Hyperventilation induced nystagmus

By Marcello Cherchi, MD PhD

For clinicians

In 1970 Tsutsui and Fukai (Tsutsui and Fukai 1970) described the effect of hyperventilation on spontaneous nystagmus. In 1972 Drachman and Hart (Drachman and Hart 1972) documented “a syndrome, not previously described, of positional vertigo occurring only after HV [hyperventilation].”

Hyperventilation by rapid, large breaths through the mouth can induce nystagmus, termed hyperventilation-induced nystagmus (HVIN). Instrumentation that eliminates fixation (ENG, VNG, VFO) are sensitive for HVIN. Methods that limit but do not eliminate fixation (optical Fresnel lenses) are less sensitive.

Most clinicians have the patient hyperventilate for 30 seconds, though some recommend 90 seconds (Baloh and Honrubia 2001; Bance et al. 1998; Robichaud, DesRoches, Bance 2002) or longer (Wilson and Kim 1981). The nystagmus induced by hyperventilation is generally weak. The fast phase of HVIN is usually directed contraversive to (away from) the diseased side — suggesting that the lesion is paretic (inhibitory); this behavior is rarely useful. However, in some disease processes the fast phase is directed ipsiversive (towards) the diseased side — suggesting that the lesion is irritative (excitatory) (Choi et al. 2005; Minor et al. 1999); in this circumstance it can be directed oppositely to the nystagmus associated with the head-shaking test or vibration test. HVIN is usually horizontal, less commonly vertical, and rarely torsional (Rosignoli, Almadori, Maurizi 1984). It can be delayed and follow hyperventilation rather than appearing during the hyperventilation itself.

Several possible mechanisms (Cherchi and Hain 2009) have been proposed for hyperventilation-induced nystagmus. Hyperventilation primarily affects blood oxygenation and pH, but has other metabolic effects as well. Hyperventilating alert patients during testing can increase spontaneous nystagmus and also may affect central compensatory mechanisms (Sakellari et al. 1997). Ideally a hypothesis regarding the underlying mechanism of HVIN would account for why its fast phase is sometimes directed towards the lesioned side, while in other instances is directed away from the lesioned side.

The most plausible explanation for hyperventilation-induced nystagmus is the direct effect of hyperventilation, which induces hypocapnia, raising the serum pH, and thereby improving neural conduction (Minor et al. 1999; Somjen et al. 1987). Transient improvement of vestibular function on the lesioned side (physiologically, probably an increase in the tonic firing rate along the vestibular nerve) would resemble rotating the head towards the lesioned side, resulting in the slow phase of nystagmus directed away from the lesion and the fast phase towards the lesion; in other words, this mechanism would account for HVIN whose fast phase is directed ipsiversive to a subtotal paretic lesion, and thus explain the pattern observed in diseases that limit (but do not completely destroy) the function of the vestibular nerve (e.g., subtotal vestibular neuritis, a small vestibular schwannoma). Minor and colleagues (Minor et al. 1999) performed electronystagmography on six patients with vestibular schwannomas and concluded that the vector of hyperventilation-induced nystagmus corresponds to the plane of the semicircular canal whose partially demyelinated afferent fibers exhibit a transient increase in activity — in other words, the fast phase of the nystagmus was directed ipsiversive to the lesion. Hyperventilation can also induce a nystagmus whose fast phase is directed contraversive to the side of a complete vestibular lesion (Sakellari et al. 1997). This can be seen, for example, in persons who are post-labyrinthectomy or vestibular neurectomy, and who thus have no remaining peripheral vestibular system on that side; thus there is no opportunity for that residual vestibular function to “improve” with hyperventilation. Other potential explanations for this pattern include augmentation of vestibular nystagmus through alerting or another mechanisms (Monday and Tetreault 1980; Theunissen, Huygen, Folgering 1986) and disruption of central compensation (Sakellari et al. 1997).

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