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Biomedical subjects

G M Halmagyi

Publications and source records attributed to G M Halmagyi.

At least 19 recordsLinked to original sources
PubMed1992

Behavioural and neural correlates of vestibular compensation.

Sudden complete loss of input from one labyrinth results in a massive change in behaviour. A vigorous horizontal ocular nystagmus occurs together with postural changes. These dramatic changes are short-lived and within about a week they have almost disappeared. This very rapid recovery has been the basis for the postulation that vestibular compensation is a textbook model for the study of neural plasticity in the central nervous system. Whilst the behavioural recovery is dramatic, quantitative testing reveals the loss and the permanent asymmetry of the system (Table 1). Recordings from single neurones show that many neurones in the ipsilesional VN are silenced by the unilateral loss, but as they start to fire again, so the spontaneous nystagmus declines. The major question which is still unanswered is the cause of the return of the firing of neurones in the ipsilesional VN. The answer may be found by studies of the neurochemistry of the VN using brain slice preparations. This review shows some of the errors which have been made by attempting to infer purely vestibular function from measurements of eye movements when other sources of ocular motor control may operate.

Animals↗
PubMed1991

Human ocular torsional position before and after unilateral vestibular neurectomy.

The static ocular torsional position of both eyes of 23 patients was measured by means of fundus photographs one day before and one week after unilateral vestibular neurectomy for the treatment of acoustic neuroma, Ménière's disease or paroxysmal vertigo. The results showed that in all patients the vestibular neurectomy caused both eyes to tort (i.e. to roll around the visual axis) toward the side of the neurectomy when measured one week after operation. The extent of this torsion was an average of 9.5 degrees one week after operation and there was no statistically significant difference in the average magnitude of the torsion in the two eyes. In 8 of these patients, additional measurements were made at intervals up to one year after operation and it was found that in these patients there is a significant reduction in torsion over time from an average of 10.2 degrees one week after operation to an average of 2.8 degrees by 16 weeks after operation. The change in torsional eye position following the neurectomy was accompanied by a change in the perceived visual orientation of a small (9.5 degrees visual angle) illuminated horizontal line at a straight ahead eye level position in an otherwise completely darkened room. One week after operation when asked to adjust the line to the perceived gravitational horizontal by rotating it in roll (i.e. around an X axis), patients who had had a right vestibular neurectomy consistently set the line so that the right side of the line (from the patient's point of view) was below the true gravitational horizontal. Similarly patients after a left neurectomy consistently set the line so that the left side of the line was below the true gravitational horizontal. There is a high correlation (r = 0.95) between the direction and magnitude of the change in torsional eye position and the direction and magnitude of the change in the perceived visual horizontal one week after operation.(ABSTRACT TRUNCATED AT 250 WORDS)

Eye Movements↗
PubMed1991

The acute effects of unilateral vestibular neurectomy on sensory and motor tests of human otolithic function.

Patients were tested 1 day before and 1 week after therapeutic unilateral vestibular neurectomy (UVN) on vestibular tests which are likely determined primarily by otolithic function. UVN causes a maintained ocular torsion: fundus photographs showed that both eyes of every patients were rolled such that the upper pole of both eyes was tonically deviated towards the operated side, and there is a corresponding change in the perceived gravitational horizontal: patients set a small bar of LEDs bar down on the same side as their operation. One week after UVN, patients showed an asymmetrical sensitivity to linear acceleration vectors directed along their interaural axis in comparison to their preoperative settings for the same stimuli.

Acceleration↗
PubMed1991

See-saw nystagmus due to unilateral mesodiencephalic lesion.

See-saw nystagmus is a unique torsional-vertical eye movement disorder with a characteristic appearance. It is a pendular nystagmus with two distinct components: a conjugate torsional component and a disjunctive vertical component. In those cases of see-saw nystagmus in which a focal lesion has been identified, the lesion is usually a bilateral, symmetric lesion located at the mesodiencephalic junction. We report an unusual case of see-saw nystagmus which was due to a strictly unilateral mesodiencephalic lesion. Furthermore, the see-saw nystagmus had, in this case, a jerk wave-form rather than the usual pendular wave-form, with the torsional component of the jerk see-saw nystagmus beating toward the side of the lesion. These observations have an impact upon the localizing and lateralizing significance of torsional nystagmus in general and of see-saw nystagmus in particular.

Adult↗
PubMed1990

The human horizontal vestibulo-ocular reflex in response to high-acceleration stimulation before and after unilateral vestibular neurectomy.

The normal horizontal vestibulo-ocular reflex (HVOR) is largely generated by simultaneous stimulation of the two horizontal semicircular canals (HSCCs). To determine the dynamics of the HVOR when it is generated by only one HSCC, compensatory eye movements in response to a novel vestibular stimulus were measured using magnetic search coils. The vestibular stimulus consisted of low-amplitude, high-acceleration, passive, unpredictable, horizontal rotations of the head with respect to the trunk. While these so called head "impuses" had amplitudes of only 15-20 degrees with peak velocities up to 250 deg/s, they had peak accelerations up to 3000 deg/s/s. Fourteen humans were studied in this way before and after therapeutic unilateral vestibular neurectomy; 10 were studied 1 week or 1 year afterwards; 4 were studied 1 week and 1 year afterwards. The results from these 14 patients were compared with the results from 30 normal control subjects and with the results from one subject with absent vestibular function following bilateral vestibular neurectomy. Compensatory eye rotation in normal subjects closely mirrored head rotation. In contrast there was no compensatory eye rotation in the first 170 ms after the onset of head rotation in the subject without vestibular function. Before unilateral vestibular neurectomy all the patients' eye movement responses were within the normal control range. One week after unilateral vestibular neurectomy however there was a asymmetrical bilateral HVOR deficit. The asymmetry was much more profound than has been shown in any previous studies. The HVOR generated in response to head impulses directed away from the intact side largely by ampullofugal disfacilitation from the single intact HSCC (ignoring for the moment the small contribution to the HVOR from stimulation of the vertical SCCs), was severely deficient with an average gain (eye velocity/head velocity) of 0.25 at 122.5 deg/sec head velocity (normal gain = 0.94 +/- 0.08). In contrast the HVOR generated in response to head impulses directed toward the intact side, largely by ampullopetal excitation from the single intact HSCC, was only mildly (but nonetheless significantly) deficient, with an average gain of 0.80 at 122.5 deg/sec head velocity. At these accelerations there was no significant improvement in the average HVOR velocity gain in either direction over the following year. These results indicate that ampullopetal excitation from one HSCC can, even in the absence of ampullofugal disfacilitation from the opposite HSCC, generate a near normal HVOR in response to high-acceleration stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Acceleration↗
PubMed1990

Tonic contraversive ocular tilt reaction due to unilateral meso-diencephalic lesion.

We studied 4 patients with tonic contraversive ocular tilt reactions due to unilateral, paramedian, mesodiencephalic lesions. This is in contrast to the only 2 previously reported patients with ocular tilt reactions due to unilateral mesodiencephalic lesions, each of whom had a paroxysmal ipsiversive ocular tilt reaction. This new finding is considered in the context of previous clinical and experimental data on the various types of ocular tilt reactions that follow stimulation or destruction of the peripheral and central vestibular system. Otolithic inputs to the interstitial nucleus of Cajal from the contralateral vestibular nucleus and motor outputs from the interstitial nucleus of Cajal to cervical and ocular motoneurons could be involved in the ocular tilt reaction. We propose that in patients with unilateral meso-diencephalic lesions, a tonic contraversive ocular tilt reaction could be due to persistently decreased resting activity of ipsilateral interstitial nucleus neurons, whereas a paroxysmal ipsiversive ocular tilt reaction could be due to transiently increased activity of the same interstitial nucleus neurons. Cases of ocular tilt reaction due to unilateral meso-diencephalic lesion point to the existence of a crossed graviceptive pathway between the vestibular nucleus and the contralateral interstitial nucleus of Cajal.

Adult↗
PubMed1990

Diagnosis of unilateral otolith hypofunction.

Asymmetric vestibular function is the basis of vertigo. Whereas caloric tests can identify unilateral peripheral loss or impairment of horizontal semicircular canal function reasonably accurately, there is as yet no single accepted test of unilateral otolith hypofunction. In some advanced vestibular laboratories around the world, new and perhaps diagnostically useful tests of otolith function are being devised. The physiologic basis and the present clinical applications of these tests are reviewed.

Animals↗
PubMed1989

Lithium-induced downbeat nystagmus.

We examined six patients who developed blurring or oscillopsia as a result of downbeat nystagmus while being treated with lithium carbonate. Of these six plus six previously described similar patients, all but two developed downbeat nystagmus insidiously as an isolated disorder in the setting of otherwise satisfactory therapeutic control, without clinical or biochemical evidence of acute lithium intoxication. Only six of these 12 patients were able either to reduce or to stop taking lithium, and in only two of these six did the downbeat nystagmus improve or remit.

Adult↗
PubMed1989

Painful oculomotor nerve palsy due to dural-cavernous sinus shunt.

Two patients presented with painful unilateral oculomotor nerve palsies without evidence of ocular congestion or hypoxia. They were initially thought to have posterior communicating or distal internal carotid aneurysms, but had, in fact, dural-cavernous sinus shunts, draining posteriorly into the inferior petrosal sinus. One patient later developed a moderately severe congestive ophthalmopathy, and repeated selective carotid arteriograms showed that the shunt was now draining anteriorly into the superior ophthalmic vein. In the other patient, the oculomotor nerve palsy resolved without the development of any further signs. These observations support the concept that dural-cavernous sinus shunts produce symptoms that are dependent on the direction of drainage from the shunt. It is clear that the direction of drainage can change and that thrombosis of the posterior cavernous sinus determines the direction of drainage. The exact mechanism of the cranial neuropathy is, however, unknown.

Cavernous Sinus↗
PubMed1989

A model of otolith stimulation.

A new model of otolithic stimulation by linear acceleration is presented and compared to previous models, based upon anatomical evidence and on the ability of normal subjects to sense the direction of a linear acceleration vector acting in the coronal plane (roll-tilt perception). There are two basic methods of generating roll-tilt stimuli: 1) tilt-chairs either inside or outside a centrifuge and 2) fixed-chair centrifuges. The present model is based on consideration of the probable otoconial displacement produced by these two different methods of stimulation and the model incorporates a major role for the elastic restoring force of the otolith membrane. When this force is taken into account, and most previous models have ignored it, the model predicts that different patterns of otoconial displacement will be produced in tilt-chair and in fixed-chair centrifuge experiments. The different roll-tilt perception produced by these two methods may be caused by the different otoconial displacement patterns. It is suggested that the elastic restoring force of the otoconial membrane may contribute to space motion sickness.

Acceleration↗