Purpose To present clinical findings and etiologic investigation of two consecutive clusters of toxic anterior segment syndrome (TASS) after uncomplicated phacoemulsification cataract surgery. Case Report At the Veterans Affairs Northern Indiana Health Care System Fort Wayne campus, 11 consecutive patients on two separate days in 2011 underwent clear corneal incision phacoemulsification cataract surgery by the same surgeon. On the first postoperative day, all patients had 1+ to 2+ diffuse limbus to limbus stromal edema and 2+ to 4+ anterior chamber white blood cells. Five eyes had inflammatory plaques on the surface of the intraocular implant, six had fibrin, three had hypopyon, and one had inflammatory debris “puff ball.” Visual acuity ranged 20/70 to 20/400. Treatment included moxifloxacin four times a day, diclofenac four times a day, and prednisolone acetate 1% every 1 to 2 hours. In all patients, active inflammation and corneal edema resolved within 6 weeks, and visual outcome was 20/20. Cataract surgery was paused for 5 months after the first cluster of TASS and then immediately paused again after restarting because of a second cluster. Although no specific causes were identified, etiologic investigation resulted in the implementation of multiple changes. The changes included new replacement surgical instruments, disposable irrigation/aspirator tip and handle, risk of residue on reusable instruments minimized, preservative-free medications used when available, ophthalmic ointment eliminated, manufacturers’ recommendations followed exactly, and eye instruments processed separately. Toxic anterior segment syndrome did not occur when surgery resumed 11 months after the last cluster. Conclusions There are multiple possible etiologies of TASS. However, as in our clusters, specific causes are often not identified. Thorough review of all steps in surgery, processing of equipment and preparation of injectable solutions and materials, and adoption of best practices can prevent additional cases of TASS. Prompt diagnosis and treatment of TASS are extremely important because this leads to a desirable outcome.

The objective of this study was to evaluate visual scanning strategies in carriers of the Huntington disease (HD) gene expansion and to test whether there is an association between measures of visual scanning and cognitive performance. The study sample included control (NC, n = 23), prediagnostic (PDHD, n = 21), and subjects recently diagnosed with HD (HD, n = 19). All participants completed a uniform clinical evaluation that included examination by neurologist and molecular testing. Eye movements were recorded during completion of the Digit Symbol Subscale (DS) test. Quantitative measures of the subject's visual scanning were evaluated using joint analysis of eye movements and performance on the DS test. All participants employed a simple visual scanning strategy when completing the DS test. There was a significant group effect and a linear trend of decreasing frequency and regularity of visual scanning from NC to PDHD to HD. The performance of all groups improved slightly and in a parallel fashion across the duration of the DS test. There was a strong correlation between visual scanning measures and the DS cognitive scores. While all individuals employed a similar visual scanning strategy, the visual scanning measures grew progressively worse from NC to PDHD to HD. The deficits in visual scanning accounted, at least in part, for the decrease in the DS score. © 2008 Movement Disorder Society

Objective To evaluate quantitative measures of saccades as possible biomarkers in early stages of Parkinson disease (PD) and in a population at-risk for PD. Methods The study sample (n=68) included mildly to moderately affected PD patients, their unaffected siblings, and control individuals. All participants completed a clinical evaluation by a movement disorder neurologist. Genotyping of the G2019S mutation in the LRRK2 gene was performed in the PD patients and their unaffected siblings. A high resolution, video-based eye tracking system was employed to record eye positions during a battery of visually guided, anti-saccadic (AS), and two memory-guided (MG) tasks. Saccade measures (latency, velocity, gain, error rate, and multiple step pattern) were quantified. Results PD patients and a subgroup of their unaffected siblings had an abnormally high incidence of multiple step patterns (MSP) and reduced gain of saccades as compared with controls. The abnormalities were most pronounced in the more challenging version of the MG task. For this task, the MSP measure demonstrated good sensitivity (87%) and excellent specificity (96%) in the ability to discriminate PD patients from controls. PD patients and their siblings also made more errors in the AS task. Conclusions Abnormalities in eye movement measures appear to be sensitive and specific measures in PD patients as well as a subset of those at-risk for PD. The inclusion of quantitative laboratory testing of saccadic movements may increase the sensitivity of the neurological examination to identify individuals who are at greater risk for PD.

PURPOSE:Abnormalities in saccades appear to be sensitive and specific biomarkers in the prediagnostic stages of Huntington disease (HD). The goal of this study was to evaluate test-retest reliability of saccadic measures in prediagnostic carriers of the HD gene expansion (PDHD) and normal controls (NC).METHODS:The study sample included 9 PDHD and 12 NC who completed two study visits within an approximate 1-month interval. At the first visit, all participants completed a uniform clinical evaluation. A high-resolution, video-based system was used to record eye movements during completion of a battery of visually guided, antisaccade, and memory-guided tasks. Latency, velocity, gain, and percentage of errors were quantified. Test-retest reliability was estimated by calculating the intraclass correlation (ICC) of the saccade measures collected at the first and second visits. In addition, an equality test based on Fisher's z-transformation was used to evaluate the effects of group (PDHD and NC) and the subject's sex on ICC.RESULTS:The percentage of errors showed moderate to high reliability in the antisaccade and memory-guided tasks (ICC = 0.64-0.93). The latency of the saccades also demonstrated moderate to high reliability (ICC = 0.55-0.87) across all tasks. The velocity and gain of the saccades showed moderate reliability. The ICC was similar in the PDHD and NC groups. There was no significant effect of sex on the ICC.CONCLUSIONS:Good reliability of saccadic latency and percentage of errors in both antisaccade and memory-guided tasks suggests that these measures could serve as biomarkers to evaluate progression in HD.

The ocular motor system directs the eyes to targets of interest, maintains fixation, pursues moving targets, and stabilizes the eyes in the face of head, body, or background motion. It provides the signals for the perception of a stable world despite retinal image motion. Ocular motor disorders may take the form of nystagmus, saccadic intrusions, saccadic oscillations, or dysmetria. Eye-movement data and analysis allow differential diagnosis of these disorders, and suggestions for, and evaluation of, therapies.

Eye-head gaze pursuit-related activity was recorded in rostral portions of the nucleus reticularis tegmenti pontis (rNRTP) in alert macaques. The head was unrestrained in the horizontal plane, and macaques were trained to pursue a moving target either with their head, with the eyes stationary in the orbits, or with their eyes, with their head voluntarily held stationary in space. Head-pursuit-related modulations in rNRTP activity were observed with some cells exhibiting increases in firing rate with increases in head-pursuit frequency. For many units, this head-pursuit response appeared to saturate at higher frequencies (>0.6 Hz). The response phase re:peak head-pursuit velocity formed a continuum, containing cells that could encode head-pursuit velocity and those encoding head-pursuit acceleration. The latter cells did not exhibit head position-related activity. Sensitivities were calculated with respect to peak head-pursuit velocity and averaged 1.8 spikes/s/deg/s. Of the cells that were tested for both head- and eye-pursuit-related activity, 86% exhibited responses to both head- and eye-pursuit and therefore carried a putative gaze-pursuit signal. For these gaze-pursuit units, the ratio of head to eye response sensitivities averaged approximately 1.4. Pursuit eccentricity seemed to affect head-pursuit response amplitude even in the absence of a head position response per se. The results indicated that rNRTP is a strong candidate for the source of an active head-pursuit signal that projects to the cerebellum, specifically to the target-velocity and gaze-velocity Purkinje cells that have been observed in vermal lobules VI and VII.

OBJECTIVES:Studies of saccadic eye movement impairment in Alzheimer's disease (AD) have largely focused on simple reflexive eye movements and the antisaccade task. The effects of manipulating stimulus timing have been little studied.METHODS:Fourteen patients with mild to severe AD and 11 age-matched controls were studied on the antisaccade task, while latencies on simultaneous, gap and predictable tasks were recorded from 11 patients and 11 controls. Dementia severity was assessed with the Mini-Mental State Examination.RESULTS:As a group, patients' latencies were significantly higher and more variable on the simultaneous and gap tasks. Predictable task performance was similar in mean but significantly more variable. Grossly anticipatory responses by patients were common on the predictable, simultaneous and gap tasks. Exclusion of these from subject means revealed that AD patients, when making target-driven saccades, demonstrated a gap effect of similar magnitude to normal subjects. Patients made significantly fewer correct antisaccades and significantly more reflexive errors not followed by a corrective antisaccade than did controls.CONCLUSIONS:The frequent presence of grossly anticipatory saccades may reflect dysfunction of fixation mechanisms possibly involving projections from frontal lobe to superior colliculus. The less frequently seen, marked prolongation of latency may reflect changes in posterior parietal mechanisms mediating reflexive saccade generation. The presence of the gap effect demonstrates a continued ability to benefit from externally controlled stimulus disengagement. Patients' ability to make appropriately timed saccades to targets of known locations was particularly impaired, but the target sequence itself was at least grossly correctly learned. Larger studies may be able to identify clinically distinct populations of AD patients.

Peter Hispanus, who became Pope John XXI, wrote a book about eye diseases and their treatment in the 13th century. De Oculis was not a scholarly treatise about eye diseases, but a manual intended for general physicians. Nevertheless, Latin copies were made into the 16th century, indicating its influence and importance. We present the first published English translation of De Oculis, based on a synthesis of the medieval Latin manuscripts and a German translation from the 19th century. The sources of Peter's understanding of the causes and treatment of eye diseases were the more scholarly and complete treatises by Greek and Arab writers. Many of the diseases described then cannot be correlated precisely with ophthalmic disorders known to us today because of the limited understanding of anatomy, function and pathophysiology that existed. However, De Oculis provides us with a glimpse of the practice of medicine in the Middle Ages.

OBJECTIVESTo characterize the pathogenesis and clinical features of optic disc edema associated with obstructive sleep apnea syndrome (SAS).METHODSA series of 4 patients with SAS and papilledema (PE) underwent complete neuro-ophthalmologic evaluation and lumbar puncture. In 1 patient, continuous 24-hour intracranial pressure (ICP) monitoring was also performed.RESULTSAll 4 patients had bilateral PE that was asymmetric in 2. Three patients had optic nerve dysfunction, asymmetric in 1, unilateral in 2. Daytime cerebrospinal fluid pressure measurements were within normal range. Nocturnal monitoring performed in one patient, however, demonstrated repeated episodes of marked ICP elevation associated with apnea and arterial oxygen desaturation.CONCLUSIONSWe propose that PE in SAS is due to episodic nocturnal hypoxemia and hypercarbia resulting in increased ICP secondary to cerebral vasodilation. In these individuals, intermittent ICP elevation is sufficient to cause persistent disc edema. These patients may be at increased risk for developing visual loss secondary to PE compared with patients with obesity-related pseudotumor cerebri because of associated hypoxemia. The diagnosis of SAS PE may not be appreciated because daytime cerebrospinal fluid pressure measurements are normal and because patients tend to present with visual loss rather than with symptoms of increased ICP.

The objective of this article was to evaluate the etiologies, findings, and treatment of ocular neuromyotonia (ONM) in three case reports. The etiologies of ONM were determined by the histories, neuroradiologic tests, or biopsies. Clinical observations, videotaping, and electronic eye movement recordings documented the eye movement abnormalities. Intermittent diplopia developed several years after myelography with thorium dioxide (Thorotrast), radiation treatment for a pituitary tumor, and radiotherapy for medulloblastoma of the posterior fossa. All of the patients had intermittent, variable tropias that occurred spontaneously or were induced by eccentric gaze. One patient had a partial third nerve palsy, and another had a unilateral internuclear ophthalmoplegia (INO). ONM involved the paretic third nerve, extraocular muscles, and ipsilateral lateral rectus muscle in one patient, the paretic medial rectus muscle (INO) in one patient, a lateral rectus muscle (INO) in one patient, and a lateral rectus muscle in the last patient. Eye movement recordings were consistent with spasms of the involved muscles. Carbamazepine (Tegretol) abolished the ONM in two patients. The other patient had been taking carbamazepine for seizures and developed ONM when the dose was decreased. Increasing the dose abolished the ONM. ONM is an unusual cause of intermittent diplopia and strabismus, but its distinctive history and signs identify it easily. Damage to the peripheral cranial nerves might produce segmental demyelination, axonal hyperexcitability, and a self-perpetuating, reverberating circuit that causes spasms of the extraocular muscles.

In Reply. —Small children with nystagmus whom ophthalmologists encounter most often have congenital nystagmus (CN). However, other causes of nystagmus should be sought. The most important are neurologic disorders, since the child's general health can be at risk and early medical intervention might be needed. Therefore, I emphasize detecting neurologic disorders by seeking neurologic signs and symptoms and looking for nystagmus characteristics that are uncommon in CN, eg, vertical and torsional directions. Neuroradiologic tests are not used routinely, but are performed when neurologic disorders are suspected. I agree with Dr Brodie that electrophysiologic tests, such as electroretinography, are useful in detecting some ocular abnormalities associated with nystagmus. The nystagmus can usually be distinguished from CN. For example, nystagmus associated with rod monochromatism often has a higher frequency and/or smaller amplitude than CN.1Congenital nystagmus has characteristic waveforms that can be revealed by eye movement recordings in young children.

The analysis of vertical saccades by electrooculography (EOG) is limited by the presence of waveform artifacts that occur with both upward and downward saccades. The artifacts have been shown to increase the calculated velocities of upward saccades. For better evaluation of the nature of these artifacts, voluntary vertical saccades were recorded by EOG and magnetic search coil in five normal subjects and by EOG only in two patients who had previously undergone enucleation. All subjects demonstrated peaked EOG artifacts during vertical saccades. The amplitude of these artifacts was decreased but not completely eliminated by eyelid or eyeball fixation during the attempted saccade. Peak saccadic velocities were also decreased by eyelid fixation, but EOG measurements were generally less accurate than those obtained by search coil. There is evidence that these artifacts may be the result of a combination of eyelid electrical activity and resistance effects.

Eye-movement recordings may be helpful in the differentiation of Duane's syndrome from sixth-cranial-nerve palsy. Voluntary horizontal saccades were recorded and quantitated by electrooculography in 18 patients with unilateral type I Duane's syndrome and in 25 patients with sixth-nerve palsy. When ranges of abduction were matched, the peak velocities of abducting saccades in affected eyes were decreased equally in both groups. However, the peak velocities of adducting saccades in sound eyes were slowed in patients with Duane's syndrome. Because the standard deviations in saccadic velocities are large, computer-based, stepwise discriminant analyses were performed to identify the variables that proved to be useful in differentiating the two disorders. By entering these variables into the discriminant functions that were created, we could distinguish Duane's syndrome from sixth-nerve palsy in a statistically significant manner.

Despite the complete absence of horizontal saccades, two patients with pontine gliomas had horizontal reflex eye movements within a range of +/- 20 degrees. The gain (peak eye velocity/peak stimulus velocity) and phase of the vestibulo-ocular reflex were normal, but the optokinetic gain was decreased. The latency, accuracy, and peak velocity of vertical saccades were normal. Apparently the voluntary gaze centers in the pontine reticular formation are not crucial for generating horizontal vestibular or vertical saccadic eye movements.