Describe the characteristics of schizophrenia
SZ is a major psychotic disorder that causes a variety of possible
psychological symptoms but is typified by a lack of contact with reality. It
affects 1 in 100 people, and typically shows in men in their late teens. People
with SZ can often show prodromal symptoms prior to diagnosis, such as mild
symptoms of depression, generalized anxiety, lack of interest in personal
appearance and hygiene and avoiding the company of others. SZ is
treatable, often through the use of antipsychotic drugs, but there is no
known cure. People can have episodes of severe symptoms, alongside being
symptom free for long periods of time. Many people with SZ have difficulty
accepting their diagnosis, and often feel their delusions or hallucinations are
real, leading to social and occupational dysfunction.
Symptoms of SZ can be categorized as being either positive or negative.
Positive symptoms are symptoms/behaviors that a person is exhibiting in
addition to ‘normal behaviors’ - if they didn’t have SZ, they wouldn’t have
this symptom. Examples of positive symptoms include delusions,
hallucinations and disorganized thinking. Delusions are fixed beliefs that are
not amendable to change in light of conflicting evidence. There are a variety
of types of delusion – persecutory (where you believe someone is out to get
you), referential, somatic, religious and grandiose (e.g. you believe you are
God). Delusions are deemed bizarre if they are clearly implausible, for
example, believing an alien stole your organs but you have no scar. An
example of a non-bizarre delusion would be believing you are under
surveillance by the police – this is very unlikely, but it is possible.
Hallucinations are perceptions that are unreal, and they can be auditory or
tactile. Auditory hallucinations include hearing voices, and tactile
hallucinations are when you think something, or someone is touching you –
however hallucinations can present themselves in any sensory modality. A
rarer form of hallucination is formication, where someone has a sensation of
small insects crawling on or under their skin. Disorganized thinking/speech is
a formal thought disorder which is often shown in an individual's speech –
people will often be seen to switch randomly from 1 topic to another,
showing derailments or loose associations in speech. Speech can often be so
severely disorganized that it is incomprehensible and resembles receptive
aphasia = incoherence. Tangentiality refers to answers to questions being
either obliquely related or unrelated. Negative symptoms are
symptoms/behaviors that are inhibiting people with SZ from demonstrating
‘normal behaviors’, such as being unable to hold a conversation. Examples of
negative symptoms include catatonia, alogia, anhedonia, avolition and
,flatness of affect. Catatonic behavior can range from fast, repetitive, useless
movements to little to no movement at all - people may move for no reason
e.g. walking in circles or may be immobile for long periods of time. Waxy
flexibility is where limbs remain rigid and in an un-natural position (adapt
bizarre postures or facial contortions), and echopraxia is often seen where
someone with SZ mimics the movements of others. Alogia is another
symptom where someone has poverty of speech where they lack meaning or
have a reduction in total speech. Anhedonia is where people react
inappropriately to pleasurable experiences. Flatness of affect is where
somone appears to have no emotion – little to no facial expressions such as
smiling. Their behavior is interpreted as apathetic, where they don’t emit the
same emotions as others in their group.
The ICD-11 (UK and Europe) or DSM-5 (USA) are diagnostic manuals that can
be used for diagnosis of SZ. For diagnosis on SZ in the ICD-11, someone
must have 1 very clear symptom, or 2 if less clear cut, and this symptom can
be either positive or negative. This also has subtypes of SZ: catatonic or
paranoid. These symptoms must be present most of the time during a period
of 1 month+. For diagnosis of SZ in the DSM-5, someone must have 2 or
more symptoms of SZ, and one of these symptoms must be a positive
symptom. The DSM-5 doesn't have subtypes of SZ, and the symptoms must
be present for a significant portion of time for a month+ period.
,Describe the dopamine hypothesis explanation for schizophrenia
(BIO)
Initially the dopamine hypothesis was quite a basic concept that proposed
that individuals with SZ simply had too much of the neurotransmitter
dopamine, and as such demonstrated symptoms related to high levels of
dopamine. This hypothesis was supported by research, such as Griffith et al
induced psychosis in non-SZ volunteers via the administration of dextro-
amphetamine (a drug to increase the amount of dopamine in the brain), and
found they began to demonstrate an abrupt onset of paranoid delusions and
cold/detached emotional responses – they developed symptoms of SZ.
However, this hypothesis was found to be too simplistic – this was confirmed
by the administration of drugs to lower the levels of dopamine in the brain.
But these drugs had little to no effect on those suffering with mostly negative
symptoms of SZ, showing the hypothesis was wrong.
Multiple subtypes of dopamine receptors sites were discovered, D1 to D5
were discovered, which were found to be widely distributed in the cerebral
cortex, and also subcortically in the limbic system. The main dopamine
receptor site is the D2 receptor which is found to be primarily in the
subcortical regions and the limbic system, and became the main focus of the
dopamine hypothesis. This was found by Seeman and Lee who showed the
impact of antipsychotic drugs primarily on the D2 receptor.
The role of dopamine in the limbic system has been the main area of study in
recent years. The limbic system consists of a variety of subcortical structures
that are engaged in many functions, but most notably, emotions, memory
formation and arousal. Nerve pathways leave the limbic system to many
other subcortical structures and to the cerebral cortex; 2 of the main
pathways considered with dopamine are the mesolimbic and the
mesocortical pathways.
The revised dopamine hypothesis looks at both the mesolimbic and
mesocortical pathways. The mesolimbic pathway carries signals from the
, VTA to the nucleus accumbens – and contains too much dopamine, resulting
from too much release of dopamine due to neurons that fire too quickly, or
too often. This results in overstimulation = hyperdopaminergia. This is the
cause for positive symptoms of SZ, such as hallucinations and delusions.
Antipsychotic drugs can reduce dopaminergic neurotransmission and as such
reduce dopamine activity in this pathway, to ultimately reduce positive
symptoms of SZ. The mesocortical pathway carries signals from the VTA to
the frontal lobe. This nerve pathway is vital in emotional responses,
motivation and cognition. This pathway has too little dopamine in the D1
receptors of the frontal lobe – this results in under stimulation =
hypodopaminergia. This causes negative symptoms of SZ such as alogia and
anhedonia, and cognitive impairments. The frontal lobe is responsible for
emotion and motivation, and the lack of dopamine in this area can explain
symptoms such as flatness of affect and avolition.
Evaluate the dopamine hypothesis explanation for schizophrenia
(BIO)
A strength of the dopamine hypothesis explanation for SZ is that it has lots
of supporting research. For example, Seeman and Lee researched the effect
of antipsychotic drugs on D2 receptors in schizophrenic patients. They found
that the use of an antipsychotic drug for treatment led to reduced symptoms
of SZ in the patients. This is because the drug acted as a blocking agent of
the D2 dopamine receptor on post-synaptic neurons, preventing excess
dopamine from being received at the neuron. This is a strength as it supports
the initial dopamine hypothesis stating that excessive dopamine in the
mesolimbic pathway is a cause of SZ. Their research showed a relationship
between dopamine levels up taken by receptors, and schizophrenia
symptoms – antipsychotics decreasing dopamine levels = less symptoms of
SZ. Although this research suggests that the dopamine hypothesis is valid, it
is a very reductionist idea. This only explains dopamine as a
neurotransmitter involved in SZ, whereas Carlsson showed that this idea is
wrong, and glutamate and serotonin are also involved.
A weakness of the dopamine hypothesis explanation for SZ is that the
measurement of dopamine in the body is not always reliable, so it is not that
scientific. For psychologist's studying dopamine levels in controls compared
to schizophrenia patients, they must measure dopamine after it has been
metabolized into HVA. HVA is found in cerebrospinal fluid and is the
byproduct of dopamine metabolism, so it is not a direct measure of
dopamine. This means it is not a reliable measure of dopamine levels, as
