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Five patients with a disturbance of their preprogramming of speech (dyspraxia of speech) were exposed to a comprehensive eye-motor test-battery. The saccades were found hypometric and inaccurate with irregular intervening pauses. The finding was interpreted as due to an extension of lesions from frontal cortical speech areas into visual motor cortex disturbing the normal preprogramming of voluntary saccades. The results were interpreted as supporting the assumption that voluntary saccades are initiated in the frontal cortex. An increase of vestibular nystagmus in these cases was related to a release of vestibular nystagmus due to the disappearance of cortical inhibition on brain stem acitivty.

Peak velocities of voluntary saccades and fast phases of different qualities of nystagmus were studied in 20 normal subjects, 5 patients with pontine lesions and 5 patients with lesions in the frontal cortex. The peak velocity of saccades was related to the amplitude of the eye movement, the alertness of the subject and whether the subject could see the target or not. The effect of the age was not significant. The quick phases of caloric, optokinetic and angular acceleration induced nystagmus were equally rapid but somewhat slower than that of vestibular nystagmus recorded in standardized visual surrounding. In the same visual condition saccades were always faster than quick phases of nystagmus. Patients with cortical lesions had normal velocities in saccades and quick phases of nystagmus. Patients with pontine disorders had significantly reduced saccadic and quick phase velocity, and some of the patients exhibited dissociations between velocity mechanisms while the somewhat higher velocity in quick phase of vestibular nystagmus recorded in light is probably related to higher attention evoked by vestibular-visual interaction.

The number of saccades, vestibular gain and visual suppression as a function of smooth pursuit gain were determined in 10 cerebellar cases. Visual suppression increased and the number of saccades decreased with increasing smooth pursuit gain while a high vestibular gain was found in most cases but without relation to the gain of smooth pursuit. An eye-motor model is presented according to which all findings could be related to a disturbance of proper cerebellar processing of optic impulses and of impulses to the vestibular nuclei in the paramedian reticular formation.

The peak velocities of saccades and fast phases of nystagmus were examined and compared in 20 healthy subjects. The peak velocities of both types of eye movements increased with increase of amplitudes. The saccades were found to be fastest in light, slower in darkness and slowest behind closed eyelids. The peak velocities of the quick phases of optokinetic and of vestibular nystagmus were found to be the same. Fast phases of optovestibular (optic as well as vestibular stimulation) nystagmus produced significantly higher peak velocities than the two others. At the same amplitude and during the same visual conditions the saccades were significantly faster than any type of fast components of nystagmus. The difference in velocity between voluntary and reflexive eye movements is possibly related to differences in antagonistic activity during these eye movements, but also to specific synaptic events during the voluntary action.

In 5 healthy individuals the postrotatory, exponential constants were estimated for each of the four nystagmus qualities, viz. the velocities and durations of fast and slow components. The residual spread (Sr) of each quality in a semilogarithmic plot was also determined. The value of the constant for postrotatory decay indicated a decrease of the velocity and an increase for the duration of the slow component, both with a significant difference between individuals, while for the corresponding values of the fast components no systematic change in the postrotatory reactions was indicated, nor any difference between individuals. The constant that corresponds to the value at maximum stimulus showed differences between individuals for each of the four nystagmus qualities, while Sr presented differences between individuals only for the two slow phase qualities. This technique to describe postrotatory nystagmus reactions by the two exponential constants for each of the four nystagmus qualities together with the residual spread for each of the qualities is intended for future 'on-line' nystagmus analysis.

The maximum velocity gain of smooth pursuit and optokinetic, vestibular, and optovestibular slow phases was examined in 15 patients with pontine, 10 with medullary, 10 with cerebellar, and 5 with combined cerebello-brain stem disorders. Marked dissociations were observed between smooth pursuit and optokinetic slow phases, especially in medullary disease. A cerebellar deficit enhanced slow phase velocity gain during rotation in darkness, whereas the corresponding gain during rotation in light was normal.

The eye tracking test is today a well established part of clinical otoneurological examination. In the present paper some applications of the test in evaluating of the level of lesion within the vestibular system are reviewed.

Peak velocity of saccade, maximum velocity of smooth pursuit, and peak velocity of slow phase of vestibular and optovestibular nystagmus were measured three times daily on three separate days in 6 healthy subjects in order to estimate the intra-individual variation of the results of oculomotor tests. Analysis of variance revealed that the oculomotor performance of the individual subjects varied systematically, depending on whether the tests were performed in the morning, at noon, or late in the afternoon. In particular, the velocity of saccade displayed lowest values in the afternoon. The present results indicate that oculomotor performance may depend on the individual biological rhythm of fatigue; however, it is also possible that eye motor behaviour is coupled to an independent rhythm of motor activity. Circadian rhythmicity of oculomotor performance should be considered in follow-up studies and in examination of patients with reduced vigilance.

Tracking eye movements were studied in 20 healthy subjects and in 24 patients with vestibular neuronitis, disorders within the frontal cortex, the cerebellum or the brain stem. The tracking tests were performed at six different target velocities between 10-60 degrees s-1 and different parameters were evaluated. The maximum velocity gain of smooth pursuit as normal in the group with vestibular neuronitis but reduced in the groups with disorders within the frontal cortex, cerebellum and the brain stem. The total amplitude of tracking and amplitude of smooth pursuit were normal in the groups with vestibular neuronitis and frontal cortical disorders, while in the groups with cerebellar and brain stem disorders it was reduced. The frequency of superimposed saccades with amplitude range of 3-10 degrees was significantly increased in all groups; however, in the group with vestibular neuronitis the increase was significant only during tracking in the direction of spontaneous nystagmus. The number of superimposed saccades with amplitude range of 11-20 degrees was significantly increased only in the group with cerebellar disorders. The frequency of square waves was not significantly increased in any group. Quantitative analysis of tracking eye movements seems to be a valuable aid for evaluation of site of lesions in the central nervus system.

Eye movements in 30 patients with brain-stem lesions were evaluated with electro-oculography, and the findings were analyzed with regard to the site of the lesion in the brain stem. Eye velocities generally were reduced more severely in pontine than in medullary lesions. In medullary lesions, there even was a slight enhancement of the velocities in the fast component of optokinetic and postrotatory nystagmus. In contrast to the slow-phase velocity of OKN, which often was preserved in medullary lesions, the smooth-pursuit velocity was reduced in lesions at all levels in the brian stem. This indicates that these two types of visually induced eye movements use different mechanisms.

Mean peak velocity and accuracy of vertical saccades were measured in 15 patients with disorders in the brain stem and in 12 normal subjects. (1) In the normal group up-directed saccades were faster than down-directed and the velocity of the saccade was not dependent on the age of the subject. Up-saccades were faster whether electro-oculography or photo-electro-oculography were used. (2) In patients with brain stem disorders the velocity of vertical saccades did not significantly differ from the saccadic velocity in the normal group. This is in contrast to what was found in horizontal saccades, where a reduced velocity was characteristic.

Quantification of dysrhythmia in a nystagmus response has hitherto not been seriously attempted, possibly because the nystagmus response does not easily lend itself to description in mathematical or physical terms. Ideally the nystagmus response consists of a sequence of triangles. Each such triangle is determined by four qualities, i.e. the velocities and the durations of the fast and slow components. Thus, without serious loss of information it is possible to represent a nystagmus reaction by four sequences of values, one for each of the four above mentioned qualities. From each such sequence we have extracted relevant information and presented it in graphical form. It may be assumed that each of the four nystagmus qualitiees reflects the activity within separate 'neuronal systems'. Each of these four systems is then informed upon by three parameters for each nystagmus quality, i.e. by its mean, by its variation coefficient and by its sequential variation coefficient. It is claimed that these three diagrams contain nystagmus information not earlier considered.