Three clinical syndromes of schizophrenia in untreated subjects: relation to brain glucose activity measured by position emission tomography (PET)

Kaplan, Ronald D.; Szechtman, Henry; Franco, S.; Szechtman, Barbara; Nahmias, Claude; Garnett, E. S.; List, Stephen; Cleghorn, John M.

doi:10.1016/0920-9964(93)90037-j

Cited by 106 publications

(47 citation statements)

References 28 publications

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“…In a landmark study, Liddle demonstrated that each of the three syndrome scores was associated with a specific pattern of perfusion in paralimbic, associative cortex, and subcortical nuclei. Other studies followed that confirmed the association between these factors and unique perfusion patterns (Ebmeier et al, 1993;Kaplan et al, 1993;Siegel Jr et al, 1993;Kawasaki et al, 1996;Schroder et al, 1996;Min et al, 1999;Tamminga et al, 1992). Differences between metabolic patterns were observed as well between three different subtypes of schizophrenia: negative, paranoid, and Schneiderian (Gur et al, 1995).…”

Section: Introductionmentioning

confidence: 69%

“…Functional imaging studies seeking regional associations between brain metabolism and negative symptoms have been typically based on correlation (Wolkin et al, 1992;Sabri et al, 1997), factor analysis Kaplan et al, 1993;Yuasa et al, 1995;Kawasaki et al, 1996;Schroder et al, 1996) or categorical (ie deficit vs nondeficit schizophrenia) (Andreasen et al, 1992;Heckers et al, 1999;Lahti et al, 2001;Potkin et al, 2002;Tamminga et al, 1992) analyses. The majority of these studies have reported hypometabolism in frontal cortex during rest Wolkin et al, 1992;Kaplan et al, 1993;Yuasa et al, 1995;Sabri et al, 1997) and task-activated states (Andreasen et al, 1992;Schroder et al, 1996;Potkin et al, 2002) in association with negative symptoms. In addition, three of these studies also showed reduced functional recruitment of the inferior parietal cortex in deficit compared to nondeficit subjects either at rest (Tamminga et al, 1992) or during task performance Heckers et al, 1999).…”

Section: Hippocampal/parahippocampal Regions: Normal Function and Abnmentioning

confidence: 99%

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Correlations Between rCBF and Symptoms in Two Independent Cohorts of Drug-Free Patients with Schizophrenia

Lahti

Weiler

Holcomb

et al. 2005

Neuropsychopharmacol

122

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We report on the correlations between whole brain rCBF and the positive and negative symptoms of schizophrenia in two cohorts of patients who were scanned while free of antipsychotic medication. We hypothesized that positive symptoms would correlate with rCBF in limbic and paralimbic regions, and that negative symptoms would correlate with rCBF in frontal and parietal regions. Both cohorts of patients with schizophrenia (Cohort 1: n ¼ 32; Cohort 2: n ¼ 23) were scanned using PET with H 2 15O while free of antipsychotic medication for an average of 21 and 15 days, respectively. Both groups were scanned during a resting state. Using SPM99, we conducted pixel by pixel linear regression analyses between BPRS scores and whole brain rCBF. As hypothesized, positive symptoms correlated with rCBF in the anterior cingulate cortex (ACC) in a positive direction and with the hippocampus/parahippocampus in a negative direction in both patient groups. When the positive symptoms were further divided into disorganization and hallucination/delusion scores, similar positive correlations with ACC and negative correlations with hippocampus rCBF were found. In both cohorts, the disorganization scores correlated positively with rCBF in Broca's area. As expected, negative symptoms correlated inversely with rCBF in frontal and parietal regions. This study provides evidence that limbic dysfunction may underlie the production of positive symptoms. It suggests that abnormal function of Broca's area may add a specific language-related dimension to positive symptoms. This study also provides further support for an independent neurobiological substrate of negative symptoms distinct from positive symptoms. The involvement of both frontal and parietal regions is implicated in the pathophysiology of negative symptoms.

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Section: Introductionmentioning

confidence: 69%

Section: Hippocampal/parahippocampal Regions: Normal Function and Abnmentioning

confidence: 99%

Correlations Between rCBF and Symptoms in Two Independent Cohorts of Drug-Free Patients with Schizophrenia

Lahti

Weiler

Holcomb

et al. 2005

Neuropsychopharmacol

122

View full text Add to dashboard Cite

show abstract

“…Some research suggests that several neural activity deficits found in schizophrenia may be associated with prefrontal and inferior parietal lobe dysfunction 1 . The inferior parietal lobule (IPL) and the prefrontal cortex (PFC) have extensive interconnections and common cortical and subcortical target regions 2 .…”

Section: Introductionmentioning

confidence: 99%

Reduced oligodendroglial density in the inferior parietal lobule and lack of insight in schizophrenia

2013

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-Background and Objectives: Alterations and deficits of oligodendrocytes reported in the grey and white matter in schizophrenia may contribute to neuronal disconnectivity. Prefrontal-parietal functional disconnections have been implicated in diverse clinical symptoms of schizophrenia, including poor insight. We studied the effects of schizophrenia diagnosis and insight on numerical density (Nv) of oligodendrocytes in the inferior parietal lobule (IPL).Methods: Nissl-stained sections from the Stanley "Parietal Collection" from male schizophrenia subjects (n = 24) having poor, fair, or good insight and healthy matched controls (n = 24) were examined. The Nv of oligodendrocytes was estimated in layer 3 of BA 39 and BA 40 of the IPL and in white matter underlying layer 6 by optical dissector method.Results: In BA 39 we found a significant 15% decrease in the Nv of oligodendrocytes in layer 3 in the schizophrenia group. Nv of oligodendrocytes in the poor+fair insight subgroup was 20% lower compared to controls (p< 0.05) and to good insight subgroup (p = 0.055). Nv of oligodendrocytes in the good insight subgroup did not differ from the control group. A significant lateralization of oligodendrocyte density was detected in layer 3 (L>R) only in the control group. There were no significant group differences in the Nv of oligodendrocytes in BA 40 or in the white matter underlying BA 39/40 areas.Conclusions: Lack of insight in schizophrenia may be associated with a deficit of oligodendroglia in the grey matter of IPL.

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“…These drugs produce a state of intoxication that resembles the symptoms of acute schizophrenia (Vollenweider and Geyer, 2001). Additionally, human brain imaging demonstrates a common pattern of increased activity in the frontal cortex caused by psychotomimetic drugs and acute schizophrenia (Cleghorn et al, 1989;Hermle et al, 1992;Kaplan et al, 1993;Ebmeier et al, 1995;Vollenweider et al, 1997a, b), consistent with a role for hyperglutamatergic signaling in psychotic behaviors. Investigation of hallucinogenic drug action as a model of psychosis suggests that the behavioral effects of hallucinogens in humans are mediated by activation of serotonin (5-HT) subtype 2A (5-HT 2A ) receptors (Vollenweider et al, 1998).…”

Section: Introductionmentioning

confidence: 91%

Chronic Phenethylamine Hallucinogen Treatment Alters Behavioral Sensitivity to a Metabotropic Glutamate 2/3 Receptor Agonist

Benneyworth

Smith

Sanders‐Bush

2007

Neuropsychopharmacol

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Recent clinical studies in schizophrenic patients show that a selective agonist of group II metabotropic glutamate (mGlu) receptors has robust efficacy in treating positive and negative symptoms. Group II mGlu receptor agonists also modulate the in vivo activity of psychotomimetic drugs, reducing the ability of psychotomimetic hallucinogens to increase glutamatergic transmission. The use of mouse models provides an opportunity to investigate the dynamic action that mGlu2/3 receptors play in regulating the behavioral effects of hallucinogen-induced glutamatergic neurotransmission using genetic as well as pharmacological strategies. The current study sought to characterize the use of the two-lever drug discrimination paradigm in ICR (CD-1) mice, using the hallucinogenic 5-HT 2A/2C receptor agonist (À)-2,5-dimethoxy-4-bromoamphetamine [(À)-DOB)] as a stimulus-producing drug. The (À)-DOB discriminative stimulus was dose-dependent, generalized to the hallucinogen lysergic acid diethylamide, and was potently blocked by the 5-HT 2A receptor antagonist M100907. However, contrary to our prediction, the hallucinogen-induced discriminative stimulus was not regulated by mGlu2/3 receptors. In a series of follow-up studies using hallucinogen-induced head twitch response and phencyclidine-induced hyperlocomotion, it was additionally discovered that the repeated dosing regimen required for discrimination training attenuated the behavioral effects of the mGlu2/3 receptor agonist LY379268. Furthermore chronic studies, using a 14 day (À)-DOB treatment, confirmed that repeated hallucinogen treatment causes a loss of behavioral activity of mGlu2/3 receptors, likely resulting from persistent activation of mGlu2/3 receptors by a hallucinogen-induced hyperglutamatergic state.

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Three clinical syndromes of schizophrenia in untreated subjects: relation to brain glucose activity measured by position emission tomography (PET)

Cited by 106 publications

References 28 publications

Correlations Between rCBF and Symptoms in Two Independent Cohorts of Drug-Free Patients with Schizophrenia

Correlations Between rCBF and Symptoms in Two Independent Cohorts of Drug-Free Patients with Schizophrenia

Reduced oligodendroglial density in the inferior parietal lobule and lack of insight in schizophrenia

Chronic Phenethylamine Hallucinogen Treatment Alters Behavioral Sensitivity to a Metabotropic Glutamate 2/3 Receptor Agonist

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