S: biological explanation and characteristic Flashcards
what is schizophrenia
a psychotic disorder of the mind that affects how you think, feel and behave. mainly the sufferer will lose a sense of contact with reality
when is schizophrenia diagnosed and who does it affect
most often between the ages of 15 and 35. men and women are affected equally and it affects roughly 1% of the population
who came up with characterising symptoms
Kurt Schneider
suggested characterising the symptoms of schizophrenia as either being positive or negative
what is a positive symptom
any change in behaviour or thoughts, such as hallucinations or delusions. here the word ‘positive’ means the presence of behaviours
what are the positive symptoms
hallucinations
delusions
disordered thinking
definition of hallucinations
perceptions that are unreal. often auditory or visual and so involve seeing or hearing things that aren’t really there. they can be experienced in any sensory modality
example of a hallucination
visual- involves seeing things that aren’t real (objects, people etc.)
definition of delusions
beliefs that are unreal, usually experienced with no evidence to offer in support of the belief
example of delusions
paranoid- may believe they’re being harassed or persecuted. may believe they’re being chased, followed, watched or plotted against (often by their family and friends)
grandiose- individuals believe they are special in some ways
definition of disordered thinking
often evident through examining the speech of those individuals with schizophrenia. the persons thoughts seem to jump from one topic to another for no apparent reason and show no logical flow of discussion
example of disordered thinking
a persons train of thoughts seem to jump from one topic to another for no reason (knights move thinking)
and show no logical flow of discussion (word salad)
what is a negative symptoms
a lack of function that you would not usually expect to see in a healthy person
e.g. people with schizophrenia often appear emotionless and flat. negative symptoms refers to an absence of normal mental functioning
what are the negative symptoms
alogia
avolition
catatonic behaviour
flatness of affect
what is alogia
refers to a poverty of speech. apart from a reduction in the total amount of speech produced people with schizophrenia lack meaning, even simple, short answers can be a problem
example of alogia
you may not talk because you hear voices that tell you not to speak or because you feel nervous or paranoid around other people
what is avolition
occurs when people seem to be indifferent to or unconcerned with the goings on in their surroundings. show little desire to take part in activities (work or social) even if it is something they previously enjoyed
example of avolition
inability to care for personal hygiene or participate in work or recreational activities
what is flatness of affect
where the individual would appear to have no emotion. they may converse without the usual emotional intonation and show little or no facial expressions such as smiling or grimacing
example of flatness of affect
may speak in a dull flat voice and your face may not change
what is catatonic behaviour
issues can range widely from fast, repetitive movements to little or no movements at all. the person with schizophrenia may move for no obvious reason
example of catatonic behaviour
may remain motionless in a rigid posture for hours/days
criteria for diagnosing schizophrenia
patient is assessed against the DSM V criteria. the patient must have experienced 2 of the symptoms and at least one must be positive,
continuous signs of these disturbances must persist for at least 6 months and at least 1 month of active symptoms (may be less if successfully treated
what are the 2 biological explanations of schizophrenia
dopamine hypothesis
structural abnormalities
hero explanation of schizophrenia
dopamine hypothesis
sidekick explanation
structural abnormalities
when was a link between dopamine and schizophrenia first established
dopamine hypothesis
when it was found that a drug developed in the 1950s (L-Dopa) was successful in reducing Parkinson’s symptoms, instead sufferers developed behaviours seen in schizophrenics
what did the dopamine hypothesis initially propose
that individuals with schizophrenia simply produce too much dopamine
research supporting the dopamine hypothesis
Griffith et al. induced psychosis in non-schizophrenic volunteers with the administration of dextro-amphetamine (drug increasing the presence of dopamine in the brain) finding that volunteers demonstrated a generally abrupt onset of paranoid delusions and demonstrate a cold and detached emotional response
why has the dopamine hypothesis been labelled as being too simple
as the drug that reduced the levels of dopamine had little or no effect on those individuals who mainly suffered with the negative symptoms of schizophrenia
explain D2 receptor sites
dopamine hypothesis
Seeman and Lee were able to show the impact of anti-psychotic drugs on this particular receptor. as D2 recpetor sites are found primarily in the subcortical regions of the limbic system, this became the main focus of the dopamine hypothesis
these structures are responsible for functions such as emotion, memory formation and arousal
two pathways linked to schizophrenia
dopamine hypothesis
mesolimbic and mesocortical
explain the mesolimbic pathway
D hypothesis
dopamine is a major neurotransmitter in the mesolimbic pathway. this pathway carries signals from the ventral tegmental area to the nucleus accumbens.
hyperactivity of Dopamine D2 causes over stimulation and therefore contributes to the positive symptoms of schizophrenia like delusions and hallucinations.
how do antipsychotics work in the mesolimbic pathway
D hypothesis
reduce dopamine activity in this pathway and ultimately the positive symptoms of schizophrenia
what is the mesocortical pathway
D hypothesis
dopamine is also a major neurotransmitter in this pathway. this path carries signals from the ventral tegmental area to the frontal lobe. this pathway is essential for emotional responses, motivation and cognition
Davis et al. note that hypo-activity/too little dopamine is evident in the D1 receptor sites of the frontal lobe of many individuals with the cognitive impairments and negative symptoms of schizophrenia
one strength of the dopamine hypothesis
it makes good sense and it is possible to explain how such dopamine imbalances may come about. many researchers believe that dopamine imbalances may come about as a result of a genetic predisposition, twin and family studies are able to indicate that there is some genetic basis for schizophrenia
research evidence to support the strength of the dopamine hypothesis
Gottesman et al. looked at rates of schizophrenica in cousins, grandchildren, half-siblings, parents, siblings, non-identical and identical twins. as genetic similarity increased, so did the risk of both individuals having schizophrenia
PB point to Gottesman et als research
evaluating dopamine hypothesis
research looking for one or a few candidate genes has been dissapointing. in 2014, the Schizophrenia Working Group of the Psychiatric Genomics Consortium (300 scientists from 35 countries) reported that there were 108 genetic loci associated with schizophrenia. this suggests that although there may be a genetic basis for schizophrenia, it is a complex matter which involves more than a few abnormal dopamine genes
one weakness of the dopamine hypothesis
there is contradictory evidence available which weakens it’s propositions. dopamine is not the only neurotransmitter that has been implicated with schizophrenia. serotonin has also been identified as a potential influence. newer atypical anti-psychotics (clozapine) block the D2 dopamine receptor as well as the serotonin receptor 5-HT2A. although this may not suggest that the dopamine hypothesis is completely wrong, it suggests the action of dopamine is not sufficient to provide and explanation on its own. although our understanding of the dopamine hypothesis has led to the development of some successful treatments which has been of benefit to many, there are still unanswered questions to link neurotransmission and the onset of schizophrenia
another weakness of the dopamine hypothesis
additional problem that reduces the validity of the hypothesis is the issues with establishing cause and effect. people who believe this explanation would say that dopamine imbalances cause schizophrenia. it could also be argued that schizophrenia causes dopamine imbalances. this will remain unknown until investigative techniques become less invasive and research can take place to try and establish which comes first
what does a lack of validity suggest
dopamine hypothesis weakness
research using PET scans hasn’t yet been able to detect differences in the dopamine activity of the brains of individuals with and without schizophrenia. suggesting we are still some way off answering this fundamental question and therefore has huge implications for this explanation
final weakness of the dopamine hypothesis
some concerns over the methodological processes adopted in exploring this hypothesis. it is very difficult to make direct measurements of neurotransmitters such as dopamine so both research exploring dopamine action is based on metabolites. (what neurotransmitters get broken down into, levels can be assessed in cerebrospinal fluid)
weakness of dopamine hypothesis
problem with using metabolites to measure
a patients diet and drug use can also alter their metabolite levels and even when research is conducted under controlled conditions, results can be difficult to interpret. therefore an element of caution should be adopted when considering this explanation of schizophrenia as research using metabolite levels will have reduced validity.
briefly explain how biological explanations could be applied to methods of modifying schizophrenia
- the dopamine explanation suggests that schizophrenics produce too much dopamine
- therefore, in order to reduce suffering and the experience of symptoms such as hallucinations and delusions, it would be necessary to lower dopamine levels
- anti-psychotic drugs work by binding to, but not stimulating dopamine receptors preventing dopamine molecules from gaining access
- dopamine levels reduce as a result, bur this can cause side effects
- newer atypical antipsychotics work by binding to receptors for a brief period of time, but rapidly disassociating, this allows for some dopamine transmission and side effects are lessened as a result
explain enlarged ventricles
structural abnormalities explanation
ventricles are cavities that produce and transport certebrospinal fluid, providing protection, buoyancy and chemical stability to the brain and spine,
Andreasen studied MRI scans of individuals with or without schizophrenia and found those with schizophrenia had ventricles that were 20-50% larger than controls
how can enlarged ventricles lead to schizophrenia
structural abnormalities
ventricles enlarge when the brain has been damaged in some way, by something that has caused the brain to reduce in size. the ventricles enlarge to maintain stability. Andreasen found patients with larger ventricles showed more ‘ negative symptoms’ whilst those with slightly enlarged ventricles (smaller) showed more positive symptoms
explain cortical atrophy
structural abnormalities
cortical atrophy means loss of neurons in the cerebral cortex, looks like its shrunk. affects the cognitive functions of that area
Vita et al used CAT scans to assess 143 individuals with schizophrenia and 45 control group pps. they found 33% of individuals with schizophrenia showed moderate to severe atrophy
how might cortical atrophy explain increased ventricles size
structural abnormalities
CA make the brain shrink, brain becomes unstable as there is too much space. so the ventricles would increase in size to offer stability for the brain
explain reversed cerebral asymmetry
structural abnormalities
our brains are not symmetrical, however the usual pattern of asymmetry is not seen in the schizophrenic brain. in many schizophrenics, the right hemisphere is larger than the left (reverse of non-schizophrenic brains) as language function is located on the left hemisphere, reversed asymmetry may account for some symptoms of schizophrenia (alogia)
strength of the structural abnormalities explanation
one huge strength is that findings from studies conducted in this area are highly reliable. the same structural abnormalities are found time after time when studies are replicated. strong evidence suggesting brain abnormalities are at least partially involved in schizophrenia.
research to support structural abnormalities explanation being reliable
McCarley et al. suggests that the presence of enlarged venricles is by far the most reliable finding in research using brain scans. the link between cortical atrophy and schizophrenia has also been confirmed
PB point for the brain abnormality explanation being reliable
McCarley et al suggest factors such as age, sex and severity of symptoms can all exert a powerful influence on the prevalence and pattern of the observed brain abnormalities. suggesting either structural abnormalities are only evident in some of those individuals diagnosed with schizophrenia or that we need to assess and acknowledge more subtle differences when assessing abnormalities
weakness of the structural abnormalities explanation
an issue that weakens the validity of the research is that structural abnormalities discussed above are not only linked to schizophrenia.
research to support the weakness of the structural abnormalities explanation
Roy et al. note that individuals diagnosed with bipolar disorder and schizoaffective disorder have also been found to have schizophrenia. disorders like bipolar and schizophrenia have similar symptoms which may be as a result of the same structural abnormalities. factors such as age, gender and severity of symptoms can affect the prevalence and pattern of these structural differences. this suggests we need to acknowledge other facts that may account for the illness.
