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Biomedical subjects

A M Bronstein

Publications and source records attributed to A M Bronstein.

154 records · Page 9Linked to original sources

Suppression of visually evoked postural responses.

Normal subjects standing on an earth-fixed force platform inside a movable room displaced at velocities comparable to those accompanying spontaneous body sway, exhibit a visually evoked postural response (VEPR) some 600 ms after the start of the room movement. It consists of a displacement of the centre of force of the body in the direction of the stimulus (primary component), followed shortly by a corrective displacement in the opposite (secondary component). On second presentation of the stimulus VEPR is markedly reduced, but only if full proprioceptive information from the lower limbs is available to the subjects. A patient deprived of this information showed much enhanced VEPR which he was unable to suppress, in contrast to a patient with absent vestibular function who presented normal VEPR. The results show that in the presence of conflict between different sensory clues, vision is initially dominant in sway control, although adaptive processes can quickly rearrange this hierarchy.

Adolescent↗

Vestibular involvement in spasmodic torticollis.

Vestibular findings in a group of 35 patients with spasmodic torticollis without other otological or neurological symptoms were reviewed. The most consistent abnormality, present in more than 70% of cases, was a directional preponderance of vestibular nystagmus in the dark in a direction opposite to the head (chin) deviation. Rigidly clamping the head to a rotating chair did not abolish the directional preponderance. In the presence of optic fixation the directional preponderance was less frequent and its severity tended to diminish as a function of the duration of the disease. Smooth pursuit and optokinetic nystagmus were only occasionally affected. The results are indicative of primary involvement of the vestibular system in spasmodic torticollis and are discussed in terms of a break-down of the central mechanisms conveying sensory information responsible for head and eye orientation.

Adult↗

Predictive ocular motor control in Parkinson's disease.

A comparison was made of predictive eye movements of both the saccadic and pursuit ocular motor systems in parkinsonian patients and aged-matched normal controls. In a predictive task our patients, who were mildly or moderately affected, showed a reduced tendency to make anticipatory saccades compared with normal controls. Although there was some impairment of pursuit during a nonpredictive task as shown by an increased phase lag, a normal amount of improvement took place with a predictive task. This difference between prediction in the saccadic and pursuit system is possibly explained by an increased reliance on a visual input by parkinsonian patients which prevents them making use of verbal instruction to generate anticipatory (eye in advance of target) saccades. Improvement of pursuit with a predictive target track is possible in such patients since normally in these circumstances the target is mainly followed rather than anticipated. The metrics of saccadic and smooth pursuit eye movements (saccadic velocity and pursuit turnover velocity) were normal.

Aged↗

Cervical nystagmus due to loss of cerebellar inhibition on the cervico-ocular reflex: a case report.

Studies of the cervico-ocular reflex and the vestibulo-ocular reflex have been carried out separately and in combination on a patient with gait ataxia due to a cerebellar tumour. With the head fixed in space, body rotation to the right (left neck torsion) induced marked nystagmus to the left in darkness. Vestibulo-ocular responses to sinusoidal rotation were symmetrical while the neck was immobilised and asymmetric when it moved freely. It is suggested that the cervical nystagmus seen in this case was the result of removal of cerebellar inhibition upon the cervico-ocular reflex and that abnormal interaction of cervical and vestibular inputs could have played a role in the patient's unsteadiness.

Adenocarcinoma↗

Bilateral loss of vestibular function: clinical findings in 53 patients.

The clinical presentations and aetiologies of a series of 53 cases of bilateral vestibular failure (BVF) seen by the authors over a decade were evaluated by retrospective review of the medical records. Thirty-nine per cent of patients had associated neurological disease; 13% had a progressive cerebellar syndrome with disabling gait ataxia, abnormal eye movements and cerebellar atrophy on neuro-imaging. BVF was usually unsuspected. Nine per cent had cranial or peripheral neuropathies and in this group there was no abnormality of brain stem/cerebellar oculomotor function, but hearing loss was common. Eleven per cent revealed BVF and hearing loss secondary to meningitis, and 6% had other neurological disorders. Idiopathic BVF was found in 21% of cases, characterised by paroxysmal vertigo and/or oscillopsia, but no abnormal clinical signs. Gentamicin ototoxicity accounted for a further 17%, while autoimmune disease was present in 9% of patients. Otological or neoplastic disease was diagnosed in the remaining 13% of patients. It was concluded that neurological, audiological and ocular motor assessments allow the probable cause of BVF to be defined in approximately 80% of cases. A group of BVF related to autoimmune pathologies is reported for the first time, indicating the need for immunological screening. Idiopathic BVF may present with only minor visual or vestibular symptoms, while in patients with cerebellar degeneration, BVF may be unsuspected and, thus, underdiagnosed.

Adult↗

Visual influences on balance.

This paper discusses the impact of vision on balance and orientation in patients with vestibular disorders and in anxiety patients with space and motion discomfort (SMD). When the vestibular system is impaired, vision has a greater influence on standing postural control, resulting in greater sway when individuals are presented with erroneous or conflicting visual cues. Studies have shown that individuals with other motion sensitivities, such as motion sickness, also tend to rely on vision for balance and do not disregard erroneous visual cues. Recently, patients with anxiety disorders that include SMD also have been shown to have increased postural sway in conflicting visual environments, similar to patients with vestibular disorders. Thus, while specific vestibular deficits are not always directly associated with SMD, data regarding the impact of vision on balance suggest that some patients with SMD may have an underlying balance disorder.

Anxiety↗

Reduced duration of a visual motion aftereffect in congenital nystagmus.

Congenital nystagmus (CN) is a primarily horizontal, involuntary, conjugate eye movement which can be observed soon after birth or during the first half-year of life. Individuals with CN rarely complain of oscillopsia. Using a motion aftereffect (MAE), we investigated if individuals with CN have abnormalities in motion perception and if any such abnormality could be due to nystagmus or to compensatory mechanisms to avoid oscillopsia. In task A, patients (n=10) and control subjects (n=10) indicated the direction, duration and relative velocity of MAEs. The subjects binocularly viewed a high contrast, grey scale grating (0.23 cyc/deg; visual angle: 18.3 deg) moving upward or downward at 1, 3, and 6 deg/sec for 60 sec. Vertical optokinetic nystagmus (OKN) was monitored. In task B, patients (n=8) and control subjects (n=8) viewed similar spatial frequency gratings (visual angle: 40.7 degs; 0.5, 0.2, 0.08 cyc/deg) which moved at 4, 10, and 16 deg/sec for 60 sec. In task C, five control subjects, with induced vestibular nystagmus, viewed a grating (0.2 cyc/deg; visual acuity: 28.5 deg), moving upward for 40 sec. In all three tasks, after adaptation with the moving grating, subjects viewed the then static grating and reported the duration and direction of the MAE. One CN patient and eight control subjects reported MABs at all three test velocities in task A. When patients exhibited OKN, the gain was close to one, as in the control group. In task B, seven of the eight patients and all of the control subjects had MABs at the faster adaptation velocities. CN patients had less MAEs at an adaptation velocity of 4 deg/sec and when MAEs were observed, the duration of the illusory motion was reduced by approximately 48%. Control subjects, with induced vestibular nystagmus, reported MAEs at 4 deg/sec (task C). These findings indicate that nystagmus cannot be the only factor accounting for the suppression of motion perception and suggest that compensatory mechanisms used to avoid oscillopsia contribute to the differences found between the groups.

Adaptation, Ocular↗

Oscillopsia of peripheral vestibular origin. Central and cervical compensatory mechanisms.

Eight patients with absent vestibular function categorized into four grades according to the disability they suffered from oscillopsia have been studied with a view to correlating its severity with the development of gaze stabilizing compensatory mechanisms. Eye movements were recorded while the following sinusoidal rotational stimuli were delivered: 1) trunk on head oscillation in the dark (COR); 2) head on trunk oscillation in the dark; 3) head on trunk and whole body (head and trunk) oscillation in the light in the presence of optic fixation. The COR was potentiated in all the patients regardless of their clinical status. Velocity gains (peak slow phase eye velocity/peak head velocity) during whole body rotation were significantly lower than head on trunk gains in the light in the better compensated patients. Since in the absence of vestibular function whole body rotation involves only the otokinetic system (OKN), this finding implies a depression of the OKN in these patients which can be corrected during head on trunk movements by virtue of a dynamic input from the neck. The results suggest that the processes of recovery from oscillopsia are dependent, in the main, upon the development of central mechanisms by means of which undesirable image movement across the retina is perceptually suppressed. Depression of OKN may be secondary to this perceptual rearrangement.

Adolescent↗

Evidence for a vestibular input contributing to dynamic head stabilization in man.

Horizontal head movements in response to unpredictable horizontal oscillations of the trunk were studied in 6 patients lacking vestibular function and in 6 normal subjects. In order to obtain compensatory (i.e. stabilizing with respect to earth) head movements, all subjects were required to look at an earth-fixed target, using their eyes and head. The turning points (maxima and minima) were determined from head and trunk position records. It was found that normal subjects reversed the direction of head movements in advance of trunk movements (mean lead = 82 ms) whereas the patients reversed head direction after the trunk (mean lag = 169 ms). The coherence function between head and trunk movements, measured with a spectral analyser in an additional labyrinthineless patient, was considerably lower than in normal controls. It is concluded that patients lacking vestibular function have impaired stabilization of the head in space, which can be taken as indirect evidence of the existence of active dynamic vestibulo-collic reflex (VCR) mechanisms in normal man. The lead found in normal subjects, notwithstanding the unpredictability of the stimuli, may reflect the detection of early acceleration signals by the vestibular apparatus to organize compensatory head movements.

Adult↗