By Marcello Cherchi, MD PhD
For clinicians
Horizontal optokinetic testing is a standard part of most ocular motor testing protocols, whereas assessment of vertical optokinetic nystagmus is not.
In healthy subjects, vertical optokinetic nystagmus shows asymmetrical gain in the slow phase velocity; specifically, upward gain (i.e., with the stimulus moving toward the subject’s forehead) is higher than downward gain (i.e., with the stimulus moving toward the subject’s feet) (Murasugi and Howard 1989; Ogino et al. 1996; Takahashi et al. 1978; Wei et al. 1992, 1994). This asymmetry persists whether the subject is upright (i.e., earth vertical), lying on their side (Böhmer and Baloh 1990), or at some other tilt angle (Correia et al. 1997); some investigators report that the asymmetry is actually more pronounced when the subject is lying on their side or is upside-down (Clément and Lathan 1991).
In microgravity this asymmetry initially reverses (Clement et al. 1986) and then disappears (Clément 2003). Most investigators hypothesize that this is related to the influence of otolithic input (Clément 2003; Ogino et al. 1996), or perhaps due to microgravity-induced changes in the velocity storage mechanism (Clement and Berthoz 1990). These microgravity-induced changes in vertical optokinetic responses disappear when astronauts return to earth (Clément et al. 1993).
Vertical optokinetic responses may be abnormal in patients with congenital strabismus; specifically, a horizontal component emerges (Garbutt et al. 2003), resulting in a diagonally-oriented pattern of nystagmus (Economides et al. 2020).
Abnormalities of vertical optokinetic nystagmus have modest value in neuroanatomical localization. Garbutt and colleagues suggest that the differential diagnosis includes, “neurometabolic disease or an abnormality involving the cortex, brainstem, and /or cerebellum. Abnormal VOKN [vertical optokinetic nystagmus…] is highly suggestive of a rostral midbrain lesion” (Garbutt and Harris 2000). Abnormal vertical optokinetic nystagmus has been reported in progressive supranuclear palsy (Garbutt et al. 2004), idiopathic Parkinson’s disease (Knapp et al. 2009) and mercury toxicity (Mizukoshi et al. 1975; Mizukoshi et al. 1989; Mizukoshi et al. 2002).
References
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