# Evolution of Hyperventilation-Induced Nystagmus in Acute Unilateral Vestibulopathy—Interpretative Model and Etiopathogenetic Hypotheses

## TL;DR

This study examines how hyperventilation-induced nystagmus changes over time in patients with acute unilateral vestibulopathy, offering insights into the condition's underlying causes.

## Contribution

The paper introduces a new interpretative model linking hyperventilation-induced nystagmus patterns to the etiology of acute unilateral vestibulopathy.

## Key findings

- In the acute phase, the excitatory pattern of nystagmus was more common than the inhibitory pattern.
- Over time, the excitatory pattern decreased while the inhibitory pattern increased.
- The model suggests that excitatory patterns are linked to viral causes, while inhibitory patterns may indicate viral or vascular causes.

## Abstract

Hyperventilation induces metabolic changes that can elicit nystagmus (hyperventilation-induced nystagmus, HVIN) in various vestibular disorders, revealing vestibular imbalance and bringing out central or peripheral asymmetries. In acute unilateral vestibulopathy (AUVP, namely vestibular neuritis), hyperventilation can induce different patterns of nystagmus (excitatory, inhibitory, or negative), disclosing or modifying existing static vestibular asymmetries through its ability to invalidate compensation or increase peripheral excitability. In this context, we followed the evolutionary stages of HVIN in AUVP across 35 consecutive patients, with the goal of assessing alterations in the oculomotor pattern caused by hyperventilation over time. In the acute phase, the incidence of the excitatory pattern (and the strongly excitatory one, consisting of a reversal nystagmus evoked by hyperventilation) was significantly higher compared to the inhibitory pattern; then, a progressive reduction in the incidence of the excitatory pattern and a concomitant gradual increase in the incidence of the inhibitory one were observed in the follow-up period. Assuming the role of the ephaptic effect and the transient loss of vestibular compensation as opposing mechanisms, i.e., excitatory and inhibitory, respectively, the oculomotor pattern evoked by hyperventilation is the result of the interaction of these two factors. The data obtained allowed us to hypothesize an interpretative model regarding the pathogenetic aspects of responses evoked by hyperventilation and the etiologies of the disease: according to our hypotheses, the excitatory pattern implies a neuritic (viral) form of AUVP; instead, the inhibitory (and negative) one can be an expression of both the neuritic (viral) and vascular forms of the disease.