Pathways of referred pain from the nose

Fenton, Ralph A.

doi:10.1016/s0002-9610(38)91168-7

Cited by 3 publications

(2 citation statements)

References 7 publications

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“…Phylogenetically, the forward development of the cerebral hemispheres and forward turning of the orbits have created narrow conditions in the nasal and retroorbital area, especially in man. [98][99] The continuation of the internal maxillary artery, the sphenopalatine artery, curls worm-like over the anterior aspect of the sphenopalatine ganglion in the pterygopalatine (pterygomaxillary) fossa, 17,100 before its main branch passes through the sphenopalatine foramen together with nerve branches from the maxillary nerve and the sphenopalatine ganglion (Figure 3). Apart from visceromotor and sensory fibres to the nose, palate and lacrimal gland, the sphenopalatine ganglion has vasomotor connections through rami orbitales with vessels in the posterior and anterior parts of the eye (choroidal and conjunctival vessels), 101 with the internal carotid artery through other rami orbitales 64-65,69,102 (Figure 2 and 3), and with the superficial temporal artery.…”

Section: Pain Fibres and Vessels Of The Pterygopalatine Fossa And Nasmentioning

confidence: 99%

On Pain Mechanisms in Cluster Headache

Hardebo

1991

Headache

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Various possible pathophysiological mechanisms to explain the pain in cluster headache are reviewed. Several locations for the initiation of pain along the primary afferent pathways in cranial nerves are discussed, together with the local mechanisms that might be responsible. These include neurogenic inflammation of large cranial vessels, irritation of vascular pain fibres by compression of dilated vessels in bony canals, and irritative foci in or around cranial sensory ganglia. In particular, recent neuroanatomical and pharmacological findings on nociceptive innervation of the intracranial segment of the internal carotid artery are commented upon. The possibilities for referred pain to explain the location of pain is illustrated. Evidence for involvement of central pain modulatory systems in the pain production is discussed. Finally a synthesis is made of the probable peripheral and central pain mechanisms in the disease.

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Section: Pain Fibres and Vessels Of The Pterygopalatine Fossa And Nasmentioning

confidence: 99%

On Pain Mechanisms in Cluster Headache

Hardebo

1991

Headache

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“…The pain of a cluster attack is mainly located in or behind the eye. Rarely, the painful area reaches outside the distribution of the ophthalmic and maxillary branches of the trigeminal nerve, and may then be explained as referred pain of sensory input from facial or cervical nerve roots, 3,27 except in rare cases where the pain is also distributed in the distribution of the mandibular branch. Surgical resection of the trigeminal nerve root or destruction of the Gasserian ganglion, or strong blockade of nerve transmission through the ganglion by alcohol or glycerol result in prompt relief from all symptoms of a cluster attack.…”

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confidence: 99%

The Involvement of Trigeminal Substance P Neurons in Cluster Headache. An Hypothesis

Hardebo

1984

Headache

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SYNOPSIS Substance P (SP) neurons, with bipolar axons from the cell body, in sensory ganglia, exhibit unique properties in that impulses may travel either orthodromically or antidromically in the various ramifications of the axons, and that the transmitter may be released both in the central and peripheral ends of the neuron. Thus, these nerves are not only sensory, carrying nociceptive impulses from the periphery, but also motor with ability to dilate blood vessels, constrict smooth muscle cells and cause protein extravasation, glandular secretion, release from mast cells and excitation of autonomic ganglion cells. Within the individual neuron several local reflex arches ‐ axon reflexes ‐ are established in this way. An hypothesis is forwarded about the pathophysiology of cluster headache, against the background of recent morphological and functional evidence for SP neurons in the ipsilateral trigeminal nerve and its connections to various cranial structures including the sphenopalatine (pterygopalatine) ganglion and internal carotid perivascular nerve plexus. Activation of SP fibers in the ophthalmic and maxillary divisions may give rise to practically all symptoms of an attack of cluster headache. This provides a rational explanation for the beneficial effect on both pain and vegetative symptoms achieved by blockade of the Gasserian or sphenopalatine ganglia in this disease. A temporary arrest of central inhibitory serotonergic impulses presynaptically on the SP neurons in the caudal trigeminal nucleus is, with our present knowledge, a likely explanation for such an activation, even if it may not be the only factor. A comparison is made with the present opinion on activation of parasympathetic and blockade of sympathetic nerves to explain the various symptoms of a cluster attack.

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Atypical Facial Neuralgia

Martin¹

1942

Archives of Otolaryngology - Head and Neck Surgery

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A large group of patients have atypical facial neuralgia characterized by severe boring, at times burning, pain, not limited to the distribution of a cranial nerve but occurring back of the eye, over the zygoma, cheek or nose and occasionally over the mastoid region and down the neck. It cannot be brought on by touching or moving the area and is not lancinating as is trigeminal neuralgia. This syndrome is often temporarily relieved by cocainizing the sphenopalatine ganglion, and Sluder, who first described the condition, thought that permanent relief was sometimes obtained by the injection of alcohol into that ganglion. I have seen patients relieved after cocainization but not after injection of alcohol.Hypotheses as to the production of this pain are many. Davis and Pollock 1 stated the belief that they had disproved experimentally the existence of afferent sympathetic fibers. It was their opinion that stimulation of the efferent sympathetic fibers in turn stimulates the accepted pathways in the cranial nerves and produces the pain. Davis 2 expressed the belief that failure to relieve atypical neuralgia by section of the superior cervical ganglion and the sensory root of the fifth nerve shows that sensibility to pain on deep pressure is transmitted by the seventh nerve. Kuntz 3 stated the belief that there are no afferent fibers in the sympathetic nervous system. Because in some cases of atypical neuralgia there is a distribution of pain which corresponds not to the area of any sensory nerve but rather to areas of arterial supply, Fay 4 has advanced the possibility of another mechanism. He stated that sectioning of various combinations of nerves had led to the impression that the vascular pain fibers of the head and neck find entry to the cranial nerves through the vagus, for the most Read at the Forty

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Pathways of referred pain from the nose

Cited by 3 publications

References 7 publications

On Pain Mechanisms in Cluster Headache

On Pain Mechanisms in Cluster Headache

The Involvement of Trigeminal Substance P Neurons in Cluster Headache. An Hypothesis

Atypical Facial Neuralgia

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