Reduction of cortical volume in schizophrenia on magnetic resonance imaging

Harvey, Ian; Maymon, Ron; Boulay, George du; Wicks, David; Lewis, Shôn; Murray, Robin M.

doi:10.1017/s003329170002537x

Cited by 200 publications

(99 citation statements)

References 81 publications

(99 reference statements)

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“…The deficits in gray matter volume were most prominent in the frontal and temporal lobes. These findings are consistent with findings in other patients with schizophrenia (Gur et al 2000a;Gur et al 2000b;Harvey et al 1993;Lim et al 1996;Sullivan et al 1998;Zipursky et al 1992). These results raise the possibility that genetic abnormalities underlying 22qDS may provide clues to the pathogenesis of the brain abnormalities associated with schizophrenia.…”

Section: Discussionsupporting

confidence: 90%

“…In schizophrenia, the most consistent structural neuro-imaging findings are larger lateral and third ventricles and smaller gray matter volumes (Gur et al 2000a;Gur et al 2000b;Harvey et al 1993;Lim et al 1996;Zipursky et al 1998;Zipursky et al 1992;Zipursky et al 1997). White matter volumes in patients with schizophrenia tend not to be different from controls (Lim et al 1996;Zipursky et al 1998;Zipursky et al 1992).…”

Section: Introductionmentioning

confidence: 93%

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Structural brain abnormalities in patients with schizophrenia and 22q11 deletion syndrome

Chow

Zipursky

Mikulis

et al. 2002

Biological Psychiatry

100

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Background-22q11 Deletion Syndrome is a genetic syndrome associated with an increased risk for developing schizophrenia. Brain abnormalities have been reported in 22q11 Deletion Syndrome, but little is known about whether differences in brain structure underlie the psychotic disorders associated with this syndrome. In the current study, we used magnetic resonance imaging to characterize the structural brain abnormalities found in adults who have both 22q11 Deletion Syndrome and schizophrenia.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 93%

Structural brain abnormalities in patients with schizophrenia and 22q11 deletion syndrome

Chow

Zipursky

Mikulis

et al. 2002

Biological Psychiatry

100

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“…For example, Egan et al (1994) used only a 1-cm slice to measure the whole parietal lobe, and two other studies measured the parietal lobe combined with other brain regions (e.g. Harvey et al, 1993;Zipursky et al, 1994).…”

Section: Parietal and Occipital Lobesmentioning

confidence: 99%

“…We call particular attention to the white matter fiber tracts of the corpus callosum, because we think they strongly illustrate the power of this technique in visualizing heretofore unseen fiber tracts in vivo. Summary of MR studies seporting positive and negative findings in schizophenia (Table is updated Gur et al, 1994Gur et al, , 1998bGur et al, , 1999Jernigan et al, 1991;Nasrallah et al, 1990;Rajarethinam et al, 2000;Sanfilipo et al, 2000a;Whitworth et al, 1998] − Bilder et al, 1994;Blackwood et al, 1991;Breier et al, 1992;Buchanan et al, 1993Buchanan et al, , 1998Cannon et al, 1998;Colombo et al, 1993;Dauphinais et al, 1990Flaum et al, 1995;Goldstein et al, 1999;Harvey et al, 1993;Hazlett et al, 1999;Hirayasu et al, 1998Hirayasu et al, , 2000…”

Section: Summary Of Mri Findings and Future Directions For Researchmentioning

confidence: 99%

A review of MRI findings in schizophrenia

Shenton

Dickey

Frumin

et al. 2001

Schizophrenia Research

2,110

118

1,310

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After more than 100 years of research, the neuropathology of schizophrenia remains unknown and this is despite the fact that both Kraepelin (1919/1971: Kraepelin,E., 1919/1971. Dementia praecox. Churchill Livingston Inc., New York) and Bleuler (1911/1950: Bleuler, E., 1911/1950. Dementia praecox or the group of schizophrenias. International Universities Press, New York), who first described 'dementia praecox' and the ' schizophrenias', were convinced that schizophrenia would ultimately be linked to an organic brain disorder. Alzheimer (1897: Alzheimer, A., 1897. Beitrage zur pathologischen anatomie der hirnrinde und zur anatomischen grundlage einiger psychosen. Monatsschrift fur Psychiarie und Neurologie. 2, 82-120) was the first to investigate the neuropathology of schizophrenia, though he went on to study more tractable brain diseases. The results of subsequent neuropathological studies were disappointing because of conflicting findings. Research interest thus waned and did not flourish again until 1976, following the pivotal computer assisted tomography (CT) finding of lateral ventricular enlargement in schizophrenia by Johnstone and colleagues. Since that time significant progress has been made in brain imaging, particularly with the advent of magnetic resonance imaging (MRI), beginning with the first MRI study of schizophrenia by Smith and coworkers in 1984 (Smith, R.C., Calderon, M., Ravichandran, G. K., et al. (1984). Nuclear magnetic resonance in schizophrenia: A preliminary study. Psychiatry Res. 12, 137-147). MR in vivo imaging of the brain now confirms brain abnormalities in schizophrenia.The 193 peer reviewed MRI studies reported in the current review span the period from 1988 to August, 2000. This 12 year period has witnessed a burgeoning of MRI studies and has led to more definitive findings of brain abnormalities in schizophrenia than any other time period in the history of schizophrenia research. Such progress in defining the neuropathology of schizophrenia is largely due to advances in in vivo MRI techniques. These advances have now led to the identification of a number of brain abnormalities in schizophrenia. Some of these abnormalities confirm earlier postmortem findings, and most are small and subtle, rather than large, thus necessitating more advanced and accurate measurement tools. These findings include ventricular enlargement (80% of studies reviewed) and third ventricle enlargement (73% of studies reviewed). There is also preferential involvement of medial temporal lobe structures (74% of studies reviewed), which include the amygdala, hippocampus, and parahippocampal gyrus, and neocortical temporal lobe regions (superior temporal gyrus) (100% of studies reviewed). When gray and white matter of superior temporal gyrus was combined, 67% of studies reported abnormalities. There was also moderate evidence for frontal lobe abnormalities (59% of studies reviewed), particularly prefrontal gray matter and orbitofrontal regions. Similarly, there was moderate evidence for parietal lobe ab...

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“…The relationship among the PFC, executive dysfunction, and schizophrenia symptoms has been studied, and several studies have shown the existence of abnormalities in the PFC. MRI studies have revealed a decrease in the volume of PFC in schizophrenic patients [10][11][12][13] , and a postmortem anatomical study found that the cortex of prefrontal area 46 is thinner and the density of neurons in this area is increased [14][15][16] . In as early as 1986, to study the relationship between prefrontal dysfunction and schizophrenia, medication-free chronic schizophrenia patients and normal controls were used, and the regional cerebral blood flow (rCBF) was measured during performance of a PFCspecifi c cognitive test, the Wisconsin Card Sorting (WCS) or a simple number-matching (NM) test as the control.…”

mentioning

confidence: 99%

Prefrontal dysfunction and a monkey model of schizophrenia

et al. 2015

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The prefrontal cortex is implicated in cognitive functioning and schizophrenia. Prefrontal dysfunction is closely associated with the symptoms of schizophrenia. In addition to the features typical of schizophrenia, patients also present with aspects of cognitive disorders. Based on these relationships, a monkey model mimicking the cognitive symptoms of schizophrenia has been made using treatment with the non-specific competitive N-methyl-D-aspartate receptor antagonist, phencyclidine. The symptoms are ameliorated by atypical antipsychotic drugs such as clozapine. The benefi cial effects of clozapine on behavioral impairment might be a specifi c indicator of schizophrenia-related cognitive impairment. Keywords: prefrontal cortex; schizophrenia; monkey model ·Review· IntroductionOne percent of the adult population, particularly young adults, are affected by schizophrenia. Schizophrenic patients typically present with hallucinations, delusions, withdrawal from social activities, loss of personal care skills, and flat or inappropriate emotional responses to situations [1] . Although many factors have been associated with schizophrenia, including genetic factors, early environmental influences, and neurobiological, psychological, and sociological processes [2][3][4] that are very important contributory factors, the mechanism underlying this disorder is unknown. Patient data are insufficient for understanding the pathology and etiology of schizophrenia.Further, direct experimentation on human subjects is ethically unacceptable. Thus, animal models have become an indispensable tool for pathological research. Unlike other neurological diseases such as stroke, epilepsy, and Parkinson's disease that can be easily replicated in animals, some of the symptoms of schizophrenia human patients, such as thinking disorders, delusions, and hallucinations, are difficult to replicate in animals.For many years, there has been no appropriate nonhuman primate model of schizophrenia. In addition to the typical features of schizophrenia, patients present with aspects of prefrontal cognitive disorders involving, e.g., working memory, selective attention, initiating movement, and planning. Based on these relationships, a monkey model of schizophrenia could be developed by mimicking its cognitive symptoms. In this review, we introduce schizophrenia and the prefrontal cortex (PFC) as well as their relationship and discuss the development of a monkey model of schizophrenia, including the methods and behavioral tests of the model. The Prefrontal Cortex and SchizophreniaThe volume of the human brain is twice that of the chimpanzee, and the PFC, which is the most rostral component of the primate cortex, has expanded most in humans [5,6] . In other species, the PFC functions in voluntary motor control, whereas in primates, it has developed [5][6][7] . The PFC has broad connections with many parts of the brain, particularly the sub-regions of the limbic system [10] . The human PFC, which is better developed than in other primates, is the primary ...

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Reduction of cortical volume in schizophrenia on magnetic resonance imaging

Cited by 200 publications

References 81 publications

Structural brain abnormalities in patients with schizophrenia and 22q11 deletion syndrome

Structural brain abnormalities in patients with schizophrenia and 22q11 deletion syndrome

A review of MRI findings in schizophrenia

Prefrontal dysfunction and a monkey model of schizophrenia

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