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Enxaqueca/Cefaléia/Dor de cabeça

Reflexos neurovasculares extracranianos aumentam susceptibilidade à enxaqueca

12/03/2004
 

 

Em neurologia, existe a hipótese de que sintomas como náuseas e cefaléia possam interagir entre si durante crises de enxaqueca. Os mecanismos fisiopatológicos propostos para sustentar a associação seriam relacionados a descargas trigeminais determinadas pela estimulação dolorosa da região temporal na face. Estudo publicado no periódico Brain testou a hipótese através da estimulação optocinética e dolorosa (com aplicação de gelo nas têmporas) de 27 pacientes migranosos e 23 controles. Os autores, da Faculdade de Psicologia da Murdoch University, na Austrália, encontraram resultados sugestivos de que mecanismos desencadeadores de reflexos neurovasculares extracranianos podem aumentar a susceptibilidade à enxaqueca.

Brain

Brain Advance Access published January 28, 2004, 10.1093/brain/awh061
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Brain, Vol. 127, No. 3, 526-534, March 2004
© 2004 Guarantors of Brain
doi: 10.1093/brain/awh061

Facial pain increases nausea and headache during motion sickness in migraine sufferers

Peter D. Drummond and Anna Granston

School of Psychology, Murdoch University, Western Australia, Australia

Correspondence to: Dr Peter Drummond, School of Psychology, Murdoch University, 6150 Western Australia, Australia E-mail: drummond@central.murdoch.edu.au

The aim of this study was to determine whether trigeminal nerve discharge associated with painful stimulation of the temple would intensify symptoms of motion sickness in migraine sufferers. If so, this would support the notion that symptoms such as nausea and headache interact with each other during attacks of migraine. Symptoms of motion sickness were rated at 2 min intervals during 15 min of optokinetic stimulation in 27 migraine sufferers and 23 age- and sex-matched controls. To document changes in frontotemporal blood flow, pulse amplitude was monitored with photoelectric pulse transducers. To induce facial pain, ice was applied to the temple for 30 s, three times at 4 min intervals during optokinetic stimulation. On another occasion, pain was induced during optokinetic stimulation by immersing the non-dominant hand in 2°C ice water for 30 s, three times at 4 min intervals. On a third occasion, measures were obtained during optokinetic stimulation alone. Migraine sufferers rated themselves as being generally more susceptible to motion sickness than controls. In addition, symptoms of motion sickness provoked by optokinetic stimulation were greater in migraine sufferers than in controls. Painful stimulation of the temple intensified nausea and headache during optokinetic stimulation, whereas painful stimulation of the hand did not. Since nausea also intensifies facial pain during motion sickness, nausea and headache may reinforce each other in a vicious circle. In the absence of painful stimulation, increases in pulse amplitude during optokinetic stimulation were greater in migraine sufferers than controls, possibly because the discomfort associated with motion sickness triggered extracranial vasodilatation in migraine sufferers as part of a fight-or-flight (defense) response. Extracranial vasodilatation did not differ between migraine sufferers and controls when ice was applied to the temple or hand during optokinetic stimulation, implying that the additional discomfort associated with painful stimulation of the head and hand evoked a defense response in controls. These findings suggest that a mechanism which boosts extracranial neurovascular reflexes to stress and which heightens symptoms of motion sickness, increases susceptibility to migraine.


 


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