Stimulation of the greater occipital nerve increases metabolic activity in the trigeminal nucleus caudalis and cervical dorsal horn of the cat

Abstract

Patients with primary headache syndromes often describe a distribution of pain that involves both frontal and occipital parts of the head. Such a distribution of pain does not respect the cutaneous sensory innervation of the head which would divide it into anterior (trigeminally innervated) and posterior (spinal nerve root innervated) regions. Studies of pain-producing intracranial structures, such as the superior sagittal sinus, have demonstrated that second order neurons as caudal as C2 are activated after either electrical or mechanical stimulation. For this study cats were anaesthetised with halothane (during surgery) and alpha-chloralose (60 mg/kg, i.p., then 20 mg/kg intravenous maintenance), paralysed (gallamine 6 mg/kg) and ventilated. The greater occipital nerve was isolated bilaterally and stimulated unilaterally using hook electrodes with stimuli of 100 V at 0.3 Hz. Metabolic activity in the caudal brain stem and upper cervical cord was measured using 2-deoxyglucose autoradiography and quantitative densitometry. Stimulation of the greater occipital nerve increased metabolic activity by 220% ipsilateral to stimulation and by a lesser amount contralaterally. Increases in metabolic activity were seen in the dorsal horn at the level of C1 and C2 as might be predicted from the cervical origin of the nerve. Neuronal activation appeared contiguous with the trigeminal nucleus caudalis and was in the same distribution as is seen when trigeminally-innervated structures are stimulated. These data suggest that the well recognised clinical phenomenon of pain at the front and back of the head and in the upper neck are likely to be a consequence of overlap of processing of nociceptive information at the level of the second order neurons.

Cervical Referral of Head Pain in Migraineurs: Effects on the Nociceptive Blink Reflex

“…19 Notwithstanding the effectiveness of GON blockades for migrainuers, 20-22 the mechanism(s) for the successful outcome remain uncertain. 23 It has been postulated that GON blockade influences central pain processing mechanisms by modulating responses to convergent synaptic input from cervical and trigeminal nociceptive afferents. 23 In our clinical experience, patients often report lessening of their referred, usual pain as the examination of the cervicospinal segment is sustained.…”

“…23 It has been postulated that GON blockade influences central pain processing mechanisms by modulating responses to convergent synaptic input from cervical and trigeminal nociceptive afferents. 23 In our clinical experience, patients often report lessening of their referred, usual pain as the examination of the cervicospinal segment is sustained. The pain usually lessens (to a variable degree, but often with complete resolution) within 90 seconds.…”

Targeting CGRP: A New Era for Migraine Treatment

“…The SSN, in turn, activates postganglionic parasympathetic neurons in the sphenopalatine ganglion, resulting in vasodilation and local release of inflammatory molecules that activate meningeal nociceptors [16]. This pathway, often referred to as trigeminocervical complex, has been studied extensively in animal models by Goadsby and colleagues [17][18][19].…”

Bloqueio anestésico do nervo occipital maior na profilaxia da migrânea

“…A ausência de mecanismos de convergência, não especificamente ao nível dos receptores do NMDA, foi descartada por estudos recentes 2,[33][34][35] . Se os mecanismos de convergência existem, esta convergên-cia poderia ser inibitória?…”

“…Pesquisas recentes mostraram que ele também participa ativamente na modulação nociceptiva encefálica, atuando diretamente, em conjunto com o nervo trigêmeo (NT), sobre neurô-nios nociceptivos secundários, localizados ao nível do tronco cerebral 2 . A influência do NOM sobre os mecanismos fisiológicos da migrânea não foram até o momento, adequadamente esclarecidos.…”