s: biological explanations and characteristics Flashcards

1
Q

what is schizophrenia

A

a psychotic disorder of the mind that affects how you think, feel and behave, sufferer will lose a sens of contact with reality

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2
Q

who does it affect

A

about 1% of the population, most often diagnosed between the ages of 15 and 35. Men and women are equally affected

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3
Q

who came up with the characteristics of addiction

A

Kurt Schneider

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4
Q

what is a positive symptom

A

any change in behaviour or thoughts, such as hallucinations or delusions. the word ‘positive’ means the presence of a behaviour

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5
Q

what are the positive symptoms

A

hallucinations
delusions
disordered thinking

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6
Q

what is hallucinations
example

A

perceptions that are unreal. often auditory or visual and so involve seeing or hearing things that aren’t really there. however, they can be experienced in any modality
e.g. visual hallucinations may involve seeing things that aren’t there (people, objects)

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7
Q

what are delusions
example

A

beliefs that are unreal, usually experienced with no evidence to offer in support of the belief
e.g grandiose - individuals believe they are special in some way

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8
Q

what is disordered thinking
example

A

often evident through examining the speech of 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
e.g persons train of thought seem to jump from one topic to another for no reason (knights move thinking) and show no logical flow of discussion (word salad)

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9
Q

what is a negative symptoms

A

a withdrawal or 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 refer to an absence or lack of normal mental functioning involving thinking, behaviour or perception

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10
Q

what are the negative symptoms

A

alogia
avolition
flatness of affect
catatonic behaviour

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11
Q

what is alogia
example

A

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
e.g. they may not talk because they hear voices telling them not to speak

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12
Q

what is avolition
example

A

occurs when people seem to be unconcerned with whats going on in their lives, little desire to take part in activities, work or things they once enjoyed
e.g inability to care for personal hygiene or participate in work or recreational activities

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13
Q

what is flatness of affect example

A

where the individual would appear to have no emotion. may show little to no facial expressions such as smiling
e.g. may speak in a dull flat voice and their face may not change

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14
Q

what is catatonic behaviour
example

A

issues can range widely from fast, repetitive useless movements to little or none at all. schizophrenic may move for no obvious reason
e.g. may remain motionless in a rigid posture for hours/days

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15
Q

criteria for diagnosis

A

DSM V
patient must have experience at least 2 of the symptoms (1 must be positive)
must have persisted for at least 6 months and at least 1 month of active symptoms

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16
Q

what is the first biological explanation of schizophrenia

A

the dopamine hypothesis

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17
Q

a link between dopamine and schizophrenia

A

was first established in the 1950s when a drug L-Dopa was successful in reducing Parkinsons symptoms. it was suggested that individuals with schizophrenia simply produce too much dopamine

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18
Q

who supported the link between dopamine and schizophrenia

A

Griffith et al. induced psychosis in non-schizophrenic volunteers finding that volunteers demonstrated a generally abrupt onset of paranoid delusions and a cold and detached emotional response

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19
Q

explain D2 receptor sites

A

are found primarily in the subcortical regions of the limbic system (containing structures such as the prefrontal cortex and the amygdala which are responsible for functions such as emotion, memory formation and arousal)

20
Q

what did Seeman and Lee find

A

able to show the impact of anti-psychotic drugs on this particular receptor. as D2 receptors found primarily in the subcortical regions of the limbic system,became the main focus of this hypothesis

21
Q

explain the 2 pathways

A

2 pathways linked to this explanation of schizophrenia; mesolimbic and mesocortical. dopamine is a major neurotransmitter in both pathways

22
Q

explain how the mesolimbic pathway links to schizophrenia

A

carries signals from the ventral tegmental area to the nucleus accumbens. hyperactivity of dopamine D2 in this pathway are linked to positive symptoms (hallucinations and delusions) in individuals with schizophrenia

23
Q

how do antipsychotic drugs work in the mesolimbic pathway

A

reduce dopamine activitiy in this pathway and so the positive symptoms will subside

24
Q

explain how the mesocortical pathway link to schizophrenia

A

the mesocortical pathway carries signals from the ventral tegmental area to the frontal lobe. this pathway is responsible for emotional responses, motivation and cognition.
Davis et al. reported hypofunctionality of dopamine D1 receptor contributed to negative symptoms of schizophrenia

25
Q

a strength of the dopamine hypothesis

A

it makes good sense and it is possible to explain how such dopamine imbalances come about. many researchers believe that dopamine imbalances may come about as a result of a genetic predisposition

26
Q

what evidence supports the strength of the dopamine hypothesis

A

twin and family studies are able to indicate that there is some genetic basis for schizophrenia. Gottesman et al. looked at the rates of schizophrenia 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 (risk inreased to 50% if you have an identical twin who had been diagnosed with schizophrenia)

27
Q

PB point for the strength of the dopamine hypothesis

A

research looking for one or few candidate genes has been disappointing. In 2014, the Schizophrenia Working Group of the Psychiatric Genomics consortium reported that there were 108 genetic loci associated with schizophrenia

28
Q

what does the PB point for the strength of the dopamine hypothesis suggest

A

that although there may be a genetic basis for schizophrenia, it is a complex matter which must involve more than a few abnormal dopamine genes

29
Q

one weakness of the dopamine hypothesis of schizophrenia

A

is that there is contradictory evidence available which weakens its propositions. dopamine is not the only neurotransmitter that has been identified as a potential influence of schizophrenia. serotonin also identified. newer atypical antipsychotics e.g. clozapine block the D2 dopamine receptor as well as the seretonin receptor

30
Q

what does other neurotransmitters suggest about the dopamine hypothesis

A

this may not suggest the dopamine hypothesis is completely wrong, it does suggest the action of dopamine is not sufficient to provide an explanation on its own. therefore although we have developed some successful treatment on the back of this hypothesis, there are still unanswered questions as to the link between neurotransmission and the onset of schizophrenia

31
Q

second weakness of the dopamine hypothesis explanation of schizophrenia

A

issue establishing cause and effect which reduces the validity of the hypothesis. although this explanation says the dopamine imbalance causes schizophrenia, it could be argued that dopamine imbalances are an affect that are created after the onset of schizophrenia. this will remain unknown until investigative techniques become less invasive and research can establish what comes first

32
Q

research the supports the issue of finding cause and effect
dopamine hypothesis

A

research using PET scans (Copolov and Crook) hasn’t been able to detect differences in the dopamine activity of the brains of individuals with schizophrenia and those without. this suggests we are some way off being able to answer the question of cause and effect which has huge implications for this explanation

33
Q

final weakness of the biological explanation of schizophrenia

A

some concerns over the methodological processes adopted when exploring the hypothesis, very difficult to take direct measurements of dopamine, most research on dopamine action is based on metabolites, (however it is also known that a patient’s diet and drug use could also alter their metabolite levels. the results can be difficult to measure when levels can vary from patient to patient.

34
Q

what does the weakness of problems with methodological processes suggest
(dopamine hypothesis)

A

an element of caution should be adopted when considering this explanation of schizophrenia as much research may have reduced validity if based on metabolite levels instead of the actual neurotransmitter

35
Q

briefly explain how biological explanations could be applied to MOM schizophrenia (5)

A
  • the dopamine explanation suggests that schizophrenics produce excessive amounts of the neurotransmitter dopamine
    -so 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, but this can cause side effects
    -newer atypical antipsychotics work by binding to receptors for a brief period, but rapidly disassociating. this allows for dopamine transmission and side effects are lessened as a result
36
Q

what is the second biological explanation of schizophrenia

A

structural abnormalities

37
Q

what has been found about large ventricles

A

in some individuals with schizophrenia, their ventricles appear larger than those of non-schizophrenics. Andreasen studies MRI scans of individuals with or without schizophrenia, found that those with schizophrenia had ventricles that were 20-50% larger than in controls

38
Q

how does enlarged ventricles lead to schizophrenia

A

ventricles enlarge when the brain has been damaged, different factors caused the brain to reduce in size so the ventricles have to enlarge to maintain stability. Andreasen found patients with larger ventricles showed more ‘negative symptoms’ whilst those with slightly enlarged (smaller) ventricles showed more positive symptoms

39
Q

what is cotrical atrophy

A

means the loss of neurons in the cerebral cortex, atrophy makes the brain look like its shrunk, atrophy affects the cognitive functions of that area of the cerebral cortex
Vita et al used CAT scans to assess 143 individuals with schizophrenia and 45 control group pps. found 33% of individuals with schizophrenia showed moderate to sever atrophy

40
Q

how might cortical atrophy explain the increased venticle size

A

ventricles would increases in size to offer stability after cortical atrophy makes the brain shrink

41
Q

what is reversed cerebral asymmetry

A

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) reversed may account for some of the symptoms of schizophrenia such as alogia

42
Q

strength of structural abnormalities explanation of schizophrenia

A

one strength is related to structural abnormalities in the brain is that the findings from the studies conducted are highly reliable. the same abnormalities have been found time after time. this is strong evidence that structural brain abnormalities are at least partially involved in schizophrenia

43
Q

what did McCarley et al. suggest
(brian abnormalities explanaiton)

A

suggests that the presence of enlarged ventricles is by far the most reliable finding in research that uses brain scans. the link between cotrical atrophy and schizophrenia had also been confirmed (Flashman and Green)

44
Q

PB point of the strength of structural abnormalities explanation

A

however, 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 are only evident in some of those individuals diagnosed with schizophrenia, or we also need to asses more subtle differences when assessing structural abnormalities.

45
Q

one weakness of structural abnormalities explanation

A

an issue which weakens the validity of the explanation is that structural abnormalities such as the ones discussed above are not only linked to schizophrenia and have been found in individuals suffering from conditions other than schizophrenia

46
Q

evidence to support the weakness of the structural abnormalities explanation

A

Roy et al. noted that individuals diagnosed with bipolar disorder and schizoaffective disorder have also been found with enlarged ventricles. bipolar and schizophrenia also have many overlapping symptoms so may result in similar structural abnormalities of the brain

47
Q

what does Roy et al. research suggest

A

age,gender and severity of symptoms can also affect the prevalence of these structural differences. we need to acknowledge there may be other factors that may account for the illness. so as scanning techniques improve in their sophistication, diagnosis of some conditions may become more dependent on the scans as opposed to just resultant behaviours.