Mark J. Morrow

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.

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 Brodmanns 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

Article abstract-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. NEUROLOGY 1996;46: 264-266

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. NEUROLOGY 1996;46: 514-521

Effects of fixation target timing on smooth-pursuit initiation.

We measured smooth pursuit and anticipatory smooth eye movements in four normal subjects, using step-ramp stimuli. Between trials, subjects fixated a motionless central target which disappeared before, after, or at the same time as the ramp stimulus appeared. We found that gaps or overlaps in the relative timing of fixation target offset and ramp onset neither expedited nor delayed the initiation of smooth pursuit. In contrast, anticipatory and smooth pursuit eye accelerations were influenced by the presence of a stationary foveal target; both were significantly higher when the fixation stimulus disappeared before ramp onset than when it disappeared after ramp onset.

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 ipsilatera1 horizontal saccades caused by pontine damage.

Recurrent Chemical Meningitis Due to Parasellar Epidermoid Cyst

Intracranial epidermoid cysts are exceedingly rare lesions that result from a disorder of gastrulation. They are seen only in the pediatric patient population. We describe a 44-year-old Hispanic woman who presented with acute confusion. The family reported two months of progressive headaches and two weeks of fever, blurred central vision, and restricted visual fields. On examination, the patient appeared ill, with a low-grade fever and stiff neck. Neurological testing was limited but grossly non-focal. Computerized tomography (CT) of the head and magnetic resonance imaging (MRI) of the brain showed a large cystic mass arising in the sella, where it displaced the normal pituitary gland. Cerebrospinal fluid (CSF) showed mildly elevated opening pressure with high protein, low glucose, and neutrophilic pleocytosis. Extensive serum and CSF evaluation were negative for infectious agents. The patient was initially started on empiric treatment for presumed infectious meningoencephalitis. As tests for bacterial and viral pathogens were normal, she was switched to fluconazole. The mental status returned to normal and she was discharged home with close follow up. She returned one month later with a recurrent headache, nausea, and stiff neck. The examination showed meningismus but was otherwise non-focal. MRI of the brain showed no change in the parasellar mass. Repeat CSF showed an even higher white blood cell (WBC) count and protein with continued hypo-glycorrhachia. She underwent trans-nasal trans-sphenoidal hypophysectomy and pathology revealed a squamous epithelium-lined keratin-filled cyst suggestive of an epidermoid cyst. The patient responded well to surgery and was discharged on pituitary hormone supplements alone. To our knowledge, this is a first adult case of recurrent chemical meningitis secondary to a ruptured epidermoid cyst in the sella.

Should Oral Corticosteroids Be Used to Treat Demyelinating Optic Neuritis

Isolated demyelinating optic neuritis is the most common cause of acute optic nerve dysfunction in adults. Although the natural history is one of spontaneous recovery of vision for most patients, treatment with corticosteroids is often offered to speed recovery and relieve pain. The type, dose, route, and duration of administration of corticosteroids vary considerably among providers and there is an ongoing discourse about the role of oral versus intravenous steroid therapy. Two experts debate this topic. For the purposes of this discussion, the authors have adopted the following definitions of steroid dosing: low-dose #100 mg methylprednisolone [MP] or equivalent per day; moderate-dose 101–499 mg MP or equivalent per day; high-dose