Schizophrenia
❖ Clinical Characteristics: Positive/negative symptoms and ICD 11
❖ Biological Explanations: Dopamine hypothesis → brain structure (enlarged
ventricles)
❖ Individual Differences Explanations: Cognitive explanation →
psychodynamic explanation
❖ Social Psychological Explanations: Dysfunctional families →
sociocultural factors
❖ Methods of Modifying Behaviour: Antipsychotics → CBT
Clinical Characteristics
Positive symptoms= Concerning behaviour with loss of touch from reality. It’s type 1 which
relates to acute schizophrenia. Responds well to medication and it occurs in short episodes.
Hallucinations (unreal perceptions of environment):
➔ Auditory→ hearing voices that others cant hear
➔ Visual→ seeing light, objects, faces others cant see
➔ Olfactory→ smelling things others can't smell
➔ Tactile→ feeling that bugs etc are crawling on or under your skin,
FORMICATION is the name for this sensation
Delusions (bizarre beliefs that seem real but isn’t):
➔ Reference→ events in environment appear to be directly related to them, like
special personal messages through tv
➔ Grandeur→ beliefs that their someone famous or have powers (elphaba)
➔ Persecution→ beliefs that people are plotting against them or being spied upon
(guy fawkes even tho it was real)
Third example is Thought disorder
The person’s thoughts seem to jump from 1 topic to another without a logical flow of discussion.
Additionally, Thought insertion is when thoughts in one’s head aren’t their own or placed by a
third party
Negative symptoms= Concerning behaviours, disrupting normal emotions and actions. This is
type II which relates to chronic schizophrenia. They are resistant to medication
➔ Inappropriate affect= silliness or laughter in the wrong context. For example, laughing
when hearing sad news
, ➔ Cataleptic stupor= Reduced motor activity, they stand motionless like a statue or make
fast, useless movements
➔ Anhedonia= where the individual doesn’t react appropriately to pleasurable
experiences. Like, football fan isn’t happy when their team wins
➔ Echopraxia= they mimic the movements of others around them
➔ Echolalia= they repeat the echoing of words spoken by others
ICD 11
To be diagnosed with schizophrenia, a person’s behaviour is assessed to the criteria in the ICD-
11. This is a medical classification list which aims to clarify the symptoms in order to diagnose a
patient.
→ 2 of the symptoms must be present from the list, most of the time or at least a month
→ One of the symptoms must be present from item a) through d) from positive symptoms
(persistent delusions - experiences of influence, passivity or control) and one clear negative
symptom from item e) through g) (negative symptoms - psychomotor disturbances).
Biological explanation: Dopamine Hypothesis
In order: excessive dopamine, dopamine receptor sites, limbic system
Excessive Dopamine
People with Parkinson’s (condition that causes tremors) have been given a drug called L-dopa
which increases dopamine in the brain. It reduced Parkinson’s symptoms but increased
symptoms of schizophrenia.
THEREFORE, THIS WAS THE FIRST LINK BETWEEN DOPAMINE AND SCHIZOPHRENIA
Led to 3 findings:
➔ Delay, Deniker and Harl discovered antipsychotic drugs
➔ Carlsson and Lindqvist realised that these drugs increased the metabolism of
dopamine
➔ Studies that showed that amphetamine could induce psychotic symptoms and
reserpine could treat them. This is significant because amphetamine could increase
monoamine levels and reserpine could block the reuptake of dopamine
Dopamine Receptor Sites
In 1970s, the focus moved to DA Receptor Sites D1-D5.
→ At first, D2 receptors were important as there was a greater volume of them in
schizophrenics
→ However, questions were raised about D1 receptors because they were important
for its presence in the prefrontal cortex, which is implicated in schizophrenia
Davis et al proposed that abnormal dopamine activity affects different areas of the brain. For
example, low dopamine activity results of fewer D1 receptors in the prefrontal cortex which
, leads to negative symptoms. Increased dopamine activity results in excess D2 receptors in the
striatal areas which leads to positive symptoms.
Further supported by Owen and Falkai. Owen found excess receptor sites in schizophrenia, on
the left amygdala. Falkai found increased dopamine in striatal areas like putamen.
Limbic System
Responsible for emotional, arousal and memory formation.
2 main pathways associated with schizophrenia:
➔ Mesolimbic pathway. Dopamine is a major neurotransmitter in this pathway and it
carries signals from VTA to nucleus accumbens. If there’s too much dopamine, it can
cause overstimulation and positive symptoms. Antipsychotic drugs reduce the dopamine
activity and reduces positive symptoms
➔ Mesocortical pathway. Dopamine is a major neurotransmitter in this pathway and
carries signals from VTA to frontal lobe. This nerve pathway is vital in motivation,
cognition and emotional response
Frankle and Laruelle stated that imaging can show the blocking of the elevated activity by
blocking dopamine release of the postsynaptic receptors.
Talkowski et al said that 4 of the top 10 genes thought to be involved, are involved with
dopamine activity.
Biological explanation: Brain Structure (enlarged ventricles)
In order: Enlarged ventricles, Cortical atrophy
First finding that indicated brain damage was connected to schizophrenia came from the
enlarged ventricles from CT scans. Ventricles maintain brain pressure that keeps the neurons
in place and if they enlarge, there’s damage
CT scans by Johnstone and Weinberger showed significant ventricular enlargement when
schizophrenic brains were compared to those of control. This indicated that brain damage is
present in schizophrenics and could be the cause of their symptoms.
Cortical atrophy
Loss of neurons. Brain damage is present in patients with schizophrenia is cortical atrophy in
their brains. This type of damage appears in 20%-35% of people with chronic schizophrenia.
→ Jenkinson conducted an MRI scan and found that significant cortical atrophy in the
prefrontal regions reflects underlying reduction in grey matter. This was shared by at-risk
patients who then converted to psychosis.
❖ Clinical Characteristics: Positive/negative symptoms and ICD 11
❖ Biological Explanations: Dopamine hypothesis → brain structure (enlarged
ventricles)
❖ Individual Differences Explanations: Cognitive explanation →
psychodynamic explanation
❖ Social Psychological Explanations: Dysfunctional families →
sociocultural factors
❖ Methods of Modifying Behaviour: Antipsychotics → CBT
Clinical Characteristics
Positive symptoms= Concerning behaviour with loss of touch from reality. It’s type 1 which
relates to acute schizophrenia. Responds well to medication and it occurs in short episodes.
Hallucinations (unreal perceptions of environment):
➔ Auditory→ hearing voices that others cant hear
➔ Visual→ seeing light, objects, faces others cant see
➔ Olfactory→ smelling things others can't smell
➔ Tactile→ feeling that bugs etc are crawling on or under your skin,
FORMICATION is the name for this sensation
Delusions (bizarre beliefs that seem real but isn’t):
➔ Reference→ events in environment appear to be directly related to them, like
special personal messages through tv
➔ Grandeur→ beliefs that their someone famous or have powers (elphaba)
➔ Persecution→ beliefs that people are plotting against them or being spied upon
(guy fawkes even tho it was real)
Third example is Thought disorder
The person’s thoughts seem to jump from 1 topic to another without a logical flow of discussion.
Additionally, Thought insertion is when thoughts in one’s head aren’t their own or placed by a
third party
Negative symptoms= Concerning behaviours, disrupting normal emotions and actions. This is
type II which relates to chronic schizophrenia. They are resistant to medication
➔ Inappropriate affect= silliness or laughter in the wrong context. For example, laughing
when hearing sad news
, ➔ Cataleptic stupor= Reduced motor activity, they stand motionless like a statue or make
fast, useless movements
➔ Anhedonia= where the individual doesn’t react appropriately to pleasurable
experiences. Like, football fan isn’t happy when their team wins
➔ Echopraxia= they mimic the movements of others around them
➔ Echolalia= they repeat the echoing of words spoken by others
ICD 11
To be diagnosed with schizophrenia, a person’s behaviour is assessed to the criteria in the ICD-
11. This is a medical classification list which aims to clarify the symptoms in order to diagnose a
patient.
→ 2 of the symptoms must be present from the list, most of the time or at least a month
→ One of the symptoms must be present from item a) through d) from positive symptoms
(persistent delusions - experiences of influence, passivity or control) and one clear negative
symptom from item e) through g) (negative symptoms - psychomotor disturbances).
Biological explanation: Dopamine Hypothesis
In order: excessive dopamine, dopamine receptor sites, limbic system
Excessive Dopamine
People with Parkinson’s (condition that causes tremors) have been given a drug called L-dopa
which increases dopamine in the brain. It reduced Parkinson’s symptoms but increased
symptoms of schizophrenia.
THEREFORE, THIS WAS THE FIRST LINK BETWEEN DOPAMINE AND SCHIZOPHRENIA
Led to 3 findings:
➔ Delay, Deniker and Harl discovered antipsychotic drugs
➔ Carlsson and Lindqvist realised that these drugs increased the metabolism of
dopamine
➔ Studies that showed that amphetamine could induce psychotic symptoms and
reserpine could treat them. This is significant because amphetamine could increase
monoamine levels and reserpine could block the reuptake of dopamine
Dopamine Receptor Sites
In 1970s, the focus moved to DA Receptor Sites D1-D5.
→ At first, D2 receptors were important as there was a greater volume of them in
schizophrenics
→ However, questions were raised about D1 receptors because they were important
for its presence in the prefrontal cortex, which is implicated in schizophrenia
Davis et al proposed that abnormal dopamine activity affects different areas of the brain. For
example, low dopamine activity results of fewer D1 receptors in the prefrontal cortex which
, leads to negative symptoms. Increased dopamine activity results in excess D2 receptors in the
striatal areas which leads to positive symptoms.
Further supported by Owen and Falkai. Owen found excess receptor sites in schizophrenia, on
the left amygdala. Falkai found increased dopamine in striatal areas like putamen.
Limbic System
Responsible for emotional, arousal and memory formation.
2 main pathways associated with schizophrenia:
➔ Mesolimbic pathway. Dopamine is a major neurotransmitter in this pathway and it
carries signals from VTA to nucleus accumbens. If there’s too much dopamine, it can
cause overstimulation and positive symptoms. Antipsychotic drugs reduce the dopamine
activity and reduces positive symptoms
➔ Mesocortical pathway. Dopamine is a major neurotransmitter in this pathway and
carries signals from VTA to frontal lobe. This nerve pathway is vital in motivation,
cognition and emotional response
Frankle and Laruelle stated that imaging can show the blocking of the elevated activity by
blocking dopamine release of the postsynaptic receptors.
Talkowski et al said that 4 of the top 10 genes thought to be involved, are involved with
dopamine activity.
Biological explanation: Brain Structure (enlarged ventricles)
In order: Enlarged ventricles, Cortical atrophy
First finding that indicated brain damage was connected to schizophrenia came from the
enlarged ventricles from CT scans. Ventricles maintain brain pressure that keeps the neurons
in place and if they enlarge, there’s damage
CT scans by Johnstone and Weinberger showed significant ventricular enlargement when
schizophrenic brains were compared to those of control. This indicated that brain damage is
present in schizophrenics and could be the cause of their symptoms.
Cortical atrophy
Loss of neurons. Brain damage is present in patients with schizophrenia is cortical atrophy in
their brains. This type of damage appears in 20%-35% of people with chronic schizophrenia.
→ Jenkinson conducted an MRI scan and found that significant cortical atrophy in the
prefrontal regions reflects underlying reduction in grey matter. This was shared by at-risk
patients who then converted to psychosis.
