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U Büttner

Publications and source records attributed to U Büttner.

At least 19 recordsLinked to original sources
PubMed1995

Saccade-related Purkinje cell activity in the oculomotor vermis during spontaneous eye movements in light and darkness.

Saccade-related Purkinje cells (PCs) were recorded in the oculomotor vermis (lobules VI, VII) during spontaneous eye movements and fast phases of optokinetic and vestibular nystagmus in the light and darkness, from two macaque monkeys. All neurons (n = 46) were spontaneously active and exhibited a saccade-related change of activity with all saccades and fast phases of nystagmus. Four types of neurons were found: most neurons (n = 31) exhibited a saccade-related burst of activity only (VBN); other units (n = 7) showed a burst of activity with a subsequent pause (VBPN); some of the units (n = 5) paused in relation to the saccadic eye movement (pause units, VPN); a few PCs (n = 3) showed a burst of activity in one direction and a pause of activity in the opposite direction. For all neurons, burst activity varied considerably for similar saccades. There were no activity differences between spontaneous saccades and vestibular or optokinetically elicited fast phases of nystagmus. The activity before, during, and after horizontal saccades was quantitatively analyzed. For 24 burst PCs (VBN, VBPN), the burst started before saccade onset in one horizontal direction (preferred direction), on average by 15.3 ms (range 27-5 ms). For all these neurons, burst activity started later in the opposite (non-preferred) direction, on average 4.9 ms (range 20 to -12 ms, P < 0.01) before saccade onset. The preferred direction could be either with ipsilateral (42% of neurons) or contralateral (58%) saccades. Nine burst PCs had similar latencies and burst patterns in both horizontal directions. The onset of burst activity of a minority of PCs (n = 5) lagged saccade onset in all directions. The pause for VBPN neurons started after the end of the saccade and reached a minimum of activity some 40-50 ms after saccade completion. For all saccades and quick phases of nystagmus, burst duration increased with saccade duration. Peak burst activity was not correlated with saccade amplitude or peak eye velocity. PCs continued to show saccade-related burst activity in the dark. However, in 59% of the PCs (VBN, VBPN), peak burst activity was significantly reduced in the dark (on average 28%, range 15-36%) when saccades with the same amplitude (but longer duration in the dark) were compared. For VBP neurons, the pause component after the saccade disappeared in the dark.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

Gaze-evoked nystagmus and smooth pursuit deficits: their relationship studied in 52 patients.

Gaze-evoked nystagmus occurs with cerebellar and brainstem lesions and reflects a deficiency of the so-called common neural integrator. Experimental data show that loss of the neural integrator also abolishes slow conjugate eye movements, i.e. smooth pursuit eye movements and the vestibulo-ocular reflex (VOR). Since the smooth pursuit system has its own premotor circuits, a smooth pursuit deficit can be either the result of a premotor smooth pursuit lesion or the consequence of a gaze-holding deficit. To study this question DC eye movement recordings of 52 patients with horizontal gaze-evoked nystagmus and/or smooth pursuit deficits were studied in detail. It was found that the majority (71%) had a combined smooth pursuit and gaze-holding deficit. Thirteen patients (25%) had a smooth pursuit deficit only. Only 2 patients (4%) had an isolated gaze-evoked nystagmus, which was comparatively weak. Thus a major finding is that each substantial gaze-evoked nystagmus is combined with a smooth pursuit deficit; the two deficits are well correlated (coefficient r = 0.81). In all patients with a smooth pursuit deficit, visual suppression of the VOR was similarly impaired, when comparing the groups with and without gaze-evoked nystagmus. It is argued here that, although gaze-holding and smooth pursuit deficits are well correlated, the gaze-holding deficits seen in patients are not severe enough to explain the smooth pursuit deficit solely as a consequence of the gaze-holding deficit. Rather it probably reflects the close anatomical vicinity of gaze-holding and smooth pursuit mechanisms in the floccular region, the vestibular nuclei/nucleus prepositus complex and its connecting pathways.

Adult↗
PubMed1995

Eye movements.

Several areas with different saccade-related functions in the frontal cortex are outlined in this review: the frontal eye field, the supplementary eye field, the supplementary motor area, and the dorsolateral prefrontal cortex. Other recent findings that are discussed are that cerebellar midline lesions, including the oculomotor vermis (lobulus VI and VII), and the caudal fastigial nucleus lead to saccadic dysmetria and smooth pursuit deficits.

Animals↗
PubMed1994

Saccadic lateropulsion in Wallenberg's syndrome may be caused by a functional lesion of the fastigial nucleus.

One of the clinical oculomotor hallmarks of lateral medullary infarction (Wallenberg's syndrome) is the so-called saccadic lateropulsion. In man and in animals, cerebellar lesions lead to dysmetric saccades and underline the importance of cerebellar control on saccadic accuracy. In order to study the lesion site responsible for saccadic lateropulsion we prospectively examined 12 patients with Wallenberg's syndrome who did not show a cerebellar lesion on CT or MRI. All patients consistently showed hypermetric saccades to the ipsilateral side and hypometric contralateral saccades comparable with the effects of cerebellar lesions in monkeys on saccadic accuracy. Based on the most recent experiments involving recordings from saccade-related neurons in the deep cerebellar nuclei of monkeys (oculo-motor region of fastigial nucleus), we hypothesize that saccadic lateropulsion in lateral medullary infarction is essentially identical with cerebellar saccadic dysmetria and results from a disruption of afferent olivocerebellar climbing fibres that gives rise to functional disinhibition of the cerebellar cortex and to increased inhibition of the deep cerebellar nuclei.

Adult↗
PubMed1992

["Abducens neuromyotonia" with partial oculomotor paralysis].

Paroxysmal involuntary spasms of extraocular eye muscles which can lead to reversible pathological eye positions and limitations of eye movements are etiologically heterogenous. Despite the diagnostic difficulty, they are important as a neurological sign because of the usually good response to treatment. We report on a patient with the unusual combination of ocular neuromyotonia with brief paroxysmal tonic lateral deviation of the left eye and a concomitant partial third nerve palsy. The paroxysmal episodes disappeared with carbamazepine therapy. Possible pathomechanisms are discussed.

Abducens Nerve↗
PubMed1992

Neuroanatomy of the ocular motor pathways.

Oculomotor-related structures in the brain stem extend from the rostral mesencephalon to the hypoglossal nucleus in the caudal medulla. This chapter reviews their location in man, their connections and some basic features of their function; these are summarized in Table 1. In addition to the extraocular motor nuclei (the oculomotor, trochlear and abducens nuclei) the brain stem contains premotor areas responsible for all five different types of eye movements and for gaze-holding. These premotor structures include the riMLF and PPRF for the generation of vertical/torsional and horizontal saccades, respectively. The role of the vestibular nuclei in the VOR and optokinetic responses is well established, and they probably also mediate smooth pursuit eye movements along with the dorsolateral pontine nuclei and the floccular region. In contrast, there is only scanty evidence for the function of the accessory optic nuclei relaying optokinetic information in man. Little is known about the neuroanatomy of the premotor areas for convergence. There is accumulating evidence that the INC and the vestibular and perihypoglossal nuclei are essential for the maintenance of gaze.

Animals↗
PubMed1991

Differential effects of bicuculline and muscimol microinjections into the vestibular nuclei on simian eye movements.

1.) Eye movements were recorded in four Java monkeys (M. fascicularis) after unilateral microinjections (1 microliter, concentration 1 micrograms/microliter) of the GABA antagonist, bicuculline, and the GABA agonist, muscimol, into oculomotor related regions of the vestibular nuclei. Eye movements were investigated in the dark and light during spontaneous eye movements, vestibular stimulation (sinusoidal: 0.2 Hz, +/- 40 deg/s, and velocity trapezoid: 40 deg/s2 acceleration, 120 deg/s constant velocity), and visual-vestibular conflict stimulation. 2.) Bicuculline and muscimol injections consistently led to specific eye movement changes, which were maximal 5-10 min after bicuculline injection (muscimol 10-30 min), and lasted 90-120 min (muscimol 2-4 h). Control injections with NaCl (0.9%) into the responsive area and with bicuculline 2-3 mm more lateral showed no effect. 3.) Bicuculline induced a spontaneous nystagmus of 40.9 deg/s (average, range 10.5-93 deg/s), beating in 60% of the cases to the contralateral and in 40% to the ipsilateral side. The analysis of the slope of the slow phase gave no evidence for an additional gaze holding deficit. The VOR gain in the dark showed a slight decrease (pre: 0.96; post: 0.86) on average. The time constant of decay for slow phase nystagmus velocity after vestibular ramp stimulation was reduced, reflecting a 'velocity storage' deficit. After bicuculline injections nystagmus suppression in the light and during visual-vestibular conflict stimulation was generally well preserved. 4.) After muscimol injections horizontal gaze holding was severely affected. Each saccade was followed by an exponentially decreasing postsaccadic drift with a time constant as short as 250 ms (average 414 ms). The eyes always drifted towards a null-position, which generally did not coincide with the midposition of the eye. The null-position could move up to 35 deg to the contralateral or ipsilateral side. The highly distorted eye movements after muscimol injections prevented VOR-measurements based on eye velocity. Instead vestibular stimulation led to a shift of the null-position with an amplitude corresponding to a gain (eye position/stimulus position) of 0.17 (average) at 0.2 Hz (+/- 40 deg/s). Vertical eye movements did not show a major gaze holding deficit. 5.) From the experiments it can be concluded that the inhibitory transmitter GABA plays an important role for eye movement generation within the vestibular nuclei. Bicuculline induces mainly a vestibular imbalance with little evidence for a neural integrator deficit. In contrast unilateral muscimol injections lead to a complete, reversible loss of function for the common horizontal neural integrator, which converts eye velocity into eye position signals. The accompanying shift of the null-position reflects an additional vestibular imbalance.

Animals↗
PubMed1991

The effects of baclofen and cholinergic drugs on upbeat and downbeat nystagmus.

The GABAergic drug baclofen and the cholinergic drug physostigmine were administered to patients with upbeat and downbeat nystagmus. Baclofen (orally, 5 mg three times daily) reduced nystagmus slow phase velocity and distressing oscillopsia by 25-75% in four out of five patients (two upbeat nystagmus; two downbeat nystagmus). Physostigmine (1 mg single intravenous injection) increased nystagmus in five additional patients with downbeat (1) or positional downbeat nystagmus (4) for a duration of 15-20 minutes. The different interactions of baclofen and physostigmine on neurotransmission subserving vertical vestibulo-ocular reflex could account for these effects. The response to baclofen appears to be a GABA-B-ergic effect with augmentation of the physiological inhibitory influence of the vestibulo-cerebellum on the vestibular nuclei. Similarly baclofen has an inhibitory effect on the velocity storage mechanism. Cholinergic action may cause the increment of nystagmus by physostigmine.

Adult↗
PubMed1991

Fastigial nucleus activity in the alert monkey during slow eye and head movements.

1. Single units were recorded extracellularly from the fastigial nucleus of three macaque monkeys. Two untrained animals were subjected to whole-body yaw rotations in the light and dark and to full-field horizontal optokinetic stimuli provided by a drum with vertical stripes. The third also was subjected to sinusoidal yaw rotations but, in addition, was trained to follow a small spot, which moved in various ways relative to the animal, to reveal possible smooth pursuit and vestibular sensitivities. 2. On the basis of their responses to vestibular and optokinetic stimuli and their responses during smooth pursuit, fastigial neurons could be divided functionally into a rostral and a caudal group. 3. Most rostral neurons exhibited an increased firing for contralateral head rotations and ipsilateral optokinetic stimuli. A few had the opposite combination of directional preferences. The average firing rates increased monotonically both with contralateral head velocity and ipsilateral drum velocity and decreased monotonically for the oppositely directed movements. There was no change in firing rate for either spontaneous saccades or smooth pursuit of a small moving spot. 4. In contrast, neurons in the caudal fastigial nuclei not only have a robust vestibular sensitivity, but respond during smooth pursuit as well. Most discharge during contralateral head velocity and contralateral smooth pursuit so that they exhibit very little modulation during the vestibuloocular reflex (VOR) or when the rotating animal is fixating a target stationary in the world (SIW). The remaining neurons discharge during contralateral head rotations but ipsilateral eye rotations; these units exhibit their greatest modulation during the SIW condition. 5. Because they respond during quite different behavioral situations, it seems likely that rostral fastigial neurons are involved with descending control of the somatic musculature, whereas the caudal neurons are involved in oculomotor control. The sparse anatomic and lesion data that is available is consistent with this idea.

Animals↗
PubMed1989

Dissociated nystagmus as a common sign of ocular motor disorders in HIV-infected patients.

In order to determine if ocular motor disturbances due to brainstem and cerebellar dysfunction provide a frequent and early marker for HIV infection of the brain, neurological examination was performed in 133 HIV-infected persons who were consecutively admitted to our hospital. In 22 patients (17%) we found no other reason for cerebellar or pontomesencephalic signs than HIV encephalopathy. Ocular motor disorders accounted for the most frequent signs of cerebellar and pontomesencephalic dysfunction. Ocular motor disorders mainly consisted of dissociated nystagmus (n = 12), gaze-evoked nystagmus (n = 10) and impaired smooth pursuit (n = 6). Cerebellar ataxic gait and dysmetria were present in 3 patients. Since dissociated nystagmus was the primary ocular motor disorder, we assume that the medial longitudinal fasciculus may be a predilected circumscribed area for HIV infection of the brain. We suppose that cerebellar and pontomesencephalic disorders may be an early marker for HIV encephalopathy because they were the only neurological signs found in 12 patients.

AIDS Dementia Complex↗
PubMed1989

Ptosis and supranuclear downgaze paralysis.

A patient developed the unusual combination of a supranuclear downward gaze paralysis and bilateral ptosis. It was caused by a single midbrain glioma. Other ocular motor functions were intact. The neuropathologic examination showed a tumor growing mainly around the third ventricle and the aqueduct. The findings agree with recent experimental evidence that a network of neural elements involved in eyelid control lies in the supraoculomotor area immediately dorsal to the oculomotor nucleus.

Aged↗
PubMed1989

The role of the cerebellum in smooth pursuit eye movements and optokinetic nystagmus in primates.

Experimental evidence demonstrates that the primate cerebellum plays an essential role in the generation of smooth pursuit eye movements (SPEM). The same neural elements also take part in the generation of the 'direct' component of OKN, which is responsible for an initial jump in slow phase eye velocity during constant velocity stimulation and the optokinetic response above 0,05 Hz. In addition to the extensively studied floccular region, recent experiments also indicate a role of the mid-vermis (lobule VI and VII) in SPEM control. The 'indirect' or 'velocity storage' component of OKN produces more gradual changes in slow phase eye velocity, and basically depends only on brainstem mechanisms. It is, however, under the inhibitory control of the nodulus and ventral uvula. The loss of this control after lesions could explain disorders like periodic alternating nystagmus.

Animals↗
PubMed1988

Neuronal activity in the flocculus of the alert monkey during sinusoidal optokinetic stimulation.

1. Activity of single units was recorded in the flocculus of alert, behaving monkeys during sinusoidal optokinetic (0.02-5.0 Hz), constant velocity optokinetic, vestibular and visual-vestibular conflict stimulation. The maximal stimulus velocity for sinusoidal optokinetic stimulation at different frequencies was 40 deg/s or less (at frequencies above 1 Hz). For an amplitude series at 0.2 Hz, stimulus velocity was varied between +/- 10 to +/- 80 deg/s. In one trained monkey activity was also investigated during smooth pursuit eye movements and suppression of the vestibulo-ocular reflex by visual fixation (VOR-supp.). Only neurons which responded to 0.2 Hz (+/- 40 deg/s) optokinetic stimulation were included in the study. 2. The majority of neurons (44 out of 59) were type I Purkinje cells (PCs), which increased their simple spike activity during optokinetic cylinder rotation to the ipsilateral recording side. The responses during other, vestibular related, paradigms allowed all these neurons to be classified as so called 'gaze velocity' PCs. Three type II PCs were encountered, which responded similarly, but were only weakly modulated. 3. All type I PCs were modulated at frequencies of sinusoidal optokinetic stimulation between 0.05 and 2.5 Hz. PC's showed little or no modulation at 0.03 and 0.02 Hz. About half of the PC's still responded at 5.0 Hz. 4. Relative to eye velocity, the PC activity had a phase advance of about 30 deg between 0.1 and 2 Hz. It became larger at lower, and smaller at higher, frequencies. Eye velocity related sensitivity (imp/s/deg/s) was small at low stimulus frequencies and increased monotonically, on average from 0.16 at 0.02 Hz to 2.0 at 3.3 Hz. 5. Ten (out of 12) mossy fiber related input neurons were classified as visual neurons, since their activity could be related to the amount of retinal slip in all conditions. Neurons were clearly modulated at sinusoidal optokinetic stimulation up to 5 Hz. One input neuron, investigated during sinusoidal OKN, smooth pursuit eye movements, VOR and VOR-supp., behaved qualitatively like a 'gaze velocity' PC. The remaining input neuron encoded eye velocity at 0.2 Hz optokinetic, vestibular and visual-vestibular conflict stimulation. 6. The results show that during sinusoidal and constant velocity optokinetic stimulation 'gaze velocity' PC's do not encode eye velocity and/or eye acceleration. 7. The vestibular nuclei-flocculus complementary hypothesis (Waespe and Henn 1981) can explain PC responses to a large extent.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1988

Neuroanatomy of the oculomotor system. The reticular formation.

The afferent and efferent connections of specific subdivisions of the reticular formation involved in the control of gaze are reviewed. Three regions of the medial brainstem reticular formation: the paramedian pontine reticular formation (PPRF), the dorsomedial rostral medullary reticular formation and the rostral interstitial nucleus of the MLF (riMLF) have direct projections to the extraocular motor nuclei, and play a well-defined role in the generation of saccadic eye movements only. The interstitial nucleus of Cajal (iC) also has direct premotor control of vertical extraocular motoneurons and is probably involved in the maintenance of vertical eye position. Reticulospinal neurons, which modulate the activity of neck and postural musculature, originate from all these regions. The neuroanatomy of other cell groups associated with the reticular formation are also described: the central mesencephalic reticular formation (cMRF), the posterior commissure nuclear complex (nPC), nucleus reticularis tegmenti pontis (nrtp), nucleus intercalatus (nic), nucleus of Roller (Ro) and nucleus interfascicularis hypoglossi (ifh), nucleus supragenualis (sg) and finally the cell groups lying within the paramedian tracts (pmt) of the pons and medulla. These have diverse and generally less well understood roles in the control of gaze.

Afferent Pathways↗
PubMed1988

Present concepts of oculomotor organization.

An introduction to the oculomotor system, which should provide a framework for the 10 anatomical reviews in the following chapters, this chapter describes the characteristics of the 5 basic types of eye movement and outlines the structures that are involved in the generation of each. Some common eye movement deficits, and concepts such as 'the neural integrator' and the 'velocity storage mechanism', for which anatomical substrates are still sought, are introduced.

Animals↗
PubMed1987

Paroxysmal spontaneous nystagmus and vertigo evoked by lateral eye position.

Prolonged lateral eye position to the extreme left for 5 to 20 seconds, without vestibular stimulation, induced intense attacks of nystagmus and rotational vertigo lasting 50-90 seconds in a patient. During the attacks the nystagmus beat to the right and counterclockwise, while the patient could look freely around. Clinical data were suggestive of repeated strokes in the vertebrobasilar territory, mainly affecting the right dorsolateral medulla oblongata including the vestibular nuclei. A paroxysmal attack of nystagmus and vertigo evoked by voluntary lateral eye position is an unusual clinical finding. This is discussed in the light of multisensory integration within the vestibular system, which also includes eye position information.

Brain↗