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for Quality Eye Care without any external financial support. Authors and reviewers of the guidelines are volunteers and do not receive any financial compensation for their contributions to the documents. The guidelines are externally reviewed by experts and stakeholders before publication.

for Quality Eye Care without any external financial support. Authors and reviewers of the guidelines are volunteers and do not receive any financial compensation for their contributions to the documents. The guidelines are externally reviewed by experts and stakeholders before publication.

Sensorimotor gating, measured by prepulse inhibition (PPI) of the startle reflex, is reduced in schizophrenia patients and in rats treated with dopamine agonists. Strain differences in the sensitivity to the PPI-disruptive effects of dopamine agonists may provide insight into the genetic basis for human population differences in sensorimotor gating. We reported strain differences in the sensitivity to the PPI-disruptive effects of the D1/D2 agonist apomorphine in adult rats, with greater sensitivity in Harlan Sprague Dawley (SDH) versus Wistar (WH) rats. However, Kinney et al. (1999) recently reported opposite findings, using Bantin-Kingman Sprague Dawley (SDBK) and Wistar (WBK) rats; in fact, SDBK rats did not exhibit clear apomorphine-induced reductions in sensorimotor gating. These new findings of Kinney et al. (1999) directly conflict with over 15 years of results from our laboratories and challenge interpretations from a large body of literature. The present studies carefully assessed drug effects on sensorimotor gating in SD versus W strains, across rat suppliers (H vs BK). Significantly greater SDH than WH apomorphine sensitivity in PPI measures was observed in both adult and 18 d pups, confirming that these strain differences are both robust and innate. These strain differences in apomorphine sensitivity were not found in adult BK rats. Supplier differences in sensitivity (SDH > SDBK) were also evident in the PPI-disruptive effects of D1 but not D2-family agonists; PPI was clearly disrupted by quinpirole in both SDH and SDBK rats. These findings demonstrate robust, innate, neurochemically specific, and apparently heritable phenotypic differences in an animal model of sensorimotor gating deficits in human neuropsychiatric disorders.

To study mood disturbance in Graves ophthalmopathy. Methods: Forty-eight patients (mean age, 55 years; 40 women and 8 men) with Graves ophthalmopathy from a university-based referral center were classified into two groups, 24 with moderate/severe disease (study group) and 24 with negligible/mild disease (control group). The groups were matched with regard to demographic and medical characteristics. All participants completed a mood survey to assess differences in degree of emotional distress. Main Outcome Measure: The Profile of Mood States survey, a 65-item self-reported inventory designed to assess emotional distress, was the primary outcome measure. A total mood disturbance score was assigned by summing the scores derived on the 6 subscales of the survey-tension, depression, vigor, confusion, fatigue, and anger. Results: Analysis of variance revealed that patients with moderate/severe Graves ophthalmopathy showed significantly greater emotional distress than patients with mild/negligible Graves ophthalmopathy on the Profile of Mood States mean total score (PϽ.001). Additionally, patients who had disfigurement (proptosis) as the predominant clinical feature had significantly elevated emotional distress compared with the control group (P=.01), whereas no significant difference was detected between the control group and patients with diplopia as the predominant clinical feature (P =.20). Conclusion: Patients with moderate to severe Graves ophthalmopathy have significant mood disturbance, especially when disfiguring signs are predominant. We propose that evaluation of the psychological burden of the disease should be considered in routine follow-up and in decisions regarding treatment.

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