Longitudinal Neuropsychological Follow-Up Study of Patients With First-Episode Schizophrenia

Hoff, Anne L.; Sakuma, Michael; Wieneke, Mary; Horon, Robert; Kushner, Maureen; DeLisi, Lynn E.

doi:10.1176/ajp.156.9.1336

Cited by 317 publications

(23 citation statements)

References 20 publications

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“…[19][20][182][183][184] The available evidence suggests that neuropsychological functions are not progressive after illness onset and may improve. [185][186][187][188][189] Further, more recent findings from the UHR studies indicate that deficits, particularly of executive functions, are evident before illness onset. [155][156]158 One possible explanation is that there is ''development arrest'' of those functions that should be developing during adolescence, namely, frontal executive abilities.…”

Section: Discussionmentioning

confidence: 99%

Structural Brain Imaging Evidence for Multiple Pathological Processes at Different Stages of Brain Development in Schizophrenia

Pantelis

2005

Schizophrenia Bulletin

500

291

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The underlying neurobiology of emerging psychotic disorders is not well understood. While there is evidence from structural imaging and other studies supporting the popular notion that schizophrenia arises as a consequence of an "early neurodevelopmental" lesion, more recent findings challenge this notion. Evidence, including our own data, suggests that dynamic brain changes occur during the earliest stages of a psychotic illness, including around the time of transition to illness. In this article we review the available longitudinal and relevant cross-sectional structural neuroimaging studies focusing on both the very early neurodevelopmental markers (pre- or perinatal origin) and the later markers (late neurodevelopmental) around the period of transition to illness. Based on our review of recent findings, we suggest that the onset of psychosis is a time of active brain changes, wherein, for a proportion of individuals, (i) an early (pre- and perinatal) neurodevelopmental lesion renders the brain vulnerable to anomalous late (particularly postpubertal) neurodevelopmental processes, as indicated by evidence for accelerated loss of gray matter and aberrant connectivity particularly in prefrontal regions; and (ii) these anomalous neurodevelopmental processes interact with other causative factors associated with the onset of psychosis (e.g., substance use, stress, and dysregulation of the hypothalamic-pituitary-adrenal axis function), which together have neuroprogressive sequelae involving medial temporal and orbital prefrontal regions, as suggested by imaging studies around transition to active illness. However, the pathological processes underlying such progressive changes during "late neurodevelopment" remain unclear but may reflect anomalies of synaptic plasticity, abnormal brain maturation, the adverse effects of stress, or other environmental factors. In this context, the features of schizophrenia, including the neuropsychological deficits and behavioral manifestations, can be understood as direct effects of these multiple pathological processes at various neurodevelopmental stages, including genetic and nongenetic etiological factors.

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Section: Discussionmentioning

confidence: 99%

Structural Brain Imaging Evidence for Multiple Pathological Processes at Different Stages of Brain Development in Schizophrenia

Pantelis

2005

Schizophrenia Bulletin

500

291

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“…Groups were matched for age, gender, parental social economic status, and premorbid IQ, measured by the vocabulary component of the Wechsler Abbreviated Scale of Intelligence (WASI) (Table 1 ). The WASI vocabulary subtest is a measure of semantic knowledge, an IQ measure relatively resistant to psychosis, neurodegeneration, and deterioration over time (Bilder et al, 1988 ; de Oliveira et al, 2014 ; Eberhard et al, 2003 ; Heaton et al, 2001 ; Hoff et al, 1999 ; Kremen et al, 1995 ; Mohn‐Haugen et al, 2022 ). All participants had healthy hearing confirmed with audiometry.…”

Section: Methodsmentioning

confidence: 99%

Attentional M100 gain modulation localizes to auditory sensory cortex and is deficient in first‐episode psychosis

Curtis

Ren

Coffman

et al. 2022

Human Brain Mapping

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Selective attention is impaired in first‐episode psychosis (FEP). Selective attention effects can be detected during auditory tasks as increased sensory activity. We previously reported electroencephalography scalp‐measured N100 enhancement is reduced in FEP. Here, we localized magnetoencephalography (MEG) M100 source activity within the auditory cortex, making novel use of the Human Connectome Project multimodal parcellation (HCP‐MMP) to identify precise auditory cortical areas involved in attention modulation and its impairment in FEP. MEG was recorded from 27 FEP and 31 matched healthy controls (HC) while individuals either ignored frequent standard and rare oddball tones while watching a silent movie or attended tones by pressing a button to oddballs. Because M100 arises mainly in the auditory cortices, MEG activity during the M100 interval was projected to the auditory sensory cortices defined by the HCP‐MMP (A1, lateral belt, and parabelt parcels). FEP had less auditory sensory cortex M100 activity in both conditions. In addition, there was a significant interaction between group and attention. HC enhanced source activity with attention, but FEP did not. These results demonstrate deficits in both sensory processing and attentional modulation of the M100 in FEP. Novel use of the HCP‐MMP revealed the precise cortical areas underlying attention modulation of auditory sensory activity in healthy individuals and impairments in FEP. The sensory reduction and attention modulation impairment indicate local and systems‐level pathophysiology proximal to disease onset that may be critical for etiology. Further, M100 and N100 enhancement may serve as outcome variables for targeted intervention to improve attention in early psychosis.

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“…There is a possibility that we were unable to discern the differences due to a small sample size, but another explanation is that the cognitive change is of comparable magnitude in the two groups. In their longitudinal study on first-episode schizophrenia, Hoff et al (1999) Table 2 The best fitting models for the cognitive domains. have demonstrated that patients scored below controls on all cognitive domains on baseline, and although many cognitive domains improved over time, the cognitive deficits remained 1 to 2 standard deviations below controls throughout a five-year period.…”

Section: Discussionmentioning

confidence: 99%

Cognitive improvement in first-episode schizophrenia and healthy controls: A 6-year multi-assessment follow-up study

Czajkowski

Torgalsbøen

2018

Psychiatry Research

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Longitudinal Neuropsychological Follow-Up Study of Patients With First-Episode Schizophrenia

Cited by 317 publications

References 20 publications

Structural Brain Imaging Evidence for Multiple Pathological Processes at Different Stages of Brain Development in Schizophrenia

Structural Brain Imaging Evidence for Multiple Pathological Processes at Different Stages of Brain Development in Schizophrenia

Attentional M100 gain modulation localizes to auditory sensory cortex and is deficient in first‐episode psychosis

Cognitive improvement in first-episode schizophrenia and healthy controls: A 6-year multi-assessment follow-up study

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