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Biomedical subjects

A M Bronstein

Publications and source records attributed to A M Bronstein.

At least 145 records · Page 8Linked to original sources
PubMed1990

Convergence nystagmus associated with Arnold-Chiari malformation.

A case of convergence nystagmus associated with an Arnold-Chiari type I malformation is presented. The nystagmus appeared in the absence of fixation, was provoked during Valsalva's maneuver and neck flexion and extension, and attenuated on deep inspiration. Sagittal magnetic resonance images showed that the diameter of the cerebral aqueduct increased with the neck in full flexion and in full extension. Surgical foramen magnum decompression considerably reduced the nystagmus and abolished the postural variation of aqueduct diameter. It is postulated that this nystagmus was due to a combination of mechanical distortion and abnormal transmission of cerebrospinal fluid pressure to the aqueductal region.

Adolescent↗
PubMed1990

Visual control of balance in cerebellar and parkinsonian syndromes.

The role of vision in the control of balance in patients with Parkinson's disease (PD) and cerebellar disease (CD) was studied by measuring body sway with eyes open, closed, and in response to visual stimuli generated by discrete lateral displacements of a moveable room which enclosed the subjects. In response to room movement, normal subjects swayed by an amount intermediate between sway with eyes open and eyes closed and their response attenuated on repetition of the movement, a process depending on shifting from predominantly visual to proprioceptive control. CD patients swayed more than controls with eyes open or closed and as shown by high 'Romberg quotients' (eyes closed/eyes open sway ratio) were able to use visual information to control much of their unsteadiness. CD patients had a normal attenuation of response to repetition of the room movement. PD patients had normal sway with eyes open or closed but their responses to room movement were abnormal, being proportionately larger and failing to attenuate during successive stimuli. The results indicate that cerebellar lesions seem largely to spare the visuopostural loop and also spare the ability to shift from a visual to a proprioceptive control of postural sway. In contrast, the findings in PD suggest that the visuopostural loop is hyperactive and that its influence cannot easily be de-emphasized when visual information is misleading. The latter finding suggests that basal ganglia participation in posture is concerned with the reweighting of the various sensorimotor loops controlling posture in the process of adapting to novel situations.

Adaptation, Physiological↗
PubMed1990

Abnormalities of horizontal gaze. Clinical, oculographic and magnetic resonance imaging findings. I. Abducens palsy.

Fifty one patients with abnormalities of horizontal gaze were studied with magnetic imaging of the brain (MRI) and eye movement recordings to identify the loci of lesions responsible for isolated abducens palsy, conjugate gaze palsy and different types of internuclear ophthalmoplegias. The lesions responsible for a particular disorder were identified by overlapping enlarged drawings of the individual scans at comparable brain-stem levels and identifying the areas where the abnormal MRI signals intersected. A statistical procedure was devised to exclude the possibility that the areas of overlap occurred by chance. In this paper, the findings in the group of patients with VI nerve palsy are reported since the location of their lesions could be predicted from known anatomy, so validating the procedure. The results were independently obtained with the overlapping technique and the statistical procedure and showed that the lesions were located in a region corresponding to the posterior part of the abducens fasciculus. This confirms that central lesions producing isolated lateral rectus weakness spare the abducens nuclei. The agreement between the procedures used and earlier clinical and experimental results suggest that the method we describe can be applied to locate the site of lesions on MRI scans in other groups of patients with more complex gaze disorders.

Abducens Nerve↗
PubMed1990

Abnormalities of horizontal gaze. Clinical, oculographic and magnetic resonance imaging findings. II. Gaze palsy and internuclear ophthalmoplegia.

The site of lesions responsible for horizontal gaze palsy and various types of internuclear ophthalmoplegia (INO) was established by identifying the common areas where the abnormal MRI signals from patients with a given ocular-motor disorder overlapped. Patients with unilateral gaze palsy had lesions in the paramedian area of the pons, including the abducens nucleus, the lateral part of the nucleus reticularis pontis caudalis and the nucleus reticularis pontis oralis. Patients with abducens nucleus lesions showed additional clinical signs of lateral rectus weakness. Lesions responsible for bilateral gaze palsy involved the pontine tegmental raphe. Since this region contains the saccadic omnipause neurons, this finding suggests that damage to omnipause cells produces slowing of saccades rather than opsoclonus, as previously proposed. All INOs, regardless of the presence of impaired abduction or convergence, had similar MRI appearances. Frequently the lesions in patients with INO, were not confined to the medial longitudinal fasciculus (MLF) but also involved neighbouring structures at the pontine and mid-brain levels. There was a statistically significant association between the clinical severity of the INO and the presence of abnormal abduction or convergence. The findings suggest that the lesions outside the MLF, which may affect abducens, gaze or convergence pathways, are responsible for the presence of features additional to INO, depending on the magnitude of functional disruption they produce.

Abducens Nerve↗
PubMed1990

Saccadic function in spasmodic torticollis.

Twelve patients with idiopathic spasmodic torticollis were compared with 19 normal controls on tests of saccadic eye movements thought to depend upon normal basal ganglia function. The patients were able to make random, predictive, remembered, and self-paced saccades equally as well as control subjects. This suggests that those parts of the basal ganglia which may be damaged in spasmodic torticollis, are separate from pathways responsible for the normal initiation and execution of saccades.

Adult↗
PubMed1990

The neurological complications of Anderson-Fabry disease (alpha-galactosidase A deficiency)--investigation of symptomatic and presymptomatic patients.

Anderson-Fabry disease is an X-linked inborn error of metabolism characterized by subnormal activity of the lysosomal hydrolase, alpha-galactosidase A. We have assessed the incidence and nature of neuropathy in 12 patients (seven affected men and five carrier females). Abnormalities of cutaneous thermal sensation were common, even in asymptomatic carriers, with a unique predilection for cold sensitivity which suggests involvement of small myelinated nerve fibres. Intracranial abnormalities were frequently detected by magnetic resonance imaging (MRI) in males, both with and without overt cerebrovascular disease, and were more extensive in older patients. Such abnormalities were not detected in carriers. Auditory and vestibular abnormalities were present in six patients, only one of whom was symptomatic. Cranial MRI and assessment of cutaneous thermal thresholds are sensitive techniques which can identify neurological involvement in asymptomatic patients. They may be of benefit in monitoring the effectiveness of enzyme replacement therapy and excluding the carrier state for the defective gene.

Adolescent↗
PubMed1989

Ataxia telangiectasia: a reappraisal of the ocular motor features and their value in the diagnosis of atypical cases.

The eye movements of four patients with ataxia telangiectasia (AT), three of whom had an unusual neurological presentation, were studied. All had striking abnormalities of saccadic generation with markedly hypometric saccades, increased saccadic latency, but normal saccadic velocity. Three patients used head thrusts to aid refixation. In addition, there was absence of smooth pursuit and optokinetic nystagmus, and hyperactive vestibular responses. Two of the four patients had, in addition, periodic alternating nystagmus. This combination of an ocular motor apraxia with superadded cerebellar ocular motor abnormalities, and possibly periodic alternating nystagmus, should strongly suggest the diagnosis of AT, even if the clinical syndrome is otherwise atypical.

Adult↗
PubMed1989

Vestibulo-ocular abnormalities in spasmodic torticollis before and after botulinum toxin injections.

In order to establish whether vestibular abnormalities often found in spasmodic torticollis are secondary to the abnormal head posture, the vestibulo-ocular reflex (VOR) was studied in eight patients before and after correction of head posture with botulinum toxin. Eye movements were recorded in the dark during sinusoidal and velocity step rotation. Four patients showed a significantly asymmetric response, with the slow phase of the VOR more active ipsilateral to the torticollis (chin). Despite significant improvement of the head posture in all patients for up to 10 weeks following treatment, no correction of the vestibular asymmetry occurred. This suggests that the VOR abnormalities are not caused by the head posture itself. We interpret the findings as evidence of primary involvement of the vestibular system in torticollis and we postulate a widespread derangement of the sensory-motor mechanisms controlling head posture in this disease.

Adult↗
PubMed1988

Short latency compensatory eye movement responses to transient linear head acceleration: a specific function of the otolith-ocular reflex.

Normal subjects were exposed to 0.26 g linear acceleration steps along the inter-aural axis whilst they fixated an earth stationary target at 110 cm distance. The stimulus evoked slow phase eye movements at a mean latency of 34 ms which attained the relative target velocity in 113 ms. In contrast, visual following with head fixed, of identical relative target motion, had significantly longer latencies and time to match target velocity. The short latency responses to linear acceleration were absent in an alabyrinthine subject. It is concluded that the otolith-ocular reflex is responsible for the short latency responses to linear head movement and functions to stabilise vision during sudden head movement before visually guided compensatory eye movements take effect.

Acceleration↗
PubMed1987

Eye movement responses to combined linear and angular head movement.

Lateral eye movements evoked by linear head motion were evaluated in human subjects by subtracting the eye movement responses to head-centred angular oscillation in the dark, about a vertical axis, from the responses evoked by similar oscillation with the head displaced 30 cm eccentrically from the axis. The centred oscillation gave a purely angular stimulus whereas the eccentric oscillation gave an additional tangential linear acceleration acting laterally to the head. The stimuli used were relatively unpredictable, enveloped sinewaves at 0.02 to 1.2 Hz, 60 degrees/s peak angular velocity, 0.004 to 0.24 g peak tangential acceleration, and subjects were either given no instructions or were told to imagine fixating on targets at 60 cm or 5 m distance. Eye movements of significantly higher velocity were evoked in the eccentric position, particularly at the higher frequencies and when subjects imagined near targets. The increase in velocity of eye movement was attributed to the linear stimulus and probably derives from stimulation of the otolith organs. The frequency response of the gain (degree/s/g) of these movements gave an approximate slope of -1, indicating that the eye velocity bears a constant proportionality to linear head velocity. The findings are in accord with the theoretical prediction that eye movements compensating for linear head motion should only be required for viewing near targets. These otolithic influences on eye movements could either the mediated by a direct "otolith-ocular reflex" which is subservient to viewing conditions, or, alternatively, the otolith signals may modify the activity of other oculomotor mechanisms.

Acceleration↗
PubMed1987

Down beating nystagmus: magnetic resonance imaging and neuro-otological findings.

Twenty-four patients with down beating nystagmus (DBN) underwent magnetic resonance imaging (MRI) of the head. MRI provided diagnostic images in Arnold-Chiari malformation (6 cases), cerebellar atrophy (6 cases), 1 case with a prepontine-medullary epidermoid tumour and was helpful in the diagnosis of 2 patients with multiple sclerosis and 1 with a ponto-cerebellar infarct. Multiple cerebral hemisphere lesions were found in 6 patients (5 of them over 60 years of age) in whom no diagnosis was made. All cases of DBN, plus 3 additional patients with Arnold-Chiari malformation and other types of nystagmus, were neuro-otologically assessed. Sensitivity of the nystagmus to head tilt with respect to the gravity vector had no localizing value. Impaired horizontal vestibulo-ocular reflex suppression occurred more frequently in those patients with abnormal posterior fossa MRI. Pure torsional nystagmus, and DBN with a strong torsional component, in patients with Arnold-Chiari malformation was associated with syringomyelia. Magnetic resonance is the imaging method of choice for investigating patients with DBN.

Adolescent↗
PubMed1987

Predictive eye saccades are different from visually triggered saccades.

The metrics of eye saccades in response to random and predictable target motion were determined in 8 normal young subjects. The peak velocity of predictive saccades (PS) was significantly reduced when compared with randomly elicited saccades (RS) of equal amplitude. Saccadic gain (initial saccadic amplitude/target amplitude) was also decreased in PS. Saccadic inaccuracy was extremely frequent in PS and, in contrast to RS, it was independent of target amplitude displacement. These stimulus-dependent changes in saccadic characteristics may reflect activation of the saccadic pontine generators by different supranuclear pathways.

Adolescent↗
PubMed1987

Spasmodic torticollis following unilateral VIII nerve lesions: neck EMG modulation in response to vestibular stimuli.

Three patients with spasmodic torticollis following VIII nerve lesions (VIII-ST) underwent quantitative assessment of their sternomastoid EMG during vestibular (otolith and semicircular canal) stimulation. The results were compared with a normal control group and with six patients with idiopathic spasmodic torticollis (ST). Backwards tilt of the VIII-ST patients resulted in a marked increase in the EMG, especially in the more affected sternomastoid, whereas this manoeuvre did not have a significant effect in normal subjects, or had a variable effect in the ST group. These results suggest that those with torticollis following VIII nerve lesions are a distinct group. Since there was no relationship between the side of the VIII nerve lesion and the direction of the torticollis a direct aetiological link between the two is, however, unlikely. The unusual EMG/tilt responses are explained on the basis of peripheral imbalance of utricular signals (maximal in the supine position) in the presence of central deranged processing of information concerning head posture.

Electromyography↗
PubMed1987

Testing the vestibular-ocular reflexes: abnormalities of the otolith contribution in patients with neuro-otological disease.

Conventional vestibular rotation testing with the head centered on the axis stimulates the semicircular canals evoking compensatory eye movements. If the head is placed forwards of the axis in an eccentric position the otoliths are also stimulated by a tangential linear acceleration acting laterally to the skull. In normal subjects the additional otolithic stimulus evokes compensatory eye movements with a higher gain than with head centred, particularly for high frequency (greater than 0.1 Hz) stimuli. The responses with head centred and eccentric in various patients with known/suspected neuro-otological abnormalities have been compared. Patients with vestibular neurinectomies who have asymmetrical head centred responses showed greater asymmetry with head eccentric at higher stimulus frequencies. Some patients with cerebellar lesions showed abnormally enhanced or depressed and asymmetrical responses with head eccentric in comparison with head centred responses, which could be normal. The enhancing effects could be specific to low frequency stimuli. All patients who showed abnormal responses with head eccentric also had positional nystagmus provoked by the gravity acceleration vector when the head was tilted laterally. The direction of the positional nystagmus with respect to the gravity vector was not necessarily the same as the direction of the effect on eye movements of lateral acceleration during eccentric oscillation. Patients with benign paroxysmal vertigo or chronic linear vertigo in whom otolithic abnormalities are suspected were not found to have abnormal responses with head eccentric. We conclude that this method of testing may be useful in elucidating pathophysiology but is not a decisive clinical test for the presence of disordered otolith function.

Acceleration↗
PubMed1986

The cervico-ocular reflex in normal subjects and patients with absent vestibular function.

The role of the cervico-ocular reflex (COR) has been studied in 12 patients with absent vestibular function and 13 normal subjects. Ramp and sinusoidal displacement stimuli were applied with trunk on head and head on trunk movements. In all patients, trunk on head movements evoked a marked slow-phase compensatory COR while in normal subjects it was weak and variable in direction. Fast components of the COR induced gaze shifts in the direction of the relative head movement ('anticompensatory' direction) which could be suppressed by imagining an earth fixed targed. No tonic component could be identified instead, in the case of ramp stimuli, a residual eye deviation was noted which was significantly enhanced in the patients and resulted from activity dynamically generated during the course of the trunk movement and not from its final angular displacement. Head on trunk ramp displacements in the dark evoked initial anticompensatory saccades followed by slow compensatory components, a pattern of eye movements remarkably similar to that seen during active head-eye target seeking. Thus, in the absence of labyrinthine function, the COR appears to take on the role of the vestibulo-ocular reflex in head-eye coordination in the initiation of the anticompensatory saccade which takes the eyes in the direction of the target, and the generation of the subsequent slow compensatory eye movements. Central pre-programming, as revealed by comparing the effect of different instructions and active versus passive neck-induced eye movements, has a profound influence on COR functioning.

Adult↗
PubMed1986

Otolith stimulation evokes compensatory reflex eye movements of high velocity when linear motion of the head is combined with concurrent angular motion.

Previous investigations have failed to find significant compensatory eye movements in response to linear motion of the head. However, the fact that visual acuity is essentially preserved during natural head movements, which combine both linear and angular components, is evidence that there must be compensation for linear translation. Hence we examined the lateral eye movements produced by angular oscillation, in the dark, in yaw at 0.5 and 1.5 Hz, 80 degrees/s peak, with the head both centred and positioned 30 cm eccentric from the axis of rotation in order to produce an additional linear acceleration acting tangentially. The combined stimuli produced high velocities of eye movement which were much greater than those produced by angular motion alone. The findings are evidence or a linear-compensatory reflex which is probably otolithic. The dependency of otolithic eye movements on concurrent stimulation of the semicircular canals is a possible explanation of positional nystagmus in neuro-otological disease in which it may be released by a pathological imbalance of canal function.

Adult↗