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PubMed2001

Abnormal exploratory eye movements in schizophrenic patients vs healthy subjects.

OBJECTIVE: We examined previously described exploratory eye movements abnormalities as biologic markers in schizophrenic patients in comparison with age-matched healthy subjects. MATERIAL AND METHODS: Using an eye-mark recorder, eye movements were analysed for mean gazing time, total number of gazing points, mean eye scanning length, total eye scanning length, and total gazing times as subjects viewed six simple pictures in preparation for copying them. RESULTS: In-patients, and to a lesser extent, out-patients, with schizophrenia showed a longer gazing time, fewer gazing points, a shorter mean and total eye scanning length. and longer gazing time than healthy subjects. In schizophrenic patients. negative symptom scores were positively correlated with mean gazing time (r = 0.33), and negatively correlated with the total number of gazing points (r = -0.29) as well as, the mean (r = -0.40) and total scanning length (r = -0.46). CONCLUSION: Exploratory eye movements are a biologic marker useful for evaluation of schizophrenia.

Adult↗
PubMed2000

Eye movements and the search for the essence of schizophrenia.

Clinical Schizophrenia has eluded precise description because of its protean phenotypic manifestations and variable clinical course, a variability that also makes it difficult to discover genetic linkages. Co-familial traits have higher recurrence risk rates than schizophrenia itself and might serve as pointers to the underlying physiology of schizophrenic illness. A dysfunction of smooth pursuit eye movements is one such co-familial trait that occurs in about 40 to 80% of schizophrenic patients and about 25 to 40% of their first degree relatives. The eye movement abnormality appears only when the subject tracks a moving target. We have traced this abnormality to a deficit in velocity sensitivity, a function that is regulated by a specific central nervous system network that includes the middle temporal and medial superior temporal areas of the extra-striate cortex. The higher familial recurrence risk of abnormal eye tracking, compared with that of clinical schizophrenia (about 5 to 8%), suggests that schizophrenic psychosis may be the rare form of a more prevalent disorder whose symptoms are much milder and more benign than the cognitive and behavioral disturbances of the clinical psychosis. From this vantage point, abnormal eye tracking can be viewed as one pleiotropic manifestation of schizophrenia, considered broadly, just as the café-au-lait spots of neurofibromatosis are a more benign and more frequent manifestation of that disease than are the neurofibromata.

Animals↗
PubMed1994

Correlation of regional cerebral blood flow equivalents measured by single photon emission computerized tomography with P300 latency and eye movement abnormality in schizophrenia.

Single photon emission tomography with the intravenous blood flow marker 99mTc-exametazime was carried out in 14 acutely ill drug-free schizophrenic patients from whom P300 event-related potential, smooth eye pursuit eye tracking and verbal fluency were measured within a few days of scanning. Smooth pursuit eye movement abnormality correlated significantly with abnormal tracer uptake in superior pre-frontal cortex on the right and left and inferior pre-frontal cortex on the left. Abnormal eye movement was also associated with higher tracer uptake in left anterior cingulate and left posterior cingulate. P300 latency was significantly correlated with higher tracer uptake in left superior pre-frontal and left parietal regions. Verbal fluency performance was negatively correlated with tracer uptake in left frontal region. Eye tracking abnormality in schizophrenia is associated with bilateral frontal lobe disturbance and P300 latency increase with left-sided frontal and temporoparietal dysfunction. There was, however, a significant inverse relation between eye tracking abnormalities and abnormal perfusion in the left anterior cingulate region.

Adult↗
PubMed1995

Eye movement abnormalities in systemic lupus erythematosus.

OBJECTIVE: To describe eye movement abnormalities in patients with systemic lupus erythematosus (SLE). DESIGN: Between January 1, 1970, and June 30, 1995, 113 patients with a clinical diagnosis of SLE were examined. Of these, 33 had ocular motor abnormalities and a diagnosis of SLE as defined by the revised criteria of the American College of Rheumatology. SETTING: Patients hospitalized on the wards of the Los Angeles County-University of Southern California Medical Center, Los Angeles. SUBJECTS: Thirty-three patients, 82% women, ranging in age from 19 to 58 years (mean, 33.5 years). The average duration of SLE was 3.5 years, and 10 patients had been symptomatic for 5 years or longer. RESULTS: Of 55 ocular motor signs, 33 involved limitation of eye movements or abnormal eye position at rest; abnormal spontaneous eye movements occurred 12 times; ptosis was seen in eight patients and psychogenic signs in two. Sixteen patients (48%) had brain-stem infarcts; 11 had other known causes, including three with meningitis, two with hysteria, and one each with ocular myositis, pseudotumor cerebri, both ocular myositis and pseudotumor cerebri, Guillain-Barré syndrome, hyperosmolality, and hypoxic encephalopathy. In four patients with isolated sixth nerve palsies and two with isolated ptosis, the cause remained unknown. CONCLUSIONS: Ocular motor signs in SLE are uncommon and often transitory. When present, they help to ascertain the location, and often the cause, of neurologic involvement.

Adult↗
PubMed1981

Eye movement abnormalities in rod monochromacy.

Eye movements were studied quantitatively using electro-oculography in seven patients with rod monochromacy. Attention was given to eye movement abnormalities that could help to differentiate rod monochromacy from other forms of congenital nystagmus. Horizontal nystagmus in center gaze had pendular and jerk waveforms with much lower amplitude than that in patients with other forms of congenital nystagmus and visual acuity of 20/200-20/400. Slow build-up of slow component velocity over many seconds and directional asymmetry of optokinetic nystagmus (OKN) were observed during monocular optokinetic stimulation. The directional asymmetry of OKN was characterized by a higher OKN gain (eye velocity/OKN drum velocity) during rotation of the OKN drum in the temporal-to-nasal direction in the visual field, than that during drum rotation in the nasal-to temporal direction. Similar directional asymmetry and slow build-up are found in afoveate animals, such as the rabbit, during monocular optokinetic stimulation, but are not found in normal human subjects or in patients with other forms of congenital nystagmus.

Adolescent↗
PubMedDate not supplied

Abnormal supranuclear eye movements in the child: a practical guide to examination and interpretation.

Abnormal eye movements in the infant or voting child can be congenital or acquired. They may be a result of abnormal early visual development or a sign of underlying neurologic or neuromuscular disease. It is important to be able to detect these abnormalities and to distinguish them from normal but immature eye movements. The spectrum of disease in children differs from that in adults. Serious, potentially fatal but treatable disorders can be acquired in infancy, and abnormal eye movements in a sometimes apparently well child should never be labeled as congenital or benign without careful investigation. Eye movement analysis can indicate the presence of an underlying condition and help the clinician to classify different neurologic diseases. It is important to carefully examine the ocular motor system in any children at risk of neurologic disease. This review provides a practical guide to the examination and interpretation of eye movements in the child and includes recent literature on eye movement disorders of childhood. We describe supranuclear abnormalities of the ocular motor system in the order in which we would normally examine it: saccades, pursuit, convergence, vestibulo-ocular reflex, and optokinetic nystagmus. Nystagmus, internuclear ophthalmoplegia, cranial nerve abnormalities, and "miswiring" phenomena (such as Duane's syndrome and synergistic divergence) are not discussed.

Child↗
PubMed1998

Eye tracking abnormalities in schizophrenia: evidence for dysfunction in the frontal eye fields.

BACKGROUND: Eye tracking deficits are robust abnormalities in schizophrenia, but the neurobiological disturbance underlying these deficits is not known. METHODS: To clarify the pathophysiology of eye tracking disturbances in schizophrenia, we tested 12 first-episode treatment-naive schizophrenic patients and 10 matched healthy individuals on foveofugal and foveopetal step-ramp pursuit tasks. RESULTS: On foveopetal tasks, the initiation of pursuit eye movements was delayed in schizophrenic patients, and their steady-state pursuit gain was reduced particularly at slower target speeds (8 and 16 deg/sec). In foveofugal step-ramp tasks, their primary catch-up saccades were normal in latency and accuracy, but their postsaccadic pursuit in the first 100 msec after the primary catch-up saccade was significantly reduced even relative to their slow steady-state pursuit, especially during and immediately after an acute episode of illness. CONCLUSIONS: These observations indicate that motion-sensitive areas in posterior temporal cortex provide sufficiently intact information about moving targets to guide accurate catch-up saccades, but that the sensory processing of motion information is not being used effectively for pursuit eye movements. Low-gain pursuit after the early stage of pursuit initiation suggests that the use of extraretinal signals about target motion (e.g., anticipatory prediction) only partially compensates for this deficit. The pattern of low-gain pursuit, impaired pursuit initiation, and intact processing of motion information for catch-up saccades but not pursuit eye movements, was consistent in the schizophrenic patients tested at five time points over a 2-year follow-up period, and implicates the frontal eye fields or their efferent or afferent pathways in the pathophysiology of eye tracking abnormalities in schizophrenia.

Adult↗
PubMed1998

Eye movement abnormalities in myotonic dystrophy.

We studied saccade and smooth pursuit eye movements in 31 patients suffering from myotonic dystrophy (MD). On the basis of mean value comparisons, saccades were slower and hypometric and smooth pursuit eye movements performed worse in MD patients than in controls. On an individual basis, saccade duration was prolonged in 67.7%, saccades were hypometric in 19.4%, saccade latency was delayed in 9.7%, and the smooth pursuit performance index was decreased in 9.7% of patients. Eye movement abnormalities did not correlate with those detectable by visual, brain-stem auditory and somatosensory evoked potentials. We attempted to classify eye movement abnormalities as myogenic or neurogenic on the basis of differences in combination of eye movement abnormalities and the occurrence of D5/D35 dissociation; the latter consists of a prolonged duration for large (35 degrees) but not for small (5 degrees) saccades. Since D5/D35 dissociation occurred in 26/33 multiple sclerosis patients with increased saccade duration, we considered it to be a neurogenic pattern attributable to a central nervous system (CNS) dysfunction. A prolonged duration without dissociation especially in combination with saccade hypometria, is interpreted as a myogenic pattern, although the lack of dissociation may also occur with CNS impairment in case of a marked increase in saccade duration. Accordingly we classified the oculomotor abnormalities detected as neurogenic in 11 MD patients and as myogenic in another 10, but in some subjects belonging to the second group concomitant CNS impairment is not to be excluded.

Adolescent↗
PubMed1983

Eye tracking abnormalities in patients with cerebrovascular disease.

Ten patients with disequilibrium, ataxia, and cerebrovascular abnormalities were studied using computer aided eye tracking and vestibular function tests. The patients had severe abnormalities in smooth pursuit (decreased gain) and saccade tests (increased delay, decreased accuracy). Optokinetic responses were less affected. The gain of the vestibulo-oculomotor reflex was sometimes affected. Patients with eye tracking abnormalities frequently had symptoms of difficulty reading and watching television. When the lesion was asymmetrical, abnormal eye tracking tests usually pointed to the side of the lesion. Computer aided eye tracking tests are a useful adjunct to the evaluation of the patient with suspected vascular disease. They help to locate areas of central nervous system dysfunction, and produce an objective measurement of the severity of impairment. Conversely, when impairment of the smooth pursuit or saccade system is detected in patients being evaluated for disequilibrium, an assessment of the patients' cerebrovascular system should be considered.

Adult↗
PubMed1988

Eye movement abnormalities as a predictor of the acquired immunodeficiency syndrome dementia complex.

Using infrared oculography, we recorded the eye movements in a group of patients with acquired immunodeficiency syndrome (AIDS), with or without the AIDS dementia complex (ADC). Our aim was to determine whether the severity of dementia could be correlated with abnormalities of eye movement and whether eye movement abnormalities could be detected prior to the onset of clinical dementia. Abnormalities of eye movement were present in seven of seven patients with mild, moderate, or severe ADC and in six of seven AIDS or asymptomatic human immunodeficiency virus-seropositive patients without clinical dementia, but at risk for ADC. The eye movement abnormalities detected included disturbances of both saccadic and smooth-pursuit function, and their severity correlated strongly with the severity of dementia. The abnormalities were qualitatively similar to those that occur in Alzheimer's disease but quantitatively less severe. Recording of eye movements may be a valuable, noninvasive technique for the early detection of neurologic dysfunction in asymptomatic patients who are seropositive for human immunodeficiency virus or in patients with AIDS, even prior to other clinical evidence of ADC. In particular, it may be of use in selecting high-risk patients requiring antiviral therapy and in monitoring the neurologic response to such treatment.

Acquired Immunodeficiency Syndrome↗
PubMed2000

Saccadic eye movement abnormalities in relatives of patients with schizophrenia.

Recent studies note abnormalities in saccadic eye movements of relatives of patients with schizophrenia. The current study examined which aspects of the saccadic system are affected, whether these saccadic abnormalities are associated with schizophrenia spectrum personality symptoms (SSP), and whether such an association is dependent on a family history of schizophrenia. Furthermore, the study examined what proportion of relatives have the saccadic abnormality(ies). Fifty-five first-degree relatives with no DSM-III-R Axis I diagnosis participated in the study. Twenty-one of these relatives experienced SSP symptoms and 34 had no Axis II diagnosis. Sixty-two subjects with no Axis I diagnosis were recruited from the community. Twenty-five experienced SSP symptoms and 37 had no Axis II diagnosis. Prosaccades (saccades toward the target) and antisaccades (saccades made in the opposite direction of the target jump) were examined. Relatives, particularly those with SSP, had difficulties with the antisaccade task as suggested by higher error rates and longer antisaccade latency. Prosaccades were not different in relatives compared to the community subjects, although the effects of field were different in the two groups on some measures. The antisaccade latency was 'abnormal' in only a small proportion (1.6%) of community subjects compared to 14.9% of all relatives (35.3% of SSP relatives and 3.3% of non-SSP relatives). Relatives of patients with schizophrenia have deficits in aspects of the saccadic system involved in generating internally driven saccades and inhibition of unwanted saccades. These deficits implicate frontal ocular motor neuronal circuitry involving frontal cortical and basal ganglia areas. These deficits are associated with SSP symptoms, but not in the absence of a blood relationship to schizophrenia. The relatively high prevalence rate of the abnormality in at-risk subjects may have relevance for use of these measures in linkage analysis.

Adult↗
PubMed1986

Total occlusion does not disrupt photoreceptor alignment.

Previous measurements of the photopic Stiles-Crawford function (SCF) in human observers prior to, during, and after (1) total occlusion, and (2) displacement of the eye's pupil, indicate by inference the presence of a phototropic mechanism which actively maintains photoreceptor alignment. In an attempt to replicate and expand the conclusions of these experiments, full SCFs were measured on three normal eyes and one abnormal eye prior to and after at least 6 days total occlusion. Counter to previous reports, total occlusion induced few if any alterations in the SCF rho value in both the normal and abnormal eyes.

Darkness↗
PubMed1994

Eye movement abnormalities in carriers of blue-cone monochromatism.

PURPOSE: Although impaired color vision and ERG changes have been detected in carriers of blue-cone monochromatism (BCM), no eye movement abnormalities have been identified. Quantitative eye movements of three obligate carriers of BCM were analyzed. METHODS: Horizontal and vertical eye movements of three obligate carriers of two families with BCM with visual acuity of 20/20 or better were recorded using the magnetic search coil technique. Subjects were examined fixing in primary and eccentric gaze and during horizontal and vertical smooth pursuit at 20 degrees, 40 degrees, and 80 degrees per second. RESULTS: All carriers displayed fixation instability. In two subjects, fine-amplitude upbeat, jerk-type nystagmus was detected. Reduced pursuit gain was found in the carriers. The third subject had small downbeat nystagmus. CONCLUSION: Abnormal eye movements are described for the first time in carriers of BCM. The nystagmus is clearly distinct from congenital or latent nystagmus and is similar to the nystagmus reported in BCM. Because all carriers had excellent visual acuity, in BCM, nystagmus is intrinsic to the disease and can appear independently of the visual defect.

Adult↗
PubMed1997

Eye movement abnormalities in a case of Tourette syndrome.

Tourette syndrome (TS) is a neuropsychiatric disorder that is characterised by the presence of multiple vocal, facial, and motor tics which change with time, and a number of other behavioural phenomena. Previous studies have not revealed any ocular-motor abnormalities. We report the eye movement studies of a patient with TS, using electrooculography and simultaneous video recording. Intrusive saccades occurred during smooth pursuit and optokinetic nystagmus. Reflexive and voluntary saccades were dysmetric and there was a complete failure of antisaccades. These abnormalities are characteristic of disease of the frontal lobes and basal ganglia. We review the literature with respect to the eye movement abnormalities associated with TS.

Adolescent↗
PubMed1999

The effect of abnormal fixational eye movements upon visual acuity in congenital nystagmus.

PURPOSE: The purpose of this study was to investigate the role that abnormal eye movements play in the degradation of visual acuity. METHODS: Visual acuity was measured monocularly in 10 normal subjects (26.7+/-4.3 years) and 5 subjects with congenital nystagmus (34.9+/-8.8 years), using Regan Repeat Letter charts (RRL) and a logMAR based test (LogMAR Crowded Acuity Test (CAT)) while eye movements were continuously recorded using a commercially available infrared limbal eye tracker (Type 54, Optoelectronic Developments, UK). The eye tracker was controlled via a virtual oscilloscope (Viewdac, Keighly Instruments, UK) on an IBM PC clone (Opus Technology 486). RESULTS: The mean visual acuity obtained with RRL was significantly higher than that obtained by CAT in the subjects with congenital nystagmus. A significant correlation was found between the root mean square value of the nystagmus waveform and the angular extent of CAT. Linear regression analysis revealed a correlation between the duration of the foveation periods and the linear acuity of the subjects with congential nystagmus. The nystagmus waveforms also demonstrated increased amounts of high frequency components (HFC: >3.0 Hz) when compared to the normal eyes. CONCLUSIONS: The results of this study reveal 1) RRL charts provide a measure of a subjects resolution limit which is less dependent on eye movements; 2) the duration of foveation periods has a significant effect on visual acuity measurements obtained using a linear test chart format; 3) the predominance of high frequency components in the congenital nystagmus waveforms lead to short foveation periods adding to the degree of fixation instability.

Adult↗
PubMed1994

Eye tracking dysfunction in schizophrenia: characterization of component eye movement abnormalities, diagnostic specificity, and the role of attention.

To characterize oculomotor components and diagnostic specificity of eye tracking abnormalities in schizophrenia, we examined a large consecutively admitted series of psychotic patients and matched controls. The most common abnormality in schizophrenic patients was low gain (slow) pursuit eye movements (47% of cases). Pursuit and saccadic eye movement abnormalities were no more severe in schizophrenic Ss than in those with affective psychoses, except that high rates of catch-up saccades were unique to schizophrenic Ss (17% of cases). These findings indicate that impaired pursuit eye movements are a major cause of eye tracking impairments in schizophrenia, that tracking dysfunctions commonly occur in affective psychoses, and that markedly high rates of catch-up saccades during eye tracking may be specific to schizophrenia.

Adult↗