The Autonomic Nervous System and Its Relation to Headaches

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    The Autonomic Nervous System and its Relationship to Headache

    by Dr. Dietrich Klinghardt, M.D., PhD

    Thomas Willis, the "father" of modern neurology, proposed the vascular theory of headache in 1!.#e suggested that the source of pain $as not the brain itself but nerve fibers being pulled by the

    distended vessels%1&

    #arold Wollf reported in 1'() on the autonomic nervous system %*+& involvement in migraine

    headaches- he postulated that the primary cause of migraine is vasoconstriction of the etracranial

    arteries in the early phases of the headache follo$ed by vasoconstriction /$ith associated peripheralvasoconstriction in the limbs%&. 0ther signs suggesting *+ involvement in headache include nausea,

    diarrhea%(&,constipation %&, coldness in hands and feet, paroysmal tachycardia %2&, chest pain %&,

    variant angina %!&, paraesthesia and numbness of the s3in and others. The vascular theory of migraine$as the generally accepted $or3ing model until the cell receptor theory came along around 1'!). 4n

    1')5 +obel pri6e laureate Paul 7hrlich postulated the eistence of cell receptors, $hose interaction

    $ith specific agents $as a mechanism responsible for many illnesses. 8eceptor biochemistry has

    become the basis for most pharmacological approaches. * recent eample is the development of thedrug sumatriptan $hich attaches to the 2/#T1 receptor. 0ther receptors involved in headache include

    the alpha/ receptors, u/opioid receptors and somatostatin receptors. 9ntil today there are numerous

    theories on the neurophysiology of headache, none of $hich are completely proven%5&.

    Anatomy

    To understand the role of the *+ in headache, the anatomy has to be understood. The *+ servesthree basic functions in the brain-

    1. 4nnervation of the smooth muscleof the vascular tree $ithin the brain. * stress signal $ithin the

    sympathetic nervous system $ill generally lead to vasoconstriction in the affected area of the brain.

    . Transport of neuropeptidesand informational substances $ithin the aons of the *+ into the

    terminals $ithin the vascular endothelium. everal do6en substances travel via the *+ aons to theendothelium and are released into the bloodstream, causing both local and systemic effects. erotonin,

    en3ephalin, nitric oide and the inflammatory peptides such as substance P, neuro3inin * and

    calcitonin gene related peptide are thought to be involved in the genesis of migraine pain.

    (. 5): of *+ fibers are thought to be sensory in nature and may be directly involved in painperception. ensory autonomic nerves are present in the cranial membranes %dura, arachnoid,

    tentorium&, in the connective tissue and in the $alls of the larger blood and lymphatic vessels. The*+ is 3no$n to have a $ind/up effect %sensiti6ing effect& on the $ide dynamic range%WD8& cells in

    the spinal chord, $hich modulate the pain path$ay. 4f pain originates for eample in the trigeminal

    system, this message has to pass through the WD8 cells. 4f the threshold is lo$ered by arousal of thesympathetic nervous system in the same segment, the pain message passes through the WD8 cell up

    into the brain. *rousal in the *+ can be caused by any ecitatory stimulus acting on the aons, nerve

    endings or ganglia of the *+. ;ommon in the dental arena are abnormal electrical signals %"abnormalsignaling"& arising from dysfunctional scars %from tooth etractions or surgical procedures& or from

    dysfunctional teeth %decay, incompatible restoration materials, mechanical stress, toicity from filling

    materials and infections etc.&. The dental pulp has its o$n autonomic nervous system mostlycomprised of sympathetic fibers traveling piggybac3 on the arteries, veins and lymphatic vessels of the

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    tooth pulp. The fibers are post/ganglionic and arise in the anterior cervical ganglia %stellate, middle/and upper cervical sympathetic ganglia& and travel to the teeth piggybac3 on the vessels and trigeminal

    nerve fibers&. *ny dysfunction in a tooth or related structure %muscles of mastication, periosteum,

    dental ligaments,

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    "iagnosis

    The follo$ing diagnostic approaches have emerged in the last () years, that are able to assess

    dysfunction of the *+ and>or locate a focal area-

    1. #eart rate variability testing. Thermography(. 7lectrodermal screening %7*&

    . *utonomic response testing %"3inesiology", "muscle testing"&

    2. Palpation>clinical eam. ;hinese pulse diagnosis %also *&

    Treatment

    The treatment consists in an appropriate intervention that eliminates or treats the disturbing factor.

    #ere is a list of common solutions that have emerged in the 7uropean +eural Therapy contet -

    1. !luster headache#the focus is usually a small area inside the nose, $here the middle turbinatetouches the nasal septum. Treatment is either in

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    %iterature

    1. ac3s,0.- Migraine / 9nderstanding a ;ommon Disorder. ?er3eley 9niversity of ;al.Press, 1'52-1/

    5, 5

    . Dalessio, D.=.- WolffEs #eadache and other #ead Pain. th ed.+e$ For3. 0ford 9niv.Press, 1'5)(. elbyu,@. 0bservations on 2)) cases of Migraine and *llied ascular #eadache.

    =.+eurol.+eurosurg.Psychiatry 1'), (-(/(. ;ady,8.-Treating the #eadache Patient. Marcel De33er, 4+;, +e$ For3 1''2, pg.2. Thomas, W*- Paroysmal Tachycardia in Migraine. =*M* 1'2. 5-2'/2!)

    . ?riggs,=C- Precordial Migraine. is;hest 1'2. 1- (2/)

    !. Miller,D.- 4s ariant *ngina the coronary Manifestation of a @enerali6ed asospastic DisorderG+e$ 7ngl = Med 1'51. ()- !(/!

    5. 8.;ady- Treating the #eadache Patient. Marcel De33er, +.F., 1''2