Dizziness and Vertigo _________________________________________________________________________
Isolated attacks of spontaneous dizziness are the most common symptom of an imminent posterior circulation TIA and are frequent in the days to weeks preceding posterior circulation stroke [8; 36]. TIA presenting with isolated dizziness is eas- ily missed; 90% of patients who seek medical attention for transient dizziness that preceded vertebrobasilar stroke are initially misdiagnosed [108]. Dizziness is the most common presenting symptom of basilar artery occlusion and vertebral artery dissection. Prompt diagnosis is critical; 5% of patients with TIA suffer a stroke within 48 hours, but the risk is much greater with posterior circulation TIA. Prompt treatment low- ers stroke risk after TIA by 80% [8; 117; 118]. The clinical presentation of vestibular migraine is highly vari- able. The duration of attacks ranges from seconds to days. Nystagmus (peripheral or central), headache, and nausea, vomiting, photophobia, phonophobia or visual auras can be present or absent during an attack. Hearing loss or tinnitus can occur, mimicking Ménière disease [8]. Vestibular migraine is diagnosed by clinical findings of recur- rent migraine headache episodes: five or more episodes char- acterized by moderate-to-severe vestibular symptoms; ≥50% of episodes have pulsating, impairing headache; photo- or phonophobia; and/or visual aura [48]. The prevalence of migraine syndrome is high in patients with Ménière disease, and when such patients present with attacks of s-EVS, the diagnostic attribution may seem difficult. The presence of low frequency hearing loss favors the diagnosis of Ménière disease [18; 48]. Cardiac arrhythmia should be suspected when syncope or exertion is the precipitating factor for the onset of dizziness. Clinical features may increase or decrease the odds of a danger- ous cardiac cause, but cardiac specialist testing is often required for diagnostic confirmation [8; 36].
Bilateral vestibulopathy is a CVS characterized by unsteadi- ness when walking or standing that worsens in darkness, on uneven ground, or during head motion. Patients may describe head or body movement-induced blurred vision or oscillopsia. Symptoms usually remit when sitting or lying down. Bilateral vestibulo-ocular reflex function is significantly impaired or absent in bilateral vestibulopathy and is assessed using the HIT, video-HIT, or other tests [40]. As discussed, PPPD is a newly defined CVS that unifies key features of chronic subjective dizziness, phobic postural vertigo, and related disorders. Patients with PPPD often develop gait dis- order, anxiety, avoidance behaviors, and severe disability [121]. A PPPD diagnosis requires dizziness, unsteadiness, or non- spinning vertigo present on most days for at least three months, exacerbated by posture, movement, and/or moving/complex visual stimuli. Symptoms are precipitated by any condition that causes vertigo, unsteadiness, dizziness, or problems with balance and cause significant distress or impairment [62]. In addition to timing and triggers, the diagnostic approach should also capture the dynamic features of patient history to uncover the nuances of psychologic distress, maladaptive cop- ing, and differential diagnosis. Patients who fulfill diagnostic criteria for PPPD after a TBI or whiplash should receive the diagnosis. The presence of other injury sequelae determines additional diagnoses [62].
According to the Bárány Society, the differential diagnosis of PPPD includes chronic sequelae of acute precipitants, recurrent attacks of episodic precipitants, ongoing manifestations of chronic precipitants, other chronic vestibular
syndromes, medical or psychiatric disorders that produce persistent unsteadiness or dizziness, and adverse effects of regularly consumed prescription or non-prescription medications. (https://content.iospress.com/articles/journal-of- vestibular-research/ves622. Last accessed September 30, 2024.) Level of Evidence : Expert Opinion/Consensus Statement
CHRONIC VESTIBULAR SYNDROME Triggered CVS
Central compensatory mechanisms can ameliorate vestibular symptoms over time, but to an unpredictable extent, and last- ing vestibular compensation does not develop or incompletely develops. Thus, some vestibular syndromes become chronic, with persistent dizziness or unsteadiness lasting months to years, with oscillopsia, nystagmus, and/or gait disturbance. CVS develops from poorly compensated unilateral or bilateral vestibulopathy or cerebellar degeneration [119]. Other etiolo- gies include PPPD, autoimmune or neoplastic disease, central vestibular syndromes with downbeat or upbeat nystagmus, and dizziness due to isolated causes [120]. In t-CVS, dizziness or vertigo is provoked by head movement (as in uncompensated vestibular loss), medication side effects, and/or anxiety, depres- sion, or other psychiatric conditions [119].
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