b. Altered Cerebral Asymmetries
• Reduced Physical Asymmetry in the Brain:
Cerebral physical asymmetry can be observed in several parts of the brain. In
the normal population the brain displays asymmetry with larger right hemisphere prefrontal and frontal regions, and larger left hemisphere occipitoparietal, occipital, and sensorimotor regions (Falkai, Schneider, Greve, Klieser, & Bogerts, 1995; Sharma et al., 1999). These asymmetries have been found to be reduced or absent in people with schizophrenia and their first degree family members (Bilder et al., 1994; Falkai, et al., 1995; Sharma, et al., 1999; Sommer, André, Ramsey, Bouma, & Kahn, 2001; Turetsky et al., 1995).
The role of the temporal lobe in schizophrenia has been of interest in the study of schizophrenia as direct stimulation has been demonstrated to invoke auditory hallucinations (Penfield & Perot, 1963).
• Functional Asymmetry in the Brain:
Further cerebral asymmetry can be observed in the functional specialisation of each hemisphere. This is demonstrated in the lateralisation of language to the left hemisphere in more than 90% of right-handers (Springer et al., 1999), 85% of ambidextrous people, and 73% of left-handers in the normal population (Knecht et al., 2000). People with schizophrenia have been found to have decreased cerebral lateralisation of language.
• Schizophrenia as a By-Product of Cerebral Lateralisation and Language:
It has been proposed that schizophrenia should have been selected against
during human evolution as it is inherently non-adaptive due to people with
schizophrenia having reduced fecundity compared with people without schizophrenia (Crow, 2000; Haverkamp, Propping, & Hilger, 1982; Nanko & Moridaira, 1993; Svensson, Lichtenstein, Sandin, & Hultman, 2007). However, due to the continued stable incidence of schizophrenia it has been postulated that schizophrenia is linked to genes that are fundamentally involved in the speciation event that led to the evolution of Homosapiens (Crow, 2000).
• Handedness and Cerebral Functional Asymmetry
More evidence for altered asymmetries in the schizophrenia population comes from studies in human handedness. Approximately 90% of the normal population is right-handed (Dragovic & Hammond, 2008; Hardyck & Petrinovich, 1977), which is linked with the functional lateralisation in the cerebral cortex (Corballis, 1991; Springer, et al., 1999).
Left-handed people with schizophrenia have higher levels of thought disorder
and higher rates of disorganised type schizophrenia, when compared with righthanded people with schizophrenia (Dollfus, Buijsrogge, Benali, Delamilleure, & Brazo, 2002; Manoach, Maher, & Manschreck, 1988).
c. Left Hemisphere Dysfunction:
Left hemisphere dysfunction in people with schizophrenia is evidenced in physiological and behavioural differences. Functional magnetic resonance imaging (fMRI) has shown people with schizophrenia with prominent negative symptoms have anatomical abnormalities in the left neocortical and limbic regions, and related white matter tracts (Sigmundsson et al., 2001). People with schizophrenia have also been shown to exhibit reduced left hemisphere advantage during a dichotic fused words task, and this was correlated with higher levels of positive symptoms (Bruder et al., 1995). Studies using fMRI found decreased activity in Wernicke’s area, an area linked to formal thought disorder, in people with schizophrenia (Kircher et al., 2001).
d. Right Hemisphere Dysfunction
Researchers looking at the right hemisphere in people with schizophrenia have also found evidence of differences between the schizophrenia population and the normal population. The right hemisphere is thought to be involved in speech prosody, recognition of facial affect, and the interpretation of metaphors (Brownell, Potter, ; Michelow, 1984; Kucharska-Pietura ; Klimkowski, 2002; Ross ; Monnot, 2008), skills that are often disturbed in people with schizophrenia (Addington, Penn, Woods, Addington, ; Perkins, 2008; Kucharska-Pietura ; Klimkowski, 2002; Murphy ; Cutting, 1990).
In addition, people with right hemisphere damage can experience
delusional misidentification (Capgras Syndrome) (F?rstl, Almeida, Owen, Burns, ; Howard, 1991), break-down of self/other boundaries (Bogousslavsky ; Regli, 1988), and loss of will (Coslett ; Heilman, 1989), all of which are symptoms of schizophrenia (Cutting, 1994).
Moreover, right hemisphere lesions can result in the loss of the ability to use
prosody and emotional gesticulation when speaking (Ross ; Marek-Marsel, 1979). Right hemisphere damage is also linked to deficits in the ability to express and perceive emotion (Borod, 1992; Borod, Koff, Perlman, ; Nicholas, 1986), and removal of the right hemisphere can result in deficits in perceiving negative emotional expressions, lies, and sarcasm (Fournier, Calverly, Wagner, Poock, ; Crossley, 2008).
8. Electroencephalography and Schizophrenia:
EEG creates an attenuated view of the synchronous excitatory and inhibitory
neuronal post-synaptic potentials in the cerebral cortex (Barlow, 1993; Olejniczak, 2006). Experimentally its basic function is to observe the physiological output, or change in neural activity in the cortex, as a function of different stimuli or behaviour, thus allowing for the inference of the role of different cortical areas to various sensory or behavioural functions (Lopes da Silva, 2005). The recorded activity is the summation of the electrical activity primarily from groups of pyramidal neurons, which creates a picture of temporal brain activity (Barlow, 1993; Olejniczak, 2006).
C. Medication Effect on EEG:
Comparison between studies of people with schizophrenia is confounded by
some studies using medicated individuals and others using non-medicated individuals. Furthermore, there exists a range of possible antipsychotic medications available, further confounding comparisons between studies, as participants in different studies may be medicated differently. There appears to be a lack of recent literature addressing this issue from which to draw upon.
The effect of medication on EEG is a complex issue. As such the influence
that it has on EEG signals should be reviewed on a case by case basis.
D. Source Localization of the EEG:
One technique for source localisation is ‘Low Resolution Electromagnetic
Tomography’ (LORETA). This creates a three dimensional image of the electricalnactivity within the cortex from the 2-dimensional scalp recordings (Pascual-Marqui, et al., 1994). This technique creates a topographic map of the EEG oscillations byncalculating the smoothest “3-dimensional current distributions” between thenoscillations based on the data (Pascual-Marqui, et al., 1994, p. 49). Subsequently, we will reconstruct the current density dynamics from each estimated source. The peak energy at each source (within a particular time window) can then be used as a potentially more accurate estimate of the latency differences between activation of particular areas of the brain.
9. Event Related Potentials (ERPs)
ERPs are the summation of synchronous activation of pyramidal neurons that
consist of negative and positive wave forms (Epstein, 2003). They are considered to be the neurobiological response or transient change of regularly occurring wave forms as a function of sensory stimulation or internal event processing (Celesia ; Peachey, 2005), and are considered to be indicative of cortical information processing (Pfurtscheller ; Lopes da Silva, 2005).
10.Exposure to early biological risks
There is now a growing evidence indicating that certain environmental factors to
which a baby may be exposed in the mother’s womb or at birth are related to
vulnerability in developing schizophrenia. (Mueser & Gingerich, 1994). Perhaps
exposure to early biological risks explains how a person who does not have the
inherited tendency becomes the first person in his family to have schizophrenia.
Exposure to early biological risks can be via two ways: viral infection or birth
(a) Viral infection:
Several studies have shown that schizophrenia may be associated with prenatal
exposure to influenza. For example, Sarnoff Mednick and his colleagues (1991)
followed a large number of people after a severe influenza epidemic in Helsinki,
Finland and found that those whose mothers were exposed to influenza during their
pregnancy were much more likely to have schizophrenia than others. This observation has been confirmed by some researchers (eg. O’Callaghan et al., 1991; Venables, 1996). However, there are also researchers who did not agree to this observation (Torrey, Rawlings, ; Waldman, 1988). (Cited in Barlow ; Durand, 2002)
(b) Pregnancy and Birth complications:
More convincingly are the evidence of birth complications in identical twins. Carson ; Sanislow (1993) found that birth complications such as the loss of oxygen (anoxia) could affect only one of the identical twins. McNeil (1987) found that obstetrical complications appear often among twins with schizophrenia in discordant identical pairs, and among the more severely affected if both twins have schizophrenia. (Cited in Barlow ; Durand, 2002.) Other examples of birth complications reported are forceps delivery and fetal distress. Some scientists suggested that exposure to these types of environmental “insult” may cause small amounts of brain damage which only become apparent later in the person’s development. (Mueser & Gingerich, 1994.)
If a person has a biological vulnerability/predisposition to schizophrenia, excessive
stress can trigger the symptoms of schizophrenia according to the Stress-Vulnerability Model. Excessive stress can be in the form of traumatic life events such as the death of a loved one, marital or boy-girl relationship break up, or loss of job. Living in an environment in which there is a great deal of conflict, hostility, criticism or negativity between the patient and others (either family members or professional staff) can be stressful to patients and increase their risk of relapse. (Mueser & Gingerich; Brown, 1959; Brown et al., 1962). Also, an environment that places heavy demands on the patient can be stressful. (Mueser & Gingerich, 1994).
Coping skills refers to a patient’s ability to handle stress effectively and thereby
reduce the negative effects of stress. Some evidences of poor coping skills are a lack of social skills and the inability to relax. Having had a biological vulnerability to schizophrenia, the excessive stress a person experiences and is unable to cope with will trigger an onset of schizophrenia or a relapse. (Mueser ; Gingerich, 1994.)
(e) Drug abuse:
Drugs don’t directly cause schizophrenia, but studies have shown drug misuse
increases the risk of developing schizophrenia or a similar illness.
Certain drugs, particularly cannabis, cocaine, LSD or amphetamines, may trigger
symptoms of schizophrenia in people who are susceptible.
Using amphetamines or cocaine can lead to psychosis, and can cause a relapse in
people recovering from an earlier episode.
Three major studies have shown teenagers under 15 who use cannabis regularly,
especially “skunk” and other more potent forms of the drug, are up to four times
more likely to develop schizophrenia by the age of 26.
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