The Cluster Phenomenon: An Unspecific feature?

Sjaastad, Ottar; Carvalho, Diana Paula de Souza Rêgo Pinto; Fragoso, Yára Dadalti

doi:10.1046/j.1468-2982.1988.0802061.x

Cited by 10 publications

(8 citation statements)

References 17 publications

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“…Summed up, they seem to minimize the chances that one is faced with ordinary cluster headache in this case (15,16). The role of the giant aneurysm in this picture is dubious.…”

Section: Anterior Communicating Artery Aneurysm and Cluster Headache-mentioning

confidence: 96%

“…However, manifold atypical traits were also present, like the age of onset (around 14 years), the duration of the solitary attack (up to 5-6h), vomiting during severe attacks, and so forth. Summed up, they seem to minimize the chances that one is faced with ordinary cluster headache in this case (15,16). The role of the giant aneurysm in this picture is dubious.…”

Section: Anterior Communicating Artery Aneurysm and Cluster Headache-mentioning

confidence: 96%

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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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“…Summed up, they seem to minimize the chances that one is faced with ordinary cluster headache in this case (15,16). The role of the giant aneurysm in this picture is dubious.…”

Section: Anterior Communicating Artery Aneurysm and Cluster Headache-mentioning

confidence: 96%

Section: Anterior Communicating Artery Aneurysm and Cluster Headache-mentioning

confidence: 96%

Cluster Headache: The Possible Significance of Midline Structures

Sjaastad¹

1988

Cephalalgia

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“…Two patients had the "mild form" of cluster headache (16) and were able to work during pain attacks. One of the patients had a "primary chronic type of cluster headache", and is still under investigation for a possible neurological disease leading to a "symptomatic cluster headache" (17). This case as well as two others were studied during bouts, and two of them had taken analgesics 12 h prior to blood sampling.…”

mentioning

confidence: 99%

Increased Incorporation of L-(U-14C)serine into Phosphatidylserine in Polymorphonuclear Cells from Cluster Headache Patients

Fragoso¹,

Stovner²,

Bjerve³

et al. 1989

Cephalalgia

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It has recently been demonstrated by our group that polymorphonuclear cells (PMNs) from cluster headache patients incorporate more arachidonic acid (AA) into phosphatidylserine (PS) than PMNs from controls. In the present report, the incorporation of L-(U-14C)serine into PS in PMNs from 14 healthy volunteers and 12 cluster headache patients was studied. PMNs from controls incorporated 1194 +/- 578 (mean +/- SD) cpm of L-(U-14C)serine into PS, 268 +/- 292 cpm into phosphatidylethanolamine, and 57 +/- 71 cpm into sphingomyeline. The corresponding figures in cluster headache patients were 2365 +/- 841 cpm, 291 +/- 207 cpm, and 88 +/- 66 cpm, respectively. Incorporation of L-(U-14C)serine into PS was significantly increased (p less than 0.0004) in PMNs from cluster headache patients, whereas no significant difference was seen in other lipids. The results confirm that patients with cluster headache have an increased incorporation of precursors into PS in isolated PMNs, and they indicate that this is due to an increased de novo synthesis of PS.

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“…the occurrence of attacks within a relatively limited time-span, which led to the commonly used appellation cluster headache, is actually not an exclusive feature of this headache, but is also quite typical for other unilateral headaches [16], including SUNCT. Ipsilateral, localized autonomic phenomena during attacks are obligatory for the diagnosis of CH as well as SUNCT [3,15].…”

Section: Clinical Variablesmentioning

confidence: 99%

Cluster headache and SUNCT: similarities and differences

Kruszewski

Pareja

Caminero³

et al. 2001

J Headache Pain

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IntroductionOur first case of SUNCT was found in 1978 [1], and a total of three cases were later published under the common name "shortlasting, unilateral, neuralgiform headache attacks with conjunctival injection and tearing" in 1989 [2]. Currently, SUNCT is defined by the International Association for the Study of Pain (IASP) as "Repetitive paroxysms of unilateral shortlasting pain, usually 15-120 seconds duration, mainly in the ocular and the periocular areas, of a neuralgiform nature and moderate to severe intensity, usually appearing only during daytime and accompanied by ipsilateral marked conjunctival injection, lacrimation, a low to moderate degree of rhinorrhea, and subclinical forehead sweating", and belongs to the group of neuralgias of the head and face [3]. Furthermore, the pain paroxysms accompanied by autonomic phenomena tend to appear in cluster periods, and there is a clear male preponderance in SUNCT [3]. Thus, SUNCT has even been considered to be in the same group as cluster headache (CH) [4,5]. Abstract SUNCT is probably a distinct syndrome, although it shares some common features with cluster headache (CH): male sex preponderance, clustering of attacks, unilaterality of headache without sideshift, pain of non-pulsating type with its maximum in the periocular area, ipsilateral autonomic phenomena (e.g. conjunctival injection, lacrimation, rhinorrhea, increased forehead sweating), systemic blood pressure increment with heart rate decrement, blood flow velocity decrement in the middle cerebral artery, and hyperventilation. In spite of these similarities, SUNCT syndrome differs clearly from CH as regards a number of clinical variables, such as duration, intensity, frequency, and nocturnal preponderance of attacks. The two syndromes also differ markedly as regards precipitation of attacks, the usual age at onset, and efficacy of various treatment alternatives.Laboratory investigations have disclosed differences as regards presence or absence of Horner-like picture and possibly also the respiratory sinus arrhythmia pattern. All in all, these differences seem sufficiently ponderous to make it likely that SUNCT syndrome and CH differ essentially. SUNCT seems to be a "neuralgiform" headache, but different from trigeminal neuralgia.

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The Cluster Phenomenon: An Unspecific feature?

Cited by 10 publications

References 17 publications

Cluster Headache: The Possible Significance of Midline Structures

Cluster Headache: The Possible Significance of Midline Structures

Increased Incorporation of L-(U-14C)serine into Phosphatidylserine in Polymorphonuclear Cells from Cluster Headache Patients

Cluster headache and SUNCT: similarities and differences

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