Central Integration of Canal and Otolith Signals is Abnormal in Vestibular Migraine: A Commentary.

摘要: This is a very interesting and well-written article describing possible mechanisms that may contribute to the vestibular symptoms motion intolerance are most commonly seen in migraine. (1) The discussion cogent, based on experimental results presented, exemplifying idea of multiple potential interactions between migraine system, thus suggesting vertigo multifactorial include peripheral (e.g., labyrinthine), as well brain components (vestibular nuclei locus coeruleus). Vestibular said be second frequent cause and, fact, appears commonest spontaneous episodic (2). In study by Neuhauser colleagues (3, 4), evaluating presence both lifetime vertigo, authors found significant percentage migraineurs complained vertigo. addition, sufferers, symptomatology apparently occurs without headache itself. Migraine attacks also begin earlier life than appearance or, contrary, patients report years before regular occurrence headaches (5). It noteworthy specific antimigraine drugs (triptans) when used relieve trigger (6). Taken together, these considerations lead us presume distinct at work “typical” forms migraine. Even today, there still much debate pathophysiology migraine, particularly concerning initial anatomical location brain, where attack triggered – cortex vs. brainstem. considering cerebellum another initiation crisis intriguing. If this indeed case, more caudal part cerebellar vermis, i.e., nodulus uvula, would seem involved mechanism linked presentation plausible example strongly suggests hypothesis (or brainstem) origin attack. On other hand, activation occur later on, during course such an attack. Neuroimaging studies have demonstrated lesions can (7, 8), addition periventricular white matter abnormalities (9). Brainstem detected patients. indicates not benign disease previously believed (Figure ​(Figure1)1) (10). Subclinical dysfunction was reported (11). Does accumulation throughout alter severity disorder? explanation for new same individual or could one causes transformation into chronic one. abovementioned suggest disorders changes (12), which initially biochemical, neuroimaging findings, but some with severe form disease, comorbid conditions present dyslipidemia), “specific,” occasionally encountered MRI (7–10). said, concept disorder harbored particular progresses different presentation, females, owing hormonal fluctuations, namely childhood its equivalents, becoming apparent menarche period, attenuating pregnancy lactation, oligosymptomatic absent post-menopausal period. Figure 1 MRI 69-year-old woman long history attacks. Note abnormalities, frequently migraineurs. It common knowledge clinical phenomenology covers spectrum ranging from mild extremely incapacitating form, among subjects. syndrome consists variety symptoms, auras, autonomic manifestations, pain, auditory complaints, etc., each involve neuronal networks nervous system innervated tissues, those vascular (13). We largely ignorant exactly how why occurs. Another point genetically similar we, specialists, pooling single entity. Owing multiplicity manifestations grouping together several “migraine disorders,” precise physiopathogenesis has clarified. being published King coworkers selected highly population evaluate physiopathology focusing subset population. In conclusion, relatively condition fully understood recognized medical community general.