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5. Neurodevelopmental Hypothesis:

Some gestational and perinatal factors have been found to significantly
increase the risk of developing schizophrenia in later life. These include prenatal famine; high levels of maternal distress in the first trimester; low birth weight; and shorter gestation (Jones, Rantakallio, Hartikainen, Isohanni, & Sipila, 1998; Khashan et al., 2008; St Clair et al., 2005; Susser et al., 1996).

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Obstetric complications have also been linked to the later development of schizophrenia. These include preeclampsia (which is linked to foetal malnutrition); caesarean section due to foetal distress, manual extraction of the baby; haemorrhage during delivery; and premature delivery (Byrne, Agerbo, Bennedsen, Eaton, & Mortensen, 2007; Dalman, Allebeck, Cullberg, Grunewald, & Köster, 1999).

It has been proposed that these events confer some form of brain damage, such as hypoxia to the foetus, which is linked to the later development of the disorder (Geddes et al., 1999; Marenco & Weinberger, 2000).

Winter and spring birth and older paternal age at conception are also linked to the development of schizophrenia (Davies, Welham, Chant, Torrey, & McGrath, 2003; Wohl & Gorwood, 2007; Wu, Liu, Zhao, Ma, & Li, 2011).

Foetal exposure to a virus during the first two trimesters has also been linked
to the development of schizophrenia.

Anatomical abnormalities present in schizophrenia, such as increased
ventricular size and decreased brain volume, lend further support to the
neurodevelopmental hypothesis (McCarley et al., 1999).

6. Cortical Dysconnection Syndrome Hypothesis:

The dysconnection hypothesis states that schizophrenia is caused by
disturbance (decrease or increase) in the connections between brain regions due to reduced synaptic plasticity and structural aberrations in the brain (Stephen, Baldeweg, & Friston, 2006). This results in a lack of functional integration between brain regions and a reduction in the ability of synapses to modulate plasticity in memory systems, emotions, and learning, which results in a lack of reinforcement of adaptive behaviorv(Friston, 1998, 1999).

In people with schizophrenia there appears to be a disruption in the anterior
cingulate cortex’s (ACC) modulation of the temporal and the prefrontal areas
(Fletcher, McKenna, Friston, Frith, ; Dolan, 1999).

Fletcher et al. (1999) propose that the lack of integration between these two areas by the ACC may result in the deficits in attention (Bench, Grasby, ; Friston, 1993), performance monitoring (Carter et al., 1998), and willed action (Frith, Friston, Liddle, ; Frackowiak, 1991) found in people with schizophrenia.

(2005) showed people with schizophrenia had altered functional networks between the ACC, and the cerebellum and the pre- and post-central gyrus.

Positron emission tomography has demonstrated aberrant cortical connections between semantic processing areas in the cerebellum, and temporal and occipital lobes (Kim et al., 2005), and between the prefrontal and parietal lobes during a working memory task performed by people with schizophrenia (Kim et al., 2003).

Deficits in parieto-motor area interactions have also been found in a study of
medicated and non-medicated people with schizophrenia using a trascranial magnetic stimulation (Koch et al., 2008).

There is evidence that there may be alterations in the connections and communication between the hemispheres in people with schizophrenia (Barnett, Corballis, ; Kirk, 2005; Endrass, Mohr, ; Rockstroh, 2002). These findings appear to consistently point towards an altered association or connectivity between several brain regions in people with schizophrenia.

7. Brain Anatomical Differences in Schizophrenia:

Structural differences between the brains of people with schizophrenia and
people without schizophrenia show that there is no one reliable deviation in brain structure observed in every person with schizophrenia. However, commonly found structural abnormalities include a decrease in cerebral volume and increase in ventricle size (Fannon et al., 2000; McCarley, et al., 1999; Shenton, Dickey, Frumin, ; McCarley, 2001; Steen, Mull, McClure, Hamer, ; Lieberman, 2006; Wright et al., 2000). Meta-analysis has found abnormalities in the medial-temporal lobe structures (amygdala, hippocampus, and parahippocampal gyrus), corpus callosum, and frontal
lobes, as well as reduced volume in the occipital, and parietal lobes (McCarley, et al., 1999; Shenton, et al., 2001). One meta-analysis also reported that 20% of the studies they reviewed found an increase in the size of the fourth ventricle (Shenton, et al., 2001). Another meta-analysis, however, found no enlargement of the fourth ventricle in people with schizophrenia (McCarley, et al., 1999).

a. Corpus Callosum

The corpus callosum (CC) is the largest of the commissures in the brain
(Keshavan et al., 2002). Its primary role is to facilitate the rapid transfer of
information between homologous regions, and beyond, in the left and right
hemispheres of the brain (Aboitiz, Scheibel, Fisher, ; Zaidel, 1992; Jarbo, Verstynen, ; Schinder, 2012).

The size of the CC increases into adult years (Pujol, Vendrell, Junqué, Martí-Vilalta, ; Capdevila, 1993). Meta-analysis has found that people with
schizophrenia have reductions in the size of the corpus callosum (Woodruff,
McManus, ; David, 1995).

Moreover, a meta-analysis of MRI studies found 67% of the studies reviewed reported people with schizophrenia had differences in the CC when compared to the normal population (Shenton, et al., 2001).

Specifically, reductions in the width and volume of the splenium, genu, isthmus, and area of the anterior midbody of the CC have been reported in people with schizophrenia (Bersani, Quartini, Iannitelli, Paolemili, ; Ratti, 2010; Knöchel et al., 2012; Walterfang et al., 2009; Walterfang et al., 2008).

Investigations into the integrity of the white matter of the CC in people with
schizophrenia using FA have found decreased white matter FA bilaterally in the CC (Mitelman, et al., 2007), with specific decreases found in the genu, isthmus and splenium (Knöchel, et al., 2012; Price et al., 2007).

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