medical model

• medical model

  View that psychological disorders occur due to biological disruption/malfunction eg brain chemistry, electrical activity in brain region. It assumes that mental disorder can be understood as illnesses in the same way as physical conditions - therefore can be classified, diagnosed and treated by medical personnel in the same way as physical disease. Approaches to treatment are based on the idea that we can correct/reduce the effects of these malfunctions or disruption.
• treatments according to medical model

  biologically based, including drugs, surgery and the application of electric shocks, magnetic fields and bright light
• explanations for mental health provided by medical model

  biochemical, genetics, brain abnormality
• biochemical explanation

  suggests that mental illness is due to abnormal neurotransmitter levels/action
• biochemical more info

  *Our brain cells must transmit info via electrical impulses around the brain for us to be able to think, feel or make a decision

  *At each synapse (gap between two brain cells) chemicals known as neurotransmitters must pass across, for information to pass across cells
• monoamines

  group of neurotransmitters: dopamine, noradrenaline and serotonin
• dopamine

  regulates mood
• noradrenaline

  regulates activity levels
• serotonin

  regulates dopamine and noradrenaline levels
• monoamine hypothesis of depression


  Depression involves lowered mood & disruption to activity levels leaving patients more/less active than they'd be under normal circumstances. Dopamine plays an important role in regulating mood, noradrenaline is implicated in activity levels. and serotonin is important in controlling both dopamine and noradrenaline. Two versions of such hypothesis:

  1. Reductions in serotonin levels (typically following stressful events) lead to failure to regulate normal dopamine and noradrenaline function which disrupts mood and activity levels

  2. Disruptions to monoamine levels is a result of abnormally high levels of an enzyme that breaks down monoamine, reducing their action
• dopamine hypothesis of schizophrenia

  Dopamine is widely believed to be important in the functioning of several brain systems that may be implicated in the symptoms of schizophrenia: early DA hypotheses identified possible role for high levels of DA in certain lower parts of the brain, which could account for some symptoms of schizophrenia (eg excess in those centres of brain responsible for speech production may cause hallucinations with voices). Newer DA hypothesis focuses on reduced DA levels/activity in brain's cortex (low levels/activity in pre-frontal cortex (responsible for thinking and decision-making) may explain other symptoms of schizophrenia - eg apathy and incoherent speech & thoughts)
• genetic explanation

  we are predisposed to mental health disorders if our parents are (as we inherit 50% of genetics from each parent) - it's probable that genes exert an influence on individual psychological characteristics (eg mental issues) by influencing the nature of physical structures of chemical levels in CNS
• genotype consists of

  randomly inherited genetic material from our parents (50% mother, 50% father)
• genes

  sections of DNA that contain instructions for producing physical structure
• interactionism (genetics)

  genetics unlikely to be only cause for mental illness, but may increase vulnerability to developing mental health problems (genetic vulnerability)
• genetic vulnerability to depression

  serotonin transporter gene (responsible for producing serotonin) - 3 forms varying in length of its two strands: long-long, long-short, short-short. it's believed that short form leads to inefficient serotonin production, making people with this less resilient to stress, increasing their vulnerability to depression
• genetic vulnerability to schizophrenia

  runs in families, a number of genetic variations makes people slightly more vulnerable - disorder can be described as polygenic and aetiologically heterogeneous. ripke et al (2014), 108 separate genetic variations were found to be associated with increased risk of schizophrenia
• polygenic

  multiple genes (factors) impact it
• aetiologically heterogeneous

  different combinations of factors can lead to similar symptoms
• genetic vulnerability and dopamine hypothesis together

  genes associated with increased vulnerability to developing schizophrenia included those coding for the functioning of a number of neurotransmitters, including dopamine
• brain abnormality explanation

  certain brain structures may not function properly (eg have different size, shape, levels of electrical activity), which causes mental health disorders
• brain abnormality in depression

  mean frontal lobe (region at front of the brain cortex particularly involved in thinking) volume in depressed patients is significantly smaller (Coffey et al (1993) compared size of frontal lobes of depressed and non-depressed patients using MRI). also, frontal lobes may not draw blood flow as they would usually (hyperfusion), but can be improved immediately after ECT (Milo et al (2001) PET-scanning)
• brain abnormality in schizophrenia

  left hemisphere doesn't function normally, but can be aided by antipsychotic drugs (Purdon (2001), compared force applied with right and left hand in patients with schizophrenia and control group - 1- given anti-psychotics, and those untreated were significantly weaker in right hand - effect disappeared after treatment). also, negative symptoms may be related with less activity in ventral striatum (Juckel et al (2006) measured activity in VS in schizophrenia - found lower levels of activity than those observed in controls, and also negative correlation between VS activity and severity of overall negative symptoms)