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Arquivos de Neuro-Psiquiatria

Print version ISSN 0004-282X

Arq. Neuro-Psiquiatr. vol.55 no.2 São Paulo June 1997

http://dx.doi.org/10.1590/S0004-282X1997000200001 

ON the pathogenesis of headache following TIA

 

A respeito da fisiopatologia da cefaléia pós-ataque isquêmico transitório

 

 

Charles AndréI; Maurice B. VincentII

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.

 

 

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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.

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