Subclinical vestibulopathy in migraineurs may be related to multiple potential interactions between the trigeminal and vestibular systems at various levels. In migraine patients, stimulation of the trigeminal nuclei has produced spontaneous nystagmus [40]. Conversely, vestibular nuclei receive both serotonergic inputs from the dorsal raphe nucleus and noradrenergic inputs from the locus coeruleus, and activation of these pain structures during migraine can affect central vestibular processing [3]. These reciprocal connections between the vestibular nuclei and trigeminal nucleus caudalis may provide a mechanism whereby vestibular signals influence trigeminovascular pathways and trigeminal information processing during migraine attacks [41]. Additionally, studies using functional MRI showed that the vestibular system is represented at a cortical level [42]. The presence of descending cortical projections on vestibular nuclei has been demonstrated in cats. Researchers concluded that neurons in cortical areas were able to modulate vestibular reflexes [43]. Minor cerebellar abnormalities related to eye and arm movements have also been described in asymptomatic migraine patients [20, 35]. Although semicircular canal and otolith afferents terminate in the vestibular nuclei region, both inputs project to the caudal vermis of the cerebellum and Purkinje cells in the cortex of the nodulus/uvula inhibit the vestibular nuclei [44]. These various potential interconnections between migraine and the vestibular system can cause abnormalities in vestibular function tests in migraineurs during the interictal period. A recent blood oxygen level-dependent (BOLD) functional MRI study conducted in patients with VM, patients with migraine without aura, and healthy controls during the interictal period, revealed that caloric vestibular stimulation elicited statistically significant activation in the bilateral insular cortex, thalamus, cerebellum, and brainstem of all subjects [36]. In particular, discrete activation in the periaqueductal gray matter was observed in migraine patients, suggesting a peculiar relationship between vestibular stimulation and the activation of brain areas that play key roles in pain processing [45]. This reciprocal connection between brainstem vestibular nuclei and structures involved in modulation of trigeminal nociceptive inputs may explain the VEMP abnormalities in migraineurs.