OCR Psychology A Level Book 2 sample

Cognitive neuroscience explanation of schizophrenia We discussed cognitive deficits in schizophrenia earlier in this chapter, on page 37. Cognitive neuroscience goes a step further and aims to explain these cognitive deficits in terms of brain activity. Hallucinations One positive symptom of schizophrenia is hallucinations which may be explained in terms of neural circuits. For example, we described Chris Frith’s cognitive explanation for schizophrenia on page 37. In a more recent version (Frith 2005) he proposed a neurocognitive explanation—a breakdown in the neural circuit that links the prefrontal cortex with the septo-hippocampal system is responsible for delusions associated with schizophrenia. The septo-hippocampal system is a brain circuit that includes the hippocampus and amygdala, both involved in emotional processing. This system stops being regulated by the executive functions of the prefrontal cortex. The cognitive impairment that results is one in which the patient with schizophrenia cannot tell the difference between an externally generated stimulus and an internally generated intention. One outcome is the experience of third-person auditory hallucinations. The patient hears voices, as if from outside their head, commenting on their behaviour, appearance, etc. Language abnormalities Another common cognitive symptom of schizophrenia is language difficulties, such as poverty of speech ( alogia ) and loose associations, in which words in a sentence have little meaningful relationship to each other. These difficulties are thought to originate from structural and functional abnormalities in a temporal-prefrontal neural circuit . This links the primary auditory cortex in the temporal lobe with areas in the prefrontal cortex responsible for executive functions. Both are central to processing the meaning of language. Research evidence Gina Kuperberg et al. (2007) used fMRI to scan the brains of 17 patients with chronic schizophrenia while showing them semantically related words. There was increased activity in both the temporal cortex and inferior prefrontal cortex compared with a matched control group of participants without schizophrenia. This suggests that the loose associations produced by people with schizophrenia may be due to hyperactivity in the areas of the brain that deal with language. This may reflect abnormal functioning of the temporal- prefrontal neural circuit that connects them. A review by André Aleman (2014) reported increases in prefrontal activity during difficult working memory tasks in participants with schizophrenia compared with controls. However, when the tasks became too hard to complete, participants with schizophrenia showed reduced activity compared with controls. These results indicate some neuronal basis for the cognitive deficits in schizophrenia. Cognitive neuroscience explanation of specific phobias The amygdala is the key brain structure involved in the neural circuits associated with specific phobia . Dual brain circuits According to Joseph LeDoux (2003), two brain circuits control the normal fear response. The shorter circuit runs from the thalamus —which integrates sensory information from the eyes, ears, etc.—to the amygdala. This is a kind of ‘early warning system’, fast but inaccurate. It responds to the broad features of any potentially threatening stimulus so we get a quick indication that there is something to be afraid of (e.g. an object that looks spider-ish). A second, longer circuit runs from the thalamus to the prefrontal cortex before connecting with the amygdala. This is a slower circuit because it involves more thorough processing of the threat in the prefrontal cortex (‘slower’ in this context means about 0.12 seconds). But it is precise—it allows us to perceive more accurately what is causing the fear response. This circuit could override or inhibit the fear response if we conclude that there is nothing to be afraid of. Impairment in phobia Both of these circuits are probably impaired in people with specific phobias. This means they have greater amygdala activity than non-phobics and therefore have a stronger fear response in the first place. But they also have decreased activity in the parts of the cortex that would normally override fear, such as the orbitofrontal cortex (OFC) (Kumari, 2006). Research evidence Stefan Dilger et al . (2003) compared the brain activity of nine women with a spider phobia and nine who had no phobias. All were shown images of spiders (phobia-related) and images of snakes and mushrooms (phobia-unrelated) while undergoing brain scanning with fMRI. The researchers found that the phobia-related images were associated with increased amygdala activity in the phobic participants but not in the non-phobic participants. This suggests that a specific phobia could result from a neurological impairment leading to a cognitive deficit in the ability to process information about fear and anxiety. check your understanding 1. Briefly summarise the cognitive neuroscience explanation of mental illness. 2. Outline how neural abnormalities can explain cognitive biases in depression. 3. Outline one piece of research that supports the cognitive neuroscience explanation of one mental illness. 4. Outline the role of the prefrontal cortex in the cognitive deficits of schizophrenia. 5. Explain how faulty neural circuits might lead to a specific phobia. 6. Identify one scanning technique and explain how this could help in our understanding of the cognitive neuroscientific basis for mental illness. Functional magnetic resonance imaging (fMRI) is perhaps the most popular current method of investigating brain activity. fMRI detects which areas of the brain are active and this allows cognitive neuroscientists to link cognitive functions or dysfunctions (e.g. memory, depression) with localised brain activity. 43 Background: The cognitive neuroscience explanation of mental illness