Migraine and motion sickness: what is the link?

The brainstem is a structurally complex region, containing numerous ascending and descending fibres that converge on centres that regulate bodily functions essential to life. Afferent input from the cranial tissues and the special senses is processed, in part, in brainstem nuclei. In addition, brainstem centres modulate the flow of pain messages and other forms of sensory information to higher regions of the brain, and influence the general excitability of these cortical regions. Thus, disruptions in brainstem processing might evoke a complex range of unpleasant symptoms, vegetative changes and neurovascular disturbances and that, together, form attacks of migraine. Migraine is linked with various co-morbid conditions, the most prominent being motion sickness. Symptoms such as nausea, dizziness and headache are common to motion sickness and migraine; moreover, migraine sufferers have a heightened vulnerability to motion sickness. As both maladies involve reflexes that relay in the brainstem, symptoms may share the same neural circuitry. In consequence, subclinical interictal persistence of disturbances in these brainstem pathways could not only increase vulnerability to recurrent attacks of migraine but also increase susceptibility to motion sickness. Mechanisms that mediate symptoms of motion sickness and migraine are explored in this paper. The physiology of motion sickness and migraine is discussed, and neurotransmitters that may be involved in the manifestation of symptoms are reviewed. Recent findings have shed light on the relationship between migraine and motion sickness, and provide insights into the generation of migraine attacks

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

Population-based study of vestibular symptoms in migraineurs

Conclusion: The differences between migraineurs with vertigo or motion sickness or both, and migraineurs with neither might reflect differences in migraine pathophysiology. Objective: To assess vestibular symptoms in 871 definite migraineurs. Methods: Data were gathered using a structured questionnaire. We considered responses to only 2/150 questions: (1) 'have you had vertigo with or apart from your headaches?' and (2) 'have you experienced motion sickness most of your life?'. The target groups were: (a) migraineurs with either vertigo or motion sickness, 'migraine with vestibular symptoms' (MwVS), their control group being migraineurs with neither vertigo nor motion sickness, 'migraine without vestibular symptoms' (MwoVS); (b) migraineurs who reported vertigo, 'migraine with vertigo' (MwV); their control group being migraineurs without vertigo (MwoV). Results: Among the 871 definite migraineurs, 534 had MwV, 337 had MwoV, 663 had MwVS, and 208 had MwoVS. The MwVS group had more headache, aura, nausea, vomiting, osmophobia, allergy, allodynia, headache increasing with head motion, noise as trigger for headache, days needing analgesics, and higher migraine disability scores than the MwoVS group. The pattern was the same in the MwV vertigo group as in the MwVS group, apart from migraine disability scores, which were no different