Physiologic Mechanisms and Treatment of Histaminic or Petrosal Neuralgia

Stowell, A

doi:10.1111/j.1526-4610.1970.hed0904187.x

Cited by 22 publications

(18 citation statements)

References 5 publications

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“…To the present author, cluster headache, to put it roughly, is more an "anterior" than a "posterior" disease. Midline structures such as the "posterior portions of the circle of Willis" (35) can, however, not be completely rejected as candidates.…”

Section: Trial At a Synthesismentioning

confidence: 99%

Cluster Headache: The Possible Significance of Midline Structures

Sjaastad¹

1988

Cephalalgia

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The pathogenesis of cluster headache is unknown (see, for example, Ref. 1). With regard to the main component of cluster headache, the pain itself, little information exists both as to the origin and as to the nature of the pain. Existing theories concerning cluster headache pathogenesis have been rather unproductive. In the following, evidence from seemingly totally unrelated fields that, nevertheless, possibly has a bearing on cluster headache pathogenesis will be reviewed. On the tendency to bilaterality in cluster headacheCluster headache is in principle a unilateral headache. There is, however, a tendency for the headache to shift side, either during one single bout (circa 5%) or from one bout to another (circa 10%). All in all, approximately 15% of cluster headache cases thus shift side at some point along the time axis (2). Accordingly, there seems to be a "disposition" or "anlage" for the headache to develop on both sides in cluster headache, although the headache actually most frequently manifests itself on one side only.The prevalence of cluster headache in the form that is severe enough to lead to medical consultations may seem to be around 0.7% (3) in Western countries. The tendency to develop headache on the side opposite the pain side in a cluster headache patient may, therefore, seem to be around 200 times higher than for an individual to develop this type of headache de novo (4). Side shift is thus a conspicuous feature of this disease.On rare occasions, the headache may even be bilateral (5). Several variations of bilaterality have also been observed. Ekbom (6) has thus described a case with a most peculiar pattern, in which the headache during one bout, in addition to appearing on the original side, started appearing on the contralateral side; then "the headache shifted [side] in different attacks"; thereafter, a decrescendo occurred on the original side as opposed to a crescendo on the contralateral side, and, in the ultimate phase, attacks only appeared on the contralateral side.After operations on one side, pain attacks have a tendency to recur on the opposite, previously pain-free side. This was thus the case in 1 of 12 cases treated with the "combined procedure"-that is, sectioning of the greater superficial petrosal nerve and neurolysis of the sensory root of the trigeminal nerve (7).The attack of cluster headache as such consists of (at least) two components: the pain and the autonomic phenomena. The latter also show a tendency to bilaterality (8, 9) and, in fact, much more regularly so than does the pain. In patients with side shift there is sometimes a dichotomy between pain and autonomic phenomena, the latter persisting on the previous pain side (4). The schism may even be primary; that is, the pain has always been contralateral to the autonomic phenomena (10).This tendency to bilaterality in cluster headache is intriguing. A pathogenetic model of cluster headache must also include and explain the marked tendency to bilaterality of the pain and, above all, of the autonomic manifestati...

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Section: Trial At a Synthesismentioning

confidence: 99%

Cluster Headache: The Possible Significance of Midline Structures

Sjaastad¹

1988

Cephalalgia

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“…section of the supraorbital nerve) relieves pain locally. 26,38 This may indicate that pain production in these patients involves activation of the trigeminal nerve pathways, with impulses travelling ortho-or antidromically, at or distal to this peripheral point of blockade. However, in most of these patients in which a local anesthesia or nerve section in the painful area is performed (e.g.…”

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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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“…Surgical ablation of parasympathetic pathways has resulted in varying degrees of success in alleviating cluster head ache., 12,13 Ekbom studied the distribution of pain in cluster headache and the results indicate that the pain is confined to the territory of the trigeminal nerves with the most severe pain being in the periorbital region. Kunkle 11 suggested that the cluster headache results from a para-sympathetic storm.…”

Section: Discussionmentioning

confidence: 99%

Corneal Sensitivity in Cluster Headache

Vijayan

Watson

1985

Headache

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SYNOPSIS Cluster headache pain is thought to arise from vasodilatation, but a neural origin of the pain has never been completely excluded. Some patients with cluster headache have complained of subjective diminution of sensation over the ipsilateral forehead. This is hard to quantitate and is often variable. Besides, ablation of trigeminal sensory pathways has been re sorted to for relief of pain in some intractable cases. The present study was undertaken to quantitatively assess the sensitivity of the cornea in cluster patients. Fifteen cluster headache patients were the subjects of this study. Measurement of the corneal sensitivity was undertaken using a Cochet‐Bonnet Aesthesiometer. There was no difference between the affected and the unaffected eye. There was no difference in the sensitivity when testing was done during the cluster period and later on when the patients were in remission. It is concluded from this study that there is no objective evidence for involvement of trigeminal sensory pathways in patients with cluster headache.

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Physiologic Mechanisms and Treatment of Histaminic or Petrosal Neuralgia

Cited by 22 publications

References 5 publications

Cluster Headache: The Possible Significance of Midline Structures

Cluster Headache: The Possible Significance of Midline Structures

On Pain Mechanisms in Cluster Headache

Corneal Sensitivity in Cluster Headache

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