Biomedical subjects
Publications and source records attributed to O Meienberg.
The essential clinical features of eight cases of carotidynia are outlined. As little is known about treatment, the effectiveness was evaluated of drugs used in some specific forms of vascular headache with similar pain characteristics. Indomethacin or flurbiprofen were shown to be potent drugs in the treatment of carotidynia.
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We used two simple bedside tests of saccadic eye movements between two fingers as targets to study 23 hemianopic patients. With these tests, we could provide confirmation or, in malingering, exclusion of a hemianopia. Furthermore, the amount of ocular motor compensation for the loss of one half of the visual field could be estimated, and visual hemineglect was demonstrated. The findings in some cases with chronic homonymous hemianopia suggested "extrastriate vision."
Three cases of painful ophthalmoplegia with acute onset due to an unruptured aneurysm of the intracavernous portion of the internal carotid artery are reported. The possible pathogenetic mechanisms responsible for this unusual mode of clinical manifestation are discussed and the neurovascular relationships of the cavernous sinus are analyzed in respect of ischemic versus compressive damage to the intracavernous neural structures.
Paralytic disease was observed in a 68-year-old man with non-Hodgkin lymphoma following administration of oral live poliomyelitis vaccine. The vaccine had been administered during a vaccination campaign just before the patient underwent chemotherapy with cyclophosphamide. The dangers intrinsic in vaccination campaigns, i.e. of failure to individualize risks and benefit of the vaccination, are discussed.
Pattern-evoked and flash-evoked responses were recorded from four patients with acute blindness due to occipital ischaemia. No responses could be obtained with pattern stimulation. Flash stimulation, however, yielded well-reproducible potentials in all four cases in spite of practically complete visual loss. In one patient vision recovered completely while the three others showed poor or minimal recovery in restricted visual field areas only. It is concluded that the flash method is not appropriate for differentiation of occipital blindness from psychogenic visual disorders. Furthermore, preserved flash-evoked potentials in the acute stage of occipital blindness cannot be taken as a reliable prognostic sign for visual recovery, as has been postulated by others. A possible extrastriate origin of these flash responses is discussed in view of recent theories on a second visual system.
Quantitative studies of latencies and trajectories of eye-head movements during visual search and fixation in patients with occipital hemianopia show that (1) the latency of head movement is bilaterally increased, with significantly greater delays in movements toward the blind side; (2) the compensatory eye movements (CEMs) during head movements toward the blind side have increased velocity; (3) these CEMs entail a non-vestibular anticipatory component; and (4) head movements toward the blind side are comprised of multiple steps similar to staircase eye movements documented in previous studies. Hemianopic patients seemingly simplify search and fixation strategies by minimizing or entirely eliminating head movements and relying on eye movements instead.
Electromyograms, representing samples of neurological control signals, can be used to predict head rotation that can be either time optimal or non-time optimal, depending upon a given subject's intent. Kinematic factors such as operating levels in terms of horizontal and vertical position of the head from which horizontal rotations are made, importantly influence the tonic and phasic aspects of the EMG signal. Pairs of head-rotating muscles, splenius and sternocleidomastoideus muscles, demonstrate reciprocal innervation, particularly for time optimal head rotations. Head rotations of the same amplitude but different velocities correlate with pulse height and pulse width of envelopes of the rectified EMG. Rise of the agonistic EMG correlates in detail with rise of the acceleration transient for a given fast or slow head rotation. Our data demonstrate both the optimal control of details of head movements and the influence of the stretch reflex that strongly relates to initial head position and the velocity of the movements around the primary position. The results support the idea of higher level programmed control of head rotation in human subjects.
Infrared oculographic recordings from three patients with hemianopia due to an occipital lesion showed that these patients employed a consistent set of (presumably unconscious) compensatory strategies to find and fixate objects. For targets in the blind hemifield, patients at first used a staircase strategy consisting of a series of stepwise saccadic search movements. This is safe but slow. When retested later, one patient had adopted a more efficient strategy employing one large saccade calculated to overshoot the target. Other strategies for finding targets in the blind hemifield were employed in response to specific situations presented by our experiments: a predictive strategy using past experience to anticipate where the target would be found, and special strategies for recovering a lost target and for awaiting the reappearance of the target. To fixate targets in the seeing hemifield, our subjects undershot the target to prevent losing it in the blind hemifield, then held it off-fovea on the seeing side of the macula.
Flash-evoked visual responses of two patients from a family with congenital nystagmus showed marked asymmetry between the recordings from the right and left occipital regions in response to monocular stimulation. The asymmetries were crossed, ie, the degree of abnormality inverted when the stimulus changed from one eye to the other. Stimulation of both eyes together evoked symmetrical responses from the two hemispheres. The patients had no signs of abnormality involving the visual pathways. The changes in the visually evoked responses were similar to those found in human albinos, who are known to have abnormal retinostriate projections and also nystagmus.
Oculographic recordings of refixation saccades and pursuit movements during nystagmus-free intervals in a patient with periodic alternating nystagmus revealed cerebellar ocular motor disturbances that support the hypothesis that cerebellar disinhibition plays a role in the pathogenesis of periodic alternating nystagmus.
The essential disturbance in five patients with vertical nystagmus was an inability to generate smooth pursuit eye movements in the direction of the quick phase of their nystagmus. As the cause of this behavior, the authors suggest an asymmetric impairment of the visual input to the pursuit system. This defect causes a 'directional preponderance' of the pursuit system detectable as a continuous drift off target. The drift is interrupted by refoveating saccades, thus resulting in a vertical nystagmus.
Upper lid and vertical eye movements are usually preserved in patients with the "locked-in" syndrome, a condition manifested by anarthria, spastic quadriparesis, and intact mental function, and caused by lesions in the ventral portion of the pons. We describe a presumed mesencephalic "locked-in" syndrome in a patient who had total bilateral ptosis at the onset of his disease and later on experienced complete bilateral oculomotor nerve paralysis.
Using a commercially available television set for stimulation of 78 healthy subjects, the upper limit of normal for the latency of the major positive wave (p 100) of checkerboard pattern reversal evoked potentials is practically the same as that obtained by employing slide projector combined with a rotating mirror. Potentials evoked by a small pattern, for purely foveal stimulation, were often difficult to evaluate exactly. Fixation of a large pattern at the upper border of the stimulus field brought no advantages as compared to the usual fixation in the center. Continuous prolonged recordings, with successive averaging of 64 pattern reversals, confirmed statements that only the major positive wave and its latency are constantly reproducible without being influenced by fatigue or inattention. Repeated examinations in the same subjects at intervals of 2 weeks showed a considerable spread of the latencies from one session to the other but the absolute values always ranged within the normal. More or less large latency differences (up to 12ms with large pattern stimulation) were found in every subject at least once. A longer latency found at a control examination, or a newly appearing latency difference, therefore do not prove a fresh optic nerve lesion as long as the absolute values are still within the limits of normal. From repeated examinations it could also be seen that foveal stimulation with a small pattern is not suitable for routine examinations because of high variation in the results.
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In a case of left inferior rectus paresis, it is demonstrated that the lesion must be prenuclear. On downward gaze, the left eye, although it reached the required target with a rapid saccade, drifted back towards the midline immediately afterwards. During the drift, several corrective saccades appeared. A dissociated "gaze paretic" nystagmus resulted. Synchronously, the right eye showed an incyclorotary nystagmus. We suspect a lesion of "tonic" fibers supplying the nuclear region of the left inferior rectus and the right superior oblique muscle.
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Continuous myoclonus in a localised area of the body was observed in three patients. In two cases the myocloni sometimes developed into motor Jacksonian convulsions. All three patients had neurological signs on the same side as their continuous twitching indicating a lesion of the contralateral hemisphere. The surface EEG did not show changes which could be directly correlated with continuous convulsions in any of the cases. The cause was found to be a malformation of the hemisphere in one case, a recent encephalomalacia in the second and a severe hyperosomolar diabetic electrolyte imbalance in the third. Epilepsia partialis continua Kozevnikov differs from motor Jacksonian epilepsy in the continuous non-attack character and the absence of a "march of convulsions". Pathophysiologically they are both forms of focal cortical status epilepticus.