Biomedical subjects
Publications and source records attributed to K Hepp.
We have tested Listing's law in the monkey using the dual search coil technique to record 3-dimensional eye positions during smooth pursuit and during spontaneous eye movements in the light. Our results indicate that during smooth pursuit the eye positions obey Listing's law with a least the same accuracy as during spontaneous eye movements or during periods of fixations.
The riMLF is a nucleus in the rostral mesencephalon whose bilateral destruction leads to a palsy of vertical and torsional rapid eye movements. A unilateral lesion leads to a loss of torsional rapid eye movements in only one direction, but vertical rapid movements can still be generated with some reduction in their velocity. Single neuron studies in monkeys and anatomy support the concept that the riMLF together with the PPRF are the critical areas in the brainstem to generate rapid eye movements in 3 dimensions.
In the case of Concise after one year 88.3% and after two years 72.8% caries-prophylactic effect was measured. In case of Delton the same values were 83.8% and 89.4%, respectively.
The role of the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) in generating the vertical and torsional components of rapid eye movements was examined. The on-directions of burst neurons in the riMLF of alert Rhesus monkeys were obtained during quick phase nystagmus in three dimensions. The distinguishing feature of these burst neurons was the torsional component of their on-directions; neurons on the right side exhibited a clockwise component, from the point of view of the subject, while those on the left had a counterclockwise component. Vertical components could have up or down directions. This organization was verified by means of unilateral reversible inactivation of the riMLF using Muscimol. An injection in the right riMLF impaired the generation of quick phases with clockwise components while one on the left impaired counterclockwise components.
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The trajectories of rapid eye movements are usually described in a Cartesian coordinate frame with a horizontal, vertical and torsional component. The sensory to motor coordinate transformations for horizontal components of rapid eye movements can be localized to neurons of the paramedian pontine reticular formation (PPRF), where long-lead and short-lead burst neurons are found. The equivalent area for recoding of vertical and torsional movement components is situated in the rostral interstitial nucleus of the MLF (rostral iMLF). Pause cells in caudal midline structures of the PPRF help to coordinate the various movement components. Experimental inactivation of these different neuron population lead to palsies of rapid eye movement generation. A unilateral PPRF lesion leads to a loss of all horizontal rapid eye movements towards the ipsilateral side. A bilateral PPRF lesion involving caudal midline structures leads to a bilateral horizontal gaze palsy in addition to a severe disruption of vertical and torsional eye movements. A bilateral rostral iMLF lesion leads to a loss of all rapid eye movements with a vertical or torsional movement component. A unilateral iMLF lesion leads to a loss of all rapid eye movements with an ipsilateral torsional component.
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Injections of the retrograde tracer [125I]wheat germ agglutinin have been placed in different areas of the paramedian pontine reticular formation (PPRF), a well known premotor center for gaze control. Experiments in 5 monkeys revealed 3 major sources of input: (1) bilateral projections from the so-called frontal eye field (FEF), which is situated in the frontal cortex around the arcuate sulcus; (2) the intermediate and deep layers of mainly the contralateral superior colliculus; and (3) ipsilateral projections from brainstem structures such as the accessory oculomotor nuclei (nucleus interstitialis of Cajal, nucleus of Darkschewitsch, and nucleus of the posterior commissure), the mesencephalic reticular formation, the vestibular nuclei, the nucleus prepositus hypoglossi, and the cerebellar fastigial nucleus. The results are compared with previous anatomical investigations and confirm the electrophysiologically demonstrated FEF-PPRF-abducens disynaptic pathway.
Static firing frequencies have been determined in extraocular motoneuronal discharge patterns for different eye positions within +/- 30 deg around the primary position. From these data iso-frequency curves were plotted stating all possible eye positions for a given firing rate. Such curves have been constructed for the lateral, medial, and inferior recti, the superior oblique and for the upward pulling muscles (without distinguishing superior rectus and inferior oblique). Fixation of eye position always involved natural synergistic action of all muscles. The iso-frequency curves of individual motoneurons are a family of almost parallel curves with mainly horizontal or vertical gradients. Especially for the superior oblique, the innervation gradients depend strongly on eye position. Motoneurons subserving the same muscle can have different innervation gradients at the same eye position.
Eye and head position, EEG, and activity of oculomotor and vestibular neurons in the brainstem were recorded during alertness and at the transition to light sleep. Characteristic changes of firing patterns were found in many neuronal populations at the sleep-wake transition and could be related to disruption of fixation and rapid and compensatory eye movement generation. Motoneurons decreased their firing rate by 20 to 50%, and their eye velocity coding deteriorated. Burst neurons had a significant drop in maximum firing rates and often showed continuous activity unrelated to rapid eye movements, but responded to vestibular stimuli. Pause neurons went completely silent. Neurons in the vestibular nuclei often reduced their level of activity, but still responded qualitatively unchanged to semicircular canal stimulation. In the framework of current models of oculomotor organization, the sleep-wake transition can be interpreted as a non-equilibrium phase transition which is driven by specific inputs and nonspecific activating systems.
Lesions were placed in the paramedian pontine reticular formation ( PPRF ) of monkeys and the resulting gaze palsies studied. Brainstem regions were identified by single cell recordings before kainic acid was injected to selectively destroy neuronal cell bodies in the vicinity. Unilateral PPRF lesions led to a loss of all rapid eye movements towards the ipsilateral side. Deficits were identical to those after experimental electrolytic lesions in monkeys, or structural lesions in humans. Bilateral PPRF lesions produced two different syndromes. Rostral PPRF lesions led to a selective loss of horizontal rapid eye movements leaving vertical movements intact. Caudal PPRF lesions led in addition to a severe disruption of vertical rapid eye movements.
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The integrity of the paramedian pontine reticular formation (PPRF) is necessary for the generation of rapid eye movements. The main saccade-related population is of the burst type with latencies between 0 and 40 ms preceding a saccade, and they can be divided into medium- and long-lead burst neurons. Burst neurons have predominantly spatially coded movement fields in the rostral PPRF, while in the caudal PPRF they increase their burst strength in temporal coding approximately in the pulling directions of extraocular eye muscles (i.e. almost horizontal or vertical). Both neuronal populations have ipsilateral on-directions and contain long-lead burst neurons. In a quantitative analysis the firing patterns of long-lead burst neurons are compared to those of medium-lead burst neurons, which form the predominant output of the saccadic pulse generator to the motoneurons. The firing patterns of temporally coded long-lead bursters are similar to those of medium-lead bursters, except for earlier on-latencies, larger statistical fluctuations, and specializations for small or large saccades in oblique directions. The spatially coded burst neurons form a motor map of saccadic vectors. The diameter of their movement field is often about the size of the saccade vector, and they encode saccadic onset and duration. These results are consistent with a model for visual saccades in eye displacement coordinates, where the spatio-temporal recording of horizontal eye movements is effected by long-lead burst neurons in the PPRF.
In all cerebellar nuclei saccade related neurons can be recorded. In the alert untrained Rhesus monkey these neurons can be classified into short-lead bursters, complex bursters, and tonic burst neurons. Short-lead bursters can be related to the onset or to the length of saccades and blinks. Complex bursters are active in the early (acceleration) or late (deceleration) phase of saccades. Tonic burst neurons, in addition, display maintained activity which is modulated in a complex manner with eye position, during periods of fixation or slow-phase nystagmus. In agreement with clinical and previous experimental data we view these cerebellar output neurons as elements which are not part of the system which basically generates eye movements, but rather as a system which could influence the execution of movements.