Biomedical subjects

Alice M Saperstein

Publications and source records attributed to Alice M Saperstein.

6 recordsLinked to original sources

PubMed2006

Neuropsychology of the deficit syndrome: new data and meta-analysis of findings to date.

The deficit syndrome is thought to characterize a pathophysiologically distinct subgroup of patients with schizophrenia. Supporting this notion, prior research examining the neuropsychological correlates of the deficit syndrome has suggested the presence of a differential impairment in frontal and parietal functions. This article reports findings from 2 studies attempting to replicate and extend previous reports of a differential neuropsychological impairment in deficit schizophrenia. In the first study, we administered a comprehensive neuropsychological battery to 20 deficit and 25 nondeficit patients with schizophrenia and 25 normal healthy controls. In the second study, a meta-analysis was conducted of 13 separate studies examining the neuropsychology of the deficit syndrome. There was little evidence from either of the present studies that the deficit syndrome is associated with a selective impairment in frontal and parietal lobe functions. The first study failed to find significant differences in frontal or parietal abilities for deficit vs nondeficit patients. The meta-analytic findings revealed that deficit patients were globally more neuropsychologically impaired than nondeficit patients (effect size [ES] = 0.41). Relative to nondeficit patients, deficit patients performed poorest on tests of olfaction (ES = 1.11), social cognition (ES = 0.56), global cognition (ES = 0.52), and language (ES = 0.51). The neuropsychological impairments associated with the deficit form of schizophrenia do not follow an obvious anatomically defined pattern of impairment. The question of whether deficit patients exhibit a unique cognitive impairment profile will require a more sophisticated and rigorous examination of the neuropsychology of the deficit syndrome.

Adult↗

PubMed2006

A new dimension of sensory dysfunction: stereopsis deficits in schizophrenia.

BACKGROUND: Schizophrenia is a neurocognitive disorder with a wide range of cognitive and sensory impairments. Early visual processing has been shown to be especially impaired. This article investigates the integrity of binocular depth perception (stereopsis) in schizophrenia. METHODS: Seventeen schizophrenia patients and 19 healthy control subjects were compared on the Graded Circles Stereo Test. Results of stereoacuity were compared between patients and control subjects using t test. RESULTS: Schizophrenia patients demonstrated significantly (p = .006) reduced stereoacuity (mean = 142 arcseconds) versus control subjects (mean = 55 arcseconds). At the normative level for adults, patients performed below chance. CONCLUSIONS: These findings demonstrate an impairment of binocular depth perception and further confirm deficits of early visual processing in schizophrenia. Findings are discussed in context of magnocellular/dorsal stream processing with implications for visual processing and cognitive deficits.

Adult↗

PubMed2006

Neuropsychological functioning and social anhedonia: results from a community high-risk study.

Social anhedonia has shown promise as a vulnerability marker for schizophrenia-spectrum pathology. Validity data have come, in part, from findings indicating that cognitive deficits occurring in schizophrenia are also evident in individuals with elevated levels of social anhedonia. However, prior research on this topic has been limited because it has been based almost exclusively on the study of selective samples of college students. The present article reports baseline findings of neuropsychological functioning in social anhedonics and controls from a representative community sample. Data on a wide array of neuropsychological abilities from 18-19 year-old participants with (n = 85) vs. without (n = 87) elevated levels of social anhedonia were analyzed. We hypothesized that, compared to controls, social anhedonics would show impairments in memory and sustained attention. Additionally, we sought to determine if more severe cognitive impairment in anhedonics was associated with greater schizophrenia-spectrum pathology and poorer overall functioning. Compared to controls, socially anhedonic participants performed more poorly on two visual-spatial memory tasks and a test of visual-spatial construction. The groups did not statistically differ on any of the other neuropsychological measures including general cognitive ability and sustained attention. Group differences were not the result of depression, bipolar or substance abuse disorders. Neuropsychological functioning showed little relationship to current clinical symptoms and functioning. Longitudinal assessment of these participants as they move through the risk period should provide important insights into the neuropsychological correlates of the schizophrenia prodrome.

Adult↗

PubMed2006

Spatial working memory as a cognitive endophenotype of schizophrenia: assessing risk for pathophysiological dysfunction.

Research suggests that first-degree relatives and individuals with schizophrenia spectrum personality disorders (SSPD) may represent nonpenetrant carriers of the genetic diathesis for schizophrenia. This study examined visuospatial working memory (SWM) as a cognitive endophenotype of schizophrenia by expanding the concept of risk for pathophysiological dysfunction beyond overt psychosis. Risk was thus defined by familial status and the presence or absence of SSPD. SWM was assessed in the following groups, in order of decreasing likelihood of genetic vulnerability: 23 patients with schizophrenia, 17 SSPD relatives of patients with schizophrenia, 23 non-SSPD relatives of patients with schizophrenia, 14 SSPD community members with no family history of psychosis, and 36 non-SSPD community members. SWM performance during a computer task was quantified by A-Prime. Relative risk ratios for SWM deficits were compared among the groups. Compared with community non-SSPD volunteers, relative risk (RR) of SWM deficits was significantly elevated in patients with schizophrenia (RR = 3.76, p = .002) and SSPD family members (RR = 2.97, p = .027), but not in the family non-SSPD (RR = 1.88, p = .241) or community SSPD (RR = 1.03, p = .971) groups. The pattern of SWM performance deficits reflected the proposed model of latent genetic liability, upholding SWM as a viable cognitive endophenotype. The results underscore the importance of including both familial liability and the schizophrenia spectrum when considering risk for schizophrenia and schizophrenia-related traits. This is particularly relevant for research efforts to identify pathophysiological components of the disease.

Adult↗

PubMed2005

Early-stage visual processing and cortical amplification deficits in schizophrenia.

BACKGROUND: Patients with schizophrenia show deficits in early-stage visual processing, potentially reflecting dysfunction of the magnocellular visual pathway. The magnocellular system operates normally in a nonlinear amplification mode mediated by glutamatergic (N-methyl-D-aspartate) receptors. Investigating magnocellular dysfunction in schizophrenia therefore permits evaluation of underlying etiologic hypotheses. OBJECTIVES: To evaluate magnocellular dysfunction in schizophrenia, relative to known neurochemical and neuroanatomical substrates, and to examine relationships between electrophysiological and behavioral measures of visual pathway dysfunction and relationships with higher cognitive deficits. DESIGN, SETTING, AND PARTICIPANTS: Between-group study at an inpatient state psychiatric hospital and outpatient county psychiatric facilities. Thirty-three patients met DSM-IV criteria for schizophrenia or schizoaffective disorder, and 21 nonpsychiatric volunteers of similar ages composed the control group. MAIN OUTCOME MEASURES: (1) Magnocellular and parvocellular evoked potentials, analyzed using nonlinear (Michaelis-Menten) and linear contrast gain approaches; (2) behavioral contrast sensitivity measures; (3) white matter integrity; (4) visual and nonvisual neuropsychological measures, and (5) clinical symptom and community functioning measures. RESULTS: Patients generated evoked potentials that were significantly reduced in response to magnocellular-biased, but not parvocellular-biased, stimuli (P = .001). Michaelis-Menten analyses demonstrated reduced contrast gain of the magnocellular system (P = .001). Patients showed decreased contrast sensitivity to magnocellular-biased stimuli (P<.001). Evoked potential deficits were significantly related to decreased white matter integrity in the optic radiations (P<.03). Evoked potential deficits predicted impaired contrast sensitivity (P = .002), which was in turn related to deficits in complex visual processing (P< or =.04). Both evoked potential (P< or =.04) and contrast sensitivity (P = .01) measures significantly predicted community functioning. CONCLUSIONS: These findings confirm the existence of early-stage visual processing dysfunction in schizophrenia and provide the first evidence that such deficits are due to decreased nonlinear signal amplification, consistent with glutamatergic theories. Neuroimaging studies support the hypothesis of dysfunction within low-level visual pathways involving thalamocortical radiations. Deficits in early-stage visual processing significantly predict higher cognitive deficits.

Adult↗

PubMed2005

Impairments in generation of early-stage transient visual evoked potentials to magno- and parvocellular-selective stimuli in schizophrenia.

OBJECTIVE: Patients with schizophrenia demonstrate significant impairments of early visual processing, potentially implicating dysfunction of the magnocellular visual pathway. The present study evaluates transient visual evoked potential (tVEP) responses to stimuli biased toward the magnocellular (M) or parvocellular (P) systems in patients with schizophrenia vs. normal volunteers first to evaluate relative contributions of M and P systems to specific tVEP components in schizophrenia and, second, to evaluate integrity of early M and P processing in schizophrenia. METHODS: Seventy-four patients with schizophrenia and schizoaffective disorder were compared with 59 control subjects using separate stimuli to assess the tVEP response to M, P and mixed M/P conditions. Stimuli were biased toward M vs. P processing by manipulation of chromatic and achromatic contrast. C1, P1, N1 and P2 components were compared between patients and controls. All subjects showed 20/32 vision or better. RESULTS: Waveforms were obtained to low contrast (M), chromatic contrast (P) and high contrast (mixed M/P) stimuli in both patients and controls. C1 was present to P and mixed M/P stimuli. Patients showed a significant reduction in amplitude and an increase in latency of the C1 component. P1 was elicited primarily by M and mixed M/P stimuli, whereas N1 was elicited primarily by P and mixed M/P stimuli. Patients showed reductions in both P1 and N1 amplitudes across conditions. However, only reductions in P1 amplitude survived covariation for between group differences in visual acuity. Further, P1 amplitude reductions in the M condition correlated with a proxy measure of global outcome. CONCLUSIONS: M- and P-selective stimuli elicit differential components of the tVEP. Patients with schizophrenia show significant reductions in response even to simple visual stimuli. Deficits, particularly within the M system, may correlate significantly with global outcome and level of community functioning. SIGNIFICANCE: Whereas deficits in high-order cognitive processing have been extensively documented in schizophrenia, integrity of early-stage sensory processing has been studied to a lesser degree. The present findings suggest that deficits in early-stage visual processing are significantly related to overall clinical outcome in schizophrenia. Further, between-group differences in visual acuity may influence VEP results, even for subjects with 'normal' vision (20/32 or better).

Activities of Daily Living↗