OCR Psychology A Level Book 2 sample

Background The medical model Topic 2 The specification requires that you know the background to the medical model of mental illness. This is divided into three parts: the biochemical explanation, the genetic explanation and the brain abnormality explanation of mental illness. On this spread we look at the first part, the biochemical explanation of mental illness. This spread covers the essential information you will need on background for the exam but you also need to link the background to issues and debates and to the key research. We will look at these links on page 30. The biochemical explanation of mental illness This is the first of three explanations of mental illness that are associated with the medical model . The medical model was discussed at the beginning of this chapter as an example of the somatogenic approach. The main assumptions of the medical model are not only that mental illness is like any other illness and has physical causes but also that mental illness can be diagnosed by listing symptoms and working out what illness a person has. The physical causes may be due to abnormal biochemistry, genes or brain structure. We begin by looking at abnormal biochemistry—the chemical components of the brain. Biochemical principles The biochemical explanation focuses on abnormal levels of neurotransmitters —too much or too little. Neurons and synapses Messages are transmitted electrically around the brain and body via neurons . There are around 100 billion neurons in the brain. Neurons link to other neurons at a synapse , a very small gap of about 0.02 microns between the branches of one neuron and another. Neurotransmitters Information is transmitted chemically at the synapse. The electrical charge in the presynaptic neuron causes neurotransmitters to be released and these activate receptors in the postsynaptic neuron. There are different kinds of neurotransmitters—some of them are excitatory and will cause the next neuron to be activated whereas others are inhibitory and prevent activation of the next neuron. In addition, the activation of the subsequent neurons depends on the quantity of the neurotransmitters at the synapse—too few and the threshold to affect the next neuron is not reached. A synapse—where the branches of two neurons meet. There are one quadrillion synapses in the brain—that’s 1,000,000, 000,000,000,000,000,000!!! (Changeux and Ricoeur 2000) Biochemical explanation of major depression The monoamine hypothesis proposes that depression is caused by low levels of a group of neurotransmitters called monoamines. The monoamines include noradrenaline , serotonin and dopamine and are especially important in regulating the function of the limbic system in the brain which controls emotion and drive states such as appetite. Each monoamine has its own functions, and when they are reduced, the effects link to the symptoms of depression. Current thinking is that depression results from a reduction in each of these chemicals rather than just depletion in one. However, serotonin is particularly implicated as it acts as a controller of a variety of brain systems and neurotransmitters. Serotonin regulates the other monoamine neurotransmitters. Without the regulation of serotonin, erratic brain functioning and thinking patterns occur because the other two neurotransmitters are not stable. Serotonin is also independently responsible for mood, well-being, stomach functioning and memory (particularly of emotions). Deficiency in serotonin appears to be related to many of the symptoms of depression such as reduced appetite and low mood. Noradrenaline is present in the hypothalamus and hippocampus , and is largely responsible for heart rate, concentration, attention, alertness and energy. Symptoms of depression such as disruption of sleep patterns and lack of energy seem to relate to deficiencies in noradrenaline. Dopamine is responsible for motivation, pleasure, reward and motor function. Low levels of dopamine are associated with reduced attention, motivation and being less interested in pleasure and reward. These symptoms are all evident in depression. Research evidence Jeffrey Meyer et al. (2006) studied 17 patients with depression, who had not taken antidepressant medication for five months. Using PET scans the researchers compared brain activity in depressed patients compared with 17 clinically normal patients who acted as a control group . They found that the depressed patients had significantly higher monoamine oxidase levels in all 11 brain areas that were tested ( monoamine oxidase is an enzyme that metabolises the monoamines—the high levels of monoamine oxidase mean that the monoamines are broken down too quickly and therefore there are lower concentrations of them in the brain). Meyer et al .’s study therefore supports the monoamine hypothesis because it demonstrates that the depressed patients had lower levels of monoamines in their brains than the control group. postsynaptic receptor sites postsynaptic neuron axon presynaptic neuron neurotransmitter synaptic vesicle synaptic cleft The specification requires explanations of mental illness, but specific disorders such as major depression can be used as examples. The biochemical explanation of mental illness Chapter 1: Issues in mental health 22