Mental Disorders

A situation in which a person “experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others” that provoked a response that “involved intense fear, helplessness, or horror.”

• Recurrent dreams or recollections of the event, feelings that the traumatic event is recurring (“flashback” episodes), and intense psychological distress.
• These dreams, recollections, or flashback episodes can lead the person to avoid thinking about the traumatic event.
• This results in diminished interest in social activities, feelings of detachment from others, suppressed emotional feelings and a sense that the future is bleak and empty
• Particular psychological symptoms include difficulty falling or staying asleep, irritability, outbursts of anger, difficulty in concentrating, and heightened reactions to sudden noises or movements.
• Sufferers also tend to have generally poor physical health

• Yes 
• Although men are exposed to traumatic events more often than women are, women are more likely to develop PTSD after being exposed to such events (Fullerton et al., 2001)

• Yes 
• The risk for PTSD appears to depend on bothgenetic and environmental factors.
• Kolassa et al.(2010) studied 424 survivors of the genocide inthe Rwanda.
• They found that the likelihood of developing PTSD increased with the number of traumatic events the person had experienced.

• Yes 
• Evidence from twin studies suggests that genetic factors play a role in a person’s susceptibility to develop PTSD.
• Genetic factors influence not only the likelihood of developing PTSD after being exposed to traumatic events, but also the likelihood that the person will be involved in such an event (Stein et al., 2002).
• Could be due to genetic differences in the production of dopamine D2 receptors, dopamine transporters, and serotonin transporters (Nugent, Amstadter, and Koenen, 2008).

• Earlier age at the time of the traumatic event;
• Exposure to more than one traumatic event;
• A father with a depressive disorder;
• A low educational level;
• Poor social support
• Preexisting conduct disorder, panic disorder, Generalized anxiety disorder, or depressive disorder

• The hippocampus is known to be involved in the stress response (HPA-axis)
• At least two MRI studies have found evidence of hippocampal damage in veterans with combat-related post traumatic stress disorder (Bremner et al., 1995; Gurvits et al., 1996).
• In the study by Gurvits et al., the volume of the hippocampal formation was reduced by over 20 percent, and the loss was proportional to the amount of combat exposure the veteran had experienced.
• Lindauer et al. (2005) found that police officers with PTSD had a smaller hippocampus than those who had also been exposed to trauma but had not developed the disorder.

• We don't really know, BUT:
• Gilbertson et al (2002) studied forty pairs of monozygotic twins in which only one member went to Vietnam and experienced combat.
• Almost half of the men who experienced combat developed PTSD.
• As expected, the hippocampal volumes of these men were smaller than those of the men who did not develop PTSD after their combat experience.
• In addition, a smaller hippocampus was associated with more severe PTSD.
• The interesting fact is that the hippocampal volumes of the twin brothers of the PTSD patients who stayed home also showed smaller-than-average hippocampal volumes
• Given that monozygotic twins are genetically identical and usually have very similar brains, this finding suggests that a person with a small hippocampus is more likely to develop PTSD after exposure to psychological trauma.

• Several studies have found evidence that the amygdala is responsible for emotional reactions in people with PTSD
• The prefrontal cortex plays a role in these reactions in people without PTSD by inhibiting the activity of the amygdala (Rauch, Shin, and Phelps, 2006).
• For example, a functional-imaging study by Shin et al. (2005) found that when shown pictures of faces with fearful expressions, people with PTSD show greater activation of the amygdala and smaller activation of the prefrontal cortex than did people without PTSD

• Brewin (01)
• Many of the features and details of some traumatic event-the sounds, smells, and sights, for example-are initially retained in a system called situationally accessible memory, somewhat akin to episodic memory.
• When individuals reflect upon this information consciously, attempting to understand or to integrate these features and details, the ensuing insights are retained in another system instead, called verbally accessible memory, somewhat akin to semantic memory
• Cues or stimuli in the environment that are associated with this traumatic event will tend to activate or prime the contents of this memory system. Individuals will thus experience intrusive images and flashbacks-hallmarks of PTSD.
• Brewin et al (10) replaced VAM with C-reps (contextual representations) and SAM with S-reps (sensory representations) which are activated during flashbacks

A serious mental disorder characterized by disordered thoughts, delusions, hallucinations, and often bizarre behaviors

A symptom of schizophrenia evident by its presence: delusions, hallucinations, or thought disorders

• Arguably the most important symptom of schizophrenia 
• Defined by disorganized, irrational thinking

• Delusions of persecution: false beliefs that others are plotting and conspiring against
• oneself.
• Delusions of grandeur: false beliefs in one’s power and importance, such as a conviction that one has godlike powers or has special knowledge that no one else possesses.
• Delusions of control: related to delusions of persecution; the person believes (for example) that he or she is being controlled by others through such means as radar or a tiny radio receiver implanted in his or her brain.

• Hallucinations 
• Often auditory, but sometimes visual

The absence or diminution of normal behaviours: flattened emotional response, poverty of speech, lack of initiative and persistence, anhedonia (inability to experience pleasure), and social withdrawal.

• Cognitive deficits such as: difficulty in sustaining attention, deficits in learning and memory, poor abstract thinking, and poor problem solving
• Often very similar to negative symptoms, suggesting the brain regions responsible could be the same

• The symptoms of schizophrenia typically appear gradually and insidiously, over a period of three to five years.
• Negative symptoms are the first to emerge, followed by cognitive symptoms.
• The positive symptoms follow several years later.

• Pharmacological evidence suggests that the positive symptoms of schizophrenia are caused by abnormalities in Dopamine (DA) neurons.
• The dopamine hypothesis suggests that the positive symptoms of schizophrenia are caused by overactivity of DA synapses.
• Chlorpromazine, a drug that reduces dopamine levels by blocking D2 and D3 receptors, also leads to symptomatic relief in schizophrenics
• Amphetamine, cocaine, and methylphenidate (which block the reuptake of dopamine) and L-DOPA (which stimulates the synthesis of dopamine) all lead to symptomatic increase

• Schizophrenia is caused by the possession of a greater number of D2 receptors 
• More binding, more release, more symptoms 
• Postmortem measurements in the brains of deceased schizophrenic patients and PET scans after treatment with radioactive ligands for dopamine receptors have showed that there might be modest increases in the numbers of D2 receptors in the brains of schizophrenics, but that it seems unlikely that these increases are the primary cause of the disorder

• Neuropsychological testing and brain imaging technologies such as fMRI and PET have been used to examine functional differences in brain activity have shown that differences seem to most commonly occur in the frontal lobes, hippocampus and temporal lobes.
• Reductions in brain volume, smaller than those found in Alzheimer's disease, have been reported in areas of the frontal cortexand temporal lobes.
• It is uncertain whether these volumetric changes are progressive or preexist prior to the onset of the disease.

• Probably not
• New antipsychotic medication is as (or more effective) as older ones, and they focus on serotonin, not dopamine 
• Could be due to differences in NMDA glutamate receptors instead 
• Abnormally low levels of glutamate receptors found in the postmortem brains of those diagnosed with schizophrenia
• Glutamate-blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition.
• Reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function.
• Glutamate can affect dopamine function.
• Thus – it has been suggested glutamate pathways play an important mediating (and possibly causal) role in schizophrenia.
• However, positive symptoms fail to respond to glutamatergic medication.