In addition to abnormalities of saccades velocity, saccadic latency or reaction time (the interval between the impulse to move and movement) is prolonged in Huntington chorea and Parkinson disease. Saccadic latency is also increased in corticobasal ganglionic degeneration (see Chap. 38), in which case it seems to correspond to the degree of motor apraxia. The obligate need to initiate eye movements with a blink is often a subtle sign of disordered supranuclear control of conjugate movements that is evident in these same diseases and in other processes including frontal lobe lesions.
Yet another saccadic disorder takes the form of an inability to initiate voluntary movements, either vertically or horizontally. This abnormality may be congenital in nature, as in the ocular “apraxia” of childhood (Cogan syndrome, see in the following text) and in ataxia-telangiectasia; an acquired difficulty in the initiation of saccadic movements may be seen in patients with Huntington disease or with a lesion of the contralateral frontal lobe or ipsilateral pontine tegmentum.
Fragmentation of smooth pursuit movement, a frequent finding, is a jerky irregularity of tracking that has been called “saccadic pursuit.” Asymmetrical impairment of smooth pursuit movements is indicative of a parietal or a frontal lobe lesion. Pursuit is impaired toward the side of a parietal lesion and away from a frontal lesion. This clinical phenomenon can be elicited by optokinetic testing as explained further on.
In addition, impaired pursuit can arise from vestibulocerebellar and extrapyramidal disorders. The former is commonly the result of sedative drug intoxication—with barbiturates, diazepam, and others as well as from a lesion of the vestibulocerebellar apparatus. There can be gaze directed nystagmus that seemingly interrupts pursuit movements as well.
A similar-appearing phenomenon, but one that does not manifest nystagmus, nicely called “cogwheel eye movements,” is seen in certain extrapyramidal diseases such as Parkinson disease, Huntington disease, and progressive supranuclear palsy. In these diseases, there is a ratchet-like impairment of smooth pursuit movements in association with slow, hypometric saccades (“saccadic pursuit”). Indeed, according to Vidailhet and colleagues, smooth pursuit movements are impaired in all types of basal ganglionic degenerations.
The VOR is tested by moving the patient’s head either horizontally or vertically while the individual maintains visual fixation on a distant stationary point. When the VOR is functioning normally, the eyes move automatically in the opposite direction to head turning (in fact they remain motionless in relation to the room and move only relative to the head). If the vestibular system is impaired, a head thrust will not elicit the normal contraversive eye movement. Instead, the eyes turn with the head, and the patient subsequently makes a “catch-up” saccade to return the eyes to the target of fixation. The saccade that refixates the eyes is observed more easily than is the slippage of the eyes from the target. Stimulation of the labyrinths by caloric or electrical activation also elicits reflexive eye movements, as described in Chap. 16 on Coma. When cold water is instilled into one ear, it simulates the physiology of the head turning the opposite direction. They eyes, therefore, make a reflexive slow movement toward the cold stimulus. In an awake patient, this is accompanied by fast-phase movements (nystagmus) in the opposite direction, away from the cold stimulus.