Can cognitive coordination be extended to explain
disorganised affect in Schizophrenia?
In order to identify subtypes of schizophrenia, symptoms in each subtype need to be identified. The
cognitive coordination theory put forward by Phillips and Silverstein paper specifically discusses
cognitive disorganisation. Neuroimaging research has discovered links between brain areas involved in
affect and cognition. My suggestion is that cognitive coordination could also be extended to explain
disorganised affect, which is commonly categorised under disorganisation syndrome. A link between
these theories supports the notion that disorganisation syndrome is a subtype of schizophrenia.
Phillips and Silverstein (2003) provide a fascinating insight into the ways in which
cognitive context models can be combined with neuroscience research to extend
knowledge of schizophrenia. The link between difficulties in perceptual grouping and
contextual disambiguation provides a logical explanation for cognitive disorganisation
symptoms of schizophrenia. However, definitions of disorganisation syndrome often
include disorganised emotion as well as speech difficulties and problems with thought
processes. Phillips and Silverstein’s theory does not explain how affect could be
disrupted in disorganisation syndrome. I suggest that, based on the findings of recent
research linking cognition and emotion, effects of cognitive disorganisation on affect
should be considered. A review by Ochsner and Gross (2005) of neuroimaging
research shows that there are many ways emotion can be modulated by cognitive
factors such as attention and memory. The findings suggested that pre-frontal cortex
(PFC) and orbitofrontal cortex (OFC) systems could be involved in interpreting
context of stimuli and directing emotional reactions.
Ochsner and Gross found two main ways emotion can be directed by cognition. These
are attentional control and cognitive change. Research reviewed showed that
attending to emotional stimuli and being distracted from emotional stimuli could
affect the way a person responds emotionally. Also changing the way an emotional
stimulus is perceived could cause a healthy individual to perceive a harmless stimulus
as painful or induce placebo effects in pain relief. These findings could be applied to
the study of schizophrenia because they show that changing cognitive responses can
influence emotional responses. In the studies reviewed, changes were brought about
by conscious activities. My argument is that these influences could also be induced by
chemical changes in cognitive structures. This could provide the link between NMDA
activity and disorganised affect.
The OFC is likely to link perception and emotion as it receives information about
taste, odours and visual stimuli (Rolls, 1996) and is linked with reward behaviour and
punishment behaviour. Therefore, sensory information is processed in this part of the
brain to influence behaviour. The process is likely to be mediated by positive and
negative emotions. Previous research suggests that the OFC and PFC are both
involved in a process of linking emotion and attention (Fragopanagos and Taylor,
2004). The PFC is also important for emotional processing and links with cognitive
processes (Gray, Braver and Raichle, 2002). Gray et al. suggest that this part is the
centre of where emotion and cognition integrate and each have a role in modulating
the other. Ochsner and Gross (2005) discuss the many ways in which the PFC can be
linked to the control of emotion. These include regulating amygdala activity in
attention tasks and tasks where participants had to interpret stimuli to manipulate
emotional responses.
The OFC can be impaired in schizophrenia (Pantellis and Brewer, 1995). Pantellis and
Brewer found that schizophrenics were unable to identify smells despite being able to
distinguish between smells. This suggests that schizophrenics are receiving the
sensory information but there is a problem in processing it. Further investigation
suggested an executive function problem. This could be compared to the cognitive coordination model as it involves the inability to identify a stimulus. The information
required to identify the smell (the external stimulus and internal knowledge) would
need to be coordinated in order for recognition to occur. If inability to recognise the
smell resulted from a lack of coordination, the NMDA model should be relevant to
abnormalities of affect in schizophrenia. This also applies if a combination of longterm memory and attentional deficits disrupt perception. If either of these apply an
NMDA antagonist, which disrupts cognitive coordination, should also change the way
an individual responds to emotional stimuli.
This has been found in a number of cases. NMDA receptors in the amygdala play an
important role in conditioning of fear (Walker and Davis, 2000). Campeau et al.
(1992, cited in Walker and Davis, 2000) and other researchers (Fanselow & Kim,
1994; Miserendino et al., 1990, cited in Walker and Davis, 2000) showed that when
auditory, visual and contextual cues stimuli were used, conditioned fear was affected
by blocking NMDA receptors. Other research into the effects of NMDA on emotion
implicates the ventral tegmental area, frontal regions (Borowski and Kokkinidis) and
hippocampal regions (Young, Bohenek and Fanselow, 1994) in fear responses. Given
that existing research focuses mainly on fear responses, further research into other
emotional responses would be required to clarify these findings. Also, the emotional
influences of the OFC and PFC have not specifically been investigated with NMDA
antagonists.
A possible link between the affective and cognitive symptoms of disorganisation
syndrome support the theory of a subtype of schizophrenia. My suggestion is that the
link should be investigated further. If no link is found, the way the symptoms are
classified needs to be reconsidered. Further research into a wider range of emotions
and sensations beyond pain and fear would be required to increase knowledge of
cognition and emotion. Also, more knowledge is required about interactions between
the ORC, PFC and emotional centres (such as the amygdala) in relation to NMDA
receptors. The cognitive coordination model could provide more detail to clarify how
cognitive change and attentional control could be altered by cognitive disorganisation.
It is possible that investigating cognition and affect in schizophrenia could provide
insight into the cognitive architecture to regulate emotion.
References
Fragopanagos JG. Taylor N (2004) Modelling the Interaction of Attention and
Emotion, BICS, Aug 29 - Sept 1
Ochsner KN, Gross JJ (2005) The cognitive control of emotion, Trends in Cognitive
Sciences, Vol. 9 (5), p242-249
Pantelis C, Brewer W (1995) Neuropsychological and olfactory dysfunction in
schizophrenia: relationship of frontal syndromes to syndromes of schizophrenia,
Schizophrenia Research, 17, p35-45
Phillips WA and Silverstein SM (2003) Convergence of biological and psychological
perspectives on cognitive coordination of schizophrenia, Brain and Behaviour
Sciences, Vol. 26, p65-138
Rolls ET (1996) The orbitofrontal cortex, Philos Trans R Soc Lond B Biol Sci., 351
(1346), p1433-1444
Walker DL and Davis M (2000) Involvement of NMDA Receptors Within the
Amygdala in Short- Versus Long-Term Memory for Fear Conditioning as Assessed
With Fear-Potentiated Startle, Behavioral Neuroscicnce, Vol. 114 (6) p1019-1033