Ocular and head movements in infarctions of the thalamic region

Oculomotor disorders in 22 infarctions in the thalamic region are recorded. Clinical examination and electro-oculography (17 cases) showed that paramedian thalamo-subthalamic lesions were responsible for clear deficits: upgaze paralysis and in some cases downgaze paralysis, partial paresis of the oculomotor nerve, deficits of lateral eye movements, myosis, paralysis of head flexion combined with downgaze paralysis. Postero-median choroid artery infarction was associated with upgaze paresis, slight deficit of lateral eye movements and myosis. Postero-lateral choroid artery infarction resulted in a partial visual field defect and in some cases, a contralateral hypometria; myosis was slight and inconstant. Infarctions of the internal capsule (anterior choroid artery, deep branches of the middle cerebral artery) were associated with a deficit of contralateral saccades. Ocular pursuit, when possible, was often saccadic, whatever the site of the infarction. This prevailed with gaze towards the lesion side.     

Ocular motor abnormalities in progressive supranuclear palsy

Eleven patients, 7 males and 4 females, of progressive supranuclear palsy (PSP) were examined neuro-otologically for the purpose of elucidating the characteristics of ocular motor abnormalities. All cases were admitted to our hospital and age at onset was from 52 to 71 years old, duration of illness was 2 to 11 years. Range of voluntary eye movements and abnormal eye movements including nystagmus were examined on naked eyes and with electronystagmography (ENG). Smooth pursuit movements and saccadic eye movements were tested both horizontally and vertically by using visual tracking method with ENG recordings. Optokinetic nystagmus test and caloric test with visual suppression test were also performed. These neurotological examinations were made repetitively in 5 cases and their progressions were observed. Vertical gaze palsy and convergence palsy were observed in all cases as the initial symptom. In this study downward gaze was more severely disturbed than upward gaze. Using ENG, saccadic eye movements (saccades) were disturbed earlier than smooth pursuit movements. Hypometric saccades and decreased saccadic velocity were common abnormalities. In the later stage of the disease, horizontal eye movements were also disturbed. In four cases bilateral adduction palsy was added to vertical gaze paralysis so that the lesion of the MLF to oculomotor nucleus was suggested to exist. These voluntary eye movements were worsened gradually as the disease progressed. By using ENG we could find so called abnormal eye movements more frequently than the previous reports. Eight patients demonstrated horizontal gaze nystagmus, and rebound nystagmus were observed in four cases.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pathophysiologic mechanism of convergence nystagmus

The convergent eye movements in convergence nystagmus are reported to be opposed adducting saccades under excessive convergence drive. What occurs is a horizontal saccade of the adducting eye and a quick reversal of the abducting eye immediately after initiation of the original saccade. Accordingly, the opposed adducting saccades of the abducting eye have been explained by the dynamic overshoot mechanism. However, by electro-oculographic analysis of eye movements in a patient with convergence nystagmus, we found that the opposed adducting saccades of the abducting eye occurred not only after but also just before initiation of the original saccade. Our observation indicates that the opposed adducting saccades can occur without dynamic overshoot as the starter mechanism. Possibly, cessation of the discharge of omnipause neurons may lead to firing of the burst neurons for the medial rectus subnucleus via activation by the excessive convergence drive.     

The ocular motor defects in progressive supranuclear palsy

The results of quantitative infrared horizontal eye movement recordings in 8 patients with progressive supranuclear palsy are presented. Some of the patients had total paralysis of vertical movements, but none had completely lost the ability to perform horizontal eye movements. All patients had a defect in ocular fixation previously undescribed in this condition: the universal presence of square-wave jerks. Analysis of refixation sacades demonstrated hypometria, slow velocity/amplitude relationships, and profound prolongation of duration. The pursuit abnormality, characterized clinically by “cogwheel” eye movements, represented the inability to match eye velocity to target velocity. The ratio of peak eye velocity to peak target velocity (pursuit gain) was 0.2 to 0.5. Defects in the vestibuloocular reflex included inability to increase the gain of the reflex (ratio of peak eye velocity to head velocity) during viewing of a visible, stationary target and failure to suppress the reflex when viewing a target rotating with the head.     

Paralysis of upward gaze as a presenting symptom of vitamin B12 deficiency

A 47-year-old woman presented with paralysis of upward gaze associated with Addison's pernicious anaemia. Administration of cyanocobalamin resulted in significant improvement of eye movements and haematological parameters. Isolated paralysis of upward gaze may be a feature of vitamin B12 deficiency.     

Supranuclear lateral gaze palsy of pontine origin. Report of 2 clinicopathologic cases with electrooculographic and electromyographic data

Electro-oculographic, electromyographic and pathological findings in two cases of supranuclear lateral gaze palsy of pontine origin have allowed us to define the clinical and physiopathologic features of the Pontine Reticular Formation (PRF) syndrome, and to formulate hypothesis about the terminal portion of the Occipito-Pontine Tract (OPT) involved in horizontal pursuit eye movements. The unilateral PRF syndrome is characterized by abnormal eye movements in the direction of the lesion. In the ipsilateral hemifield of movement there is paralysis of all movements from midline to extreme ipsilateral side, except oculo-cephalic reflex which remains intact (dissociated palsy); in the contralateral hemifield all saccades from extreme contralateral side to midline are suppressed, and this constitutes a specific abnormality of the PRF syndrome: quick phase of optokinetic and vestibular nystagmus are absent, while voluntary gaze is preserved but remarkably slow. It is suggested that this last fact is due to simple disfacilitation arising from undamaged PRF. Electromyographic findings suggest that the division between excitatory and inhibitory fibers of descending supranuclear oculomotor tracts ending in the abducens nuclei probably occurs in the lower pans. Anatomopathologic findings in the two cases show that the OPT runs in front of the Medial Longitudinal Fasciculus or in the lateral tegmentum and that it decussates, at least once, below the upper pons.     

Eye movements in relation to rhythmic masticatory muscle activities in patients with sleep bruxism

ObjectivesTo characterize eye movements during rhythmic masticatory muscle activities (RMMAs) in patients with sleep bruxism (SB).MethodsPolysomnographic (PSG) recordings were performed on SB patients and normal controls during sleep (n = 8 for each group) and wakefulness (n = 9 for each group). The eye movements associated with episodes of RMMAs/SB during sleep and jaw movements during wakefulness were analyzed.ResultsDuring sleep, all episodes of RMMAs/SB in the SB patients and controls were associated with eye movements and most of the RMMAs/SB related slow eye movements (SB patients: 96.29%, 1583/1644; Controls: 97.49%, 543/557) were horizontal in the SB patients and controls. During wakefulness, all of the series of jaw movements were associated with eye movements. Most of cycles of jaw movements (SB patients: 88.89%, 200/225; Controls: 95.11%, 214/225) were associated with slow eye movements and most of the eye movements (SB patients: 52.50%, 105/200; Controls: 61.21%, 131/214) were vertical. There were significant correlations between the durations of episodes of eye movements and RMMAs/SB during sleep and between the duration of episodes of eye movements and duration of series of jaw movements during wakefulness in the SB patients and controls.ConclusionsMost of RMMAs/SB episodes during sleep and jaw movements during wakefulness are associated with eye movements in SB patients and normal controls.     

From the abducens nucleus to spatial memory: an ocular motor journey

Advances in our knowledge on eye movements over the last 25 years are reviewed, focusing on the author's experience. First, the advantages of binocular frontal vision, which is a common characteristic of all predator mammals, are compared to those of lateral vision, characterizing their preys. Binocular frontal vision implies a perfect parallelism of both eyes, which is ensured in the pons by means of the abducens nucleus, controlling abduction as well as adduction. The pathological example of the "one-and-a-half" syndrome, in which the abducens nucleus and the adjacent medial longitudinal fasciculus are simultaneously impaired, is described. The main brainstem syndromes involving vertical eye movements are also reviewed: in particular, the third nerve nucleus syndrome, in which both ipsilateral third nerve paralysis and contralateral superior rectus paralysis (with hypotropia) result from a unilateral third nerve nucleus lesion. A case of upbeat nystagmus (in the primary position of gaze) due to a small upper pontine lesion, probably affecting the ventral tegmental tract (VTT) is also reported. This is an opportunity to emphasize that, although a number of cases of upbeat nystagmus due to focal brainstem lesions affecting the upward vestibular pathway (UVP)--either at the upper pontine (VTT) or caudal medullary level--exist in the literature, no convincing cases with downbeat nystagmus (in the primary position of gaze) due to a focal brainstem lesion have been reported. Downbeat nystagmus could result from a UVP hyperactivity (secondary to a floccular lesion) and the notion that this pathway is physiologically predominant compared to the downward pathway, maybe due to gravity, is developed. A new hypothesis about the role of the caudal medulla in UVP is also proposed. Next, the cortical control of saccadic eye movements is reviewed, with a reminder that reflexive saccades are mainly triggered by the parietal eye field whereas intentional saccades depend upon the frontal eye field. The inhibition of reflexive saccades is mainly controlled by the dorsolateral frontal cortex (DLPFC), i.e. area 46 of Brodmann. A few examples of the use of saccades as a research tool and model in cognitive neurosciences are given. The use of memory-guided saccades allowed us to study spatial memory and led us to propose a relatively original conception of the cortical control of spatial memory in which the DLPFC, the parahippocampal cortex and the hippocampal formation could be involved successively according to specific periods of time. An experiment using functional magnetic resonance imaging in a paradigm studying decision is described, again with the involvement of the DLPFC in the decisional process. Lastly, the usefulness of eye movements in clinical neuro-ophthalmology at the bedside as well as in neurophysiological or even neuropsychological research in the laboratory is emphasized.     

Ocular bobbing: the myth of its localizing value.

Ocular bobbing is a distinctive eye movement disorder seen in patients with pontine dysfunction. The typical phenomenon consists of abrupt, spontaneous downward jerks of the eyes with a slow return to the midposition in association with paralysis of spontaneous and reflex horizontal eye movements. Bobbing was present in a patient with acute cerebellar hemorrhage in whom no intrapontine lesions could be demonstrated. The myth that this sign is specific for intrapontine destruction has to be abandoned.     

Upper visual space neglect and motor deficits after section of the midbrain commissures in the cat

The neurological deficits following section of the midbrain commissures were studied in the cat. After a lesion of the commissures between the superior and inferior colliculi, with or without involvement of the posterior commissure, the animals showed a long lasting inattention for stimuli in the upper visual space, lack of exploratory head movements towards the neglected space, head ventroflexion and vertical paralysis of gaze. After a lesion of the commissure between the superior colliculi or of its rostral part only, the same symptomatology appeared, but it was short lasting. After a lesion of the posterior commissure, the head was kept dorsiflexed, the exploratory head movements towards the lower visual space were reduced and the stimuli presented in this space were often neglected. There was a paralysis of vertical eye movements. The findings are discussed in the frame of a premotor theory of neglect.     

Abducens internuclear neurons and their role in conjugate horizontal gaze

Experimental evidence suggests that brain stem lesions producing paralysis of lateral gaze and dissociation of conjugate horizontal eye movements have certain common features. Both of these disturbances involve abducens internuclear neurons (Abd IN) or their projections. Attempts were made to determine the course and terminal distribution of Abd IN in the monkey by autoradiographic techniques. Tritiated amino acids injected in the abducens nucleus (Abd N) labeled: (1) root fibers ipsilaterally, and (2) fibers that ascended in medial parts of the contralateral medial longitudinal fasciculus (MLF). In the opposite oculomotor complex (OMC) silver grains were profuse over the ventral nucleus (VN, medial rectus muscle) and patchy over caudal parts of the dorsal nucleus (DN, inferior rectus muscle). Labeling of cells in the reticular formation nucleus to Abd N resulted in transport ipsilaterally, outside the MLF, to the rostral interstitial nucleus of the MLF (RiMLF), a cell group considered to be concerned with vertical eye movements. Bilateral labeling of Abd N and cells of the nucleus prepositus (NPP) resulted in bilateral: (1) transport of isotope via root fibers and the MLF, and (2) selective distribution of silver grains in the OMC. Bilateral silver grain distribution in the OMC suggested profuse terminations in VN, patchy terminations in DN and vertical, linear terminations in caudal parts of the medial nucleus (MN, superior rectus muscle). Comparisons with more discrete unilateral labeling of cells in Abd N suggested that cells of the NPP project selectively to terminations in MN, and may be related to upward eye movements. Two conclusions were drawn: (1) The paresis of ocular adduction which occurs in both anterior internuclear ophthalmophlegia and in paralysis of lateral gaze results from involvement of Abd IN or their ascending projections, and (2) the NPP appears to project selectively to parts of MN of the OMC, a cell group said to provide crossed innervation for the superior rectus muscle.     

Unilateral paralysis of saccades caused by pontine tuberculoma

A unilateral lesion of the paramedian pontine reticular formation results in an ipsilateral laterality paralysis with abolition of all saccadic movements directed to the side of the lesion. It is generally accepted that the oculocephalic reflex alone enables the eyes to be deviated beyond the median line of the affected side. In the present case of a paramedian pontine tuberculoma, a paralysis of laterality in accordance with the above mentioned opinion was observed initially. Treatment led to recovery of an ipsilateral pursuit of normal amplitude, contrasting with the persistent abolition of ipsilateral saccadic movements. The significance of this dissociation is discussed together with that of the later reappearance of slow voluntary movements (slow saccadic movements) towards the affected side.     

The effect of cervical and vestibular reflexes on eye movements in Huntington's chorea

In 8 patients with manifest Huntington's Chorea vestibulo-ocular (VOR) and cervico-ocular (COR) reflexes were compared with eye movements during active head turnings. Seated patients were stimulated with their eyes closed by sinusoidal swings around the vertical axis at frequencies of 0.05, 0.1 and 0.2s-1 with amplitudes of 20, 40 and 60 degrees. 1) With all stimuli and in all patients a weak nystagmus was elicited in the direction of head movements, superimposed on larger slow eye deviations. 2) The averaged total saccadic amplitudes were smaller than in normals, increased with stimulus amplitudes and were smallest for COR, followed by VOR and active head movements. 3) The gain (peak velocity of slow phase of nystagmus to peak stimulus velocity) was only slightly below norm values and decreased with increasing stimulus frequency and amplitude. 4) The peak amplitudes of average slow eye deviations increased with stimulus amplitudes. In VOR they were comparable to norm values but were below them during COR and active head movements. 5) In normal subjects these slow eye deviations were compensatory to head movements in VOR but anticompensatory in COR and during active head movements. In choreic patients during COR and more often during active head movements these slow eye movements were compensatory for the head turning.     

Combined nuclear and supranuclear defects in ocular motility. A clinicopathologic study.

A 65-year-old man suffered a midbrain infarct after coronary artery bypass surgery. He was left with a severe neuro-ophthalmologic deficit consisting of paralysis of upward and downward vertical gaze, weakness of adduction of the left eye, a dilated fixed left pupil, and partial right Horner's syndrome. He died 31 months after the episode. Postmortem examination disclosed an infarct involving parts of both oculomotor nuclei as well as supranuclear structures thought to be involved in the mediation of vertical eye movements.     

Complete bilateral horizontal gaze paralysis disclosing multiple sclerosis

Two women presented with bilateral internuclear ophthalmoplegia evolving in a few days to complete bilateral horizontal gaze paralysis. Convergence and vertical eye movements were normal. Cerebral MRI showed a few small white matter lesions in the lateral ventricle regions, and, at the brainstem level, a single, small, bilateral lesion affecting the posterior part of the medial pontine tegmentum and responsible for the clinical syndrome. The condition gradually improved in both patients, following a similar progression as at the onset: improvement first involved the adduction movements in both eyes, whereas bilateral abduction paresis still persisted for a few weeks, before complete recovery of eye movements. Bilateral damage to the medial longitudinal fasciculus and subsequent lateral extent of damage to the region of the two abducens emerging fibres may explain the clinical findings. In both cases, the cause was probably multiple sclerosis.     

Oculomotor Disturbances in Balint's Syndrome: Anatomoclinical Findings and Electrooculographic Analysis in a Case

A 67-year-old man had repeated cerebral ischemic attacks, which resulted in a clinical picture combining paralysis of visual fixation, optic ataxia and impairment of visuospatial orientation, consistent with the definition of Balint's syndrome. Postmortem examination showed multiple lesions involving the occipital cortex of both sides and the white matter underlying the right insular cortex. EOG recording demonstrated a marked impairment of refixation saccades and saccades on verbal command. Smooth pursuit movements were completely abolished. Visual fixation was randomly achieved after many erratic exploratory movements and steadily maintained on the target (spasmodic fixation). During spasmodic fixation, EOG recording detected an ocular flicker resulting in a continuous instability of eye position. It is suggested that these findings may all be accounted for by the loss of panoramic vision due to a bilateral impairment of cortical areas 18 and 19.     

Inhibition of intracranial self-stimulation in brain stem-transected cats — A proposed mechanism of aversive effects produced by brain stimulation

Effects of intracranial self-stimulation of central ‘punishment areas’ were studied on an operant conditioning of vertical eye movements in the midpontine pretrigeminal cats as well as in the ence´phale isole´cats. In 36 pretrigeminal cats, the ventromedial hypothalamus (VMH), basal amygdaloid nuclei (AMY), dorsal central gray (CG) of the midbrain and the thalamic nuclei such as the ventralis posteromedialis (VPM) and ventralis posterolateralis (VPL) were tested. No suppression of eye movements indicating a passive avoidance conditioning from stimulation of these ‘punishment areas’ was obtained in 92 electrode tip sites.In 49 ence´phale isole´cats, stimulation of the VPM associated with contraction of the facial muscles, demonstrated a marked passive avoidance effect on the eye movements. After blocking both the trigeminal (5N) and facial nerves (7N), VPM stimulation no longer produced an increase of facial EMG activity and the suppressive effect of eye movements was abolished. Extracranial blockade of 7N alone, which induced facial muscle paralysis also showed similar effects. Bilateral blockade of cranial nerves from acoustic (8N) to hypoglossal (12N) nerves had no significant effect on the avoidance conditioning. The mass neural activity recorded from the 5N showed a marked increase of discharge by VPM stimulation which was reduced significantly after 7N blockade. These results may suggest a possibility that punishing effects of brain stimulation depend on feedback from the periphery (muscles, blood vessels and visceral organs), whereas reward effects essentially depend on neural circuitry confined within the forebrain above the rostral pons.     

Rapid eye movement generation in the primate. Physiology, pathophysiology, and clinical implications

The trajectories of rapid eye movements are usually described in a Cartesian coordinate frame with a horizontal, vertical and torsional component. The sensory to motor coordinate transformations for horizontal components of rapid eye movements can be localized to neurons of the paramedian pontine reticular formation (PPRF), where long-lead and short-lead burst neurons are found. The equivalent area for recoding of vertical and torsional movement components is situated in the rostral interstitial nucleus of the MLF (rostral iMLF). Pause cells in caudal midline structures of the PPRF help to coordinate the various movement components. Experimental inactivation of these different neuron population lead to palsies of rapid eye movement generation. A unilateral PPRF lesion leads to a loss of all horizontal rapid eye movements towards the ipsilateral side. A bilateral PPRF lesion involving caudal midline structures leads to a bilateral horizontal gaze palsy in addition to a severe disruption of vertical and torsional eye movements. A bilateral rostral iMLF lesion leads to a loss of all rapid eye movements with a vertical or torsional movement component. A unilateral iMLF lesion leads to a loss of all rapid eye movements with an ipsilateral torsional component.     

Clinical spectrum of ocular bobbing

Ocular bobbing is a distinctive movement disorder occurring in a variety of related forms herein classified as `typical'', `monocular'', and `atypical''. `Typical'' ocular bobbing occurs in patients with paralysis of horizontal conjugate eye movements and consists of abrupt, spontaneous downward jerks of the eyes with a slow return to the mid position. The `monocular'' type reflects co-existing unilateral third nerve paresis in addition to the bobbing. The `atypical'' type includes either a variation unexplained by associated oculomotor palsy, or bobbing with intact spontaneous or reflex horizontal eye movements. The clinical spectrum of ocular bobbing, its varied causes, and its prognostic significance are exemplified in a report of nine cases.     

Pontine metastasis with dissociated bilateral horizontal gaze paralysis.

A clinicopathological case of pontine metastatic tumour is reported with an oculomotor syndrome including bilateral horizontal gaze paralysis affecting saccades and foveal pursuit. During full-field pursuit, oculocephalic movement, and after caloric stimulation, the right eye alone was able to move slowly only 30 degrees to the right of the midline. Convergence and vertical eye movements were unaffected in either eye. The lesion lay in the whole left pontine tegmentum and partly in the right pontine tegmentum which was also strongly compressed and displaced to the right. The bilateral horizontal gaze paralysis resulted from damage to both paramedian pontine reticular formations. The unusual combination of an absence of foveal pursuit with the persistence of a rightward full-field pursuit analysed in the light of recent experimental work, suggested a clear separation between the brainstem pathways of these two types of pursuit movement. Lastly, according to our data and other clinicopathological findings previously reported, it appeared also that the paramedian pontine reticular formation role in the triggering of voluntary vertical saccades is less significant in man than in the monkey.