When one is watching a moving object (e.g., the passing landscape from a train window, a rotating drum with vertical stripes, or a strip of cloth with similar stripes), a rhythmic jerk nystagmus called optokinetic nystagmus (OKN) normally appears. This phenomenon is explained by a slow involuntary pursuit movement iteratively followed by a quick saccadic movement in the opposite direction in order to fixate the next new target that is entering the visual field. With unilateral lesions of the parietal region, the slow pursuit phase of the OKN may be lost or diminished when the stimulus—for example, the striped OKN drum—is moving toward the side of the lesion, whereas rotation of the drum to the opposite side elicits a normal response. (A prominent neurologist of our acquaintance in past days correctly made the diagnosis of parietal lobe abscess on the basis of fever and absent pursuit to the side of the lesion.) In contrast, patients with hemianopia caused by an occipital lobe lesion show a normal optokinetic response bilaterally. The loss of the pursuit phase with a parietal lesion presumably results from interruption of efferent pathways from the parietal cortex to the brainstem centers for conjugate gaze. On the other hand, individuals with a frontal lobe lesion will track a moving target in either horizontal direction but show little or no fast-phase correction in the direction opposite the lesion.
An important additional fact about OKN is that the ability to evoke it proves that the patient is not blind. Each eye can be tested separately to exclude monocular blindness. Thus the test is of particular value in the examination of hysterical patients and malingerers who claim that they cannot see, and of neonates and infants (a nascent OKN is established within hours after birth and becomes more easily elicitable over the first few months of life). Demonstration of an intact OKN, however, merely demonstrates that some vision is preserved, and does not prove that the visual function is actually normal.
Labyrinthine stimulation—for example, irrigation of the external auditory canal with warm or cold water, or “caloric testing”—produces a marked nystagmus. Cold water induces a slow tonic deviation of the eyes toward the irrigated ear and a compensatory nystagmus in the opposite direction in a conscious, awake patient; warm water does the reverse. Thus the acronym taught to generations of medical students: COWS, or “cold opposite, warm same,” to refer to the direction of the fast phase of the induced nystagmus. The slow tonic component reflects impulses originating in the semicircular canals, and the fast component is a corrective movement. Comatose patients with an intact VOR will demonstrate the slow phase gaze deviation without the fast phase nystagmus to which this mnemonic refers. Chapter 14 discusses the production of nystagmus by labyrinthine stimulation and other features of vestibular nystagmus.
Brainstem lesions often cause a coarse, unidirectional, gaze-evoked nystagmus, which may be horizontal or vertical, meaning that the nystagmus is exaggerated when the eyes sustain an eccentric position of gaze. Vertical nystagmus, for example, is brought out usually on upward gaze, less often downward. Unlike the vestibular nystagmus discussed above, the central type usually also changes direction depending on the direction of gaze. Vertigo is less common or less intense than with labyrinthine nystagmus, but signs of disease of other nuclear structures and tracts in the brainstem are frequent.