Pain, Motion Sickness and Migraine: Effects on Symptoms and Scalp Blood Flow

Migraine, a neurovascular disorder, is associated with disturbances in brain stem activity during attacks. Interictal persistence of these disturbances might increase vulnerability to recurrent attacks of migraine. To explore this possibility, effects of motion sickness and pain on migrainous symptoms and extracranial vascular reponses were investigated in 27 migraine sufferers in the headache-free interval, and 23 healthy age/sex matched controls. Symptoms of migraine and motion sickness are remarkably similar. As both maladies involve reflexes that relay in the brain stem, they most probably share the same neural circuitry. Furthermore, migraineurs are usually susceptible to motion sickness and, conversely, motion sickness-prone individuals commonly experience migraine. Participants in the present study were exposed to optokinetic stimulation (OKS), a well-established way of inducing symptoms of motion sickness in susceptible individuals. Sensitivity to painful stimulation of the head and hand was also explored. Head pain is a hallmark of a migraine attack and cutaneous allodynia has been observed elsewhere in the body during attacks. The trigeminal nerve is associated with head pain in migraine, and trigeminal activity evokes reflexes that relay in the brain stem. To stimulate the trigeminal nerve, ice was applied to the temple. To stimulate nociceptors elsewhere in the body the participant immersed their fingers and palm in ice-water. Procedures used in this study were physically stressful and probably psychologically stressful. The impact of stress in relation to the development of symptomatic and vascular responses, particularly anticipatory stress-responses, was explored. This research involved one central experiment that consisted of six experimental conditions. On separate occasions participants were exposed to optokinetic stimulation and painful stimulation of the head or limb, individually and in combination. In migraine sufferers, symptomatic responses were enhanced during all procedures involving OKS and during temple pain after OKS, in the presence of residual motion sickness. During trigeminal stimulation independent of OKS, headache initially developed followed by nausea as the procedure progressed. In contrast, symptoms barely developed in controls during any of the six procedures except for slight dizziness, self-motion and visual-illusion during conditions involving OKS, and slight nausea when the temple was painfully stimulated during OKS and during OKS alone. Trigeminal stimulation during OKS intensified nausea and headache in migraine sufferers compared to during OKS alone or limb pain during OKS. However, the remaining symptomatic ratings were not affected by temple pain during OKS, suggesting a specific association between nausea and head pain. It may be that these cardinal symptoms compound one another during a migraine attack. Enhanced symptomatic responses in migraine sufferers during the headache interval may indicate activation of hypersensitive neural pathways that mediate symptoms of motion sickness or migraine. Migraineurs found procedures generally more unpleasant, and ice-induced pain ratings more intense and unpleasant, than controls, which may further indicate hyperexcitable nociception in this group, or a difference in their criterion of discomfort. Vascular responses, particularly during OKS alone, and during painful stimulation independent of OKS, were greater in migraine sufferers than in controls. The added stress of painful stimulation during OKS appeared to boost facial blood flow in controls to approach levels obtained in migraine sufferers. Enhanced vasodilatation was observed in migraineurs prior to painful stimulation, presumably due to anticipatory anxiety. For both groups ipsilateral vascular responses were greater than contralateral responses when the hand was painfully stimulated. During limb pain before OKS asymmetry was minimal in migraine sufferers but more apparent in controls. An enhanced stress response in migraineurs may have drawn ipsilateral and contralateral responses closer together. The development of symptoms during the procedures of this study provides an insight into how symptoms might develop sequentially in a migraine attack. Once the headache is in motion, nausea and headache may mutually exacerbate one another. In turn, trigemino-vascular responses and stress appear to be associated with the migraine crisis. Given the interactive nature of symptomatic, vascular, and stress responses, it may be more effective to target multiple, rather than individual, symptoms, in prophylactic or acute chemical and psychological interventions.