain substance. Postganglionic fibers also
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distribute to the middle meningeal artery. The plexuses along the common
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carotid and the internal carotid are not continuous with those on the
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external carotid, so that stripping the plexuses from the common and
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internal carotids will not destroy the sympathetic supply to the blood
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vessels of the face and the head. Postganglionic fibers from the
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stellate ganglion ascend along the vertebral arteries and the basilar
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artery….
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</p>
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<p>
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A parasympathetic innervation to some of the blood vessels of the head
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likewise has been demonstrated. Preganglionic parasympathetic fibers of
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the facial nerve turn off in the region of the geniculate ganglion to
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run in the great superficial petrosal nerve to the plexus on the
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internal carotid artery. Postganglionic fibers from small clusters of
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ganglion cells on the blood vessels distribute as vasodilators of the
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vessels.
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</p>
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<p>
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The vascular tone (sympathetic-parasympathetic influence) appears to be
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mediated through the forebrain with connections in the hypothalamic
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nuclei. Crosby and associates (11) wrote:
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</p>
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<p>
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The pathways by which these impulses are discharged to hypothalamic and
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midbrain segmental areas . . . constitute the various
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cortico-hypo-thalamic . . . systems and the cortico-thalamo-hypothalamic
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tracts by way of the dorsomedial thalarnic nucleus.
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</p>
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<p>
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It seems probable, as others have suggested, that the cortical paths are
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regulatory over the hypothalamic systems…. The pathways in general
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provide for emotional accompaniments to cortically initiated motor
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responses carried over pyramidal and extrapyramidal systems. . . .
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Evidence has been forthcoming that pyramidal as well as extrapyramidal
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systems carry corticofugal fibers for autonomic centers of the spinal
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cord.
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</p>
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<p>
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Before proceeding to a discussion of the types of stimuli that may be
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interpreted as pain, the character of nerve endings present in the
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meninges and associated structures of the head and neck should be
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considered in order to clarify the types of stimuli that may give rise
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to pain. Crosby and associates (11) wrote:
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</p>
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<p>
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The sensory terminations in the aura have been studied by various
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observers…. The nerve endings at the base of the skull are less numerous
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than on the convexity. They are in the form of end-branches knob- or
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club-shaped terminations, or are like balls of twine.
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</p>
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<p>
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They reported that Meissner corpuscles are associated with the finest
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tactile sensation. The Golgi-Mazzoni receptor is said to be a pressure
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receptor, of similar function to the Pacini corpuscle. The Krause
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corpuscle has been associated with discrimination of low temperatures.
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It has been suggested (11) that it may function to distinguish cool
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rather than cold. Ruffini end organs appear to serve in more than one
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type of receptor. The larger Ruffini endings serve as pressure endings,
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while smaller endings of this type are present in the subcutaneous
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connective tissue and are regarded as receptors of warmth. (11) Golgi,
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Meissner, and Pacini corpuscles have been described as receptors of
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discrimination in joint motion. They are credited with reporting motion
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characteristics in regard to rate of position change, direction of
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motion, and force required to produce position change. (12)
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</p>
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<h2>Characteristics</h2>
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<p>
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Now that the involved circuitry has been described, pain itself may be
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considered. Pain may result directly from factors originating outside
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the body (a sharp object or excessive heat), from pathophysiologic
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changes within the body (sustained muscle tension or a tumor) or from
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abnormally mediated psychologic factor~ through autonomic response. Pain
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may result from mechanical or psychologic stimulation or a combination
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of these. It may be described, then, as a response to stimuli that
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threaten tissue integrity or organizational integrity of the body unit.
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</p>
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<p>
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Various authors have classified pain according to the particular portion
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of the nervous system immediate!! Responsible for the transmission of
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the stimulus to the central nervous system. As Boshes and Arieff (3)
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said pain may be classified as being at the receptive, the conductive,
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the perceptive, or the apperceptive level, at a combination of these.
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</p>
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<p>
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Pain must be discerned as a local, projected, or referred phenomenon.
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Localized pain is restricted to the immediate area of reception, as in
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pain in a toot from an apical abscess. Projected pain in the head may be
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exemplified by trigeminal neuralgia, which Magoun (13) stated is . . .
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</p>
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<p>
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apparently due to restriction in the aural investiture of the root as
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passes over the petrous ridge, in Meckel's cave housing the ganglia or
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in the sleeves around the three branches as they exist from the skull.
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</p>
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<p>
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ain is projected at times over the entire hemiface served by the nerve.
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Referred pain may be exemplified by reference to the face of thrombosis
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of the posterior inferior cerebellar artery. (4)
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</p>
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<p>
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Although these classifications of pain overlap to some degree, the use
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of a combination of classification helps to explain various phenomena of
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pain production. The Patient waiting for the attention of the dentist or
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surgeon may suppress pain mentally and say, “It doesn't hurt as it did
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yesterday,” until the approach of the time for local anesthetic
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preparation. Then a touch by any object may produce a unique response in
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the area of attention. The apperceptive mechanisms, mediated through the
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nuclei of the thalamus and modified through the cortifugal control
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systems of the cerebellum, (14-17) plus the pituitary-adrenal
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hyperfunction due to fear, cause pain uniquely individualized by the
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patient's level of apprehension. The cortifugal controls exerted through
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the cerebellum modify the intensity of activity occurring both on a
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motor level and through the thalamic nuclei. It appears that damage to
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or suppression of the control system may be responsible for the
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rigidity, hyperactivity, dysmetria, ataxia, and epileptiform activity
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exhibited by patients with brain damage or trauma.(15)
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</p>
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<p>
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Sutherland (18) described his observations and conclusions in reference
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to stress mechanisms involving the aura mater and cranial sutures. The
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observations of the various types of nerve endings in the leptomeninges
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make the information supplied by stress on the aura mater and pie mater
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available to the centers of perception, apperception, and motor
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activity. It has been demonstrated (19) that the recurrent meningeal
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nerves in the spinal area (especially the branches that enter through
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the foremen magnum along with the internal carotid artery) are derived
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from the sympathetic trunk and supply the aura mater lining the
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posterior cranial fossa. This distribution makes available to this area
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information from the outer layers of the cranial aura mater, which forms
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the periosteum of the cranium, and the inner layer, which forms the
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investing aura of the brain (the tentorium cerebelli, falx cerebri, and
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falx cerebelli), and from the spinal cord meninges and supporting
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ligaments.
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</p>
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<p>
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Ray and Wolff (20) in 1940 studied the probable causes of headache or
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head pain in relation to the aura mater from observations made on 30
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patients during surgical procedures on the head; they concluded that the
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pains result primarily from inflammation, traction, displacement, and
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distention of pain-sensitive structures, of which cranial vascular
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structures are most frequent and widely distributed. Unfortunately, they
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failed to mention until Wolff's later work (10) that the actual pain
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sensitive nerve endings are located in the aura mater, the arachnoid,
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and the pie mater supporting the vascular structures. These factors cast
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new light on the observations of Sutherland, especially since the aura
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mater on the internal surface of the cranium is continuous with the
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periosteum of the head.
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</p>
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<p>
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No studies have been published to support the possibility of a strain
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gauge type of reporting across the sutures, but the observation of the
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sensory distribution to the internal and external surfaces of the
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cranial vault would appear to make such an arrangement feasible. (4, 6)
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</p>
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<p>
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The information available indicates that essentially the same types of
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stimuli elicit painful reactions whether they arise inside or outside
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the cranium. Psychologic modification, through mechanisms mentioned, is
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most likely to affect those areas of reception most easily observed
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through the special senses, such as sight and hearing.
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</p>
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<p>
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Since involvement of the special senses introduces the possibility of
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modification of afferent stimuli by the limbic system, Aird (21) stated:
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</p>
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<p>
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Neurophysiologic evidence has suggested that this portion of the nervous
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system is concerned with smell, taste, and other special senses, the
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gastrointestinal system and other autonomic functions, and behavioral
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reactions.
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</p>
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<p>
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This brings pain into the area of psychoneurophysiologic processes of
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reception, conduction, and perception to the stage of apperception or
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total integration of the process of interpreting pain, and a possible
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introduction of the subject of pain threshold (which is beyond the scope
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of this paper).
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</p>
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<p>
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It should be mentioned that there are definite interrelations between
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the cortifugal system, mentioned earlier, and the limbic system, which
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as yet are not clearly defined.
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</p>
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|
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<h2>Osteopathic Approach</h2>
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||
|
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<p>
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The foregoing discussion has described the circuitry necessary for the
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identification and response to head pain. Feedback mechanisms necessary
|
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to establish a cybernetic model have been outlined. On the basis of this
|
||
description it should not be difficult for the knowledgeable physician
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to apply therapeutic measures. The knowledgeable osteopathic physician
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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.
|
||
</p>
|
||
|
||
<p>
|
||
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:
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>Harvey (25) stated:</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
Stress patterns of considerable duration complicated by numerous
|
||
overlying injuries have responded in a surprising manner to treatment
|
||
applied in this manner.
|
||
</p>
|
||
|
||
<h2>Case Report</h2>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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
|
||
</p>
|
||
|
||
<h2>Treatment Discussion</h2>
|
||
|
||
<p>
|
||
The treatment of this patient was carried out according to the
|
||
principles already described.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<h2>Comments</h2>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<p>
|
||
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.
|
||
</p>
|
||
|
||
<h2>References</h2>
|
||
|
||
<p>
|
||
Dorland's illustrated medical dictionary. Ed. 24. W.B. Saunders Co.,
|
||
Philadelphia, 1965
|
||
</p>
|
||
|
||
<p>
|
||
1. Emery, H.G., and Brewster, K.G., editors: New century dictionary of
|
||
the English language. Appleton-Century-Crofts, Inc., New York, 1959
|
||
</p>
|
||
|
||
<p>
|
||
2. Boshes, B., and Arieff, A.J.: Clinical experience in the neurologic
|
||
substance of pain. Med Clin North Am 52:111-21, Jan 68
|
||
</p>
|
||
|
||
<p>3. Smith, B.H.: Anatomy of facial pain. Headache 9:7-13, Apr 69</p>
|
||
|
||
<p>
|
||
4. Larsell, O.: The nervous system. In Human anatomy. By H. Morris. Ed.
|
||
11, edited by J.P. Schaeffer. Blakiston Co., New York, 1953
|
||
</p>
|
||
|
||
<p>
|
||
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
|
||
</p>
|
||
|
||
<p>6. Gooddy, W.: On the nature of pain. Brain 80:11831, 1957</p>
|
||
|
||
<p>
|
||
7. Netter, F.H.: Nervous system. Vol. 1. Ciba collection of medical
|
||
illustrations. Ciba Pharmaceutical Co., Summit, N.J., 1953
|
||
</p>
|
||
|
||
<p>
|
||
8. Finneson, B.E.: Diagnosis and management of pain syndromes. Ed. 2.
|
||
W.B. Saunders Co., Philadelphia, 1969
|
||
</p>
|
||
|
||
<p>
|
||
9. Wolff, H.G.: Headache and other headpain. Ed.2. Oxford University
|
||
Press, New York, 1963
|
||
</p>
|
||
|
||
<p>
|
||
10. Crosby, E.C., Humphrey, T., and Lauer, E.W.: Correlative anatomy of
|
||
the nervous system. Macmillan Co., New York, 1962
|
||
</p>
|
||
|
||
<p>
|
||
11. Korr, I.M., and Buzzell, K.A.: Personal communication to the author
|
||
</p>
|
||
|
||
<p>
|
||
12. Magoun, H.I.: Osteopathy in the cranial field. Ed.2. Journal
|
||
Printing Co., Kirksville, Mo., 1966
|
||
</p>
|
||
|
||
<p>
|
||
13. Steriade, M.: The cerebello-thalamo-cortical pathway. Ascending
|
||
(specific and unspecific) and corticofugal controls. Int J Neurol
|
||
7:177-200,1970
|
||
</p>
|
||
|
||
<p>
|
||
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
|
||
</p>
|
||
|
||
<p>
|
||
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
|
||
</p>
|
||
|
||
<p>
|
||
16. Ito, M.: Neurophysiological aspects of the cerebellar motor control
|
||
system. Int J Neurol 7:162-76, 1970
|
||
</p>
|
||
</Article>
|
||
);
|
||
};
|
||
|
||
export default ArticleOsteopathicHeadPain;
|