Decoupling of Sleep-Dependent Cortical and Hippocampal Interactions in a Neurodevelopmental Model of Schizophrenia

Borderline Personality Disorder (BPD) is a complex psychological condition characterised by affective instability, cognitive impairment, problematic behaviours and social dysfunction. Due to the variability in symptomatic profiles, efforts have recently been directed towards comprehending the disorder from a neurological standpoint within the aforementioned domains. Although adolescent-onset BPD is now reliably diagnosed as the adult-onset variant, a limited number of studies address the neural correlates of first presentation BPD. Moreover, research investigating the outcomes of therapeutic interventions on brain function and morphology is scarce. Preliminary findings consistently cite the involvement of grey matter deficiencies of the orbitofrontal cortex, hippocampus and amygdala in the neuropathology of BPD. Additionally, frontolimbic white matter deficits are thought to be implicated. Functionally, over-activity in limbic regions such as the cingulate cortices and amygdala are believed to partially account for emotion dysregulation, though the neural correlates of cognitive, social and behavioural impairments are relatively poorly understood. The present review will endeavour to evaluate the existing neurobiological evidence for BPD in adolescence as well as adulthood. Finally, a rudimentary neurodevelopmental model of BPD will be proposed.

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An overview on Hebephrenia, a diagnostic cornerstone in the neurodevelopmental model of Schizophrenia

History of Psychiatry ◽

10.1177/0957154x211062534 ◽

2022 ◽

pp. 0957154X2110625

Author(s):

Carlo Maggini ◽

Riccardo Dalle Luche

Keyword(s):

Nineteenth Century ◽

Cognitive Impairment ◽

Dementia Praecox ◽

The Core ◽

Neurodevelopmental Model ◽

Psychic Energy ◽

Progressive Cognitive Impairment

Pre-Kraepelinian observations converged in Kahlbaum’s and Hecker’s description of Hebephrenia. For Kraepelin, Hebephrenia was an ‘idiopathic incurable dementia whose onset is in adolescence’. It became the core of ‘Dementia Praecox’, and then Bleulerian ‘Schizophrenia’. In recent decades, the resurgence of the ‘late neurodevelopment’ hypothesis of schizophrenia has brought into focus Hecker’s clinical reports of adolescents who, as a result of a putative loss of psychic energy, showed a rapidly progressive cognitive impairment leading to functional and behavioural disorganization. This paper summarizes the nineteenth-century conceptualization of Hebephrenia as a developmental illness.

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Genetic and perinatal influences in the etiology of schizophrenia: A neurodevelopmental model.

Origins and development of schizophrenia: Advances in experimental psychopathology. ◽

10.1037/10305-003 ◽

2004 ◽

pp. 67-92 ◽

Cited By ~ 3

Author(s):

Tyrone D. Cannon

Keyword(s):

Neurodevelopmental Model

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Neurodevelopment and Schizophrenia

Neurobiology of Mental Illness ◽

10.1093/med/9780199934959.003.0025 ◽

2013 ◽

pp. 327-337

Author(s):

Ester J. Kwon ◽

Takahiro Soda ◽

Li-Huei Tsai

Keyword(s):

Nervous System ◽

Brain Development ◽

Neural Circuitry ◽

Dendritic Trees ◽

Neurodevelopmental Model ◽

Key Aspects

A neurodevelopmental model of schizophrenia postulates that some of the key aspects of brain development that normally occur both pre- and post-natally are not occurring correctly, either in time or space. Complex neural circuitry needs to form and be modulated by experience. Classically, proliferation, migration, arborization and myelination occur prenatally. Elaboration and refining of dendritic trees and synapses as well as myelination of the nervous system continues through the first two-decade of life. There are opportunities for genetic and environmental abnormalities and variation to profoundly influence the trajectories of all of these critical functional processes.

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Neurodevelopmental Model of Schizophrenia

Archives of General Psychiatry ◽

10.1001/archpsyc.1988.01800350085014 ◽

1988 ◽

Vol 45 (11) ◽

pp. 1051 ◽

Cited By ~ 1

Author(s):

Richard Lewine

Keyword(s):

Neurodevelopmental Model

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Could Stress Cause Psychosis in Individuals Vulnerable to Schizophrenia?

CNS Spectrums ◽

10.1017/s1092852900022240 ◽

2002 ◽

Vol 7 (1) ◽

pp. 33-42 ◽

Cited By ~ 16

Author(s):

Cheryl Corcoran ◽

Lilianne Mujica-Parodi ◽

Scott Yale ◽

David Leitman ◽

Dolores Malaspina

Keyword(s):

Structural Changes ◽

Time Frame ◽

Environment Interaction ◽

Synaptic Remodeling ◽

Gene Environment Interaction ◽

Neurodevelopmental Model ◽

Gene Environment ◽

Plausible Model ◽

Neurotoxic Effects ◽

The Impact

ABSTRACTIt has long been considered that psychosocial stress plays a role in the expression of symptoms in schizophrenia (SZ), as it interacts with latent neural vulnerability that stems from genetic liability and early environmental insult. Advances in the understanding of the neurobiology of the stress cascade in both animal and human studies lead to a plausible model by which this interaction may occur: through neurotoxic effects on the hippocampus that may involve synaptic remodeling. Of late, the neurodevelopmental model of SZ etiology has been favored. But an elaboration of this schema that credits the impact of postnatal events and considers a role for neurodegenerative changes may be more plausible, given the evidence for gene-environment interaction in SZ expression and progressive structural changes observed with magnetic resonance imaging. Furthermore, new insights into nongliotic neurotoxic effects such as apoptosis, failure of neurogenesis, and changes in circuitry lead to an expansion of the time frame in which environmental effects may mediate expression of SZ symptoms.

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