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In certain conditions patients with schizophrenia make markedly smaller (hypometric) saccades than controls. This hypometria has been thought to reflect dopaminergic blockade as a result of antipsychotic medication. We tested this hypothesis by comparing the performance of an antipsychotic‐naïve group and an antipsychotic‐treated group of first‐episode schizophrenic patients on a predictive saccade paradigm. We explored the possibility that hypometria reflects a spatial working memory deficit by correlating performance on neuropsychological tests of mnemonic function with saccadic accuracy. Both the drug‐naïve and treated schizophrenic patients made hypometric saccades when compared with a group of matched controls. Primary saccade amplitude also correlated significantly with performance on some of the neuropsychological tests. These results are discussed in terms of the roles of cortical dopamine and working memory deficits in schizophrenic patients.

Rationale: Smooth pursuit abnormalities have been observed in antipsychotic naive first-episode patients, suggesting that they are intrinsic to the illness. However, it is not clear whether these abnormalities are as severe as those observed in more chronic patients. In addition, although research suggests that there are no short-term effects of conventional antipsychotic medication, the effects of long-term antipsychotic medication on smooth pursuit eye movements are relatively unknown. Objectives: To determine the short and long term effects of antipsychotic medication on the smooth pursuit performance of first-episode and chronic patients with schizophrenia. Methods: We compared the smooth pursuit performance of antipsychotic-treated and untreated first-episode and chronic schizophrenic patients with healthy controls using a comprehensive range of performance measures. This included velocity gain, the number, type and size of intrusive and corrective saccades, and the average time between the change in direction of the target and the change in direction of the eye movement, a measure of subjects’ ability to predict target movement. Results: Chronic schizophrenic patients had significantly reduced velocity gain, took longer to respondto the change in target direction and made more catch-up saccades than both first-episode schizophrenic patients and controls. First-episode patients were impaired relative to controls only on the measure of velocity gain. There were no differences between antipsychoticnaive and treated first-episode patients. Antipsychoticfree chronic patients were significantly less impaired on velocity gain than matched continuously treated chronic patients. These results were not influenced by group differences in age and symptom severity. Conclusions: These results show that: 1) the main index of smooth pursuit, velocity gain, is impaired early in the course of schizophrenia; 2) whereas velocity gain is unaffected by short-term (weeks) medication

In certain conditions patients with schizophrenia make markedly smaller ~hypometric! saccades than controls. This hypometria has been thought to reflect dopaminergic blockade as a result of antipsychotic medication. We tested this hypothesis by comparing the performance of an antipsychotic-naïve group and an antipsychotic-treated group of first-episode schizophrenic patients on a predictive saccade paradigm. We explored the possibility that hypometria reflects a spatial working memory deficit by correlating performance on neuropsychological tests of mnemonic function with saccadic accuracy. Both the drug-naïve and treated schizophrenic patients made hypometric saccades when compared with a group of matched controls. Primary saccade amplitude also correlated significantly with performance on some of the neuropsychological tests. These results are discussed in terms of the roles of cortical dopamine and working memory deficits in schizophrenic patients.

Whilst most laboratory smooth pursuit tasks are performed in the dark, in everyday life pursuit commonly occurs over a structured background. This background provides a powerful stimulus to the optokinetic reflex (OKR), inducing a background “drag” on pursuit eye movements. An inability to inhibit the influence of the OKR may be a contributing factor to the dysfunctional pursuit performance observed in many schizophrenic patients. Smooth pursuit performance was measured in 23 first-episode schizophrenic patients and 23 healthy controls matched for age and estimated IQ, both in the dark and over a structured background (a random checkerboard of black and white squares). Velocity gain was measured, as well as the number and size of corrective saccades (catch-up saccades) and intrusive saccades (anticipatory saccades and square wave jerks). Overall, schizophrenic patients had lower velocity gain and made more catch-up saccades than controls. The effect of the background was to lower velocity gain and increase the number of catch-up saccades to the same extent in schizophrenic patients and controls. There were no significant interactions between group and background effect. These results suggest that, although their overall level of performance was worse, the schizophrenic patients were as able as controls to inhibit the effect of the OKR. Since lesion studies show that inhibition of the OKR requires intact inferior parietal regions in man (Lawden et al., 1995), one hypothesis is that the parietal component of smooth pursuit may be intact in schizophrenia.

A series of molecular adducts of 2-aminothiazole derivatives - 2-aminothiazole, 2-amino-2-thiazoline and 2-aminobenzothiazole with the carboxylic-acid-substituted heterocyclics indole-2-carboxylic acid, N-methylpyrrole-2-carboxylic acid and thiophene-2-carboxylic acid - have been prepared and characterized using X-ray powder diffraction and in five cases by single-crystal X-ray diffraction methods. These five compounds are the adducts of 2-amino-2-thiazolium with indole-2-carboxylate [(C3H7N2S)+(C9H6NO2)-], and N-methylpyrrole-2-carboxylate [(C3H7N2S)+-(C6H6NO2)-], 2-aminobenzothiazolium with indole-2-carboxylate [(C7H7N2S)+(C9H6NO2)-], N-methylpyrrole-2-carboxylate [(C7H7N2S)+(C6H6NO2)-] and thiophene-2-carboxylate [(C7H7N2S)+(C5H3O2S)-]. All complexes involve proton transfer, as indicated by IR spectroscopy, while the five crystal structures display similar hydrogen-bonding patterns with the dominant interaction being an graph set dimer association between carboxylate groups and the amine/heterocyclic nitrogen sites. Futhermore, in each case a subsiduary interaction between an amino proton and a carboxylate oxygen completes a linear hydrogen-bonded chain. In addition to this, the indole-2-carboxylate molecules in the adduct structure with 2-amino-2-thiazolium form associated dimers which add to the hydrogen-bonding network.

Attempts to determine the physiological nature of smoothpursuit dysfunction in schizophrenia have included many investigations of saccade rates, but the findings have been variable. The present investigation tested the hypothesis that the misclassification of blinks as saccades affects saccade rates in studies using only infrared oculography (IROG). Both IROG and vertical electro-oculography (VEOG), the latter of which provides an objective measure of blinking, were collected while 17 schizophrenia patients and 19 healthy control subjects were presented 0.4 Hz sinusoidal stimuli. Of the blinks identified with the VEOG, 42% were not identified, and 37% were misclassified as saccades when only the IROG was used. Most misclassified saccades masqueraded as catch-up saccades (CUS)(66%) and anticipatory saccades (AS) (34%). However, CUS and total saccade rates were significantly elevated in schizophrenia patients both before and after correction for misclassified blinks. Rates of other saccade subtypes and blinks did not differ. Therefore, the misclassification of blinks as saccades is likely to introduce some measurement error into estimates of saccade rates, but it is unlikely to account for the variability in estimates evidenced in the literature. However, when the blinkto-saccade ratio is larger, as it is in saccadic paradigms, saccade metrics may be vulnerable to the effects of blink misclassification

Background. Previous studies of oculomotor dysfunction in schizophrenia have tended to concentrate on abnormalities of smooth pursuit eye tracking in chronic medicated patients. We report the results of a study of smooth pursuit, re¯exive and antisaccade performance in drug naive and antipsychotic treated ®rst-episode schizophrenic patients. Methods. Smooth pursuit and saccadic eye movements were recorded in 36 ®rst-episode schizophrenic patients and 36 controls matched for age and estimated IQ. The schizophrenic patients were divided into drug-naive (N¯17) and antipsychotic treated groups (N¯19). Results. Smooth pursuit velocity gain was signi®cantly lower than controls only in the drug-naive patients. The treated patients did not differ signi®cantly from either the controls or the untreated group. In an antisaccade paradigm both treated and drug-naive schizophrenic patients demonstrated an increased number of errors, but only drug-naive patients also demonstrated an increased latency in initiating correct antisaccades. Conclusions. These impairments are unlikely to be due to a generalized de®cit in oculomotor function in the schizophrenic groups, as there were no differences between the groups in saccadic metrics on a re¯exive saccade task. The results show that both smooth pursuit and saccadic abnormalities are present at the onset of schizophrenia and are integral to the disorder.