PMC:4630263 / 19532-29346 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/4630263","sourcedb":"PMC","sourceid":"4630263","source_url":"https://www.ncbi.nlm.nih.gov/pmc/4630263","text":"Discussion\nIn our study, significantly prolonged latency in oVEMP was detected in migraine without aura versus TTH and control groups. However, there was no significant difference in cVEMP parameters among the migraine, TTH and control groups. These results suggest pathology within the oVEMP pathway or the ascending utriculo-ocular reflex in migraineurs. Thus, migraineurs showed subclinical vestibulopathies with oVEMP abnormalities during a headache-free period.\ncVEMP and oVEMP provide valuable information regarding the location and nature of the lesion(s) affecting central vestibular pathways because the vestibulo-collic and vestibulo-ocular reflex pathways diverge beyond the nerve root entry zone [4, 28]. Using oVEMP and cVEMP together allows for the evaluation of both ascending and descending vestibular pathways, resulting in the identification of a higher percentage of abnormalities [4, 28–30]. Patients who have brainstem involvement in multiple sclerosis or internuclear ophthalmoplegia show higher abnormality rates in oVEMP than in cVEMP [29, 31]. Additionally, oVEMP is more sensitive than cVEMP for detecting silent brainstem lesions in multiple sclerosis patients and vestibular dysfunction in VM patients [14, 29]. Furthermore, because oVEMP latencies are dependent primarily on afferent and efferent reflex limbs and central transmission, prolonged latencies are likely due to the degradation of central vestibular processing of otolith signals rather than a decline in peripheral vestibular function [26]. VEMP amplitudes can be used as independent quantitative measures of otolith function [4]. Thus, peripheral vestibular disorders frequently involve an absence of oVEMPs or decreased amplitudes, whereas prolonged latencies may indicate central vestibular lesions [32]. Significantly prolonged oVEMP latencies in our study suggest an underlying functional abnormality in the central vestibular system.\nHerein, bilaterally or unilaterally absent oVEMP responses were observed in 21 % of patients in the migraine group, while absent cVEMP responses were found in 10.5 % of patients in the migraine group. Several previous reports showed absent oVEMP responses in the migraine group (53.3 %) and VM group (28 %), whereas absent cVEMP responses were detected in 8 % of VM patients [14, 16]. Similar to previous studies, a high unresponsive rate of oVEMP in migraineurs was observed in our study, although the difference did not reach statistical significance. These findings also suggest defective oVEMP pathways in migraineurs.\nVarious vestibular function test studies have been conducted on patients with migraines during the interictal period. Several works reported vestibular abnormalities in the form of involvement of peripheral or central vestibular pathways or both [18, 19, 33]. One study reported dysfunction in the vestibulo-ocular reflex, whereas another indicated underlying dysfunction in the vestibulospinal system [21, 34]. Other reports showed interictal dysfunction of vestibulocerebellar origin in migraineurs [20, 35]. These findings suggest that migraineurs without vestibular symptoms exhibit vestibular abnormalities, generally indicating subclinical vestibulopathies in patients with migraines. Additionally, the distribution between central and peripheral vestibular findings did not differ between VM and migraine patients [18]. More recently, in a report evaluating cVEMP and oVEMP pathways in patients with VM, the rates of abnormal oVEMPs were significantly higher without cVEMP abnormalities, similar to our study, although the subjects suffered symptoms on the same day of testing [14]. Thus, subclinical vestibular dysfunction may be an integral part of migraine pathophysiology and could be related to fundamental pathophysiological similarities between migraine and VM. Recently, positron emission tomography (PET) studies have demonstrated thalamo-cortical involvement or increased thalamic activation in VM patients [36, 37]. Additionally, voxel-based morphometry studies have identified gray matter volume reductions in patients with VM [38]. These functional and structural alterations in patients with VM resemble those previously described in patients with migraine. VM likely represents the pathophysiological paradigm of a connection between migraine and the vestibular system [39].\nSubclinical 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.\nDue to the measurement method and/or technical factors, oVEMP is more valuable in assessing vestibular function in patients with headache compared to cVEMP. During cVEMP recordings, amplitude-related parameters change according to the degree of tonic contraction of the SCM showing a direct correlation; the more tonic the muscle tension, the larger the cVEMP amplitude response [4]. Decreased response rate and amplitude or prolonged latencies on cVEMP and oVEMP occur with age increase over 60 years [24, 26]. Regarding the influence of gender on oVEMPs, one study found oVEMPs to be independent of gender [31], whereas another study reported that the mean oVEMP amplitude in males was significantly larger than in females [25]. Thus, in our study, we only included females 20–60 years of age based on these known age and gender effects. To control the amount of muscle tension between right and left muscles, we used a feedback method with a blood pressure manometer and analyzed VEMP parameters following EMG rectification in cVEMP [27, 46]. Many patients with primary headache disorders, such as TTH and migraine, also have accompanying pericranial, neck and shoulder muscle tenderness and/or associated myofascial pain syndrome. These conditions can affect muscle tension or posture during cVEMP measurements. Thus, the cVEMP method may provide inaccurate information in patients with migraine and TTH because the degree of muscle contraction affects the cVEMP result and its interpretation. Consequently, oVEMP may be the more sensitive method for evaluating the vestibular system in primary headache disorders.\nOur study had several limitations. First, highly selected patients from a neurology clinic at a regional university hospital were recruited. The sample size was small, and the study used a cross-sectional design that provided limited causal information. Second, the present data did not identify statistically significant correlations between VEMP parameters and headache clinical parameters such as frequency, duration, and intensity (data not shown). Additionally, this study was based on outpatient subjects and only administered the headache questionnaire at the first visit; therefore, detailed headache characteristics recorded using a headache diary should be considered in future studies to more accurately identify the correlations between electrophysiological data and headache parameters. Furthermore, prospective longitudinal studies including information regarding impact or disabilities due to headache may be warranted. Third, sound stimulation was applied at 500 Hz, which showed a 100 % response rate in both oVEMP and cVEMP of healthy subjects [47]. However, VEMPs were not obtained in approximately 8-10 % of subjects in the control group, as previous studies showed similar results [14, 16]. oVEMP and cVEMP predominantly represent saccular stimulation, and bone vibration activates both utricular and saccular afferents [4]. 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