Abnormalities of Cerebral Blood Flow Distribution in Patients With Chronic Schizophrenia

Ingvar, David H.; Franzén, Göran

doi:10.1111/j.1600-0447.1974.tb09707.x

Cited by 633 publications

(210 citation statements)

References 40 publications

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“…Characterizing compensatory mechanisms and their potential modulation is important for the social rehabilitation of schizophrenic patients. But it is well known that schizophrenia involves frontal function deficits (Jeste et al 1996;Ingvar and Franzen 1974;Weinberger et al 1986;Callicott et al 1998;Heckers et al 1999); in fact, prefrontal and inferior frontal abnormalities we will report elsewhere co-occurred in our patient's sample. What then is the relationship between the mechanisms described here and the prefrontal abnormalities observed in schizophrenia?…”

Section: Discussionmentioning

confidence: 55%

A Compensatory Mirror Cortical Mechanism for Facial Affect Processing in Schizophrenia

Quintana

2001

Neuropsychopharmacology

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Section: Discussionmentioning

confidence: 55%

A Compensatory Mirror Cortical Mechanism for Facial Affect Processing in Schizophrenia

Quintana

2001

Neuropsychopharmacology

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“…Results from many of these imaging studies suggest that PFC regional hypoperfusion are mainly observed in chronic schizophrenics exhibiting psychomotor poverty (with negative symptoms and a prolonged duration of illness). Hypoperfusion was found both at rest and when challenged by cognitive tasks that specifically test the functions of the PFC (e.g., Wisconsin Card Sorting Test), regardless of whether patients were drug-naive or medicated (Ingvar and Franzen 1974;Franzen and Ingvar 1975;Berman et al 1986;Weinberger et al 1986;Mathew et al 1988;Andreasen et al 1992;Buchsbaum et al 1992;Liddle et al 1992;Wolkin et al 1992). However, in several subgroups of schizophrenics with acute psychosis (including some who were unmedicated), investigators have detected increased PFC activity at rest, with no failure of activating PFC in cognitive tasks, such as verbal fluency and executive tasks (Chua and McKenna 1995;Ebmeier et al 1993;Heckers et al 1998).…”

Section: Possible Mechanisms Underlying Thought Disorganization (mentioning

confidence: 99%

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

Yang

Seamans

Gorelova

1999

Neuropsychopharmacology

164

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This review covers some recent findings of the electrophysiological mechanisms through which mesocortical dopamine modulates prefrontal cortical neurons. Dopamine has been shown to modulate several ionic conductances located along the soma-dendritic axis of prefrontal cortical pyramidal neurons. These ionic currents include high-voltage-activated calcium currents and slowly inactivating NaReceived May 12, 1998; revised May 27, 1998; accepted May 29, 1998. 162 C.R. Yang et al. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 21 , NO Schizophrenia strikes one in one hundred people worldwide, regardless of cultural or racial origins. As the illness progresses and if it remains unattended, patients are frequently trapped in psychological, social, and economic devastation (Gottesman 1991;Jablensky 1995). Currently, our incomplete understanding of the neurobiological bases of schizophrenia suggests that defects in the genetic controls of brain development in such limbic regions (including temporal lobe structures such as hippocampus and the amygdala) as well as the prefrontal cortex (PFC) lead to cell loss or deformation, cytoarchitectural disorganization, and abnormal innervation in these brain regions (Roberts and Bruton 1990;Stevens 1992; Bogerts 1993;Shapiro 1993; Akbarian et al. 1993 Akbarian et al. , 1996Ross and Pearlson 1996;Weinberger 1996; Karayiorgou and Gogos 1997; Lewis 1997;Selemon et al. 1995Selemon et al. , 1998.Some results from recent imaging studies of brains from living schizophrenics have suggested that there are defective functional communications between the interconnected cortical (PFC and cingulate cortex) and limbic subcortical structures (thalamus, striatum, and temporal lobe limbic structures)(see reviews of Liddle 1996; Pfefferbaum and Marsh 1995; Andreasen 1997; Heckers et al. 1998). Findings from these studies suggest that in schizophrenics, abnormal recruitment of several interconnected cortical and subcortical structures may underlie such symptom clusters as psychomotor poverty, thought disorganization, and reality distortion (Liddle et al. 1992; Liddle 1996; Fletcher 1998; Heckers et al. 1998).As noted in Figure 1, the PFC receives converging limbic, association cortical, and mesocortical dopamine inputs. These inputs interact in the PFC and are involved functionally in high-level cognitive processes (Fuster 1995). Among the many brain regions that PFC output innervates, two important subcortical regions are emphasized in this review. These are the nucleus accumbens (where mesoaccumbens dopamine neurons terminate) and the ventral tegmental area (VTA, where the midbrain dopamine neurons reside) Groenewegen et al. 1990; Berendse et al. 1992a Berendse et al. , 1992bSesack and Pickel 1992;Gorelova and Yang 1997b). Several of the interconnected limbic, cortical, and subcortical structures known to be affected in schizophrenia are targets of the ascending midbrain dopamine systems that normally provide functional modulation of neurotransmission (Björklund and Lindvall 1984;Mogenson et ...

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“…Brain imaging studies have revealed functional [1,10,14,15] as well as structural abnormalities [12] in the PFC of schizophrenic patients. Furthermore, clinical response to clozapine, an atypical APD, was inversely related to prefrontal atrophy [7].…”

mentioning

confidence: 99%

Haloperidol and clozapine increase neural activity in the rat prefrontal cortex

Kim¹,

Jang²,

Chung³

et al. 2001

Neuroscience Letters

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Abnormalities of Cerebral Blood Flow Distribution in Patients With Chronic Schizophrenia

Cited by 633 publications

References 40 publications

A Compensatory Mirror Cortical Mechanism for Facial Affect Processing in Schizophrenia

A Compensatory Mirror Cortical Mechanism for Facial Affect Processing in Schizophrenia

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

Haloperidol and clozapine increase neural activity in the rat prefrontal cortex

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