Psychiatric Disorders Flashcards Preview

Developmental and Biological Psychology > Psychiatric Disorders > Flashcards

Flashcards in Psychiatric Disorders Deck (44)
Loading flashcards...

 How is schizophrenia diagnosed?

Despite current technology, we still cannot objectively diagnose someone with a mental illness based upon brain scans alone. That’s why we must rely on symptoms to help us diagnose disorders.

The DSM-5 has labeled schizophrenia as schizophrenia spectrum disorders.

Affects 1% of the adult population.  Starts in adolescence or early childhood



Positive Symptoms of Schizophrenia

Hallucinations - A sensory experience in the absence of an external stimulus. Can be any one of the five sensory modalities, but mostly auditory (e.g. hearing voices despite the absence of any environmental cause).

Delusions - Firmly held beliefs that are not grounded in reality. Examples of delusions include delusions of control (the belief some force is controlling the persons thoughts, feelings or behaviours), delusions of grandeur (the belief in being all powerful and even Godlike), and delusions of reference (the belief insignificant events or objects hold personal significance).

Disorganised Speech/Thought - Making bizzare connections between ideas and difficulty organising words into sentences that others understand. 

Inappropriate Affect - Inappropriate emotional responses (e.g. crying when someone tells a joke).


Negative Symptoms of Schizophrenia

Avolition - Lack of motivation or interest in engaging with routine activities.

Alogia - A poverty in speech. 

Anhedonia - Loss of pleasure in doing activities that were previously pleasurable.

Flat Affect - Lack of emotional expression.

Catatonia - This presents as motor abnormalities and is seen in those with catatonic schizophrenia. A person with catatonic schizophrenia may go into a catatonic state where they become largely immobile and display what is known as waxy flexibility. 

Waxy flexibility is where a person holds a pose for a long period of time, and similar to a mannequin, their limbs can be moved with little resistance to hold another pose.


What evidence supports genetic factors in the development of schizophrenia?

Research shows that genes play a large role in the development of schizophrenia. Studies involving families of those with schizophrenia give us an indication of how likely a person is to develop the disorder based on the amount of genetic material they share. 



What evidence supports environmental factors in the development of schizophrenia?

Adoption studies where children who have been adopted develop schizophrenia show their risk of developing schizophrenia is increased by the disorder being present only in their biological relatives but not by the presence of schizophrenia in their adoptive parents.

When one identical twin has schizophrenia and the other does not, the children of the identical twin without symptoms of schizophrenia still show the same risk of developing the disorder as the children of the twin who has been diagnosed with schizophrenia. This shows that even though one twin does not show any signs of schizophrenia, they still presumably carry and pass on the increased risk genetically to their children.


Dizygotic vs Monosygotic Twins

dizygotic twins develop from separate embryos just like regular siblings.


Environmental risk factors for schizophrenia

  • Maternal stress, prenatal nutrition and prenatal infections
  • Birth complications and childhood adversity
  • Being born and raised in urban areas
  • Exposure to toxins like marijuana or harmful alcohol use
  • Highly stressful situations (e.g. low socioeconomic status, lack of social support and isolation)


Schizophrenia is considered a neurodevelopmental disorder

Neurodevelopmental disorders are disorders in which the development of the nervous system is disturbed in some way.

Support for schizophrenia being a neurodevelopmental disorder comes from periods in history where famine has been experienced.

Further support comes from some similarities between the development of schizophrenia and other neurodevelopmental disorders, such as autism spectrum disorder. For example, autism spectrum disorders share similar causal factors to schizophrenia such as genetics (e.g. heritability) and environment (e.g. prenatal infections).



a drug that activates the receptor it binds to



a drug that binds to a receptor but does not activate it. The binding to a receptor can then block other substances from binding to, and activating, that receptor.


1950 — 1959
The first antipsychotic drugs

In 1951, surgeons used the drug chlorpromazine to help patients who were about to undergo an operation to relax. Since chlorpromazine had such a calming effect, a French surgeon suggested that it might also be useful for calming people with psychosis. Further research confirmed this to be the case, and chlorpromazine was found to alleviate the symptoms of schizophrenia.

In 1952, the active ingredient of the Indian snakeroot plant called reserpine, was extracted and used in treating schizophrenia.

Despite the positive effects of these early drugs, they were accompanied by adverse motor side effects such as involuntary movements of the arms, legs and face, and muscular rigidity. 


1960 — 1969
Dopamine Theory of Schizophrenia

In the 1960s, researchers find Parkinson's disease is partly caused by low levels of dopamine in the striatum. This findings along with the following evidence led to the dopamine theory of schizophrenia:

  • Antipsychotic drugs had side effects that resembles Parkinson's disease.
  • It was known that reperine reduces monoamines like dopamine by breaking down the synaptic vesicles where they are located.
  • Stimulant drugs (e.g. cocaine and amphetamines) increase levels of dopamine in the brain and at high doses can produce a state that closely resembles the symptoms of schizophrenia.


1970 — 1979
Dopamine Receptors

Researchers knew drugs like chlorpromazine were effective in treating schizophrenia symptoms by acting as antagonists (receptor blockers) to dopamine receptors and so by the 1970s, the role of dopamine receptors in schizophrenia was explored further. They did this by combining radioactive tracer substances with dopamine, and through measuring radiation levels were able to follow the dopamine to where it was located.

As you would expect, researchers found that less dopamine was able to bind to dopamine receptors when an effective antipsychotic drug was used (e.g. chlorpromazine). This was because effective antipsychotic drugs like chlorpromazine have a high affinity for dopamine receptors. 


1980 — 1990
Limitations of the Dopamine Theory of Schizophrenia

  1. It is unlikely that a single receptor, or even a single neurotransmitter, could account for the diversity in symptoms seen in those with schizophrenia.
  2. Antipsychotic medications are only effective in treating positive symptoms (e.g. delusions, hallucinations), but ineffective at treating negative symptoms (e.g. flat affect, anhedonia).   
  3. Antipsychotic medications exert their effects on dopamine receptors within hours of taking them, so according to the dopamine theory of schizophrenia, we would expect symptom reduction within hours. However, antipsychotic medication can take weeks to have an effect on symptoms.


Antipsychotic Medications

Attempts were made to improve upon the first generation of antipsychotic drugs (also known as typical antipsychotics) such as chlorpromazine and haloperidol. One main reason was because of the significant adverse side-effects these drugs could have.

Both reserpine and chlorpromazine can also cause Parkinson-like symptoms.

One particularly concerning and sometimes irreversible extrapyramidal symptom is tardive dyskinesia, which involves the involuntary movement of the mouth muscles, and sometimes, the entire body. Another reason to improve upon these earlier drugs was their lack of effectiveness on the negative symptoms of schizophrenia.

Second generation antipsychotics known as atypical antipsychotics were developed in order to improve upon some of the issues associated with the first generation antipsychotics. These have an affinity for D2 receptors but also strongly antagonise other dopamine receptors and some serotonin receptors.  

The first atypical antipsychotic to be developed was clozapine and this drug only had a weak affinity for D2 receptors. Clozapine also has been shown to have a high affinity for D1 And D4 dopamine receptors, along with serotonin receptors, and remains one of the most commonly prescribed atypical antipsychotics to date.  

Current research into antipsychotic medications is investigating the two neurotransmitters glutamate and glycine for their role in schizophrenia.


Brain Structure in Schizophrenia

Enlarged lateral ventricles of those with schizophrenia. The larger ventricles along with the larger fissures often found in the brains of individuals suffering from schizophrenia signifies a loss in brain volume.

Loss in brain volume occurs for both grey and white matter, and is widespread, found particularly in the prefrontal cortex and temporal cortices The structural abnormalities found in the temporal cortices include areas such as the hippocampus, amygdala, thalamus, anterior cingulate and nucleus accumbens 

the loss in volume is because neurons are more tightly packed together in someone suffering from schizophrenia.

It is thought some of the disorganised symptoms seen in schizophrenia (e.g. disorganised speech) could be due to a disruption of neural communication due to a reduction in dendritic branches and spines. 

After diagnosis, meta-analyses show that the brain damage caused by schizophrenia continues to develop and this brain damage can develop at different rates in different areas of the brain. 


genetic aetiology of schizophrenia is polygenetic

  1. research has found dysfunctions in genes associated with synaptic pruning which causes increased elimination of synapses.
  2. Abnormalities in genes crucial in regulating neural proliferation and migration have been found which could change brain circuitry by preventing stems cells from developing into neurons or causing neurons to migrate to irregular areas of the brain. 
  3. Abnormalities in genes related to the dopamine D2 receptor and glutamatergic transmission help explain the effectiveness of antipsychotic medication.


Hallucinogenic Drugs and Schizophrenia

  1. Classic hallucinogens like LSD and Psilocybin cause positive schizophrenia-like symptoms by acting as an agonist at serotonin receptors. In other words, they bind to these receptors and activate them. This suggests excessive serotonin may also play a role in some of the positive symptoms we see in schizophrenia.   
  2. Dissociative hallucinogens like Ketamine cause negative schizophrenia-like symptoms by acting as an antagonist at glutamate receptors. In other words, they bind to these receptors but do not activate them. Glutamate is an excitatory neurotransmitter and this suggest some schizophrenia symptoms might be related by reduced levels of glutamate activation in the brain. 


Clinical Depression

  • About 10% of people suffer from clinical depression at some point in their lifetime.
  • Twin studies place heritability estimates of depression around 30-40 percent. 
  • Two loci (physical location of a gene) on chromosome 10 have been found to increase the risk of depression.
  • Epigenetic effects (events that turn the effects of genes 'on' or 'off') have been found to be mediators in depression onset.

  • Stressful or traumatic life events can change how genes are 'read' by cells (an epigenetic effect) that causes the onset of depression in those susceptible. 


Events that trigger Depression

Depression triggered by a negative experience  is called Reactive Depression. In cases where the cause is not apparent, that is it seems to begin without any apparent trigger, it is called Endogenous Depression.

Seasonal Affective Disorder (SAD) is where depression is linked to certain seasons (usually winter) and is thought to be caused by a reduction in sunlight.

Peripartum Depression much like SAD also has a clear cause and effects some women during and/or after pregnancy. 

​​​​​​​Around 19 percent of pregnancies are associated with peripartum depression.



Loss of ability to experience pleasure from activities that were once pleasurable


Monamine Oxidase Inhibitors

This class of drug was discovered accidentally in the 1950s when it failed to treat tuberculosis as intended, but left patients feeling less concerned about their illness. Iproniazid became the first drug to be marketed as an antidepressant in 1957. Monoamine Oxidase Inhibitors (MAOIs) have one particularly dangerous side effect called the cheese effect that causes foods rich in tyramine (e.g. cheese, wine) to cause potentially life threatening elevations in blood pressure. The effects of tyramine on blood pressure are usually minimal because it is quickly metabolised in the liver but if taking MAOIs it cannot be broken down like it usually is.

Examples: Iproniazid, Tranylcypromine

Function: As the name suggests, these drugs work to inhibit the activity of Monoamine Oxidase (MAO), an enzyme which helps break down monoamine neurotransmitters. By reducing the activity of this enzyme, this means more monoamine neurotransmitters like serotonin and norepinephrine remain in the neurons.


Tricyclic Antidepressants

Three rings of atoms that make up the structure are what gives them their name.

These drugs are safer than MAO inhibitors and work by blocking the reuptake of serotonin and norepinephrine to increase their levels in the brain.

Imipramine was the first tricyclic antidepressant developed originally to be an antipsychotic but was found to have no effect on schizophrenia but did have an effect on depression


NMDA-Receptor Antagonists

This class of drugs include Ketamine which has been found to significantly reduce depression even in low doses. These drugs have an antagonizing effect on the glutamate NMDA receptor, in other words they block the receptor and prevent agonist molecules from binding and activating it. Despite Ketamine's effectiveness, it also has undesirable side effects so researchers are trying to identify more selective NMDA-receptor antagonists that do not have such side effects.


Selective Monoamine-Reuptake Inhibitors

Selective Serotonin-Reuptake Inhibitors (SSRIs) belong to this class of drug and were discovered in the 1980s. They work by increasing the amount of serotonin in the synapses blocking its reuptake of serotonin into the presynaptic neuron.

Fluoxetine (Prozac) was the first SSRI to be developed and is a slight structural variation of tricyclic antidepressants like imipramine. Whilst they have proven to be no more effective than tricyclic antidepressants like imipramine in treating depression they have proven to be more popular. This popularity is due mostly to fewer side effects when compared to tricyclic antidepressants and MAO inhibitors. SSRIs also seem to have an effect on other psychological disorders in addition to depression.

The development of a similar drug called Selective Norepinephrine-Reuptake Inhibitors (SNRIs) were introduced following the success of SSRIs and have proven to be just as effective.


Atypical Antidepressants

This class of drug emerged in the 1980s and includes all other antidepressants that do not belong in any of the other classes. Given this class of antidepressant is composed of a variety of different types of drug, they have a range of modes of action.

For example, Bupropion blocks the reuptake of dopamine and norepinephrine, and blocks nicotinic acetylcholine receptors.  

To take another example, Agomelatine works as an agonist for melatonin receptors.


How effective are antidepressants?

On average when MAO inhibitors, tricyclic antidepressants, and elective mono-amine reuptake inhibitors are compared, about 50% of patients with clinical depression improved across all classes of drug. Taking into account that 25% of the control group (patients receiving a placebo) also improved, this shows that only 25% of patients being treated with antidepressants improved. More to this, a meta-analyses found that only those who were severely depressed seemed to benefit from antidepressants, with those suffering from mild or moderate depression showing no improvement over controls.  


Monoamine theory of depression

This theory is based on the antidepressant effects of MAO inhibitors, tricyclic antidepressants, selective serotonin-reuptake and norepinephrine-reuptake inhibitors. These drugs all act as agonists of either serotonin, norepinephrine, or both.

However, this theory has been challenged due to the limited effectiveness of antidepressant drugs as we have seen, the role other neurotransmitters like glutamate have in also causing depression, and the delayed effects of drugs on symptoms. Many antidepressant drugs increase the levels of serotonin and norepinephrine in the brain fairly rapidly, yet the antidepressant effects are only seen weeks later suggesting that some other change is happening downstream, meaning the direct cause of depression is not due to neurotransmitters levels.


neuroplasticity theory of depression

that depression is a result of decreased neuroplastic processes in the brain which leads to neuron loss and other pathology. The evidence shows that depression does disrupt neuroplastic processes such as neurogenesis in the hippocampus.

Research also shows that antidepressants do increase neuroplastic processes in the brain, processes like hippocampal neurogenesis which supports the neuroplasticity theory.


Repetitive Transcranial Magnetic Stimulation (rTMS)

rTMS is a technology based on creating a magnetic pulse when you pass electricity through a metal coil. It is not the electricity that stimulates the body, it is the electromagnetic pulse that stimulates the brain. In this case, we use it to stimulate the nerves or nerve cells that have been deactivated by the depression or a damaged structure.

Repetitive magnetic pulses using rTMS are usually applied to specific areas of the brain (usually the prefrontal cortex) to stimulate (or inhibit) activity in the region of the brain they are applied. In depression, rTMS is used to stimulate neuroplastic processes in specific areas of the brain