Mechanisms for essential tremor.
Explore the source record for details and available documents.
Electrophysiology↗
Biomedical subjects
M A Gresty
Publications and source records attributed to M A Gresty.
Visually controlled spatial stabilisation of the human head: compensation for the eye's limited ability to roll.
During movements of the head in pitch (yes-yes) or in yaw (no-no) the visual scene appears stable whereas rolling the head (ear down to shoulder) induces an apparent swinging of the world in the opposite direction. This visual instability is due to the inadequacy, in the roll plane, of the reflex eye movements which are effective in stabilising the eyes in space during pitch and yaw. We investigated whether head is stabilised in roll to protect against visual instability. Human subjects were fixed in a gimbal with their heads free and were exposed to unpredictable oscillatory movement in pitch and, for comparison roll, about axes aligned with the head. With vision, during roll motion, the head was displaced from upright by approximately half the amplitude of the gimbal motion. In comparison, with eyes closed relying on vestibular and proprioceptive cues and during pitch stimuli with or without vision, the magnitude of head displacement from upright was approximately equal to that to the gimbal. The superior head stability in roll, dependent on a visual frame of reference, compensates for poverty of eye movement in this plane.
Eye Movements↗
Eye movements in response to canal and otolith signals in opposing directions.
Explore the source record for details and available documents.
Acceleration↗
Neurology of otolith function. Peripheral and central disorders.
The otolith organs detect gravitoinertial forces acting on the head providing signals to the brain which are essential for spatial orientation, sensing motion and organizing motor behaviour. Although the pathophysiology of otolithic dysfunction is poorly understood, a disorder of otolith function, at a peripheral or central level, may be suspected when a patient describes symptoms of false sensations of linear motion or tilt or shows signs of specific derangements of ocular motor and postural, orienting and balancing responses. When disorientation is severe the patient may describe symptoms which sound bizarre, raising doubts over the organic basis of the disease. Our recognition of an otolithic disorder and understanding otolithic involvement in a wider neurological context may be guided by knowledge of otolith physiology and of the characteristics of the few proven otolithic syndromes.
Brain↗
Torsional nystagmus. A neuro-otological and MRI study of thirty-five cases.
Thirty-five patients with torsional nystagmus (TN) underwent vestibular and ocular motor assessment and magnetic resonance image (MRI) scanning of the head. Patients were divided into two groups according to whether TN was predominant and present in primary gaze (Group I, 23 patients) or elicited by head positioning or gaze deviation and less prominent than other concurrent nystagmus (Group II, 12 patients). The main aetiologies in both groups were demyelination, vascular disease and posterior fossa tumours. In Group I, a frequent pattern of findings, occurring in 30-50% of cases, was a caloric canal paresis contralateral to the direction of the fast phases ('beat') of the TN, whereas the duration of horizontal caloric/rotational nystagmus and the slow-phase eye velocity of pursuit and of optokinetic nystagmus were all reduced in the direction of beating. The TN was more frequently and consistently modulated by vertical canal stimuli (head oscillation in roll) than by otolith stimuli (static tilt). Statistical analysis of the MRI showed significant overlap of abnormal MRI signals in the area of the vestibular nuclei, on the side opposite to the beat direction of TN. These results suggest that TN originates in a central imbalance of vertical semicircular canal function, resulting from lesions involving the vestibular nuclei on the opposite side of the TN. Group II was heterogeneous with no consistent pattern of neuro-otological findings, although lesions ipsilateral to the TN were frequent occurrence; in these cases cerebellar system lesions may have produced ipsilateral vestibular nuclei disinhibition.
Adolescent↗
Neurology of latent nystagmus.
We report eye movement findings in 30 patients with latent nystagmus and who were found to have a variety of associated oculomotor disorders. Latent nystagmus is defined clinically as nystagmus which appears on covering one eye and beats towards the uncovered eye. Recordings showed that the latent nystagmus in 28 patients had slow phases with linear or exponentially decreasing velocity. This nystagmus is termed 'LN'. In 13 of these patients certain manoeuvres (e.g. pursuit) provoked nystagmus with exponentially increasing slow phase velocities characteristic of the congenital form of nystagmus termed 'CN' and we propose that this is a forme fruste of CN. In two patients the nystagmus provoked by cover was latent CN. Twenty-nine patients had a history of strabismus and one had a marked phoria. Some patients had amblyopia whilst others had normal vision in each eye. Although binocular vision was usually absent, six patients had varying degrees of stereopsis. A temporonasal predominance of monocularly elicited optokinetic response previously associated with LN, was present only in a minority of patients. Some responses were bidirectionally absent or of low velocity, possibly the result of a cortical impairment of visual motion detection. The most deranged responses had slow phases which were in the opposite direction to the stimulus as described in CN. The presence of 'forme fruste' CN in many of these patients suggests that some of the derangements of optokinetic responses are due to CN. The findings indicate a greater overlap between the incidences of LN and CN than previously estimated. Thirty percent of patients had large saccadic 'square wave' intrusions. These were not present when there was marked amblyopia. They are attributed to a competitive incongruence of visual fields and eye positions. Dissociations found between the presence and severity of strabismus, stereopsis, amblyopia and optokinetic abnormalities point to these features being relatively independent although associated in typical clusterings. This is evidence against the theory that strabismus and LN are directly caused by nasotemporal optokinetic imbalance which persists because of failure to develop binocular vision. The variability of findings favours the view that LN and CN arise from a genetic or acquired embryological disorder with various degrees and directions of expression.
Adolescent↗
Pendular pseudonystagmus arising as a combination of head tremor and vestibular failure.
We describe three patients with spontaneous pendular oscillation of the eye during funduscopy. All patients had blurred, shimmering vision or oscillopsia, exacerbated by concentration, reading, or trivial head movements, and had a history of unsteadiness. Examination revealed a fine head tremor, mild unsteadiness, absent vestibulo-ocular reflex (VOR), and otherwise normal neurologic and ocular motor findings. Rigid immobilization of the head abolished the retinal oscillations. Simultaneous precision recordings of head and eye movements showed that the eye movement was in the compensatory direction to the head tremor but that, in contrast to normal VOR, it was in phase error. We conclude that the essential head tremor was provoking oscillopsia and retinal oscillation because of the absence of VOR. Recognizing the association of head tremor with absent VOR is important since in all these patients the presence of this pendular pseudonystagmus on ophthalmoscopy raised the diagnostic possibility of brainstem disease.
Aged↗
Testing otolith function.
Otolithic signals contribute to; (1) perception of orientation and linear motion, (2) generate compensatory eye movements in response to linear acceleration of the head and (3) participate in the co-ordination of movement and balance. Tests of these functions shown to be useful in identifying clinical disorders have been reviewed: (1) Evaluation of orientation to gravity, as estimated by adjustment of the visual vertical, indicates deranged otolith function at a peripheral or central level and the sensitivity of this test can be enhanced by performing estimates during centrifugation on a motorised turntable. Estimation of thresholds of self motion on a parallel swing identifies global reduction or unilateral loss of peripheral function, with central disorders awaiting study. (2) Otolith ocular reflexes to linear head translation can be used to demonstrate overall integrity of peripheral function and reveal central abnormalities. Counter-rolling responses to head roll-tilt and measurements of cyclodeviation of the eyes demonstrate functional asymmetries, with some lateralising value, particularly in central lesions. Global function and asymmetries may also be evaluated by 'head eccentric' rotational testing, which adds a tangential linear acceleration to the angular stimulus. The linear acceleration enhances the canal response by adding an otolith component. (3) Latency and amplitude of surface electro-myography (EMG) responses in the limbs to sudden falls, which can be recorded with the subject suspended on a hinged bed, indicate gross peripheral abnormality of function and can lateralize disorders of CNS motor pathways. It is concluded that some tests of otolith function can be of use in indicating global loss of peripheral otolith function, others are capable of lateralizing a marked loss of function and all have the potential to give information about central disorders. They all have to be interpreted within the clinical context and, unfortunately, none have yet been shown to be sensitive to partial, particularly unilateral, dysfunction.
Adult↗
Disorders of head-eye coordination.
Head-eye coordination subserves the rapid transference of gaze and between gaze shifts stabilizes fixation on stationary or smoothly moving targets. The coordination involves various combinations of the components of head movement, saccadic eye movements and visual and vestibular slow phase eye movement whose fine tuning may be adjusted, to an extent currently debated, by higher order mechanisms. Disorders of head-eye coordination may result in loss of acuity when slow phases are impaired or difficulty with reorientation if there is difficulty with saccades or head movement. Pathophysiology in the brain stem affecting individual components of eye movement may often be identified with success, particularly for the horizontal system, but the organization of other functions, notably pursuit suppression and vertical movements, are little understood. Similarly little is known about the disorders of the overall pattern of coordination--'gaze types'--including the apraxias, which have been attributed to cortical, basal ganglia or even cerebellar dysfunction and are reported in an almost bewildering variety of diseases. The development of coordination in infancy is a rich field in which there have been few studies with adequate observational techniques. The differentiation between congenital disorders whose severity may subsequently wax or wane, variants on normal development and acquired disorders poses a clinical problem which could largely be resolved with adequate recording techniques. For the future there is the tantalizing promise that once the principles of coordination are understood, we can move on to the more intriguing questions of how a certain 'toss of the head' and 'look in the eye' not only transfer gaze but can also be so meaningful.
Animals↗
Compensatory eye movements in the presence of conflicting canal and otolith signals.
Orbital motion of the head with the face directed towards the axis of rotation is a stimulus to the otolith organs which is in the opposite rightwards-left-wards sense to the rotational stimulus to the semicircular canals. This can be experienced, for example, by a child held at arms length "en face' and swung from side to side. As one swings, say to the right, the child's head rotates to its right yet moves linearly to its left. Eye movement responses to a transient orbital movement were observed whilst subjects fixated earth-fixed targets. i) a "near target" placed between the head and the axis whose relative displacement is in the same direction as head rotation, and ii) a "far target" placed beyond the axis whose relative motion is in the opposite direction to head rotation. The motion stimuli evoked slow phase eye movements at 45 ms latency, always in the opposite direction to head rotation, thus compensating for the motion of the far target but in the wrong direction for fixating the near target. Theoretically, fixating the near target demands a predominance of the otolith ocular-reflex, which would give an eye movement in the correct direction. However, despite visual cues, it seems that if the canal and otolith-ocular reflexes are evoked in opposing directions, the otolith reflex fails to operate at a sensitivity sufficiently high to reverse the direction of the canal-reflex.
Adult↗
Congenital-type nystagmus emerging in later life.
We describe six patients who, as teenagers or adults, developed florid nystagmus with consequent visual symptoms without any other manifestation of disease. In three patients, previous ophthalmologic examination had excluded nystagmus, and there was medically informed witness to its onset. The remainder may or may not have had a milder, unsuspected nystagmus before the development of symptoms. Ophthalmologic and neurologic investigations were negative, and follow-up of 2 to 15 years has been uneventful. Eye movement recordings showed the characteristics of the nystagmus to be indistinguishable from congenital nystagmus, which normally becomes manifest in early infancy. We conclude that a congenital-type nystagmus can emerge or enhance in later life without apparent provocation and is probably associated with a benign pathophysiology.
Adolescent↗
Compensatory otolithic slow phase eye movement responses to abrupt linear head motion in the lateral direction. Findings in patients with labyrinthine and neurological lesions.
Explore the source record for details and available documents.
Electrooculography↗
Mechanical thermostatic mixer valve for caloric irrigation.
Explore the source record for details and available documents.
Caloric Tests↗
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↗
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↗
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↗
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↗
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↗