ON the pathogenesis of headache following TIA

André, Charles; Vincent, Maurice B.

doi:10.1590/S0004-282X1997000200001

Abstracts

Twelve out of 49 patients with single or multiple transient ischemic attacks (TIAs) had TIA-related headaches, mostly in close temporal relation to the ischemic onset. Headache predominated in patients taking vasodilators when TIA occurred or with orthostatic hypotension at the first clinical examination, but arterial hypertension or a personal history of migraine were not more frequent in patients with headache. The site of the pain did not correlate with the presumed territory of cerebral ischemia. Pain during TIA is conceivably due to an interaction between cerebral vessels and the surrounding nervous system. Blood vessels have a sturdy physiological role corcerning blood flow regulation, with receptors and signaling molecules potentialy involved with pain production. Reflex mechanisms should justify pain in other areas.

transient cerebral ischemia; Cortisol; headache; neuroendocrine system; serotonin; trigeminovascular system

Em uma série de 49 pacientes com episódios únicos ou múltiplos de ataque isquêmico transitório (AIT), 12 apresentaram cefaléia em estreita associação com as manifestações isquêmicas. Cefaléia foi mais freqüente em pacientes com hipotensão ortostática ao primeiro exame pós-TIA e naqueles em uso de vasodilatadores. Não foi detectada associação com hipotensão arterial ou com história pessoal ou familial de enxaqueca. A localização da dor teve pouca correlação com o território isquêmico, em pacientes com AIT vertebrobasilar ou carotídeo. A dor durante os AITs se deve provavelmente a interação entre vasos sangüíneos e sua inervação. Os vasos têm papel central no controle do fluxo sangüíneo cerebral. A gênese da dor é provavelmente ligada à estimulação de receptores e liberação de moléculas sinalizadoras da agressão isquêmica. Mecanismos reflexos parecem justificar a dor em territórios distantes à isquemia.

cefaléia; cortisol; isquemia cerebral transitória; serotonina; sistema neuroendócrino; sistema trigeminovascular

ON the pathogenesis of headache following TIA

A respeito da fisiopatologia da cefaléia pós-ataque isquêmico transitório

Charles André^I; Maurice B. Vincent^II

^IServiço de Neurologia, Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro (UFRJ), Brasil: Professor Assistente

^IIServiço de Neurologia, Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro (UFRJ), Brasil: Professor Adjunto

ABSTRACT

Twelve out of 49 patients with single or multiple transient ischemic attacks (TIAs) had TIA-related headaches, mostly in close temporal relation to the ischemic onset. Headache predominated in patients taking vasodilators when TIA occurred or with orthostatic hypotension at the first clinical examination, but arterial hypertension or a personal history of migraine were not more frequent in patients with headache. The site of the pain did not correlate with the presumed territory of cerebral ischemia. Pain during TIA is conceivably due to an interaction between cerebral vessels and the surrounding nervous system. Blood vessels have a sturdy physiological role corcerning blood flow regulation, with receptors and signaling molecules potentialy involved with pain production. Reflex mechanisms should justify pain in other areas.

Key words: transient cerebral ischemia, Cortisol, headache, neuroendocrine system, serotonin, trigeminovascular system.

RESUMO

Em uma série de 49 pacientes com episódios únicos ou múltiplos de ataque isquêmico transitório (AIT), 12 apresentaram cefaléia em estreita associação com as manifestações isquêmicas. Cefaléia foi mais freqüente em pacientes com hipotensão ortostática ao primeiro exame pós-TIA e naqueles em uso de vasodilatadores. Não foi detectada associação com hipotensão arterial ou com história pessoal ou familial de enxaqueca. A localização da dor teve pouca correlação com o território isquêmico, em pacientes com AIT vertebrobasilar ou carotídeo. A dor durante os AITs se deve provavelmente a interação entre vasos sangüíneos e sua inervação. Os vasos têm papel central no controle do fluxo sangüíneo cerebral. A gênese da dor é provavelmente ligada à estimulação de receptores e liberação de moléculas sinalizadoras da agressão isquêmica. Mecanismos reflexos parecem justificar a dor em territórios distantes à isquemia.

Palavras-chave: cefaléia, cortisol, isquemia cerebral transitória, serotonina, sistema neuroendócrino, sistema trigeminovascular.

Texto completo disponível apenas em PDF.

Full text available only in PDF format.

Aceite: 18-novembro-1996.

Dr. Charles André - Serviço de Neurologia, Hospital Universitário Clementino Fraga Filho, UFRJ - Av. Brigadeiro Trompowsky s/nº, 10° andar - 21941-590 Rio de Janeiro RJ - Brasil.

1. André C, Novis SAP. Clinical factors adversely affecting early outcome after brain infarction. Arq Neuropsiquiatr 1994;52:153-160.
2. André C, Neves FF, Vincent MB. Headaches in transient ischaemic attacks. Funct Neurol 1996 (in press).
3. Astrup J, Siesjö BK, Symon L. Thresholds in cerebral ischemia: the ischemic penumbra. Stroke 1981:12:723-725.
4. Bakken IJ, Vincent MB, Sjaavaag 1, White LR. Vasodilation in porcine ophthalmic artery: peptide interaction with acetylcholine and endothelial dependence. Neuropeptides 1995;29:69-75.
5. Buzzi MG. Bonamini MA, Moskowitz MA. Neurogenic model of migraine. Cephalalgia 1995:15:277-280.
6. Dalkara T, Moskowitz MA. The complex role of nitric oxide in the pathophysiology of focal cerebral ischemia. Brain Pathol 1994;4:49-57.
7. Edmeads J. The headaches of ischemic cerebrovascular disease. Headache 1979; 19:345-349.
8. Edvinsson L, Goadsby P. Neuropeptides in migraine and cluster headache. Cephalalgia 1994:14:320-327.
9. Edvinsson L, Hara H. Uddman R. Retrograde tracing of nerve fibres to the rat middle cerebral artery with true blue: colocalization with different peptides. J Cereb Blood Flow Metab 1989;9:212-218.
10. Edvinsson L, Juul R, Jansen J. Perivascular neuropeptides (NPY, VIP, CGRP and SP) in human brain vessels after subarachnoid haemorrhage. Acta Neurol Scand 1994;90:324-327.
11. Ferro JM. Costa I, Melo TP et al. Headache associated with transient ischemic attacks. Headache 1995;35:544-548.
12. Gordon ML, Lipton RB, Brown S-L, van Praag HM. The neuroendocrine challenge paradigm in headache research. Cephalalgia 1995;15:292-296.
13. Gorelick PB. The secondary headaches: ischemic stroke and intracranial hematoma. In Olesen .J, Tfelt-Hansen P, Welch KMA (eds). The Headaches. New York: Raven Press, 1993:639-645.
14. Headache Classification Committee of the International Headache Society. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia 1988;8 (Suppl 7): 1-96.
15. Iverscn HK. Olesen J, Tfelt-Hansen P. Intravenous nitroglicerin as an experimental model of vascular headache: basic characteristics. Pain 1989;38:17-24.
16. Lance JW. Current concepts of migraine pathogenesis. Neurology 1993; 43(Suppl.3):Sl 1-S15.
17. Lee Y. Kawai T, Shiosaka S et al. Coexistence of calcitonin gene-related peptide in single cells of the trigeminal ganglion of the rat: immunohistochemical analysis. Brain Res 1985;330:194-196.
18. Mayberg MR, Zervas NT, Moskowitz MA. Trigeminal projections to supratentorial pial and dural blood vessels in cats demonstrated by horseradish peroxidase histochemistry. J Comp Neurol 1984;223:46-56.
19. McCulloch J, Uddinan R, Kingman TA, Edvinsson L. Calcitonin gene-related peptide: functional role in cerebrovascular regulation. Proc Natl Acad Sci USA 1986;83:5731-5735.
20. Medina JL, Diamond S, Rubino FA. Headaches in patients with transient ischemic attacks. Headache 1975; 15:194-197.
21. Mitsias P. Ramadan NM. Headache in ischemic cerebrovascular disease. Parti: Clinical features. Cephalalgia 1992;12:269-274
22. Moskowitz MA. The neurobiology of vascular head pain. Ann Neurol 1984; 16:157-168.
23. Moskowitz MA. Neurogenic inflammation in the pathophysiology and treatment of migraine. Neurology l993;43(Suppl3):SI6-S20.
24. Olesen J, Thomsen LL, Lassen LH, Olesen IJ. The nitric oxide hypothesis of migraine and other vascular headaches. Cephalalgia 1995;15:94-100.
25. Pauson OB, Standgaaicl S, Edvinsson L. Cerebral autoregulation. Cerebrovasc Brain Metab Rev 1990:2:161 -192.
26. Raskin NH, Knittle SC. Ice cream headache and orthostatic symptoms in patients with migraine. Headache 1976; 16:222-225.
27. Ray BS. Wolff HG. Experimental studies on headache: pain sensitive structures of the head and their significance in headache. Arch Surg 1940;41:813-856.
28. Uddman R, Edvinsson L. Neuropeptides in the cerebral circulation. Cerebrovasc Brain Metab Rev 1989; 1:230-252.
29. Uddman R. Edvinsson L, Ekman R, McCulloch J, Kingman TA. Innervation of the feline cerebral vasculature by nerve fibres containing calcitonin gene-related peptide: trigeminal origin and co-existance with substance P. Neurosci Lett 1985;62:131 -136.
30. Vincent MB. Ekman R, Edvinsson L. Sand T, Sjaastad O. Reduction of calcitonin gene related peptide in jugular blood following electrical stimulation of rat greater occipital nerve. Cephalalgia 1992; 12:275-279.

Publication Dates

Publication in this collection
10 Nov 2010
Date of issue
June 1997

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

[1] 1. André C, Novis SAP. Clinical factors adversely affecting early outcome after brain infarction. Arq Neuropsiquiatr 1994;52:153-160.

[2] 2. André C, Neves FF, Vincent MB. Headaches in transient ischaemic attacks. Funct Neurol 1996 (in press).

[3] 3. Astrup J, Siesjö BK, Symon L. Thresholds in cerebral ischemia: the ischemic penumbra. Stroke 1981:12:723-725.

[4] 4. Bakken IJ, Vincent MB, Sjaavaag 1, White LR. Vasodilation in porcine ophthalmic artery: peptide interaction with acetylcholine and endothelial dependence. Neuropeptides 1995;29:69-75.

[5] 5. Buzzi MG. Bonamini MA, Moskowitz MA. Neurogenic model of migraine. Cephalalgia 1995:15:277-280.

[6] 6. Dalkara T, Moskowitz MA. The complex role of nitric oxide in the pathophysiology of focal cerebral ischemia. Brain Pathol 1994;4:49-57.

[7] 7. Edmeads J. The headaches of ischemic cerebrovascular disease. Headache 1979; 19:345-349.

[8] 8. Edvinsson L, Goadsby P. Neuropeptides in migraine and cluster headache. Cephalalgia 1994:14:320-327.

[9] 9. Edvinsson L, Hara H. Uddman R. Retrograde tracing of nerve fibres to the rat middle cerebral artery with true blue: colocalization with different peptides. J Cereb Blood Flow Metab 1989;9:212-218.

[10] 10. Edvinsson L, Juul R, Jansen J. Perivascular neuropeptides (NPY, VIP, CGRP and SP) in human brain vessels after subarachnoid haemorrhage. Acta Neurol Scand 1994;90:324-327.

[11] 11. Ferro JM. Costa I, Melo TP et al. Headache associated with transient ischemic attacks. Headache 1995;35:544-548.

[12] 12. Gordon ML, Lipton RB, Brown S-L, van Praag HM. The neuroendocrine challenge paradigm in headache research. Cephalalgia 1995;15:292-296.

[13] 13. Gorelick PB. The secondary headaches: ischemic stroke and intracranial hematoma. In Olesen .J, Tfelt-Hansen P, Welch KMA (eds). The Headaches. New York: Raven Press, 1993:639-645.

[14] 14. Headache Classification Committee of the International Headache Society. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia 1988;8 (Suppl 7): 1-96.

[15] 15. Iverscn HK. Olesen J, Tfelt-Hansen P. Intravenous nitroglicerin as an experimental model of vascular headache: basic characteristics. Pain 1989;38:17-24.

[16] 16. Lance JW. Current concepts of migraine pathogenesis. Neurology 1993; 43(Suppl.3):Sl 1-S15.

[17] 17. Lee Y. Kawai T, Shiosaka S et al. Coexistence of calcitonin gene-related peptide in single cells of the trigeminal ganglion of the rat: immunohistochemical analysis. Brain Res 1985;330:194-196.

[18] 18. Mayberg MR, Zervas NT, Moskowitz MA. Trigeminal projections to supratentorial pial and dural blood vessels in cats demonstrated by horseradish peroxidase histochemistry. J Comp Neurol 1984;223:46-56.

[19] 19. McCulloch J, Uddinan R, Kingman TA, Edvinsson L. Calcitonin gene-related peptide: functional role in cerebrovascular regulation. Proc Natl Acad Sci USA 1986;83:5731-5735.

[20] 20. Medina JL, Diamond S, Rubino FA. Headaches in patients with transient ischemic attacks. Headache 1975; 15:194-197.

[21] 21. Mitsias P. Ramadan NM. Headache in ischemic cerebrovascular disease. Parti: Clinical features. Cephalalgia 1992;12:269-274

[22] 22. Moskowitz MA. The neurobiology of vascular head pain. Ann Neurol 1984; 16:157-168.

[23] 23. Moskowitz MA. Neurogenic inflammation in the pathophysiology and treatment of migraine. Neurology l993;43(Suppl3):SI6-S20.

[24] 24. Olesen J, Thomsen LL, Lassen LH, Olesen IJ. The nitric oxide hypothesis of migraine and other vascular headaches. Cephalalgia 1995;15:94-100.

[25] 25. Pauson OB, Standgaaicl S, Edvinsson L. Cerebral autoregulation. Cerebrovasc Brain Metab Rev 1990:2:161 -192.

[26] 26. Raskin NH, Knittle SC. Ice cream headache and orthostatic symptoms in patients with migraine. Headache 1976; 16:222-225.

[27] 27. Ray BS. Wolff HG. Experimental studies on headache: pain sensitive structures of the head and their significance in headache. Arch Surg 1940;41:813-856.

[28] 28. Uddman R, Edvinsson L. Neuropeptides in the cerebral circulation. Cerebrovasc Brain Metab Rev 1989; 1:230-252.

[29] 29. Uddman R. Edvinsson L, Ekman R, McCulloch J, Kingman TA. Innervation of the feline cerebral vasculature by nerve fibres containing calcitonin gene-related peptide: trigeminal origin and co-existance with substance P. Neurosci Lett 1985;62:131 -136.

[30] 30. Vincent MB. Ekman R, Edvinsson L. Sand T, Sjaastad O. Reduction of calcitonin gene related peptide in jugular blood following electrical stimulation of rat greater occipital nerve. Cephalalgia 1992; 12:275-279.