Craniotopic defects of smooth pursuit and saccadic eye movement.

I recorded smooth pursuit and saccadic eye movements in six patients with unilateral cerebral infarction. By comparing responses within the hemiranges of eye position to the right and left of the orbital midline and in rightward and leftward directions, I quantified craniotopic and directional ocular motor deficits. Two patients had ipsiversive gaze deviation and severe craniotopic defects in which they could not generate smooth pursuit or saccadic eye movement into the contralateral orbital hemirange. Three patients without gaze deviation generated worse smooth pursuit in the contralateral hemirange than in the ipsilateral hemirange, but each had symmetric saccades according to eye position. All patients with craniotopic pursuit defects also had directional smooth tracking asymmetries in which eye velocities were lower for targets moving ipsilaterally than for targets moving contralaterally. Craniotopic and directional defects were associated with damage in the frontal eye field region. Orbital position is taken into account by cerebral circuits that govern smooth pursuit and saccades.

Cerebral hemispheric localization of smooth pursuit asymmetry.

We recorded horizontal smooth pursuit in 23 patients with discrete unilateral cerebral hemispheric lesions and in 12 normal subjects. Most patients had bidirectional reduction of smooth pursuit gain, indicating that each cerebral hemisphere participates in smooth pursuit in both directions. Pursuit gain fell proportionately more with increasing target acceleration in patients than in normals. A normal phase relationship between eye and target motion in patients indicated an intact predictor mechanism for smooth pursuit. Ten patients had pursuit asymmetry with lower gain when tracking toward the side of cerebral damage; none had lower gain when tracking away. Two patients with lower ipsilateral gain had frontal lobe lesions. Areas of anatomic overlap of lesions associated with asymmetric pursuit in 8 patients provide evidence for a pursuit pathway that originates from Brodmann areas 19 and 39 and descends to the brainstem through the posterior limb of the internal capsule.

Retinotopic and directional deficits of smooth pursuit initiation after posterior cerebral hemispheric lesions.

We investigated the initiation of ocular smooth pursuit with horizontal ramp targets in 16 patients with unilateral posterior cerebral lesions. Four of the 16 patients had directional pursuit asymmetry, in which smooth eye movement velocities were reduced toward the lesion, independent of target location on the retina. Of seven patients with normal visual fields for the target, two had a retinotopic eye movement deficit consisting of impaired smooth pursuit of targets moving in both horizontal directions in the hemifield contralateral to their lesion. Patients with retinotopic deficits and normal visual fields, and those with directional deficits, had impairment of smooth pursuit similar to that caused by unilateral lesions of cortical areas MT (middle temporal) and MST (medial superior temporal) in monkeys. All but one patient with either of these defects had a lesion near the junction of Brodmann's areas 19, 37, and 39, providing evidence that this region includes the human homologues of monkey areas MT and MST. One patient with a retinotopic pursuit defect and normal visual fields had a lesion of the rostral superior temporal sulcus, which may have included the homologue of the superior temporal polysensory area of monkeys.

Superior oblique myokymia associated with a posterior fossa tumor: oculographic correlation with an idiopathic case.

Superior oblique myokymia (SOM) was the only neurologic sign in a patient with an astrocytoma involving the midbrain tectum. Oculography showed monocular bursts of tonic and phasic intorsion and depression and miniature oscillations identical to those of idiopathic SOM. SOM stopped after tumor resection.

Bilateral ocular neuromyotonia: oculographic correlations.

We observed bilateral ocular neuromyotonia in a 45-year-old woman previously treated for a pituitary adenoma. She experienced episodic diplopia attributable to dysfunction of muscles innervated by both oculomotor nerves. Oculography demonstrated episodes of tonic adduction with slowing and restriction of saccades in all directions, but no oscillatory component. A combination of impaired phasic firing in agonist muscles and tonic contraction of antagonist muscles explains the paroxysms of eye movement limitation in this disorder.

Oblique misdirection and slowing of vertical saccades after unilateral lesions of the pontine tegmentum.

Three patients with unilateral lesions of the pontine tegmentum, identified by CT and MRI, had abnormal vertical saccades and slowed ipsilateral horizontal saccades. Attempted vertical saccades were misdirected obliquely, away from the side of the lesion, and their vertical components were prolonged. Oblique saccades had curved trajectories and prolonged durations of their vertical components. Unilateral damage to excitatory burst neurons and pause cells in the medial part of the caudal paramedian pontine reticular formation may cause these abnormal vertical and oblique saccades. Misdirection and slowing of vertical saccades can accompany the paralysis or slowing of ipsilateral horizontal saccades caused by pontine damage.

Effects of eye and head position on horizontal and vertical smooth pursuit.

PURPOSE: To identify and explain the effects of eye and head position on smooth pursuit eye movements in normal humans. METHODS: Horizontal and vertical smooth pursuit were measured in different eye-in-orbit positions in normal subjects, using a magnetic search coil technique with sinusoidal and step-ramp stimuli. Pursuit also was tested in different horizontal head-on-trunk positions. RESULTS: Pursuit gain to sinusoidal targets averaged approximately 15% less with the eyes centered 30 degrees horizontally or vertically from the primary position than with the eyes near the orbital midline. In contrast, initial pursuit responses to step-ramp stimuli were similar regardless of eye position. For sinusoidal and step-ramp responses in eccentric eye positions, no significant differences were found between pursuit movements directed toward the orbital midposition and pursuit movements directed away from it. Changes in head position had no effect on smooth pursuit. CONCLUSIONS: Sinusoidal smooth pursuit function decreases modestly for horizontal and vertical motion in eccentric eye positions. This effect is not caused by reductions in gain for centrifugal movements compared to centripetal movements, implying that the pursuit nonlinearities expected to arise from orbital mechanics are largely eliminated by central processing. Eye position-related differences in retinal or eye motion feedback or in predictive input may explain the influence of eye position on smooth pursuit maintenance. Changes in target position with respect to a trunk-centered frame of reference did not produce the orbital eccentricity effects that were documented because sinusoidal pursuit gain did not vary with head rotation.

Spasm of fixation: a quantitative study.

Spasm of fixation, consisting of impaired initiation of saccades in the presence of fixation target, but normal initiation in the absence of a fixation target, was measured in a patient with cerebral hemispheric damage. When a central target was constantly present, the patient made horizontal saccades to the sudden appearance of a second target at very prolonged latencies (mean 369 ms). In the absence of a central fixation target, saccadic latency decreased to normal (197 ms). Extinction of a target for a gap interval elicited very short latency movements (122 ms), termed express saccades. The intervals between self-paced horizontal refixation saccades with the head immobile were prolonged, whereas voluntary refixation saccades with the head free to move occurred at shorter intervals. We postulate that cerebral hemispheric damage may cause spasm of visual fixation by disinhibiting the substantia nigra pars reticulata, thereby inhibiting the superior colliculus.

The relationship of anticipatory smooth eye movement to smooth pursuit initiation.

We measured anticipatory smooth eye movements and smooth pursuit initiation with predictable and unpredictable step-ramp stimuli in normal subjects. Subjects generated anticipatory eye motion before targets moved and during intervals when targets suddenly disappeared. Expectations of target trajectory modified pursuit acceleration and latency, demonstrating that pursuit initiation is not governed by visual inputs alone. Anticipatory smooth eye movements and predictive contributions to smooth pursuit had similar accelerations and velocities. Anticipation and pursuit initiation varied in parallel between subjects; anticipation was stronger in subjects who generated faster smooth pursuit. These findings imply that anticipatory and smooth pursuit eye movements are governed by a common mechanism.

Smooth pursuit initiation in young and elderly subjects.

Smooth pursuit initiation to step-ramp stimuli was investigated in normal subjects, young and elderly. Older subjects had significant reductions in initial pursuit acceleration before saccades, and in post-saccadic and peak pursuit velocities. Aging impairs the open-loop performance of the pursuit system, possibly by decreasing sensitivity to retinal image motion or by limiting the conversion of visual motion signals into commands for smooth pursuit. Lower open-loop pursuit gain degrades steady-state, closed-loop smooth pursuit in senescence. Our elderly subjects also made less accurate saccades to moving targets, implying defective use of visual motion information by the saccadic system.

Neurologic complications of vitamin E deficiency: case report and review of the literature.

A well-defined degenerative neurological condition has been associated with cholestatic liver disease in children. This syndrome, heralded by gait and limb ataxia, areflexia, and proprioceptive and vibratory sensory loss, has also been observed in abetalipoproteinemia (Bassen-Kornzweig syndrome), cystic fibrosis, and intestinal malabsorption states. A significant body of evidence suggests that vitamin E (alpha-tocopherol) deficiency is in large part responsible for this condition. In this article, a patient manifesting this syndrome is reported, and the current status of the vitamin E deficiency state is reviewed.

Function and dysfunction of supranuclear and internuclear eye movement pathways.

Recent investigations in ocular motility have shed light on the anatomical and physiological mechanisms that govern smooth pursuit, saccades, and the vestibulo-ocular reflex in normal humans and patients with neurological disorders. Functional neuroimaging and transcranial magnetic stimulation have been used in normal human subjects to draw parallels with basic investigations in animals. Quantitative studies of eye movement disorders in patients with focal brain dysfunction have added to our understanding of human pathophysiology. Finally, some of the most practical of recent work has been aimed at developing therapies to alleviate the functional limitations caused by abnormal eye movements.

Torsional nystagmus in the lateral medullary syndrome.

Torsional nystagmus was recorded in 3 patients with the lateral medullary syndrome. Magnetic search coil oculography demonstrated slow phases of nystagmus of increasing, decreasing, and constant velocity. Neural integration of torsional eye velocity commands to position commands is impaired by lateral medullary infarction. Torsional pulsion of saccades, consisting of torsional fast eye movements induced during saccades downward or away from the side of infarction, was recorded in 2 patients. All patients had skew deviation with hypotropia on the side of brainstem damage. The torsional nystagmus beat away from the side of infarction in each patient, but in one it alternated direction as the eyes drifted about a neutral position of torsion. We attribute the torsional nystagmus to an imbalance of central projections from the anterior and posterior semicircular canals and the otolith receptors that mediate ocular counterroll.

Epidural anaesthesia for caesarean section in an achondroplastic dwarf.

We describe the anaesthetic management of a parturient with achondroplasia presenting for Caesarean section under epidural anaesthesia. A block extending from T4 to S4 was established over 25 min using a total of 12 ml of 2.0% lidocaine (lignocaine) with epinephrine (adrenaline) 1:200,000 and fentanyl 37.5 micrograms. Apart from mild discomfort during peritoneal incision, her perioperative course was uneventful. Achondroplasia is reviewed and the anaesthetic implications of the condition are discussed.