Medical Model

• What is the Monoamine Hypothesis of Depression?


  • Depression caused by levels of a group of neurotransmitters called monoamines

  Includes:

  • Noradrenaline - in hypothalamus and hippocampus (responsible for heart rate, concentration etc)
  • Serotonin
  • Dopamine
  • Important in regulating the function of the limbic system which controls emotion and drives states such as appetite
• How does Meyer (2006) support the Monoamine Hypothesis?


  • Studied 17 patients with depression who had not taken anti-depressants in 5 months
  • PET scans to compare brain activity in depressed patients compared with 17 clinically normal patients
  • Found depressed patients had significantly higher Monoamine oxidase levels in all 11 brain areas
  • Supports Monoamine Hypothesis because it demonstrates depressed patients had lower levels of monoamines in their brains than the control group
• What is the Dopamine Hypothesis of Schizophrenia?


  Original - excessive amount of dopamine in the limbic system

  Revised - excessive amount of dopamine receptors at post synaptic neuron - excess of dopamine at D2 receptor

  Positive and Negative symptoms:

  • Positive - linked with hypofunction in the mesolimbic pathway
  • Negative - linked to erratic dopamine function in the mesocortical pathway
• How does Seeman (1987) support the Dopamine Hypothesis?


  Reported several strands of evidence:

  • Drugs that increase levels of dopamine increase some positive symptoms
  • Antipsychotic drugs (block dopamine) reduce schizophrenia symptoms
  • Post Mortems of schizophrenic brains show higher density of D2 receptors than neurotypical brains
• What is the Biochemical Explanation of Anxiety (Specific phobias)?

  • GABA is the most important inhibitory neurotransmitter in the CNS - it switches off next neuron reducing activity in pathway
  • GABA counterbalances excitatory action of the neurotransmitter glutamate
  • People with phobias have decreased levels of GABA meaning neuronal finding in the glutamate pathways is higher leading to feelings of anxiety
  • Medications for anxiety often contain GABA to reduce neuronal transmission in brain
• How does Pande et. al (1999) support the Biochemical Explanation of Anxiety?


  • Randomly assigned 69 patients with social phobia to an experimental condition
  • Took drug that increased levels of GABA for 14 weeks or control where they took a placebo
  • Found significant reduction in symptoms in the GABA group compared with placebo
  • This suggests that increased levels of GABA can lead to a reduction in anxiety
• How does an abnormal amygdala explain depression?

  • Increase in activity in depressed patients when presented with negative stimuli and reduced activity when presented with positive stimuli
  • This suggests the amygdala regulates emotion which is disrupted in people with depression

  Sheline (2001):

  fMRI scans to sample 11 depressed patients and 11 control, scan showed amygdala more active in depressed patients during resting states particularly when shown emotional images expressing fear rather than happiness
• How does an abnormal hippocampus explain depression?

  • Significantly smaller in patients with depression, the more severe the depression the more severe loss of grey matter

  Kronmuller (2008):

  Reported significantly smaller hippocampi in 33 female and 24 male patients that relapsed after 2 years of being treated compared to control group of 30 healthy individuals, particularly male patients

  • Implies that the volume of hippocampus is associated with likelihood of person experiencing severe depression

   
• How does enlarged ventricles explain schizophrenia?

  • Have enlarged ventricles in brain that hold cerebrospinal fluid with nutrients to protect brain from damage, ventricles have no cognitive function. Enlarged ventricles reduce grey matter

  Pol:

  Compared 159 people with schizophrenia to 158 healthy people

  Found up to 30% increase in ventricle size for patients with schizophrenia

  Larger ventricles means less grey matter meaning less functionality
• How does reduced grey matter explain schizophrenia?

  In temporal lobe – leads to auditory hallucinations

  In frontal lobe – leads to incoherent speech and delusions

  In thalamus – auditory and verbal hallucinations
• How does a smaller brain explain schizophrenia?

  • Reduced overall brain size
  • Reduction stops when taking antipsychotics
  • This suggests grey matter is associated with schizophrenia

  Hajima (2013):

  Analysed 317 studies that did MRI on 8327 patients, patients with schizophrenia had smaller thalamus and 2.6% overall smaller brain size
• How does an abnormal prefrontal cortex explain anxiety / phobias?

  • Suppresses fear response to stimuli and fails to suppress fearful urges from the amygdala if not functioning effectively
• How does an abnormal amygdala explain anxiety / phobias?

  • Detects and responds to threats in the environment and people with phobias have a smaller amygdala with increased blood flow and is associated with inability to control behavioural and psychological responses to fear

  Ahs (2009):

  PET scans to measure cerebral blood flow in the amygdala and prefrontal cortex of patients with snake or spider phobias

  Found increased activity in the amygdala

  Found reduced activity in prefrontal cortex

  Suggests reduced behavioural control of the fear reactions from the amygdala
• How does an abnormal hippocampus explain anxiety / phobias?

  • Associated with memory and learned associations
  • Reduced functioning means person only recalls link between stimulus and previous fearful experiences rather than neutral or positive feelings
• What is the genetic explanation for depression?

  Family studies:

  • Gottesman illustrates the increased risk that children have of developing bipolar if parents have that or another disorder

  Twin studies:

  • Concordance rates for major depression in monozygotic twins (MZ) are between 30-50% whereas dizygotic twins (DZ) have a corresponding range between 12-40%

  Adoption studies:

  • Relatively few conducted and results offer less consistent support of a genetic explanation compared with twins as data and information around adoption is too protected
• What is the genetic explanation for schizophrenia?

  Family studies:

  Lifetime risk 10 times greater for first degree relatives of the person with schizophrenia

  Strong but not conclusive evidence of genetic element

  Twin studies:

  Glatt (2008) – range of twin studies show concordance for schizophrenia in MZ twins around 46-53%. This is about 15% in DZ twins
• How do adoption studies show genetic influence is not important in schizophrenia?

  Adoption studies:

  • Finnish adoption study Tienari (1994) found that lifetime schizophrenia risk for adopted away children of biological mothers who had it is 9.4%.
  • The corresponding figure for depressed adopted away children of unaffected biological parents was 1.2% and this difference suggests genetic influence is not important in schizophrenia
• What is the genetic explanation for anxiety / phobias?

  Twin studies:

  • Kendler found concordance for animal type specific phobias were 25.9% for MZ twins and 11% for DZ twins implying genetic causation
  • Skre (1993) found no differences between MZ twins and DZ twins rates for any type of phobia