COGNITIVE SYMPTOMS OF SCHIZOPHRENIA
Cognitive symptoms refer to the difficulties with concentration and memory. These can include:
1. Disorganized thinking
2. Slow thinking
3. Difficulty understanding
4. Poor concentration
5. Poor memory
6. Difficulty expressing thoughts
7. Difficulty integrating thoughts, feelings and behavior.
Each schizophrenic falls under a subtype of schizophrenia defined by a unique indicator. This indicator may be one dominant symptom only or a combination of positive and negative symptoms. People with schizophrenia are classified into 5 sub-types, namely “Paranoid Type”, “Disorganized Type”, “Catatonic Type”, “Undifferentiated Type” and “Residual Type”.
For example, schizoaffective disorder exhibits schizophrenia alongside another mental disorder. Undifferentiated schizophrenia can be thought of as “general” schizophrenia, as it doesn’t display any one dominant symptom. Below are the different types of schizophrenia and their characteristics.
There are different kinds of schizophrenia. The International Classification of
Diseases (ICD-10) manual describes them as below:
1.Paranoid schizophrenia: These persons are very suspicious of others and often have grand schemes of persecution at the root of their behavior. Halluciations, and more frequently delusions, are a prominent and common part of the illness.
-Common form of schizophrenia.
-Prominent hallucinations and/or delusions.
-May develop at a later age than other types of schizophrenia.
-Speech and emotions may be unaffected.
2. Hebephrenic schizophrenia (Disorganized schizophrenia): In this case the person is verbally incoherent and may have moods and emotions that are not appropriate to the situation. Hallucinations are not usually present.
– Disorganized behavior (e.g., difficulty starting or finishing a task, difficulty acting appropriately in social situations)
-Disorganised thoughts: other people may find it difficult to understand others.
-Pranks, giggling, health complaints and grimacing.
-Short-lasting delusions and hallucinations.
-Usually develops between 15 and 25 years old.
-Disorganized speech (e.g., word salad, incoherence, perseverance)
-Flat or inappropriate affect (e.g., poor eye contact, lack of facial expressions)
3. Catatonic schizophrenia: In this case, the person is extremely withdrawn, negative and isolated, and has marked psychomotor disturbances.
-Rarer than other types.
-Unusual movements, often switching between being very active and very still.
-You may not talk at all.
4.Undifferentiated schizophrenia: Conditions meeting the general diagnostic criteria for schizophrenia but not conforming to any of the above subtypes, or exhibiting the features of more than one of them without a clear predominance of a particular set of diagnostic characteristics.
One’s diagnosis may have some signs of paranoid, hebephrenic or catatonic schizophrenia, but doesn’t obviously fit into one of these types alone.
5. Residual schizophrenia: In this case the person is not currently suffering from delusions, hallucinations, or disorganized speech and behavior, but lacks motivation and interest in day-to-day living. One may be diagnosed with this if he/she has a history of psychosis but only have negative symptoms.
6. Simple schizophrenia:
-Rarely diagnosed in the UK.
-Negative symptoms are prominent early and get worse quickly.
-Positive symptoms are rare.
7. Cenesthopathic schizophrenia:
People with cenesthopathic schizophrenia experience unusual bodily sensations.
8. Unspecified schizophrenia:
Symptoms meet the general conditions for a diagnosis, but do not fit in to any of the above categories.
9. Schizoaffective Disorder: These people have symptoms of schizophrenia as well as mood disorder such as major depression, bipolar mania, or mixed mania.
Schizoaffective disorder is a mixture of schizophrenia and either depression or bipolar disorder. This type of schizophrenia is typically hard to diagnose because of the myriad of symptoms that depression or bipolar disorder may bring.
Depression is marked by prolonged feelings of sadness and worthlessness, as well as cognitive problems like problems with concentrating and remembering details. On the other hand, bipolar disorder causes shifts in mood — one moment you may feel elated, and then you suddenly feel low, often to the point of sadness.
The cycle between high and low emotions may become so intense and frequent that they begin to interfere with your daily life and affect your relationships and work or academic performance. The two tables below indicate the symptoms for the mental disorders that may coexist with schizophrenia.
-Weight gain or loss
-Changes in sleeping patterns
-Lack of energy
-Loss of interest in hobbies or favorite activities
-Feelings of worthlessness or hopelessness
-Guilt or self-blame
-Troubles with thinking or concentration
-Thoughts of death or suicide
Bipolar Disorder Symptoms:
Bipolar Mania (High):
• Euphoria or irritability
• Increased energy and activity
• Excessive talk or racing thoughts
• Inflated self-esteem
• Unusual energy, plus a lowered need for sleep
• Reckless pursuit of gratification
Bipolar Depression (Low):
• Depressed mood and low-self esteem
• Low energy levels and apathy
• Sadness, loneliness, helplessness, guilt
• Slow speech, fatigue and poor coordination
• Insomnia or oversleeping
• Suicidal thoughts and feelings
• Poor concentration
10. Disorders Related to (or sometimes with similar symptoms to) Schizophrenia/ Schizophrenia Spectrum Disorders:
Knowing the symptoms of these disorders, and how they can be similar and different from schizophrenia, can help prevent a possible misdiagnosis. The concentration on predominant symptoms at presentation has helped mental health professionals distinguish and better treat other mental disorders that resemble schizophrenia, creating the schizophrenia spectrum of disorders.
-Schizoid Personality: Schizoid personality disorder (SPD) is a chronic and pervasive condition characterized by social isolation and feelings of indifference toward other people. Those who suffer from this disorder are often described as distant or withdrawn.
-Schizophreniform Disorder: Schizophreniform disorder has identical features to schizophrenia but the duration of symptoms is less. The patient has experienced symptoms for longer than one week but less than six months. This diagnosis is often considered the first step towards an eventual schizophrenia diagnosis, which requires continuous signs of disturbance for at least six months.
-Schizotypal Personality: develops by early adulthood and is characterized by pervasive deficits in social and interpersonal skills, eccentric behavior, discomfort forming close personal relationships, as well as cognitive and perceptual distortions. Someone with schizotypal personality disorder may have ideas of reference. These are unlike delusions of reference, in which a person’s behavior is altered by their belief that something is referential to them personally.
-Bipolar Disorder (Manic Depression) – frequently misdiagnosed as schizophrenia (and vice versa).
-Asperger’s Syndrome – a type of Autism that may be misdiagnosed
as schizophrenia in children
Recent changes in classification and diagnosis of schizophrenia:
Different subtypes of schizophrenia were there in the past, including:
• Paranoid schizophrenia
• catatonic schizophrenia
• disorganized, or hebephrenic schizophrenia
• schizoaffective disorder
• childhood schizophrenia
In 2013 the Diagnostic and Statistical Manual of Mental Disorders 5th edition (DSM-V) changed the method of classification to bring all these categories under a single heading: schizophrenia.
The decision to eliminate these subtypes was based on the conclusion they had “low reliability, limited diagnostic stability and poor validity.” It was also concluded that they did not provide better treatment or did not predict how patients would respond to treatment. (APA)
Two other important changes that was made to the diagnostic criteria in 2013.
One was the removal of the requirement for a person to experience bizarre delusions and to hear two or more voices talking during an auditory hallucination to receive a positive diagnosis. The second was that, to receive a diagnosis, a person must have at least one of the following symptoms:
• Disorganized speech
Etiology/ RISK FACTORS/CAUSES OF SCHIZOPHRENIA:
Recently, the etiology of schizophrenia is not known. There are various theories regarding its cause. These include:
• a genetic hypothesis,
• cortical disconnection syndrome,
• neurotransmitter dysfunction,
• failure to establish cerebral asymmetry, and
• A neuro-developmental syndrome. It is noted that these possible causes has been linked, and are not considered mutually exclusive. The current thesis focuses on Miller’s (1996, 2008) hypothesis.
1. Miller’s Hypothesis:
There is a strong theme of altered lateralization in the literature on schizophrenia. Miller (1996, 2008) has provided a comprehensive theory that proposes that the underlying enduring abnormal psychological traits observed in people with schizophrenia, as opposed to episodes of active psychosis, can be viewed as the result of an alteration in normal cerebral lateralization. Miller proposes that the functional specialization seen within each hemisphere, namely the location of language in the left hemisphere and visuospatial processing in the right hemisphere (in the right-handed, neurologically normal population) is due to a greater ratio of fast-conducting myelinated and large calibre axons to slow conducting unmyelinated
and small calibre axons in the right hemisphere when compared to the left
hemisphere. This greater ratio of fast conducting axons in the right hemisphere allows for fast parallel processing of visuospatial information. While the greater number of unmyelinated and small calibre axons in the left hemisphere affords the greater temporal resolution needed for speech and language functions located in that hemisphere. Furthermore, Miller proposes that this asymmetry of axonal myelination and calibre type is global within each hemisphere, as opposed to being present only within regions involved in language and visual processing (Miller, 1996). Miller also suggests that callosal projections are made up of axons projecting from one hemisphere to the other. This results in the common finding of faster right-to-left, relative to left-to-right, interhemispheric transfer times (IHTT) in the right-handed normal population (Barnett ; Corballis, 2005; Brown, Larson, ; Jeeves, 1994; Iwabuchi ; Kirk, 2009; Marzi, Bisiacchi, ; Nicoletti, 1991; Moes, Brown, ; Minnema, 2007; Norwicka, Grabowska, ; Fersten, 1996)
2. Genetic Hypothesis:
Schizophrenia tends to run in families, but no single gene is thought to be responsible.
It’s more likely that different combinations of genes make people more vulnerable to the condition. However, having these genes doesn’t necessarily mean you’ll develop schizophrenia.
Evidence that the disorder is partly inherited comes from studies of twins. Identical
twins share the same genes.
In identical twins, if one twin develops schizophrenia, the other twin has a one in two chance of developing it, too. This is true even if they’re raised separately.
In non-identical twins, who have different genetic make-ups, when one twin develops schizophrenia, the other only has a one in seven chance of developing the condition.
While this is higher than in the general population, where the chance is about 1 in
100, it suggests genes aren’t the only factor influencing the development of
3. Specific genes:-
According to, Meta-analysis of genetic linkage studies strong evidence of susceptibility for schizophrenia has found on loci 13q, 22q11-12 and 8p21-22. According to evidence for susceptibility many other loci is also there (Badner & Gershon, 2002; DeLisi, Crow, et al., 2002; Levinson, Lewis, & Wise, 2002; Lewis et al., 2003; Tandon, Keshavan, & Nasrallah, 2008).
In some individuals in the development of schizophrenia some rare specific genetic aberrations have been implicated. These are microdeletions of part of chromosome 22q11.2, which leads to a 20-fold increase in risk for schizophrenia (Bassett et al., 2005), and deletions in 1q21.1, 15q11.2, and 15q13.3 (Stefansson et al., 2008). These microdeletions accounts for up to 2% of schizophrenia (Bassett, et al., 2005).
In rare causes of schizophrenia other genes implicated include Val66Met (Gratacòs et al., 2007), GAD1 (Straub et al., 2007), and DISC1 (disrupted in schizophrenia 1) (Hennah, Thompson, Peltonen, & Porteous, 2006). Furthermore, Neuroregulin 1 (NRG1), COMPT (catechol-O-methyl-transferase), ALC6A3, DRD3, DTNBP1 (dysbindin) and SLC184 are implicated in schizophrenia (Duan et al., 2007; Nicodemus et al., 2007; Riley et al., 2009; Tan et al., 2007).
4. Neurotransmitter Dysfunction Hypotheses:
Dopamine is a neurotransmitter which is important in the pathology of schizophrenia. Drugs that block dopamine receptors, specifically D2 receptors (Carlsson, Carlsson, & Milsson, 2004), have an ameliorating effect on symptoms of schizophrenia (Creese, Burt, & Snyder, 1996), and those that increase the action of dopamine exacerbate symptoms (Snyder, 1972).
B. Serotonin, glutamate and ?-aminobutyric acid:
Cerebral serotonin imbalances have been implicated in schizophrenia. Second
generation antipsychotics are, amongst other actions, serotonin antagonists (Meltzer, Matsubara, & Lee, 1989), and are more effective for treatment resistant schizophrenia than typical antipsychotics (Bondolfi et al., 1998). Serotonin antagonists have also proved effective in the treatment of negative symptoms (Duinkerke et al., 1993). However, the exact mechanism via which serotonin plays a role in schizophrenia is not fully understood (Duncan, Zorn, & Lieberman, 1999).
Another neurotransmitter that has been implicated in schizophrenia is glutamate. This hypothesis was drawn from the ability of glutamate agonists, such as Ketamine, to produce quasi psychotic symptoms in the normal population and in people with schizophrenia (Malhotra et al., 1996, 1997).
The inhibitory neurotransmitter ?-aminobutyric acid (GABA) has also been
proposed to play a role in schizophrenia. Post-mortem studies of the brains of people with schizophrenia have found abnormalities in the GABA neurotransmitter system in the frontal lobes (Benes, Vincent, Marie, & Khan, 1996; Sherman, Davidson, Baruah, Hegwood, & Waziri, 1991). GABA plays an important function in working memory, and it has been proposed that these GABA reductions may be linked to deficits in working memory found in schizophrenia (Lewis, Hashimoto, & Volk, 2005; Lewis, Volk, & Hashimoto, 2004; Volk & Lewis, 2002).
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).
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).
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.
Consequences of schizophrenia
Although schizophrenia is not in itself a fatal disease, death rates of people
with schizophrenia are at least twice as high as those in the general population. The excess mortality has been related in the past to poor conditions of prolonged institutional care, leading to high occurrence of tuberculosis and other communicable diseases (Allebeck, 1989). This may still be an important problem wherever large numbers of patients spend a long time in crowded asylum-like institutions. However, recent studies of people with schizophrenia living in the community showed suicide and other accidents as leading causes of death in both developing
and developed countries (Jablensky et al., 1992).
2. Social disability:
According to the International classification of impairments, disability and
Handicaps (WHO, 1980) impairment represents any loss or abnormality of
psychological, physiological or anatomical structure or function, while disability
is any restriction or lack (resulting from an impairment) of ability to perform
an activity in the manner or within the range considered normal for an
individual in his or her socio-cultural setting.
In mental disorders, such as schizophrenia, disability can affect social functioning
in various broad areas (Janca et al., 1996), namely:
• self-care, which refers to personal hygiene, dressing and feeding;
• occupational performance, which refers to expected functioning in paid
activities, studying, homemaking;
• functioning in relation to family and household members, which refers to
expected interactions with spouses, parents, children or other relatives;
• functioning in a broader social context, which refers to socially appropriate
interaction with community members, and participation in leisure and other
Data from European and North American studies show persisting disability of
moderate or severe degree in about 40% of males with schizophrenia, in
contrast with 25% of females (Shepherd et al., 1989). Substantially lower
figures have been found in India, Africa and Latin America (Leff et al., 1992).
Global assessment of disability, however, hides wide variations across life
domains, which can be affected in different ways.
There is good evidence that for most patients nature and extent of social
disability are more relevant as outcome indicators than clinical symptoms.
3. Social stigma:
Social stigma refers to a set of deeply discrediting attributes, related to negative attitudes and beliefs towards a group of people, likely to affect a person’s identity and thus leading to a damaged sense of self through social rejection, discrimination and social isolation (Goffman, 1963). Stigma is strongly linked with the label of mentally ill and is, to a certain extent, unrelated to the actual characteristics or behaviours of those stigmatized. Various adverse consequences may arise from the stigmatization process: use of pejorative language, barriers to housing or employment, restricted access to social services, fewer chances for marriage, increased mistreatment and institutionalization (Desjarlais et al., 1995).
4. Impact on caregivers:
The available data show that the proportion of persons with schizophrenia
living with their relatives ranges between 40% in United States to more than
90% in China ( Torrey and Wolfe, 1986; Xiong et al., 1994). Moreover, family
involvement and distress is not necessarily lower when the sufferer lives away from home (Winefield and Harvey, 1993). Nevertheless, the burden that is often placed on families or others living in close contact with a mentally ill
person has only recently been recognized (Fadden et al., 1987).
Various aspects of impact on caregivers should be considered, including:
• the economic burden related to the need to support the patient and the loss
of productivity of the family unit;
• emotional reactions to the patient’s illness, such as guilt, a feeling of loss
and fear about the future;
• the stress of coping with disturbed behaviour;
• disruption of household routine;
• problems of coping with social withdrawal or awkward interpersonal behaviour;
• curtailment of social activities.
5. Social costs:
In recent years a major effort has been made towards the quantification of the
global social burden of all illnesses and injuries, taking into account not only
mortality but the extent of disability and allowing comparisons between
different categories of illness. The measure of disability-adjusted life years
(DALYs) lost has been used as a health status indicator (Murray and Lopez,
1996). Although this approach may not be completely suitable for most
mental disorders, including schizophrenia, because of their variable course and the fluctuating nature of the related disability, it enables social scientists and policy-makers to put the burden associated with schizophrenia within a comprehensive public health framework.
The loss in DALYs caused by schizophrenic disorders worldwide was estimated in 1990 at slightly below 13 million, which represents about 1% of the global burden of the disease deriving from all causes. Schizophrenia is 26th in the list of the diseases, ranked according to their contribution to the overall burden. However, if one takes into account the predicted modifications in social structure in most developing countries and the increase of populations at risk over the coming decades, schizophrenia is projected to be in 20th position by the year 2020, with more than 17 millions of DALYs lost, accounting for 1.25% of the overall burden (Murray and Lopez, 1996).
Management of schizophrenia is a protracted or more precisely a life time process that requires effective pharmacotherapy along with other lines of supportive
therapy especially psychotherapy. Control of the disease may become a difficult target as other health challenges interfere. Schizophrenic patients may suffer co-morbid conditions especially diabetes mellitus, increased weight and serious cardiovascular disorders. On the other hand, symptoms of the disease not only affect the patients but also affect their families and “surroundings”. Therefore, it
is sometimes important for physicians to provide guidance to all persons affected by the disease. Psychosocial and family interventions can improve outcomes.
With proper treatment, patients can lead productive lives.
Treatment can help relieve many of the symptoms of schizophrenia. However, the majority of patients with the disorder have to cope with the symptoms for life.
Psychiatrists say the most effective treatment for schizophrenia patients is usually a combination of:
Anti-psychosis drugs have transformed schizophrenia treatment. Thanks to them, the majority of patients are able to live in the community, rather than stay in a hospital.
The most common schizophrenia medications are:
• Risperidone (Risperdal) – less sedating than other atypical antipsychotics. Weight gain and diabetes are possible side effects, but are less likely to happen, compared with Clozapine or Olanzapine.
• Olanzapine (Zyprexa) – may also improve negative symptoms. However, the risks of serious weight gain and the development of diabetes are significant.
• Quetiapine (Seroquel) – risk of weight gain and diabetes, however, the risk is lower than Clozapine or Olanzapine.
• Ziprasidone (Geodon) – the risk of weight gain and diabetes is lower than other atypical antipsychotics. However, it might contribute to cardiac arrhythmia.
• Clozapine (Clozaril) – effective for patients who have been resistant to treatment. It is known to lower suicidal behaviors in patients with schizophrenia. The risk of weight gain and diabetes is significant.
• Haloperidol – an antipsychotic used to treat schizophrenia. It has a long-lasting effect (weeks).
The primary schizophrenia treatment is medication. Sadly, compliance (following the medication regimen) is a major problem. People with schizophrenia often come off their medication for long periods during their lives, at huge personal costs to themselves and often to those around them.
The patient must continue taking medication even when symptoms are gone. Otherwise they will come back.
The first time a person experiences schizophrenia symptoms, it can be very unpleasant. They may take a long time to recover, and that recovery can be a lonely experience. It is crucial that a person living with schizophrenia receives the full support of their family, friends, and community services when onset appears for the first time.
The treatment of schizophrenia is guided by three general principles that follow
directly from the stress-vulnerability model.
? Reduce biological vulnerability
Since the introduction of antipsychotic drugs in 1952 (Frith and Johnstone,
2003), help was available for people with schizophrenia. Although some patients had to go through trial and error with the psychiatrists in determining which medication suit them best or that some actually do not respond to antipsychotic drugs at all, most patients respond well to the medication. That is, on condition, they take the medication consistently (inconsistent or refusal to take medication often lead to relapses). (Barlow ; Durand, 2002). (Many patients who refuse to take medication attribute it to the unpleasant side effects experienced by some.) The antipsychotic drugs are also called “neuroleptics”, which mean “talking hold of the nerves”. When the neuroleptics are effective, they help the patients think more clearly and reduce or eliminate hallucinations and delusions. To a lesser extent, the negative and disorganized symptoms are reduced, too. Some of the neuroleptic drugs proven effective are haloperidol, risperidone, sulpiride and the most recently introduced one, clozapine which promises patients less side-effects. (Barlow ; Durand, 2002). Recently in 2000, Hoffman and colleagues tried “transcranial magnetic stimulation” on 12 patients who experienced auditory hallucinations. They found that many of the individuals experienced improvement following it. The technique uses wire coils to repeatedly generate magnetic fields – up to 50 times per second – that pass through the skull to the brain. This input interrupts the normal communications temporarily to that part of the brain. However, this research is not well-validated yet and research to assess the true value of this technique has been going on. (Cited in Barlow ; Durand, 2002.)
? Reduce environmental stress:
• Together with drug therapy, individual psychotherapy is administered to help the patient manage the psychological factors that can also contribute to the illness. (Barlow ; Durand, 2002). Most clinicians today agree that the most beneficial treatment for schizophrenia is some combination of antipsychotic medication and therapy (Sue, Sue ; Sue, 2003; Barlow ; Durand, 2002). Since this paper is for a counsellors’ conference, I shall describe individual psychotherapy at some length.
• The psychoanalytic/psychodynamic approach where the therapist helps the patient dig deep into his past to bring to surface unresolved conflicts in his childhood, for instance, has fallen out of favour. Hogarty and colleagues (1997) reported of a recently tried out “personal therapy” which is more favourable. Personal therapy equips patients with a broad range of coping techniques and skills. The therapy is staged, which means that it comprises different components that are administered at different points in the patient’s recovery. For example, in the early stages, patients examine the relationship between their symptoms and their stress levels. They also learn relaxation and some cognitive techniques. Later, the focus is on social and vocational skills. (Cited in Butcher, Mineka and Hooley, 2004.)
• A successful cognitive technique used by Chadwick, Sambrooke, Rasch, and Davies (2000) is helping patients develop the means of critically evaluating their beliefs (delusions) or hallucinations (as cited in Sue, Sue ; Sue, 2003). The initial sessions with the terrified and helpless schizophrenia patients, who usually view the voices as omnipotent, focused on exploring when the voices began, why they think the voices occurred, and how the voices affected their lives. Later, the beliefs of omnipotence were subjected to empirical testing by demonstrating that certain behaviors could reduce the voices. They also evaluated the possibility that the voice was internally generated. This process was effective in reducing the perceived power and control of the voices.
• Coping strategies such as reading aloud to combat auditory hallucinations, asking for increased medication, seeking help or distraction and relaxing when they feel their symptoms are worsening have also been used (Sue, Sue ; Sue, 2003.) With the effectiveness of drug therapy, the responsibility for mental health care has recently been delegated to the community (and the patient’s own family). More patients are treated as outpatients rather than being hospitalized (unless their illness is severe) and there are more community efforts in providing support and rehabilitation for the patients. (Haque, 2001; Barlow & Durand, 2002). It has been found that traditional institutional treatments providing custodial care have yielded poor results (Sue, Sue & Sue, 2003).
• The self-help group therapy is one example of how the community come together to help each other. (Mueser & Gingerich, 1994). A group of outpatients come together, with the supervision of skilled personnel, to share with each other how they are coping and for an exchange of ideas on reducing stress and coping skills. Group therapies are carried out in Malaysia but they are not frequent and in smaller towns, they are not available. According to Nolen-Hoeksema (2004), the self-help support groups in the U.S.A. also practice generating and role-playing solutions to social situations besides discussing the impact of the disorder on their lives, the frustrations of trying to make people understand their disorders, their fears of relapse and their experiences with various medications.
• Behavioral family therapy has been used in the U.S.A. to teach the families of persons with schizophrenia to be more supportive. Family members are taught practical facts about schizophrenia, its symptom triggers, its treatment, antipsychotic medications and its side effects; and relieved of the myth that they caused the disorder. They are also helped with communication skills to replace the harsh criticism that characterizes some family interactions. In addition, they learn problem solving skills to help them resolve conflicts that arise. (Barlow & Durand, 2002; Mueser & Gingerich, 1994.)
? Improve coping skills:
Improving coping skills can be in the form of social skills training (esp. in community settings) and rehabilitation which teaches vocational and self-care skills. (Barlow & Durand, 2002; Mueser & Gingerich, 1994). Social skills training reduces the stress brought on by a lack of social skills which is typical of schizophrenia patients. In Malaysia, there are rehabilitation such as one organized by Malaysian Care, a non-governmental organisation. Malaysian Care teaches self-care skills, social skills and spiritual coping skills (Malaysian Care is a Christian organization). Research have shown that the addition of social skills training, family intervention and vocational rehabilitation has been more effective in preventing relapse than drug treatment alone (Falloon, Brooker & Graham-Hole, 1992 as cited in Barlow & Durand, 2002 and Hogarty et al., 1997 as cited in Nolen-Hoeksema, 2004).
? PREVENTIVE MEASURES:
Since one does not know whether one has a predisposition to schizophrenia in the first place, It can be believed that it is wise for all people to take measures to prevent it from happening to oneself or to our loved ones. For those who are already afflicted with schizophrenia, the following preventive measures should work against relapses.
(a) Healthy lifestyle:
Healthy lifestyle from the physical, spiritual and mental aspect is most important. There should be a healthy exercising of the mind. Sleep must be sufficient.
(b) Avoid excessive stress / Stress management:
Excessive stress is discouraged. Learn to relax. The many stress management seminars and talks of late should be given a consideration.
(c) Happy social relationship:
Good social relationships with family and friends should be cultivated. Effective social skills can be learned.
(d) Improve prenatal care and nutrition:
Taboos for pregnant women may actually be very sound after all! Vaccinations against viruses (eg. influenza) for women of childbearing age may be a valid preventive measure.
SCHIZOPHRENIA AND PUBLIC HEALTH
Various attempts have been made to classify symptoms of schizophrenia in order to define meaningful subtypes of the disorder. In the past 20 years the distinction between the two broad categories of positive and negative symptoms gained widespread popularity (Crow, 1980). However, more recent multivariate analysis has suggested not two but three symptom clusters: reality distortion, disorganization and psychomotor poverty (Liddle, 1987).