Recall and recognition in mildly disturbed schizophrenics: the use of matched tasks

Calev, Avraham

doi:10.1017/s0033291700003676

Cited by 72 publications

(27 citation statements)

References 28 publications

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“…In addition, patients taking any medication with anticholinergic activity (either benztropine or antipsychotics) were significantly impaired relative to the other patients in free recall but not in recognition. These results are compatible with previous research (Calev, 1984 ;Perlick et al 1986;Paulsen et al 1995). Our data suggest that drugs with anticholinergic properties affect memory by impeding semantic organization at encoding, in agreement with Strauss et al (1990).…”

Section: Discussionsupporting

confidence: 94%

“…Which components of memory are specifically affected by those drugs has not been clearly established. Calev (1984) showed that anticholinergic drugs affected free recall rather than recognition. Likewise, Perlick et al (1986) and Paulsen et al (1995) reported that higher serum anticholinergic level and anticholinergic drug dosage were correlated with deficit in free recall, but not in recognition.…”

Section: Introductionmentioning

confidence: 99%

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Medications and verbal memory impairment in schizophrenia: the role of anticholinergic drugs

et al. 2004

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Section: Discussionsupporting

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Medications and verbal memory impairment in schizophrenia: the role of anticholinergic drugs

et al. 2004

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“…This is in keeping with other studies showing that impairment in the Morris maze was observed only when more than 20% of the dorsal hippocampus was damaged (Moser et al ., 1993). The experiments thus strongly indicate that memory deficit, a well‐documented feature of schizophrenia (Calev, 1984a,b; Cutting, 1985; Goldberg et al ., 1989; McKenna et al ., 1990; Gold et al ., 1992; Tamlyn et al ., 1992; Elliot & Sahakian, 1995; McKay et al ., 1996; Meltzer & McGurk, 1999; Sharma & Antonova, 2003) can result from habenula damage. Spatial memory may be particularly pertinent to schizophrenia, as spatial learning in rodents is considered as a model of declarative memory in humans (O'Keefe & Nadel, 1978), and declarative memory appears to be selectively impaired in schizophrenia (Perry et al ., 2000).…”

Section: Discussionmentioning

confidence: 87%

Habenula lesions cause impaired cognitive performance in rats: implications for schizophrenia

Lecourtier

Neijt

Kelly

2004

Eur J of Neuroscience

135

111

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Cognitive impairment is a prominent feature of schizophrenia. Currently there is no well-accepted explanation of the aetiology of this disorder, but recent evidence indicates that dysfunction of the habenula may be involved. We therefore examined whether habenula lesions in Sprague-Dawley rats cause behavioural changes resembling those of schizophrenia. Rats received either habenula lesions, a sham operation or a small lesion of the overlying dorsal hippocampus as a check that effects observed were not due to incidental damage to this structure. As there are alterations of social behaviour, sensorimotor gating and cognition in schizophrenia, we examined comparable behaviours. Social interaction time was measured during a 5-min encounter with a novel juvenile conspecific. Prepulse inhibition of an acoustic startle response, as an index of sensorimotor gating, was measured with prepulses of various amplitudes, and spatial cognitive performance was assessed in the Morris water maze task. Histological analysis showed that habenula lesions substantially damaged both medial and lateral habenula bilaterally while largely sparing neighbouring structures. Assay of choline acetyltransferase (ChAT) in the interpeduncular nucleus terminal region of the habenulo-interpeduncular tract, showed marked reduction (by 80%) in habenula-lesioned animals. Habenula-lesioned rats, but not the control group with small dorsal hippocampus lesions, showed marked impairment of Morris maze performance compared to the sham-operated control group. Social interaction time and prepulse inhibition were not significantly altered in either lesion group. The results are consistent with a role of the habenula in cognition, and with the view that pathology of the habenula may contribute to the cognitive impairments of schizophrenia.

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“…Arguing against the interpretation that this differential level of deficit is an artifact of the discriminating power of the performance measure employed (Chapman & Chapman, 1973;Chapman & Chapman, 1978) is a report that chronic non-demented schizophrenic patients showed a larger deficit on a free recall compared to a performance matched recognition task (Calev, 1984a). This result was obtained despite the higher reliability for the recognition task, which would have predicted a higher discriminating power for the recognition versus the recall task, but also see (Calev, 1984b) and (Mohamed et al, 1999). Several reviews have concluded that mean verbal recall performance is among the measures that show strong familial effects in relatives of schizophrenic patients (Sitskoorn et al, 2004;Whyte et al, 2005;Trandafir et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Verbal recall and recognition in twins discordant for schizophrenia

Erp

Therman

Pirkola

et al. 2008

Psychiatry Research

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The nature, neural underpinnings, and etiology of deficits in verbal declarative memory in patients with schizophrenia remain unclear. To examine the contributions of genes and environment to verbal recall and recognition performance in this disorder, the California Verbal Learning Test was administered to a large population-based Finnish twin sample, which included schizophrenic and schizoaffective patients, their non-ill monozygotic (MZ) and dizygotic (DZ) co-twins, and healthy control twins. Compared with controls, patients and their co-twins showed relatively greater performance deficits on free recall compared with recognition. Intra-pair differences between patients and their non-ill co-twins in hippocampal volume and memory performance were highly positively correlated. These findings are consistent with the view that genetic influences are associated with reduced verbal recall in schizophrenia, but that non-genetic influences further compromise these abnormalities in patients who manifest the full-blown schizophrenia phenotype, with this additional degree of disease-related declarative memory deficit mediated in part by hippocampal pathology.

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Recall and recognition in mildly disturbed schizophrenics: the use of matched tasks

Cited by 72 publications

References 28 publications

Medications and verbal memory impairment in schizophrenia: the role of anticholinergic drugs

Medications and verbal memory impairment in schizophrenia: the role of anticholinergic drugs

Habenula lesions cause impaired cognitive performance in rats: implications for schizophrenia

Verbal recall and recognition in twins discordant for schizophrenia

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