Does the eye modulate the clinical expression of cluster headache?
Vinod Gupta, Dubai Police Medical Services, Dubai, United Arab Emirates
17 May 2005
Sörös and colleagues studied the link between enucleation of the eye and development of ipsilateral cluster headache (CH) in the quest for insight into the vexing association – causal or coincidental – between CH and preceding brain injury or disease [1]. Despite encountering striking development of CH in close proximity (3 weeks) to orbital exenteration in one patient (six other patients reviewed) [2], these investigators conclude on the basis of epidemiological studies that removal of the eye has no role in the development of CH [1]. The authors have detailed some of the limitations of questionnaire-based retrospective studies; the assumption that CH patients would respond better than patients with other forms of headache or patients without any headaches [1] is debatable, particularly in a subset having undergone loss of a vital organ such as the eye. Only one-third of the identified patients responded to this questionnaire [1], rendering tentative any conclusions that might be derived. The second key assumption is that patients with eye-trauma and malignant or non-malignant eye disease represent a microcosm of the general populations [1]. A poorly-defined genetic vulnerability underlies CH; it is too vague to extend this susceptibility to those undergoing enucleation for malignant or non-malignant eye disease. Also, it is not essential that the subsets prone to eye-trauma must be the subsets prone to CH. In other words, the question about the role of the eye in CH is unlikely to be answered from study of an unselected cohort of patients undergoing enucleation but by study of a cohort of patients susceptible to develop CH and undergoing enucleation. Since subclinical susceptibility to develop CH can be unmasked by a vasodilator challenge, a prospective study of patients undergoing enucleation should be undertaken to determine the contribution of enucleation / evisceration / exenteration to post-surgery CH. Besides, epidemiologically, the link between the eye and CH can be better determined by disappearance or aggravation of pre-existing CH following enucleation. Finally, the exclusion of patients undergoing orbital exenteration [1] is a critical limiting factor. Limitation of follow-up period in cancer patients does not seem to apply to de novo development of CH post-operatively; a follow-up period of 4-8 weeks might well suffice to unmask the CH diathesis due to structural modifications following orbito-ocular surgery. Extrapolating retrospectively from approximately 8 years after enucleation / evisceration is both fraught with difficulties (as stated by the authors) as well as being quite unnecessary to study a direct link between enucleation / evisceration and CH. Such epidemiological data probably do not override the authors own previous observation [2] about the link between exenteration and CH. Vascular implications of enucleation / evisceration are different from those of exenteration, as will be discussed below.
Epidemiological data are intrinsically limited; associations are interesting only if they provide clues to ætiology by leading to experiments that deepen our understanding of causal mechanisms [3]. To secure clinical usefulness, epidemiological data must be knitted back into the basic sciences involved. The circulation of the ipsilateral eye is involved in CH. Prominent ocular haemodynamic alterations occur in CH; sudden vasodilatation in intraocular circulation with increased ocular blood flow and pulse-synchronous change in intraocular volume as well as intraocular pressure (IOP) has been shown in CH as well as chronic paroxysmal hemicrania [CPH) [4,5]. These changes in the intraocular circulation are bilateral but more pronounced on the symptomatic side. Whether these changes contribute to the pain itself is not certain [4]. Nevertheless, the source of sudden intraocular vasodilatation is likely to be abnormal vasodilatation in the internal carotid-ophthalmic artery segment of the cranial arterial tree. Enucleation or evisceration of the eye removes the ocular vascular bed, constituting a substantial reduction in available anterior run-off for the internal carotid artery-ophthalmic artery blood flow. This reduction is maximal following orbital exenteration as the entire orbital content including the external eye muscles are removed. Development of CH soon after exenteration [1] indicates that the orbital and ocular circulation, by keeping CH in abeyance by a tamponade-like function, was probably protective in nature. While the exact site responsible for generation of CH – vascular or neuronal – is not known, the predisposition to develop CH following removal of the entire orbito-ocular vascular bed appears to increase. In these circumstances, the orbito-ocular bed is replaced by the stump of the ophthalmic artery, which has to accommodate the directed flow from the internal carotid artery, and, post-operatively likely undergoes adhesions or dilatations or both. Consequently, previously subclinical surges of blood flow in this arterial segment might manifest as pain of CH or as head pain without the typical characteristics of CH. Autonomic features such as conjunctival injection, lacrimation, and miosis [1] are not expected to develop after loss of ocular structures. Furthermore, lowering of IOP would decrease the tamponade-like effect of ocular vasodilatation. Unlike migraine, beta-blockers do not have a therapeutic role in CH. Remarkably, beta-blockers lower IOP [6].
If the eye is truly involved in a partial decompression of rapid-to-sudden internal carotid artery-ophthalmic artery dilatation, some of the seemingly insoluble epidemiological and biological mysteries of CH might be resolved. The predominance of males (male to female ratio being 4.5:1 to 6.7:1) is the most striking epidemiological feature of CH [7]. Such a predilection for males is probably the outcome of some cranial physio-anatomic characteristic(s) that differs between males and females. Sudden alterations in intraocular haemodynamics [4,5] are inversely proportional to the ocular rigidity; greater the rigidity, lesser would be the intraocular vasodilatation or change in pulse-synchronous IOP or ocular volume. Although there does not appear to be any significant variation in ocular rigidity between the sexes, the ocular distending effect of sudden vasodilatation in CH (and CPH) is unique; alterations in tissue elasticity and tissue creep have not been studied in these entities. I predict that in this clinical situation the female corneo-scleral envelope might be relatively more distensible and possibly decompresses sudden internal carotid artery-ophthalmic artery dilatations to a larger extent than in males. Since this difference would be predominantly dynamic rather than static, it will probably be difficult if not impossible to document significant differences in ocular rigidity in CH between the sexes clinically during life. Nevertheless, what is immeasurable might be more important than what is measurable.
Whereas episodic migraine headache may persist for days, CH is sharply limited to 15-180 minutes [1]. Other variants of the trigeminal autonomic cephalagias, CPH and short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT) [8], also manifest strictly time-limited headache episodes. There is currently no satisfactory explanation for this very characteristic feature of these primary headaches. I propose that while sudden increases in intraocular volume in these three variants of primary headache accommodates the surge in internal carotid-ophthalmic artery segment, the ocular distention involved is variably limited between individuals. The differences in visco-elastic properties of the ocular globe determine the time taken to accommodate the surge, during which period antidromic activation of the pain-sensitive terminals of the trigeminal nerve can develop [9].
In summary, the question regarding the role of the eye or its removal in the occurrence of CH cannot be dissociated from known intraocular circulatory disturbances. Enucleation or evisceration eliminates the terminal circulatory bed of the internal carotid artery-ophthalmic artery blood flow, an effect maximally seen with orbital exenteration. Available clinical evidences continue to support the contention that removal of the eye might precipitate CH in a matter of weeks. These considerations do not exclude the potential role of the eye as a possible contributor to the selective activation of the ophthalmic division of the trigeminal nerve in CH, CPH, SUNCT; the primary physiological system involved in these headaches is most likely identical, the variability in duration of headache (few seconds to a few hours) [10] probably depending on the visco-elastic properties of the tissues involved.
References
1. Sörös P, Vo O, Gerding H, Husstedt IW, Evers S. Enucleation and development of cluster headache: a retrospective study. BMC Neurology 2005, 5:6 doi:10.1186/1471-2377-5-6.
2. Evers S, Sörös P, Brilla R, Gerding H, Husstedt IW. Cluster headache after orbital exenteration. Cephalalgia 1997, 17(6):680-682.
3. Skrabanek P. The poverty of epidemiology. Persp Biol Med 1992;35:182-185.
4. Hørven I, Sjaastad O. Cluster headache syndrome and migraine: ophthalmological support for a two-entity theory. Acta Ophthalmol Copenhagen 1977;55:35-51.
5. Sjaastad O, Egge K, Hørven I, Kayed K, Lund-Roland L, Russell D, Conradi IS. Chronic paraoxysmal hemicrania: mechanical precipitation of attacks. Headache 1979;19:31-36.
6. Gupta VK. Visual function impairment in migraine: cerebral versus retinal deficit. Cephalalgia. 1993;13:431-432.
8. Goadsby PJ. Trigeminal autonomic cephalalgias: fancy term or constructive change to the HIS classification? J Neurol Neurosurg Psychiatry 2005;76:301-305.
10. Gupta VK. Trigeminal autonomic cephalalgias: ‘noso-physiology’ or pathophysiology? J Neurol Neurosurg Psychiatry (22 February 2005). Available at: http://jnnp.bmjjournals.com/cgi/eletters/76/3/301
Competing interests
None declared
Symptomatic cluster headache: literature update
Peter Sörös, University of Western Ontario, London, Ontario, Canada
10 August 2007
Since the publication of our article on a possible association between the removal of an eye and the development of cluster headache in 2005, at least 3 review papers (1, 10, 18) and 15 papers presenting original research (2-9, 11-17) on symptomatic cluster headache appeared. Papers were identified through a search in the PubMed database using the keyphrase "cluster headache" on 3 August 2007.
Most of the published reports present the development of cluster headache in patients with intracranial tumours or a disorder of intracranial vessels. None of these papers present a patient who developed cluster headache after the removal of an eye. Maggioni et al., however, described a 55-year-old man who developed cluster headache after cataract surgery involving an intraocular lens implant (9). This case report suggests that, although our retrospective study did not find an association between the removal of an eye and subsequent cluster headache, severe headache after eye surgery should be examined by a specialist who is experienced in the diagnosis of headache disorders.
References
1. Favier I, van Vliet JA, Roon KI, Witteveen RJ, Verschuuren JJ, Ferrari MD, Haan J. Trigeminal autonomic cephalgias due to structural lesions: a review of 31 cases. Arch Neurol. 2007;64:25-31.
2. Favier I, Haan J, van Duinen SG, Ferrari MD. Typical cluster headache caused by granulomatous pituitary involvement. Cephalalgia. 2007;27:173-6.
3. Gentile S, Fontanella M, Giudice RL, Rainero I, Rubino E, Pinessi L. Resolution of cluster headache after closure of an anterior communicating artery aneurysm: the role of pericarotid sympathetic fibres. Clin Neurol Neurosurg. 2006;108:195-8.
4. Georgiadis G, Tsitouridis I, Paspali D, Rudolf J. Cerebral sinus thrombosis presenting with cluster-like headache. Cephalalgia. 2007;27:79-82.
6. Hardmeier M, Gobbi C, Buitrago C, Steck A, Lyrer P, Engelter S. Dissection of the internal carotid artery mimicking episodic cluster headache. J Neurol. 2007;254:672-3.
7. Lai SL, Chang YY, Liu JS, Chen SS. Cluster-like headache from vertebral artery dissection: angiographic evidence of neurovascular activation. Cephalalgia. 2005;25:629-32.
8. Levy MJ, Matharu MS, Meeran K, Powell M, Goadsby PJ. The clinical characteristics of headache in patients with pituitary tumours. Brain. 2005;128:1921-30.
9. Maggioni F, Dainese F, Mainardi F, Lisotto C, Zanchin G. Cluster-like headache after surgical crystalline removal and intraocular lens implant: a case report. J Headache Pain. 2005;6:88-90.
10. Manzoni GC, Lambru G, Torelli P. Head trauma and cluster headache. Curr Pain Headache Rep. 2006;10:130-6.
11. Massie R, Sirhan D, Andermann F. Chronic cluster-like headache secondary to an epidermoid clival lesion. Can J Neurol Sci. 2006;33:421-2.
12. Negoro K, Kawai M, Tada Y, Ogasawara J, Misumi S, Morimatsu M. A case of postprandial cluster-like headache with prolactinoma: dramatic response to cabergoline. Headache. 2005;45:604-6.
13. Palmieri A, Mainardi F, Maggioni F, Dainese F, Zanchin G. Cluster-like headache secondary to cavernous sinus metastasis. Cephalalgia. 2005;25:743-5.
14. Peterlin BL, Levin M, Cohen JA, Ward TN. Secondary cluster headache: a presentation of cerebral venous thrombosis. Cephalalgia. 2006;26:1022-4.
15. Rigamonti A, Iurlaro S, Zelioli A, Agostoni E. Two symptomatic cases of cluster headache associated with internal carotid artery dissection. Neurol Sci. 2007;28 Suppl 2:S229-31.
16. Straube A, Freilinger T, Rüther T, Padovan C. Two cases of symptomatic cluster-like headache suggest the importance of sympathetic/parasympathetic balance. Cephalalgia. 2007 [Epub ahead of print].
17. Volcy M, Tepper SJ. Cluster-like headache secondary to idiopathic intracranial hypertension. Cephalalgia. 2006;26:883-6.
18. Walker RW. Cluster headache and head trauma: is there an association? Curr Pain Headache Rep. 2007;11:137-40.
Does the eye modulate the clinical expression of cluster headache?
17 May 2005
Sörös and colleagues studied the link between enucleation of the eye and development of ipsilateral cluster headache (CH) in the quest for insight into the vexing association – causal or coincidental – between CH and preceding brain injury or disease [1]. Despite encountering striking development of CH in close proximity (3 weeks) to orbital exenteration in one patient (six other patients reviewed) [2], these investigators conclude on the basis of epidemiological studies that removal of the eye has no role in the development of CH [1]. The authors have detailed some of the limitations of questionnaire-based retrospective studies; the assumption that CH patients would respond better than patients with other forms of headache or patients without any headaches [1] is debatable, particularly in a subset having undergone loss of a vital organ such as the eye. Only one-third of the identified patients responded to this questionnaire [1], rendering tentative any conclusions that might be derived. The second key assumption is that patients with eye-trauma and malignant or non-malignant eye disease represent a microcosm of the general populations [1]. A poorly-defined genetic vulnerability underlies CH; it is too vague to extend this susceptibility to those undergoing enucleation for malignant or non-malignant eye disease. Also, it is not essential that the subsets prone to eye-trauma must be the subsets prone to CH. In other words, the question about the role of the eye in CH is unlikely to be answered from study of an unselected cohort of patients undergoing enucleation but by study of a cohort of patients susceptible to develop CH and undergoing enucleation. Since subclinical susceptibility to develop CH can be unmasked by a vasodilator challenge, a prospective study of patients undergoing enucleation should be undertaken to determine the contribution of enucleation / evisceration / exenteration to post-surgery CH. Besides, epidemiologically, the link between the eye and CH can be better determined by disappearance or aggravation of pre-existing CH following enucleation. Finally, the exclusion of patients undergoing orbital exenteration [1] is a critical limiting factor. Limitation of follow-up period in cancer patients does not seem to apply to de novo development of CH post-operatively; a follow-up period of 4-8 weeks might well suffice to unmask the CH diathesis due to structural modifications following orbito-ocular surgery. Extrapolating retrospectively from approximately 8 years after enucleation / evisceration is both fraught with difficulties (as stated by the authors) as well as being quite unnecessary to study a direct link between enucleation / evisceration and CH. Such epidemiological data probably do not override the authors own previous observation [2] about the link between exenteration and CH. Vascular implications of enucleation / evisceration are different from those of exenteration, as will be discussed below.
Epidemiological data are intrinsically limited; associations are interesting only if they provide clues to ætiology by leading to experiments that deepen our understanding of causal mechanisms [3]. To secure clinical usefulness, epidemiological data must be knitted back into the basic sciences involved. The circulation of the ipsilateral eye is involved in CH. Prominent ocular haemodynamic alterations occur in CH; sudden vasodilatation in intraocular circulation with increased ocular blood flow and pulse-synchronous change in intraocular volume as well as intraocular pressure (IOP) has been shown in CH as well as chronic paroxysmal hemicrania [CPH) [4,5]. These changes in the intraocular circulation are bilateral but more pronounced on the symptomatic side. Whether these changes contribute to the pain itself is not certain [4]. Nevertheless, the source of sudden intraocular vasodilatation is likely to be abnormal vasodilatation in the internal carotid-ophthalmic artery segment of the cranial arterial tree. Enucleation or evisceration of the eye removes the ocular vascular bed, constituting a substantial reduction in available anterior run-off for the internal carotid artery-ophthalmic artery blood flow. This reduction is maximal following orbital exenteration as the entire orbital content including the external eye muscles are removed. Development of CH soon after exenteration [1] indicates that the orbital and ocular circulation, by keeping CH in abeyance by a tamponade-like function, was probably protective in nature. While the exact site responsible for generation of CH – vascular or neuronal – is not known, the predisposition to develop CH following removal of the entire orbito-ocular vascular bed appears to increase. In these circumstances, the orbito-ocular bed is replaced by the stump of the ophthalmic artery, which has to accommodate the directed flow from the internal carotid artery, and, post-operatively likely undergoes adhesions or dilatations or both. Consequently, previously subclinical surges of blood flow in this arterial segment might manifest as pain of CH or as head pain without the typical characteristics of CH. Autonomic features such as conjunctival injection, lacrimation, and miosis [1] are not expected to develop after loss of ocular structures. Furthermore, lowering of IOP would decrease the tamponade-like effect of ocular vasodilatation. Unlike migraine, beta-blockers do not have a therapeutic role in CH. Remarkably, beta-blockers lower IOP [6].
If the eye is truly involved in a partial decompression of rapid-to-sudden internal carotid artery-ophthalmic artery dilatation, some of the seemingly insoluble epidemiological and biological mysteries of CH might be resolved. The predominance of males (male to female ratio being 4.5:1 to 6.7:1) is the most striking epidemiological feature of CH [7]. Such a predilection for males is probably the outcome of some cranial physio-anatomic characteristic(s) that differs between males and females. Sudden alterations in intraocular haemodynamics [4,5] are inversely proportional to the ocular rigidity; greater the rigidity, lesser would be the intraocular vasodilatation or change in pulse-synchronous IOP or ocular volume. Although there does not appear to be any significant variation in ocular rigidity between the sexes, the ocular distending effect of sudden vasodilatation in CH (and CPH) is unique; alterations in tissue elasticity and tissue creep have not been studied in these entities. I predict that in this clinical situation the female corneo-scleral envelope might be relatively more distensible and possibly decompresses sudden internal carotid artery-ophthalmic artery dilatations to a larger extent than in males. Since this difference would be predominantly dynamic rather than static, it will probably be difficult if not impossible to document significant differences in ocular rigidity in CH between the sexes clinically during life. Nevertheless, what is immeasurable might be more important than what is measurable.
Whereas episodic migraine headache may persist for days, CH is sharply limited to 15-180 minutes [1]. Other variants of the trigeminal autonomic cephalagias, CPH and short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT) [8], also manifest strictly time-limited headache episodes. There is currently no satisfactory explanation for this very characteristic feature of these primary headaches. I propose that while sudden increases in intraocular volume in these three variants of primary headache accommodates the surge in internal carotid-ophthalmic artery segment, the ocular distention involved is variably limited between individuals. The differences in visco-elastic properties of the ocular globe determine the time taken to accommodate the surge, during which period antidromic activation of the pain-sensitive terminals of the trigeminal nerve can develop [9].
In summary, the question regarding the role of the eye or its removal in the occurrence of CH cannot be dissociated from known intraocular circulatory disturbances. Enucleation or evisceration eliminates the terminal circulatory bed of the internal carotid artery-ophthalmic artery blood flow, an effect maximally seen with orbital exenteration. Available clinical evidences continue to support the contention that removal of the eye might precipitate CH in a matter of weeks. These considerations do not exclude the potential role of the eye as a possible contributor to the selective activation of the ophthalmic division of the trigeminal nerve in CH, CPH, SUNCT; the primary physiological system involved in these headaches is most likely identical, the variability in duration of headache (few seconds to a few hours) [10] probably depending on the visco-elastic properties of the tissues involved.
References
1. Sörös P, Vo O, Gerding H, Husstedt IW, Evers S. Enucleation and development of cluster headache: a retrospective study. BMC Neurology 2005, 5:6 doi:10.1186/1471-2377-5-6.
2. Evers S, Sörös P, Brilla R, Gerding H, Husstedt IW. Cluster headache after orbital exenteration. Cephalalgia 1997, 17(6):680-682.
3. Skrabanek P. The poverty of epidemiology. Persp Biol Med 1992;35:182-185.
4. Hørven I, Sjaastad O. Cluster headache syndrome and migraine: ophthalmological support for a two-entity theory. Acta Ophthalmol Copenhagen 1977;55:35-51.
5. Sjaastad O, Egge K, Hørven I, Kayed K, Lund-Roland L, Russell D, Conradi IS. Chronic paraoxysmal hemicrania: mechanical precipitation of attacks. Headache 1979;19:31-36.
6. Gupta VK. Visual function impairment in migraine: cerebral versus retinal deficit. Cephalalgia. 1993;13:431-432.
7. Mathew NT. Advances in cluster headache. Neurol Clin 1990 1990;8:867-890.
8. Goadsby PJ. Trigeminal autonomic cephalalgias: fancy term or constructive change to the HIS classification? J Neurol Neurosurg Psychiatry 2005;76:301-305.
9. Gupta VK. Painless Horner’s syndrome in cluster headache. J Neurol Neurosurg Psychiatry 1996;60:462-463.
10. Gupta VK. Trigeminal autonomic cephalalgias: ‘noso-physiology’ or pathophysiology? J Neurol Neurosurg Psychiatry (22 February 2005). Available at: http://jnnp.bmjjournals.com/cgi/eletters/76/3/301
Competing interests
None declared
Symptomatic cluster headache: literature update
10 August 2007
Since the publication of our article on a possible association between the removal of an eye and the development of cluster headache in 2005, at least 3 review papers (1, 10, 18) and 15 papers presenting original research (2-9, 11-17) on symptomatic cluster headache appeared. Papers were identified through a search in the PubMed database using the keyphrase "cluster headache" on 3 August 2007.
Most of the published reports present the development of cluster headache in patients with intracranial tumours or a disorder of intracranial vessels. None of these papers present a patient who developed cluster headache after the removal of an eye. Maggioni et al., however, described a 55-year-old man who developed cluster headache after cataract surgery involving an intraocular lens implant (9). This case report suggests that, although our retrospective study did not find an association between the removal of an eye and subsequent cluster headache, severe headache after eye surgery should be examined by a specialist who is experienced in the diagnosis of headache disorders.
References
1. Favier I, van Vliet JA, Roon KI, Witteveen RJ, Verschuuren JJ, Ferrari MD, Haan J. Trigeminal autonomic cephalgias due to structural lesions: a review of 31 cases. Arch Neurol. 2007;64:25-31.
2. Favier I, Haan J, van Duinen SG, Ferrari MD. Typical cluster headache caused by granulomatous pituitary involvement. Cephalalgia. 2007;27:173-6.
3. Gentile S, Fontanella M, Giudice RL, Rainero I, Rubino E, Pinessi L. Resolution of cluster headache after closure of an anterior communicating artery aneurysm: the role of pericarotid sympathetic fibres. Clin Neurol Neurosurg. 2006;108:195-8.
4. Georgiadis G, Tsitouridis I, Paspali D, Rudolf J. Cerebral sinus thrombosis presenting with cluster-like headache. Cephalalgia. 2007;27:79-82.
5. Hannerz J, Arnardottir S, Bro Skejø HP, Lilja JA, Ericson K. Peripheral postganglionic sympathicoplegia mimicking cluster headache attacks. Headache. 2005;45:84-6.
6. Hardmeier M, Gobbi C, Buitrago C, Steck A, Lyrer P, Engelter S. Dissection of the internal carotid artery mimicking episodic cluster headache. J Neurol. 2007;254:672-3.
7. Lai SL, Chang YY, Liu JS, Chen SS. Cluster-like headache from vertebral artery dissection: angiographic evidence of neurovascular activation. Cephalalgia. 2005;25:629-32.
8. Levy MJ, Matharu MS, Meeran K, Powell M, Goadsby PJ. The clinical characteristics of headache in patients with pituitary tumours. Brain. 2005;128:1921-30.
9. Maggioni F, Dainese F, Mainardi F, Lisotto C, Zanchin G. Cluster-like headache after surgical crystalline removal and intraocular lens implant: a case report. J Headache Pain. 2005;6:88-90.
10. Manzoni GC, Lambru G, Torelli P. Head trauma and cluster headache. Curr Pain Headache Rep. 2006;10:130-6.
11. Massie R, Sirhan D, Andermann F. Chronic cluster-like headache secondary to an epidermoid clival lesion. Can J Neurol Sci. 2006;33:421-2.
12. Negoro K, Kawai M, Tada Y, Ogasawara J, Misumi S, Morimatsu M. A case of postprandial cluster-like headache with prolactinoma: dramatic response to cabergoline. Headache. 2005;45:604-6.
13. Palmieri A, Mainardi F, Maggioni F, Dainese F, Zanchin G. Cluster-like headache secondary to cavernous sinus metastasis. Cephalalgia. 2005;25:743-5.
14. Peterlin BL, Levin M, Cohen JA, Ward TN. Secondary cluster headache: a presentation of cerebral venous thrombosis. Cephalalgia. 2006;26:1022-4.
15. Rigamonti A, Iurlaro S, Zelioli A, Agostoni E. Two symptomatic cases of cluster headache associated with internal carotid artery dissection. Neurol Sci. 2007;28 Suppl 2:S229-31.
16. Straube A, Freilinger T, Rüther T, Padovan C. Two cases of symptomatic cluster-like headache suggest the importance of sympathetic/parasympathetic balance. Cephalalgia. 2007 [Epub ahead of print].
17. Volcy M, Tepper SJ. Cluster-like headache secondary to idiopathic intracranial hypertension. Cephalalgia. 2006;26:883-6.
18. Walker RW. Cluster headache and head trauma: is there an association? Curr Pain Headache Rep. 2007;11:137-40.
Competing interests
None.