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Biomedical subjects

M Fetter

Publications and source records attributed to M Fetter.

72 records · Page 4Linked to original sources
PubMed1993

Compartmentalized cerebellar functions upon the stabilization of body posture.

This paper reviews the features and topodiagnostical meaning of pathological body posture in cerebellar disorders and presents knowledge as to the physiology and pathophysiology of postural disturbances attributed to the cerebellum. Lesions of the spinocerebellar (upper vermal and intermediate) part of the anterior lobe lead to spontaneous anterior-posterior body sway, with a frequency of about 3 Hz with mild or absent ataxia of the upper limbs, but prominent ataxia of the lower limbs. The tremor is provoked by eye closure and by body displacement. Increased gain and poor cerebellar control of the duration and gain of stabilizing reflexes may be the mechanisms of this oscillation. Lesions of the lower (vestibulocerebellar) vermis cause postural ataxia of the head and trunk while sitting, standing, and walking. Postural ataxia is omnidirectional, sometimes of excessive amplitude and contains frequency components below 1 Hz. Dysmetria of the upper and lower limbs is not prominent. Visual stabilization is less than in the other groups of cerebellar patients. Lesions of the cerebellar hemispheres alone, do not cause an increase of postural sway. Lesions of spinocerebellar afferents (Friedreich's disease) lead to a low frequency large amplitude lateral sway with the most of its power below 1.1 Hz. Visual stabilization is preserved. Latencies of early and late EMG responses to sudden displacements are normal in patients with cerebellar disorders. The cerebellum is, therefore, unlikely to be the primary generator of these reflexive responses. On the other hand, the temporal composition of the orderly time sequence of a complex motor program--be it a voluntary act or its postural balancing--is deranged in cerebellar lesions. It is hypothesized that the cerebellum helps to coordinate the timing not only within but also between the single components involved in each subunit of a complex movement in three-dimensional space and that is scales the size and duration of each muscular action. The cerebellum possibly specifies the cortical movement command and sends it back to the motor cortex. The basic structure of a motor program, however, does not seem to be generated within the cerebellum.

Cerebellar Diseases↗
PubMed1992

The influence of head position and head reorientation on the axis of eye rotation and the vestibular time constant during postrotatory nystagmus.

Reorienting the head with respect to gravity during the postrotatory period alters the time course of postrotatory nystagmus (PRN), hastening its decline and thereby reducing the calculated vestibular time constant. One explanation for this phenomenon is that the head reorientation results in a corresponding reorientation of the axis of eye rotation with respect to head coordinates. This possibility was investigated in 10 human subjects whose eye movements were monitored with a three-dimensional magnetic field - search - coil technique using a variety of head reorientation paradigms in a randomized order during PRN following the termination of a 90 degrees/s rotation about earth vertical. Average eye velocities were calculated over two time intervals: from 1 s to 2 s and from 7 s to 8 s after cessation of head rotation. The time constant was estimated as one third of the duration of PRN. For most conditions, a reorientation of the head with respect to gravity 2 s after the rotation had stopped did not significantly alter the direction of the eye velocity vector of PRN with respect to head coordinates. This strongly indicates that, in humans, PRN is mainly stabilized in head coordinates and not in space coordinates, even if the otolith input changes. This finding invalidates the notion that the shortening of PRN due to reorientation of the head could be due to a change of the eye velocity vector towards a direction (torsion), which is not detectable with the eye recording methods (electrooculography) used in earlier studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Three-dimensional properties of human pursuit eye movements.

For any given location and velocity of a point target, there are infinitely many different eye velocities that the pursuit system could use to track the target perfectly. Three-dimensional recordings of eye position and velocity in 8 normal human subjects showed that the system chooses the unique tracking velocity that keeps eye position vectors (a particular mathematical representation of three-dimensional eye orientation) confined to a single plane, i.e. pursuit obeys Listing's law. One advantage of this strategy over other possible ones, such as choosing the smallest eye velocity compatible with perfect tracking, is that it permits continuous pursuit without accumulation of ocular torsion. For nonpoint targets, there is at most one eye velocity compatible with perfect retinal image stabilisation, and the optimal velocity may not fit Listing's law; we observed small but consistent deviations from the law during pursuit of rotating line targets.

Adult↗
PubMed1990

Aberrant regeneration in a case of syringobulbia: selective co-activation of abducens and facial nerves during saccades.

A patient suffering from syringobulbia and syringomyelia exhibited a phasic contraction of the ipsilateral facial muscles, mainly the levator labii, whenever he looked to the left or right. Facial muscle twitches occurred exclusively with saccades. The selective co-activation of abducens and facial nerves is interpreted as the result of bilateral misrouting of regenerating neurons from the parapontine reticular formation to the facial nerve in the tegmentum pontis.

Abducens Nerve↗
PubMed1990

Stimulus characteristics influence the gain of smooth pursuit eye movements in normal subjects.

Impaired smooth pursuit eye movements are commonly believed to indicate a lesion of the central nervous system. Smooth pursuit performance, however, is strongly dependent on non-specific variables like cooperation, arousal and attentiveness. Therefore, disturbed smooth pursuit can be attributed either to lesions of the smooth pursuit system per se, or to the influence of non-controlled variables (non-structural disturbances). This renders the evaluation of smooth pursuit uncertain. In the present study we attempted to design a stimulus that yields smooth pursuit eye movements, which are not influenced by uncontrolled variations of state and input, for a better separation of structural lesions of the pursuit system and the effect of nonspecific variables. Our results suggest that a stimulus that leads to a centrally generated representation (percept) of motion is most suitable to elicit high gains of smooth pursuit (sigma pursuit), but only if attentiveness is optimal. Beta-motion (motion elicited by discrete steps of the target) or real target motion are capable to render the smooth pursuit performance optimal, even with low attentiveness, when the fixation point and its wider surroundings or enough discrete points in the neighbourhood move in the same direction in space.

Adolescent↗
PubMed1988

Recovery from unilateral labyrinthectomy in rhesus monkey.

1. We recorded eye movements in six rhesus monkeys before and after unilateral labyrinthectomy and quantified the compensation for both the static and the dynamic disturbances of the vestibuloocular reflex (VOR). 2. When first recorded after labyrinthectomy (18-20 h postlesion), all animals had a spontaneous nystagmus with mean slow-phase velocities ranging from 24 to 54 degrees/s measured in darkness and 0-4 degrees/s measured in the light. The level of nystagmus diminished quickly, and by postoperative day 25 mean values ranged from 4 to 22 degrees/s, measured in darkness. The waveform of individual slow phases was variable, but in the first postoperative week its trajectory usually showed an increasing, or an increasing then decreasing, velocity. This finding indicates that peripheral vestibular lesions can alter the function of the ocular motor eye-position integrator. 3. The VOR gain (eye velocity/head velocity, corrected for spontaneous nystagmus) during rotations (30-300 degrees/s) in the dark was diminished from nearly 1.0 preoperatively to approximately 0.5 when first measured after labyrinthectomy, except for rotations toward the lesioned side at high speeds for which the gain was even lower. Within the first few postoperative days, for rotations toward the intact side, the VOR gain increased rapidly, to approximately 0.8. For rotations toward the lesioned side similar behavior was noted for stimuli of 30-60 degrees/s, but at higher velocities compensation proceeded more slowly. By 3 mo postoperatively gains had reached values ranging from 0.77 to 1.03 for rotations toward the intact side and from 0.61 to 0.98 for rotations toward the lesioned side. Values were higher for lower-velocity stimuli. 4. Caloric testing with ice water in the unoperated ear elicited nystagmus with a mean value of maximum slow-phase velocity of 129 degrees/s preoperatively and 195 degrees/s 3 mo postoperatively. There was no caloric response on the lesioned side. From the increase in caloric responses from the intact ear we infer considerable restoration of spontaneous activity of vestibular neurons on the deafferented side. 5. The time constant of the VOR was a function of stimulus speed preoperatively with a maximum mean value of 35 s for a 60 degrees/s stimulus. After labyrinthectomy the VOR time constant was low (6.0-9.1 s) at all speeds. Subsequently, in three animals only, there was a small increase (2-3 s) in VOR time constant during the 3-mo period following labyrinthectomy. These results indicate that labyrinthectomy profoundly and persistently impairs the action of the vestibular velocity-storage mechanism.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Physiological↗
PubMed1988

Effect of lack of vision and of occipital lobectomy upon recovery from unilateral labyrinthectomy in rhesus monkey.

1. We investigated the influence of visual experience upon vestibular compensation in monkeys. Two paradigms were used to elicit vestibular adaptation: artificially imposed motion of images upon the retina during head rotation and unilateral labyrinthectomy. Two groups of animals were investigated: monkeys that underwent a bilateral occipital lobectomy and intact monkeys without a cortical lesion. Occipital lobectomy alone caused only a minor change in the vestibuloocular reflex (VOR); the gain (eye vel/head vel) decreased slightly (10-15%) for high speeds of rotation (180-300 degrees/s). 2. In response to a 4-h period of continuous oscillation of the head (0.25 Hz, 30 degrees/s) with the visual scene made to move in phase with the head (X0 viewing) or out of phase with the head (X2 viewing), intact monkeys showed an average 40% decrease or increase, respectively, of the VOR gain measured in darkness. After occipital lobectomy this adaptive capability was diminished, primarily for increasing the VOR gain after X2 viewing (42% preop to 13% postop). 3. Unilateral labyrinthectomy in either occipital-lobectomized or in otherwise intact monkeys led to a static imbalance with initial (18- to 20-h postlesion) values of spontaneous nystagmus of 22-62 degrees/s measured in darkness and to a dynamic disturbance with an approximately 50% decrease of VOR gain. Compensation for both abnormalities was studied in three groups of animals: previously occipital-lobectomized monkeys kept in the light after labyrinthectomy, intact monkeys kept in the light after labyrinthectomy, and intact monkeys kept in the dark for 4 days after labyrinthectomy and then exposed to light. Spontaneous nystagmus disappeared at the same rate in each group of animals. VOR gain increased in the intact monkeys kept in the light after labyrinthectomy but not in the intact monkeys kept in the dark after labyrinthectomy until they were exposed to light. The occipital-lobectomized monkeys showed some recovery of VOR gain (approximately 25-40%), but only at low speeds of rotation (30-60 degrees/s). Occipital lobectomy performed in monkeys after they had already compensated for a labyrinthectomy caused the VOR gain to drop to values approximately 0.5 but without any recurrence of spontaneous nystagmus. 4. Our results indicate that visual experience after labyrinthectomy is essential for recovery of VOR gain but not for resolution of spontaneous nystagmus. Furthermore, geniculostriate pathways play a major role in providing information about high velocities of retinal image motion that is necessary for the acquisition of VOR gain adaptation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Physiological↗
PubMed1986

Influence of eye and head position on the vestibulo-ocular reflex.

For the vestibulo-ocular reflex (VOR) to function properly, namely to ensure a stable retinal image under all circumstances, it should be able to take into account varying eye positions in the orbit and varying orientations of the head with respect to the axis about which it is rotating. We tested this capability by quantifying the gain and the time constant of the horizontal component of the VOR during rotation about an earth vertical axis when the line of sight (optical axis) was moved out of the plane of head rotation--either by rotating the eyes up or down in the orbit or by pitching the head up or down with respect to earth-horizontal. In either case the gain of the horizontal component of the VOR was attenuated precisely by the cosine of the angle made between the optical axis and the plane of head rotation. Furthermore, if the head was pitched up or down but the eye rotated oppositely in the orbit so as to keep the line of sight in the plane of head rotation the gain of the horizontal component of the VOR was the same value as with the head and eyes both straight ahead. In contrast, the time constant of the VOR varied only as a function of the orientation of the head and not as a function of eye position in the orbit. During rotation about an earth vertical axis, the time constant was longest (about 18 s) when the head was pitched forward to place the lateral canals near earth-horizontal and shortest (about 11 s) when the head was pitched backward to place the vertical canals near earth-horizontal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Head-shaking nystagmus in patients with unilateral peripheral vestibular lesions.

In certain patients with peripheral or central vestibular lesions, a transient nystagmus appears after shaking the head rapidly for 10 to 20 cycles. We recorded such a "head-shaking nystagmus" using the scleral eye coil in six subjects with unilateral peripheral vestibular lesions. Horizontal head shaking elicited horizontal nystagmus with slow phases that were initially directed toward the side of the lesion and upward. All subjects showed a prolonged, lower-amplitude reversal phase after the initial response following horizontal head shaking. The main features of these results can be explained by an analytic model that incorporates a central velocity-storage mechanism that perseverates vestibular inputs, Ewald's second law, and adaptation of primary vestibular afferent activity.

Adaptation, Physiological↗
PubMedDate not supplied

Cerebral vein thrombosis in a case with thromboangiitis obliterans.

Thromboangiitis obliterans is a chronic inflammatory vessel disease that involves predominantly the small and medium-sized arteries and veins of the distal extremities. Appearance and cessation of symptoms are closely related to patterns of tobacco consumption. That cerebral arteries can also be involved is shown by reports of rare cases in which cerebral artery occlusion led to infarction. We report on a 28-year-old man with thromboangiitis obliterans who developed extensive cerebral vein thrombosis after a single episode of cigarette smoking following several years of nonsmoking. Despite extensive evaluation, no other known cause or predisposition of cerebral vein thrombosis could be found. This case suggests that cerebral veins can be involved in thromboangiitis obliterans and patients with thromboangiitis obliterans might be at risk for cerebral vein thrombosis.

Adult↗
PubMedDate not supplied

The clinical significance of head-shaking nystagmus in the dizzy patient.

The clinical significance of horizontal head-shaking nystagmus (HSN) was evaluated in 85 patients who complained of dizziness and vertigo. This was done by comparison of the horizontal head-shaking test with routine rotatory and caloric vestibular testing. We found that HSN evoked by horizontal head-shaking is a highly sensitive way to detect unilateral vestibular hypofunction. Except in patients with additional central vestibular imbalance or in patients with Meniere's disease, the direction of horizontal HSN is highly significant in indicating the side of the lesion, with the fast phase beating toward the intact side. However, horizontal HSN is not specific in distinguishing peripheral hypofunction from more central vestibular imbalances. Peripheral vestibular hypofunction as well as a central asymmetry of the vestibular velocity storage mechanism can each separately or in combination produce horizontal HSN. Thus, while the head-shaking manoeuvre is an excellent bedside-test to detect unilateral vestibular hypofunction, further rotatory and caloric testing is still necessary to clarify the patient's condition.

Adult↗
PubMedDate not supplied

Head-shaking nystagmus during vestibular compensation in humans and rhesus monkeys.

Nystagmus evoked after rapid horizontal head-shaking is believed to be a sensitive indication of the existence and location of a unilateral vestibular lesion. Its origin is the directional asymmetry in vestibular responses of the healthy labyrinth (Ewald's second law). For nystagmus to appear after the head has stopped moving, however, the directionally asymmetric responses must have been stored during the head-shaking to be discharged afterwards. Our results confirm the notion that head-shaking nystagmus is most likely generated by a directional preponderance in vestibular responses but only in combination with a functioning central velocity-storage mechanism. If velocity-storage is lost completely, as may occur during the acute phase of a unilateral peripheral vestibular lesion, even a large vestibular preponderance does not lead to head-shaking nystagmus. Thus, to interpret the results of the head-shaking test the condition of the velocity-storage mechanism must be taken into account.

Adolescent↗
PubMedDate not supplied

Adaptive mechanisms of VOR compensation after unilateral peripheral vestibular lesions in humans.

To further elucidate possible central plastic adaptive processes during the recovery from a unilateral peripheral vestibular lesion, we investigated vestibular functions in humans over a period of 2 months after an acute unilateral labyrinthine lesion. A unilateral peripheral vestibular lesion creates both a tonic imbalance that causes spontaneous nystagmus and a decrease and directional asymmetry of dynamic vestibular responses. We establish that the tonic imbalance expressed by the spontaneous nystagmus rapidly decreased (similar to other species), whether the lesion remained complete or not. This rebalancing, in the case of complete lesions, is at least partly due to restoration of central vestibular tone on the lesioned side. This restoration of tone also explains, in the case of a complete lesion, the recovery of dynamic vestibular responses for high-velocity inhibitory stimulation of the remaining labyrinth. A clear recovery of the dynamic response for excitatory stimulation of the remaining labyrinth cannot be proven, as has been shown in monkeys during the first 4 days after a unilateral vestibular lesion. This is probably due to the fact that in our patients the first recording could not be performed before day 3 after the onset of symptoms. Therefore, any fast dynamic recovery may have been missed.

Adaptation, Physiological↗
PubMedDate not supplied

Recovery of postural control after an acute unilateral vestibular lesion in humans.

Postural control during stance was investigated using the EQUITEST system in 10 patients during recovery after an acute unilateral vestibular lesion and was compared to the time course of recovery of the static and dynamic vestibulo-ocular imbalance. During the acute phase the patients showed a characteristic pattern with normal upright stance as long as at least one accurate sensory input (visual or somatosensory) was provided and severe postural disturbances when they had to rely primarily on vestibular afferences. Both static vestibulo-ocular and vestibulo-spinal balance recovered very fast, showing basically normal results on postural testing within about 2 weeks after the lesion. Thereafter, no pathological pattern was detectable during postural testing even in patients with persistent complete unilateral vestibular lesions. Reflexive postural responses to unexpected rapid displacements of the support surface seemed not to be influenced by vestibular imbalance even in the acute phase of the lesion.

Acute Disease↗
PubMedDate not supplied

Effects of full-field visual input on the three-dimensional properties of the human vestibuloocular reflex.

The three-dimensional (3-D) properties if the vestibuloocular reflex (VOR) were studied in six normal human subjects during passive whole-body rotations in darkness and with full-field visual input in light. Subjects were asked to fixate a point target stationary in space straight ahead or to imagine such a target in darkness. Using a 3-D rotating chair, subjects were rotated sinusoidally (frequency .3 Hz, maximum speed 37.5 degrees/s) about an earth-vertical axis for horizontal stimulation and about an earth-horizontal axis for vertical and torsional stimulation. The subject faced forward for vertical stimulation, 90 degrees to the side for torsional stimulation, or 15 degrees to the right or left side for combined vertical and torsional stimulation. Left eye position was measured using 3-D search coils. The VOR response was quantified using the 3-D analogue of gain, a 3 x 3 matrix where each element describes the dependence of one component--torsional, vertical, or horizontal--of eye velocity on one component of head velocity. Average gain matrices were calculated for three cycles of rotation (10 s). Major findings were: (1) Gain values for the VOR were higher in light than in darkness for all directions. In light, vertical and horizontal responses were fully compensatory in both magnitude and direction, whereas the torsional responses were still weak. (2) Intersubject variability, large in the dark, was very small in the light for the vertical and horizontal responses but still considerable for the torsional.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗