Self-Appraisal of Illness Questionnaire (SAIQ): relationship to researcher-rated insight and neuropsychological function in schizophrenia.

The Self-Appraisal of Illness Questionnaire (SAIQ) is a self-report instrument designed to assess attitudes toward mental illness among persons receiving psychiatric treatment. This instrument was developed for use in community settings, adapted closely from the Patient's Experience of Hospitalization questionnaire. In order to examine the validity of the SAIQ, a factor analysis was first conducted on the items of this instrument in a sample of 59 outpatients with schizophrenia or schizoaffective illness. Three factors emerged: Need for Treatment, Worry, and Presence/Outcome of Illness. Next, to examine the concurrent validity of these three SAIQ subscales, they were correlated with researcher rated insight scales and neuropsychological tests. Results indicated that the Need for Treatment and Presence/Outcome subscales were significantly correlated with both researcher-rated insight scales and with neuropsychological tests of executive functioning. The Worry subscale was not associated with either researcher-rated insight scales or neuropsychological tests. It was concluded that the Need for Treatment and Presence/Outcome subscales may be used in combination as a brief screening instrument for clients with schizophrenia receiving outpatient psychiatric treatment who may be at risk for treatment non-compliance due to a lack of insight into illness.

Childhood sexual trauma and psychosocial functioning in adults with schizophrenia.

OBJECTIVE: This study explored the association between sexual abuse in childhood and the severity of psychosocial deficits in adults with schizophrenia. METHODS: The Quality of Life Scale, which assesses current interpersonal and work function, and the NEO personality inventory, which assesses personality dimensions relevant to social functioning, were administered to 54 individuals who had been diagnosed as having schizophrenia. Nineteen of the individuals reported having been sexually abused as children, and 35 reported no history of abuse. RESULTS: A multiple analysis of variance indicated that there were differences between the group of individuals who had a history of sexual trauma and the group that did not. Subsequent univariate analysis of variance indicated that the individuals with a history of abuse had poorer current role functioning and fewer of the basic psychological building blocks necessary for sustaining intimacy. They also demonstrated higher levels of neuroticism, which is a measure of vulnerability to emotional turmoil. The two groups did not differ in frequency of interpersonal contacts or level of extroversion. CONCLUSIONS: Sexual abuse in childhood is associated with poorer psychosocial functioning in adults with schizophrenia.

Noninvasive external pacing in the newborn.

Complete atrioventricular block in the newborn occasionally requires emergency intervention when the heart rate is too low to provide adequate cardiac output. While medications are frequently ineffective, emergent implantation of a pacemaker is not always feasible and carries a significant morbidity. We report two cases of complete atrioventricular block in newborns treated immediately after birth with an external noninvasive pacemaker system.

Neurocognitive correlates of helplessness, hopelessness, and well-being in schizophrenia.

Persons with schizophrenia are widely recognized to experience potent feelings of hopelessness, helplessness, and a fragile sense of well-being. Although these subjective experiences have been linked to positive symptoms, little is known about their relationship to neurocognition. Accordingly, this study examined the relationship of self-reports of hope, self-efficacy, and well-being to measures of neurocognition, symptoms, and coping among 49 persons with schizophrenia or schizoaffective disorder. Results suggest that poorer executive function, verbal memory, and a greater reliance on escape avoidance as a coping mechanism predicted significantly higher levels of hope and well being with multiple regressions accounting for 34% and 20% of the variance (p < .0001), respectively. Self-efficacy predicted lower levels of positive symptoms and greater preference for escape avoidance as a coping mechanism with a multiple repression accounting for 9% of the variance (p < .05). Results may suggest that higher levels of neurocognitive impairment and an avoidant coping style may shield some with schizophrenia from painful subjective experiences. Theoretical and practical implications for rehabilitation are discussed.

Neurocognitive and symptom correlates of self-reported childhood sexual abuse in schizophrenia spectrum disorders.

This study examined whether self-reported childhood sexual abuse in schizophrenia spectrum disorders is linked with severity of neurocognitive deficits. The Wisconsin Card Sorting Test, California Verbal Learning Test, and select WAIS III subtests were administered to 15 participants with schizophrenia or schizoaffective disorder who had been sexually abused and to 28 participants with no abuse history. Controlling for age and premorbid IQ, a MANCOVA indicated there were group differences (f(9, 31) = 5.53, p < .001). Subsequent ANCOVA indicated that the sexual abuse group performed more poorly on tests of working memory and information processing speed. Childhood sexual abuse is associated with more severe working memory deficits in adults with schizophrenia spectrum disorders.

Nitric oxide synthase inhibition and delayed cerebral injury after severe cerebral ischemia in fetal sheep.

After transient cerebral ischemia in fetal sheep, delayed disruptions in cerebral energetics are represented by a delayed increase in cortical impedance, a progressive decrease in the concentration of oxidized cytochrome oxidase as measured by near-infrared spectroscopy, and cortical seizures. Because the production of nitric oxide (NO), a potent mediator of neuronal death, is increased during this phase, the present study investigated whether inhibition of NO synthesis could ameliorate the delayed disruption in cerebral energetics. Eleven late gestation fetal sheep were subjected to 30 min of transient cerebral ischemia in utero. Two hours later, the treatment group (n = 5) received a continuous infusion of N(G)-nitro-L-arginine, a competitive inhibitor of NO synthase, whereas the control group (n = 6) received PBS. Changes in concentration of oxidized cytochrome oxidase, cortical impedance, and electrocortical activity were observed for 3 d. A delayed increase in cortical impedance of similar magnitude and duration commenced at 14+/-4 h in the control and at 15+/-3 h in the treatment groups. The progressive decrease in oxidized cytochrome oxidase signal, by -2.2+/-0.2 micromol/L in the control and -2.0+/-0.4 micromol/L in the treatment group at 72 h postischemia, was similar in both groups. In both groups, delayed cortical seizures were indicated by intense low-frequency electrocortical activity. In the treatment group, duration of cortical seizures was increased and the intensity of the final electrocortical activity was more depressed (-19+/-1 dB versus -10+/-2 dB). The results indicate that after cerebral ischemia in fetal sheep, NO synthase inhibition does not ameliorate the delayed disruptions in cerebral energetics. However, the effect of NO synthase inhibition on delayed cortical seizures may improve our understanding of the role of NO during this phase.

Nitric oxide synthase inhibition attenuates delayed vasodilation and increases injury after cerebral ischemia in fetal sheep.

Transient cerebral ischemia in fetal sheep is followed by a period of delayed cerebral injury associated with cerebral vasodilation. As nitric oxide (NO) can mediate both vasodilation and neuronal death, this study investigated whether inhibition of NO synthesis would attenuate the vasodilation and decrease cerebral injury. Eleven late gestation (range 122-133 d) fetal sheep were subjected to 30 min of transient cerebral ischemia in utero. Two hours later, treatment group (n = 5) received a continuous infusion of NG-nitro-L-arginine (L-NNA) at a dose of 50 mg.h-1 for 4 h followed by 20 mg.h-1 for the subsequent study period, a competitive inhibitor of NO synthase (NOS), whereas a control group (n = 6) received PBS. Inhibition of NOS activity was confirmed in the treatment group by 1) suppression of the fall in mean arterial blood pressure (MAP) associated with acetylcholine (p < 0.01), and 2) persistent increase in MAP after commencement of L-NNA (p < 0.05). Changes in cerebral blood volume (CBV) were observed for 3 d by measuring changes in concentration of total cerebral Hb ([tHb]) using near infrared spectroscopy. The delayed increase in CBV commenced at 13.1 +/- 1.0 h postischemia in the control and 12.7 +/- 2.3 h in the treatment group. Maximum increase at 30-36 h was 0.5 +/- 0.1 mL.100 g-1 in the treatment group and 1.2 +/- 0.2 mL.100 g-1 in the control (p < 0.05). Final CBV was depressed below preischemic baseline in the treatment (-0.7 +/- 0.2 mL.100 g-1) but not the control group (-0.1 +/- 0.3 mL.100 g-1) (p < 0.05). Neuronal loss, quantified histologically 3 d postischemia, indicated that cerebral injury was increased in the treatment group (p < 0.05). The results indicate that after transient cerebral ischemia in fetal sheep, NOS inhibition attenuates the delayed rise in CBV but does not decrease the extent of cerebral injury.

Obsessive and compulsive symptoms in schizophrenia: clinical and neurocognitive correlates.

Although research suggests that the presence of obsessive and compulsive symptoms in schizophrenia is associated with graver levels of psychosocial dysfunction, it is unclear whether it is also related to clinical features of illness. Accordingly, the present study compared the symptom levels and neurocognitive function of participants with schizophrenia who had and did not have significant obsessive or compulsive symptoms. Analyses of variance revealed that participants with significant levels of either obsessive or compulsive symptoms (N = 21) had higher levels of positive and emotional discomfort symptoms on the Positive and Negative Syndrome Scale (PANSS) and performed more poorly on the Wisconsin Card Sorting Test, a measure of executive function, than participants without obsessions or compulsions (N = 25). ANCOVAs controlling for level of obsessions also revealed that participants with significant levels of compulsions (N = 12) in particular had higher levels of negative and positive symptoms on the PANSS than participants without compulsions (N = 34). The impact of obsessive-compulsive phenomena on the course and outcome of schizophrenia is discussed.

Delayed vasodilation and altered oxygenation after cerebral ischemia in fetal sheep.

The study investigated the hypothesis that delayed cerebral injury after transient cerebral ischemia is associated with vasoconstriction and decreased cerebral oxygenation. Eight chronically instrumented, late gestation fetal sheep were subjected to 30 min of cerebral ischemia in utero. Cortical impedance (CI) and electrocorticogram (ECoG) were recorded to determine the time course of cellular dysfunction. Histologic outcome was assessed 4 d postischemia. Changes in cerebral vascular tone and oxygenation were observed during and for 4 d after the insult using near infrared spectroscopy to measure changes in total cerebral Hb ([tHb]), oxyhemoglobin ([Hbo2]), and oxidized cytochrome aa3 ([Cyto2]). Results are expressed as mean +/- SEM. CI increased transiently during ischemia; then a delayed increase commenced 17.5 +/- 2.3 h postischemia and peaked at 42.3 +/- 2.4 h. ECoG was depressed during and after the insult. Seizures started 13.6 +/- 3.0 h postinsult and persisted for 25.4 +/- 3.2 h. Increases in [tHb] indicated two periods of cerebral vasodilation: immediately after early reperfusion, lasting 2.3 +/- 0.4 h and peaking to 20 +/- 2.0 mumol.L-1; and a later phase, commencing 12.8 +/- 2.0 h postischemia, peaking to 43 +/- 4.0 mumol.L-1 and lasting 43.1 +/- 5.2 h. [Hbo2] was relatively elevated (18 +/- 3.0 mumol.L-1) during d 4 postischemia, demonstrating a delayed increase in mean cerebral oxygen saturation. [Cyto2] fell during the insult (-0.7 +/- 0.2 mumol.L-1); and, commencing at 28-30 h postischemia, fell progressively to reach a minimum of -5.0 +/- 2.8 mumol.L-1 at 78-80 h postischemia. A greater fall in [Cyto2] was related to worse cerebral injury (p < 0.05). Delayed cerebral injury is accompanied by vasodilation and increased mean cerebral oxygen saturation, although a progressive fall in [Cyto2] might indicate a fall in mitochondrial oxygenation, cell loss, or changes in tissue optical characteristics.