Vestibular syncope: clinical characteristics and mechanism

Abstract

Background and objectives: Vestibular syncope is a condition in which vertigo-induced hemodynamic changes cause syncope. This study investigated the clinical and laboratory findings of vestibular syncope and tried to refine our knowledge of the mechanism underlying this newly recognized entity.

Methods: This study retrospectively analyzed 53 patients (33 women, median age = 63 years [interquartile range = 54-71 years]) with vestibular syncope from January 2017 to December 2021. To explain the mechanism of vestibular syncope, we incorporated a velocity-storage model into the dual reflex pathways comprising the vestibulo-sympathetic reflex and baroreflex and predicted the cardiovascular responses.

Results: Twenty (37.7%) patients had multiple episodes of vestibular syncope, and seven (13.2%) had potentially life-threatening injuries. Meniere's disease (20.8%) and benign paroxysmal positional vertigo (9.4%) were the most common underlying vestibular disorders. Abnormal vestibular function tests included impaired cervical vestibular-evoked myogenic potentials (57.5%) and positive head impulse tests (31.0%). Orthostatic hypotension was found in 19.5% of patients. Dyslipidemia (30.2%) and hypertension (28.3%) were common medical comorbidities. The dual reflex pathways incorporating the function of the velocity-storage circuit in the brainstem and cerebellum suggest that vestibular syncope is a neurally mediated reflex syncope associated with a sudden hemodynamic change during vertigo. This change can be arterial hypertension triggered by a false downward inertial cue, as suggested previously, or hypotension driven by a false upward inertial cue.

Conclusions: Vestibular syncope is associated with various vestibular disorders and requires careful evaluation and intervention to prevent recurrent falls and significant injuries.

Figure 1

Clinical findings of the illustrated case. (A) In video‐head impulse tests, the gain (the ratio of total eye rotation in degrees to total head rotation in degrees) is 0.57 and 0.58 in the left and right posterior canals, respectively. In addition, there are asynchronous small amplitude corrective saccades during the horizontal and posterior canal head impulse tests. (B) Bithermal caloric test and pure tone audiometry show left side canal paresis of 77% and severe left‐side sensorineural hearing loss. (C) Cervical vestibular evoked myogenic potentials are normal, but ocular vestibular evoked myogenic potentials are absent.

Figure 2

Orthostatic blood pressure tests in patients with vestibular syncope. (A) Box plots (upper row) show the systolic and diastolic blood pressures and pulse rate in the supine position and the lowest systolic and diastolic blood pressures and highest pulse rate during a 5‐min orthostatic test. (B) Bar plots (lower row) show the distribution of changes in systolic and diastolic pressures and pulse rate during a 5‐min orthostatic test. The vertical red dot lines in each plot indicate the boundary of reference values, and the purple‐filled boxes represent the number of patients with abnormal values. DBP, diastolic blood pressure; PR, pulse rate; SBP, systolic blood pressure.

Figure 3

Schematic mechanism of vestibular syncope. (A) Dual neural reflex pathways for cardiovascular homeostasis. The vestibulo‐sympathetic reflex has a short (100–200 msec) latency and operates in a feed‐forward manner. The information on the head position from the canal and otolith is further refined in the velocity storage (VS) circuit and then relayed to the brainstem autonomic nuclei controlling cardiovascular tone. Of note, vertigo attacks (purple box) can change the vestibulo‐sympathetic reflex tone without postural changes. In contrast, the baroreflex, activated by blood pressure changes in the heart and major vessels, has relatively a long latency (1–2 sec) and uses a feedback strategy. (B) The VS model shows that both false rotational cues and false downward inertia can generate a downward inertial cue (left column). In this situation, the vestibulo‐sympathetic reflex increases the sympathetic outflow to counteract the preload and blood pressure drop during upward motion. However, since vertigo attacks provoke downward inertia without actual body fluid displacement, increased sympathetic activity may cause sudden ictal hypertension. As a result, baroreflex increases parasympathetic flow, which in turn causes hypotension and eventually syncope in some cases. On the contrary, when the VS circuit generates an upward inertial cue (right column), the vestibulo‐sympathetic reflex decreases sympathetic outflow to compensate for the body fluid changes associated with actual motion. However, since the body fluid remains unchanged during vertigo, ictal hypotension (a well‐known cause of reflex syncope) may follow.