Brain Anatomic Magnetic Resonance Imaging in Childhood-Onset Schizophrenia

Frazier, Jean A.; Giedd, Jay N.; Hamburger, Susan; Albus, Kathleen E.; Kaysen, Debra; Vaituzis, A. Catherine; Rajapakse, Jagath C.; Lenane, Marge; McKenna, K.F.; Jacobsen, Leslie K.; Gordon, Charles T.; Breier, Alan; Rapoport, Judith L.

doi:10.1001/archpsyc.1996.01830070065010

Cited by 198 publications

(95 citation statements)

References 66 publications

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“…Indeed, individuals with ADHD (Trommer et al 1991;Barkley 1997;Casey et al 1997a) or schizophrenia (Braff 1993;Asarnow et al 1995) have difficulty regulating and suppressing inappropriate thoughts and actions. Furthermore, these disorders, as well as drug addiction, involve deficits in cognitive control and have been shown to involve the PFC (Lou et al 1989;Castellanos et al 1994Castellanos et al , 1996Fraizier et al 1996;Casey et al 2002;Cardinal et al 2004;Feil et al 2010;Goldstein et al 2011). An interesting hypothesis is that dysregulation of the developmental events leading to functional maturation of the PFC may contribute to or trigger the onset of ADHD and schizophrenia (Woo and Crowell 2005).…”

Section: Discussionmentioning

confidence: 99%

The ontogeny of learned inhibition

Meyer

Bucci

2014

Learn. Mem.

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Previous studies have examined the maturation of learning and memory abilities during early stages of development. By comparison, much less is known about the ontogeny of learning and memory during later stages of development, including adolescence. In Experiment 1, we tested the ability of adolescent and adult rats to learn a Pavlovian negative occasion setting task. This procedure involves learning to inhibit a behavioral response when signaled by a cue in the environment. During reinforced trials, a target stimulus (a tone) was presented and immediately followed by a food reward. On nonreinforced trials, a feature stimulus (a light) was presented 5 sec prior to the tone and indicated the absence of reward following presentation of the tone. Both adult and adolescent rats learned to discriminate between two different trial types and withhold responding when the light preceded the tone. However, adolescent rats required more sessions than adults to discriminate between reinforced and nonreinforced trials. The results of Experiment 2 revealed that adolescents could learn the task rules but were specifically impaired in expressing that learning in the form of withholding behavior on nonreinforced trials. In Experiment 3, we found that adolescents were also impaired in learning a different version of the task in which the light and tone were presented simultaneously during the nonreinforced trials. These findings add to existing literature by indicating that impairments in inhibitory behavior during adolescence do not reflect an inability to learn to inhibit a response, but instead reflect a specific deficit in expressing that learning.

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Section: Discussionmentioning

confidence: 99%

The ontogeny of learned inhibition

Meyer

Bucci

2014

Learn. Mem.

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“…This approach is predicated on the belief that studying first episode patients obviates confounds such as medication, chronicity of illness, and progressive changes. Research interest in childhood schizophrenia (Frazier et al, 1996(Frazier et al, , 1997Rapoport et al, 1997;Yeo et al, 1997) and adolescent schizophrenia (Dasari et al, 1999;James et al, 1999;Friedman et al, 1999) is also increasing. While these groups are not representative of the schizophrenia population and therefore may not be generalizable, they nonetheless offer important insights into the course of the illness and in change in brain morphology.…”

Section: The Issuesmentioning

confidence: 99%

A review of MRI findings in schizophrenia

Shenton

Dickey

Frumin

et al. 2001

Schizophrenia Research

2,128

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1,332

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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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“…Neuroimaging studies of adult-onset schizophrenia have consistently reported increased lateral ventricular volume [35], reduced gray and white matter volumes [36][37][38], particularly in the prefrontal region [39], and a reduction in thalamic size [40]. Similarly, imaging studies on early-onset cases have reported enlarged ventricular size, lower regional gray matter volumes (e.g., prefrontal cortex and cerebellum), white matter abnormalities [41], increased basal ganglia volume [14,17,42] and reduced volume of the thalamus [9,43], cerebellum [42] and anterior cingulated gyrus [44]. Adult-onset studies have also reported hippo campal volume reduction [45].…”

Section: "The Neurodevelopmental Hypothesis Proposesmentioning

confidence: 97%

“…EOS lies at one end of the continuum of disease severity and genetic liability [7]. Early-onset cases show clinical, cognitive, genetic and neurobiologic continuity with adult-onset schizophrenia [7][8][9], albeit with enduring clinical morbidity and psychosocial disability [10]. Thus, the study of this enriched population is likely to provide important pointers to the neurodevelopmental origins and pathophysiological mechanisms of schizophrenia.…”

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confidence: 99%