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

医学 解剖 刺激 脊髓 三叉神经脊核 三叉神经 麻醉 伤害 内科学 精神科 受体
作者
Peter J. Goadsby,Yolande E. Knight,Karen L. Hoskin
出处
期刊:Pain [Ovid Technologies (Wolters Kluwer)]
卷期号:73 (1): 23-28 被引量:166
标识
DOI:10.1016/s0304-3959(97)00074-2
摘要

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.

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