Carlsson

Question 1

What were the 3 aims of Carlsson?

Answer 1

-Review studies into the relationship between NT levels (D and Glutamate) on symtp SZ
-Explore theory of hypoglutamatergia
-Consider need for further research into drug treatments that target NT’s other than dopamine and improve drug treatment by reducing relapse rates and side effects

Question 2

Procedure of Carlsson

Answer 2

-Literature review of findings beyond D hypothesis
-articles looked at NT and neuro chem levels in pts w SZ and studies into drugs known to induce SZ symtp (angel dust -PCP)

Question 3

How many different studies were used?

Answer 3

-33
-32 published, 1 not
-14 own research

Question 4

Methods used in the studies? (5)

Answer 4

-Animal research(rodents) to test function of NT and brain structure
-Drug studies with animals
-SPECT and PET scans to determine NT functioning
-post mortems
-human participant

Question 5

What types of SZ were included in the studies?

Answer 5

-Acute SZ
-Sz in remission
-Treatment resistant

Question 6

What type of data was used?

Answer 6

-Secondary

Question 7

Name 3 studies he used in his review?

Answer 7

-Lindstroem et al
-Carlsson and Carlsson
-Miller and Abercrombie

Question 8

Lindstroem et al

Answer 8

-Radioactively labelled L-DOPA, administered to 10 SZ and 10 healthy. PET scans used to measure activity
-L-DOPA which produces dopamine taken up quicker in SZ than normal

Question 9

Carlsson and Carlsson

Answer 9

-Animal study about MK-801 drug to change rodent behaviour

Question 10

Miller and Abercrombie

Answer 10

-looked at glutamate receptors and relationship between glutamate and dopamine
-Rodents to test NT’s levels where competitive NMDA inhibited dopamine release

Question 11

What were the 4 categories of results?

Answer 11

-Dopamine as explanation for SZ
-Glutamate as explanation for SZ
-Drug treatments
-Thalamic filter

Question 12

Dopamine:results(3)

Answer 12

-Evidence from PET
and SPECT support D hyp. SZ show more DA than controls.
-Excess dopamine too simplistic
-Serotonin, GM, GABA, noradrenaline and acetylcholine as NT’s relating to SZ
-Dopamine easier to study in live brain than others but doesn’t mean it is only one

Question 13

What brain part do SZ have more DA than controls?

Answer 13

-Basal ganglia

Question 14

What did Laruelle et al find?

Answer 14

-SZ in remission only had normal DA activity

Question 15

What did carlsson et al point out about dopamine?

Answer 15

-Pts taking anti-psychotics complained abt side effects when in remission. Here dopamine lvls normal and drugs causing low DA.

Question 16

Glutamate: results (5)

Answer 16

-PCP leads to psychosis and blocks glutamate receptors (NMDA receptors - increases dopamine Miller and Abercrombie) so low GM might explain psychoses sympt
-GM deficiency leads to cog deficits, loss flexibility leading to neg sympt
-GM failure in C.cortex leads to neg. In basal ganglia leads to pos
-PCP more likely to result in psychosis than amphetamine (GM bigger impact)
-Reduced GM increases Dopamine . D neurons controlled by GM neurons

Question 17

What did Miller and Abercrombie find?

Answer 17

-Release of dopamine increased if glutamate reduce by blocking NMDA receptors

Question 18

Thalamic filter: results

Answer 18

-Links to pathways that relate to filtering sensory info to protect from overload
-Normal ppl have overload when extreme stress, SZ filter doesn’t work effectively
-indirect pathway: too much DA or little GM reduces protective influence of thalamus = pos sympt
-Direct pathway: excitatory. need sensory info in right areas. abnormal levels of GM and DA reduce excitation = neg sympt

Question 19

Drug treatments (3)

Answer 19

-Clozapine effective. Antidopaminergic and serotonergic. Inc serotonin, inc GM. Reduced sympt. Reciprocal interaction bet S and GM in cerebral cortex. SGA better
-Effective for T resistant bc of relationship bet S and GM. Impacts on S inc GM.
-Sub group of T resistant whose SZ caused my GM

Question 20

Conclusions

Answer 20

-SZ diff types, abnormal levels of diff NT’s
-Need more research into dev drugs that avoid neg side effects. Consider role of other NT’s

Question 21

Evaluation

Answer 21

GRAVE

Question 22

Generalisability

Answer 22

-Animal research. anthropomorphic. Don’t know if suffering pos sympt, higher cog functioning. can’t explain neg
+animal. bio similarities. structure and NT’s
+Many types of SZ patients, representative of all patients.

Question 23

Reliability

Answer 23

-Secondary data. Don’t know flaws in data
+Reliable methods: PET, labexp. standardised, specific doses of drugs.
+Range of research which support each other. 32. large sample.
+Sendt et al reviewed studies, agreed with C’s summary that cog and neg sympt due to low GM, need more research

Question 24

Applications

Answer 24

+Good. Dev more effective treatment for SZ, beneficial for pts who don’t respond to current treatment

Question 25

Validity

Answer 25

-question data as used secondary. May not be same aim
-Subjective. Carlsson used own studies
-Results subj: picks out similarities and diffs that he thinks impacted. Ignore other bits. No interrater or method like thematic analysis. No structured way to analyse
-Conf v’s. Stress alters NT’s during scanning. Clinical setting, vulnerable and anxious.
+Animal data: high control of ext variable, standardised, c&e
+Obj: PET scans. numerical measurements. vol of activity
+Scientific lab research, high control
+Triangulation: in depth detailed valid conc due to amount of data.

Question 26

Ethics

Answer 26

+No ppts as already involved in the studies. No harm, need for consent, in public domains
-Ethical purpose: to improve treatment. cost/benefit analysis. can use for treatment