[Retinal information transmission by X-cells: arguments for color perimetry?].
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Biomedical subjects
Publications and source records attributed to T Brandt.
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The variety of drug induced patterns of pathological eye movements is reviewed with emphasis on hydantoins, barbiturates, carbamazepine, benzodiazepines, amitriptyline and alcohol. These different substances may be analogous or distinct in their site of action within the labyrinths, brain stem and cerebellum. Ocular oscillations are described in correlation to drug uptake or serum levels such as positional, downbeat, gaze evoked, periodic alternating nystagmus as well as saccadic pursuit, slowing down of saccades, alteration of VOR gain or suppression by fixation, internuclear and complete ophthalmoplegia. Most of the ocular motor disturbances are possibly due to a pharmacologically induced transient dysfunction of the vestibulo-cerebellar flocculus loop.
A clinical bedside test for oscillopsia is described for patients suffering from an acute deficiency of compensatory eye movements due either to inappropriate pursuit eye movements or a defective vestibulo-ocular reflex (VOR). This test involves quantitative measurement of the amplitude of apparent image motion (oscillopsia) during head oscillations with frequencies of 1 or 2 Hz, +/- 20 deg amplitude. It was found that normals show no oscillopsia at 1 Hz whereas patients with acute disorders do. In subacute diseases of eye-head co-ordination, however, recordings of head and eye movements revealed a dissociation between net retinal slip and oscillopsia, with the magnitude of the latter being appreciably smaller than the former. This was interpreted as indicating a central suppression mechanism initiated by the acute eye movement deficiency. The results are discussed in terms of an inhibitory interaction between self and object motion perception which produces elevated thresholds for the detection of image motion.
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The differential effects of vision on motion sickness in cars were tested under real road conditions using linear accelerations, in order to confirm earlier laboratory results on visual modulation of vestibular nausea induced by angular accelerations of the body. The 18 voluntary subjects were exposed to repetitive braking maneuvers (linear accelerations: 0.1-1.2 g) on a highway. The simultaneous visual stimulus conditions for the 3 separate days were: I) eyes open, visual control of car motion; II) eyes closed; III) eyes open, artificial stationary visual field (reading). The severity of motion sickness (magnitude estimation 1-10) was a function of the visual stimulus condition with significant differences among these conditions: I) moderate nausea (less than 1) with adequate visual motion perception; II) medium nausea (approximately equal to 2) with eyes closed and somatosensory-vestibular excitation only; III) strong nausea (greater than 5) with conflicting sensory input, when vestibular acceleration is in disagreement with the visual information of no movement. Providing ample peripheral vision of the relatively moving surround is the best strategy to alleviate car sickness.
Vestibular Coriolis- and Purkinje-effect, which are known to induce vertigo, were investigated with respect to body posture. One aim of this investigation was to provide information concerning clinical vertigo symptoms. Standing on a rotatable stabilometer, 25 healthy subjects had to execute lateral head tilts during (Coriolis), or after (Purkinje), rotation varied with different constant velocities. The conditions were varied with respect to eyes open vs. eyes closed, head upright vs. head tilt to the right and left, direction of rotation clockwise vs. counterclockwise, active vs. passive head tilt, and active vs. passive body rotation. The results supported the expectation that destabilization was less severe with open than with closed eyes and that sway amplitudes were increased after head tilt as well as with a higher velocity of rotation. The direction of the induced body shift was, as expected, opposite to the initial vestibular stimulus. A forward shift after stop without head tilt was frequently found, being independent of the previous direction of rotation. Reported perceptions coincided mostly not with the initial vestibular signal but rather with the actual movement of compensation. Active instead of passive movements did not produce clearly different effects. The Purkinje experiment appeared to be equivalent to the situation when a patient with an acute lesion of a horizontal vestibular canal bends his head. The stabilogram under this condition may allow a prediction of the side of the lesion.
Vertigo occurs either with motion stimulation which causes an intersensory mismatch or by a dysfunction of one of the stabilizing sensory systems, representing either a "physiological" or a "pathological" vertigo syndrome, respectively. This review emphasizes the differential effects of physical maneuvers and drugs and surgery in the prevention or treatment of motion sickness, height vertigo, head extension vertigo, as well as peripheral labyrinthine lesions, paroxysmal positional vertigo, Menière's syndrome, vertiginous epilepsy and phobic vertigo.
Head extension may cause a physiological vertigo and postural imbalance separate and distinct from basilar insufficiency. This physiological imbalance mainly is due to a vestibular sensory deficiency when the utricular otoliths are beyond their working range because of the change in head position. Since the intact visual and somatosensory control hope widely compensate for the vestibular deficiency, head-extension vertigo is of particular concern only in certain stimulus situations or diseases in which the stabilizing input from the eyes or joint receptors is reduced. Balance training on foam rubber with head extension and closed eyes improved postural-sway activity up to 50% within five days. A daily short-term training effect and a long-term training effect together form a typical exponential sawtooth curve of postural stability over time. After termination of training, learned balance skill exponentially returns to the pretraining values within weeks. The percentage of improvement through training depends on the amount of initial instability. Clinicians should treat ataxia by exposing patients to stimulus situations producing increasing body instability in order to activate sensorimotor rearrangement.
We treated 67 patients with the symptoms of benign paroxysmal positional vertigo (BPPV) by challenging them with the precipitating head positions on a repeated and serial basis. Sixty-six of the patients experienced complete relief of the vertigo within three to 14 days; in two patients, the vertigo recurred but responded to a second course of therapy. The one patient whose condition did not respond was found to have a perilymphatic fistula that mimicked BPPV. The presumed mechanism for this therapy is the loosening and ultimate dispersion of degenerated otolithic particles from the cupula of the posterior semicircular canal.
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A theory is presented supporting a geometrical explanation for physiological height vertigo being a distance vertigo through visual destabilization of postural balance when the distance between the eyes and visible stationary contrasts becomes critically large. Physiological and posturographic data obtained under natural height vertigo conditions are consistent with this hypothesis.
A critical literature review is presented on the basis of our own clinical experiences with complications and distressing side effects of the lumbar Dimer-X myelography. Severe Complications such as spinal and conuscauda-symptoms, epileptic seizures, amnestic episodes and late palsies of the Abducens nerve in literature range between 1 and 9%. Unspecific side effects which cannot clearly be differentiated from pure post-lumbal puncture complaints are reported to occur in up to 28%. The probably underlying pathogenetic mechanisms are discussed together with former animal experiments which revealed a local toxity of the contrast medium at the central nervous tissue and the surrounding membranes.
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A compelling illusion of body rotation and nystagmus can be induced when the horizontally extended arm of a stationary subject is passively rotated about a vertical axis in the shoulder joint. Lateral nystagmus with the fast phase beating in the opposite direction to the arm movement was found consistently; the mean slow phase velocity increased with increasing actual arm velocity and reached about 15 degrees/sec; the mean position of the eyes was deviated towards the fast phase as in optokinetic nystagmus, and the nystagmus continued after the cessation of stimulation (arthrokinetic after-nystagmus). The existence of an arthrokinetic circularvection and nystagmus indicates a convergence of vestibular and somatosensory afferents from joint receptors. It is concluded that information about joint movements plays an important role within the multisensory processes of self-motion perception.