Dizziness and Vertigo _________________________________________________________________________
VESTIBULAR MIGRAINE Vestibular migraine is the most common central cause of recurrent spontaneous attacks of vertigo. “Vestibular migraine” is the preferred name for this disorder, because patients may experience a range of vestibular symptoms not limited to ver- tigo (e.g., dizziness, nausea, vomiting) [18; 48]. Vestibular migraine accounts for 7% of patients seen in dizzi- ness clinics and 9% of patients seen in headache clinics, but it remains underdiagnosed [48]. It is three times more common in women and occurs most often between 20 and 50 years of age. A family history of migraine is a risk factor, and vestibular migraine may involve a genetic susceptibility to enhanced excit- ability during sensory information processing, which induces interactions of vestibular and pain pathways [7; 48]. Pain and vestibular sensory inputs converge in brainstem struc- tures that modulate pain sensitivity and anxiety responses to pain and vestibular signaling. Vestibular stimulation activates some higher cortical regions involved in pain perception. Vestibular and pain pathways also overlap at brainstem and thalamic levels. This may explain, in part, the frequent clinical overlap of migraine (including vestibular migraine), balance, and anxiety disorders [48; 49]. Vestibular migraine is a clinical diagnosis in which central and peripheral mechanisms arise from genetic and environment interactions. Mechanistic interactions cause excessive sensitiv- ity to pain perception (e.g., headache, allodynia), hearing (e.g., phonophobia), vestibular stimulation (e.g., vertigo, motion sickness, visual vertigo), vision (e.g., photophobia), and sense of smell (e.g., osmophobia) [48; 49; 50]. Vestibular migraine is diagnosed primarily by patient his- tory and exclusion of alternative causes; neurologic exams performed between episodes generally show normal findings [48]. The migraine may occur with episodic vertigo, chronic motion sensitivity, or other vestibular symptoms. Vertigo and motion sickness, with or without headache, is the common presentation, and some patients report mild, transient auditory symptoms of tinnitus, muffled hearing, or ear pressure [15; 18]. CEREBROVASCULAR ETIOLOGIES Patients with potentially serious or life-threatening stroke may present with vestibular symptoms without other focal neuro- logic signs. This acute presentation is linked to stroke involving one of several branches that supply the brainstem, cerebellum, or inner ear. Early differentiation is an area of intense research focus. Early recognition of isolated vertigo as a stroke sign allows specific intervention and secondary prevention. Mis- diagnosis of stroke-related vertigo as a peripheral cause may result in significant morbidity or mortality, and overdiagnosis of stroke as peripheral vertigo leads to expensive and unneces- sary workups, medication, and hospital admissions [51; 52].
A connection between bilateral vestibulopathy and degenera- tive cerebellar diseases has been established. A syndrome com- prised of bilateral vestibulopathy, sensory axonal polyneuropa- thy, cerebellar ataxia, and oculomotor disturbances accounts for around 30% of cases previously considered idiopathic [39; 42]. Bilateral vestibulopathy can be severely debilitating but is partially reversible with vestibular rehabilitation. It is important for clinicians not to overlook this condition when assessing patients with complaints of dizziness/vertigo [43]. VESTIBULAR PAROXYSMIA Vestibular paroxysmia is characterized by recurrent spontane- ous vertigo attacks that are brief (several seconds up to one minute), and frequent (up to 30 per day) [44]. In one study, vestibular paroxysmia accounted for 3.7% of 17,718 consecu- tive outpatients in a multidisciplinary vertigo and balance dis- orders center. Men are affected twice as often as women, and the bimodal age of onset peaks in early childhood and again between 40 and 70 years of age [45]. Vestibular paroxysmia symptoms are triggered by neurovascular compression involving the anterior inferior cerebellar artery and the 8th cranial nerve. More than 95% of cases show vessel-nerve contact at the exit point of the 8th nerve from the brainstem, but the finding is nonspecific because it may be seen in healthy, asymptomatic adults as well [46].
CENTRAL CAUSES OF DIZZINESS AND VERTIGO
The vestibular nuclei and its connections to cerebellar, brain- stem, spinal cord, and higher cortical structures comprise the central vestibular system. Dizziness, vertigo, ataxia, or disequi- librium can result from pathologies involving central vestibular structures, the most common of which are migraine-related vestibulopathy, brainstem strokes, head trauma, multiple sclerosis, and cerebellar degeneration [47]. Vertigo, vestibular dysfunction, and anxiety disorders are now recognized as co-factors, and the inter-relationship is substan- tial. Dizziness and vertigo are associated with diverse systemic disorders, trauma, and toxic exposures. Etiologies in psychiatric and systemic disorders are complex and diffuse. Central abnormalities cause about 20% of dizziness com- plaints, and patients may present with disequilibrium or ataxia rather than vertigo. Dizziness/vertigo may be the sole presenting symptom of an impending cerebrovascular event origination in the brainstem or cerebellum [7]. In these pre- sentations, distinguishing benign from potentially or immi- nently dangerous cerebrovascular causes has been the focus of extensive research effort.
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