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Correction
March 2007

Errors in Table and Figure in: Startle Gating Deficits in a Large Cohort of Patients With Schizophrenia: Relationship to Medications, Symptoms, Neurocognition, and Level of Function

Arch Gen Psychiatry. 2007;64(3):360. doi:10.1001/archpsyc.64.3.360

Errors in Table and Figure. In the Original Article titled “Startle Gating Deficits in a Large Cohort of Patients With Schizophrenia: Relationship to Medications, Symptoms, Neurocognition, and Level of Function,” published in the December 2006 issue of the ARCHIVES (2006;63:1325-1335), there are errors in Table 2 and Figure 2A. In Table 2, the third entry under the column heading “Characteristic” should have read, “Psychiatric hospitalizations, mean (range), No.” In Figure 2A, the lengths of the error bars have been corrected. The corrected Figure 2 and its legend are printed here in their entirety.

Figure 2.
Medication effects on prepulse inhibition (PPI) in patients. A, Mean PPI percentage collapsed across prepulse intervals in patients treated with no antipsychotic medication (AP), typical APs, atypical APs, or both typical and atypical APs. Mean PPI percentage for normal comparison subjects (NCSs) are shown as a single point. Analysis of variance of PPI percentage in patients revealed a significant main effect of medication subgroups (F3,95 = 7.52, P<.001), which was also significant when limited to 60-millisecond prepulse intervals (F3,99 = 6.06, P<.001). Compared with PPI among NCSs, PPI was significantly reduced among unmedicated patients (*P<.001 by Fisher protected least-significant difference) and among all patients not receiving an atypical AP (P = .001); these effects were independent of prepulse interval (all P<.01 for 30-, 60-, and 120-millisecond intervals). Error bars indicate SEM. †P<.005 vs no AP. ‡P<.001 vs no AP. B, Mean startle magnitude on pulse-alone and combined prepulse and pulse trials in patients not receiving atypical APs and case-matched NCSs; groups were balanced precisely for startle magnitude on pulse-alone trials by omitting 1 subject whose startle magnitude on pulse-alone trials was 4.3 SDs above the group mean. Error bars indicate SEM. Analysis of variance of PPI percentage across these groups revealed a significant main effect of diagnosis (F1,34 = 7.39, P<.02) († in inset) and no sex × diagnosis interaction (F1,34 = 3.05, P>.05). Analysis of variance of startle magnitude revealed a significant main effect of trial types (F3,99 = 35.77, P<.001) and a significant interaction of diagnosis × trial type (F3,99 = 5.21, P<.003). Analysis of variance limited to prepulse trials revealed significantly greater startle magnitude on prepulse trials in patients than in NCSs (F1,40 = 15.60, P<.001), reflecting a loss of sensorimotor inhibition. *Significantly greater startle on prepulse + pulse trials in patients than in NCSs after significant interaction of diagnosis × trial type by Fisher protected least-significant difference.

Medication effects on prepulse inhibition (PPI) in patients. A, Mean PPI percentage collapsed across prepulse intervals in patients treated with no antipsychotic medication (AP), typical APs, atypical APs, or both typical and atypical APs. Mean PPI percentage for normal comparison subjects (NCSs) are shown as a single point. Analysis of variance of PPI percentage in patients revealed a significant main effect of medication subgroups (F3,95 = 7.52, P<.001), which was also significant when limited to 60-millisecond prepulse intervals (F3,99 = 6.06, P<.001). Compared with PPI among NCSs, PPI was significantly reduced among unmedicated patients (*P<.001 by Fisher protected least-significant difference) and among all patients not receiving an atypical AP (P = .001); these effects were independent of prepulse interval (all P<.01 for 30-, 60-, and 120-millisecond intervals). Error bars indicate SEM. †P<.005 vs no AP. ‡P<.001 vs no AP. B, Mean startle magnitude on pulse-alone and combined prepulse and pulse trials in patients not receiving atypical APs and case-matched NCSs; groups were balanced precisely for startle magnitude on pulse-alone trials by omitting 1 subject whose startle magnitude on pulse-alone trials was 4.3 SDs above the group mean. Error bars indicate SEM. Analysis of variance of PPI percentage across these groups revealed a significant main effect of diagnosis (F1,34 = 7.39, P<.02) († in inset) and no sex × diagnosis interaction (F1,34 = 3.05, P>.05). Analysis of variance of startle magnitude revealed a significant main effect of trial types (F3,99 = 35.77, P<.001) and a significant interaction of diagnosis × trial type (F3,99 = 5.21, P<.003). Analysis of variance limited to prepulse trials revealed significantly greater startle magnitude on prepulse trials in patients than in NCSs (F1,40 = 15.60, P<.001), reflecting a loss of sensorimotor inhibition. *Significantly greater startle on prepulse + pulse trials in patients than in NCSs after significant interaction of diagnosis × trial type by Fisher protected least-significant difference.

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