Drug intoxication is certainly the most frequent cause of nystagmus. Alcohol, barbiturates, other sedative-hypnotic drugs, phenytoin, and other antiepileptic drugs are the common ones. This form of nystagmus is most prominent on deviation of the eyes in the horizontal plane, but occasionally it also may appear in the vertical plane. For no known reason, it may occasionally be asymmetrical in the two eyes.
In many normal individuals, a few irregular jerks are observed when the eyes are moved far to one side (“nystagmoid” jerks), but the movements cease once lateral fixation is attained. A fine rhythmic nystagmus may also occur normally in extreme lateral gaze, beyond the range of binocular vision; but it is bilateral and disappears as the eyes move a few degrees toward the midline. These latter movements are probably analogous to the tremulousness of skeletal muscles when maximally contracted.
Oscillopsia is the symptom of illusory movement of the environment in which stationary objects seem to move back and forth, up and down, or from side to side. It may be caused by ocular flutter (a cerebellar sign as discussed later) or coarse nystagmus of any type. With lesions of the labyrinths (as in aminoglycoside toxicity), the symptom of oscillopsia is only provoked by motion—for example, walking or riding in an automobile—and indicates an impaired ability of the vestibular system to stabilize ocular fixation during body movement (i.e., impaired VOR function). In these circumstances, cursory examination of the eyes may disclose no abnormalities; however, if the patient’s head is rotated slowly from side to side or moved rapidly in one direction while attempting to fixate a target, impairment of smooth eye movements and their replacement by saccadic or nystagmoid movements is evoked (see Chap. 14 for further discussion of these tests). If episodic and involving only one eye, oscillopsia is usually caused by myokymia of an ocular muscle (usually the superior oblique).
Nystagmus of Labyrinthine Origin (See Also Chap. 14)
This is predominantly a horizontal or vertical unidirectional jerk nystagmus, often with a slight torsional component, that is evident when the eyes are close to the central position and changes minimally with the direction of gaze. It is more prominent when visual fixation is eliminated (conversely, it is suppressed by fixation). The observation of suppression with visual fixation is facilitated by the use of Frenzel lenses, but most instances are evident without elaborate apparatus. Vestibular nystagmus of peripheral (labyrinthine) origin beats in most cases away from the side of the lesion and increases as the eyes are turned in the direction of the quick phase (the Alexander law). In contrast, as noted below, nystagmus of brainstem and cerebellar origin is most apparent when the patient tries to maintain eccentric fixation and the direction of nystagmus changes with the direction of gaze.
Tinnitus and hearing loss are often associated with disease of the peripheral labyrinthine mechanism; also, vertigo, nausea, vomiting, and staggering may accompany disease of any part of the labyrinthine-vestibular apparatus or its central connections. As a characteristic example, the intense nystagmus of benign positional vertigo (see
Chap. 14) is evoked by moving from the sitting to the supine position, with the head turned to one side. In this condition, nystagmus of vertical-torsional type and vertigo develop a few seconds after changing head position and persist for another 10 to 15 s. When the patient sits up, the nystagmus changes to beat in the opposite direction.