Intrabeat relationship of postrotatory nystagmus in normal subjects.

Intrabeat relationships between duration, amplitude and velocity of the slow phase of nystagmus and between amplitudes of the fast and slow phase of nystagmus were analysed from postrotatory responses in 10 normal subjects, using linear regression analysis. For 5 subjects, the tests were repeated five times. Highly significant correlation was found between velocity and amplitude of the slow phase in 9 of 10 subjects, whereas in one subject it was less significant. All subjects exhibited a significant correlation between velocity and duration of the slow phases. These intrabeat relationships were repeatable and representative for each individual. Highly significant correlation was found between amplitudes of the slow and fast phases of nystagmus in all subjects. No interindividual differences in these variables could be observed. The results indicate that the end-point of the slow phase of vestibular nystagmus in darkness is controlled by positional and durational corollary circuitries. The positional signal in displacement circuitry is probably derived by integration of the velocity signals from the labyrinths. The durational circuitry is presumably more dominant at high nystagmus velocities in order to permit sufficient time for fixation.

Intrabeat relationship of postrotatory nystagmus in patients with neurological disorders.

The intrabeat relationships between velocity, amplitude and duration of the slow phase of nystagmus as well as between amplitudes of slow vs. fast phase of nystagmus were analysed during a postrotatory nystagmus response by using linear regression analysis. Three groups of patients were studied, each consisting of 10 subjects with lesions either in the peripheral vestibular system, in the frontal lobe, or in the brain stem. Irrespective of the site of the lesion, all groups exhibited the same response pattern: a reduction in amplitude control of the end-point of nystagmus and an increase in durational control. The most prominent changes were observed in patients with brain-stem lesion in whom the durational control of the slow phase of nystagmus was constant, with a mean slow phase duration of 150 to 250 ms in the case of 3 to 4 fast phases per second. No alterations were observed in the relationship between amplitude of slow vis-à-vis fast phase. The results indicate that analysis of intrabeat relationship may provide additional data on the side of the disorder affecting the vestibular system.

Eye movements in patients with speech dyspraxia.

Saccades, smooth pursuit and angular acceleration induced nystagmus were analysed quantitatively in 10 patients with speech dyspraxia. The saccades were less accurate, had a prolonged reaction time and showed a tendency to reduced peak velocity, though only contralateral to the lesion. Smooth pursuit was imparied, with a reduction in maximum velocity gain. The vestibular responses tended to be hyperactive, indicating facilitated brain-stem reflexes. The findings show that a lesion in the frontal eye field can produce various oculomotor disturbances, in which the triggering of eye movements and their control, and pacing of the various movement sequences are disturbed. In addition, anticipation of a movement pattern requiring volition may be greatly impaired.

Clinical evaluation of dysrhythmia of postrotatory nystagmus.

Postrotatory responses of nystagmus were analysed in an exponential model by utilizing linear regression analysis. Four nystagmus qualities (velocity and duration of slow and fast phases) were studied in 10 patients with vestibular peripheral lesions, 10 patients with frontal lobe lesions and 10 patients with brain-stem lesions, together with 10 control subjects. In addition, pauses during the responses were quantified. Patients with frontal lobe lesions differed from other groups by scoring higher values of slow phase velocity and by exhibiting more pauses. The time constant was significantly shorter in patients with brain-stem lesion than in any other group. As regards other qualities, e.g. slow phase duration and fast phase velocity, or duration, no differences were observed. The pathological dysrhythmia may therefore be presented as changes in the gain and time constant of slow phase velocity as well as in pauses during nystagmus. Since all these changes may be encountered in normal subjects, one should be cautious in interpreting these changes as being pathological in each individual case.

The dysrhythmia and the exponential constants of the postrotatory nystagmus qualities.

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.

Dyspraxia of speech and of eye motility.

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.

Quantification of vestibular dysrhythmia.

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.