Xiberas et al (Reference Xiberas, Martinot and Mallet2001) measured D2 receptor occupancy in striatum, thalamus and temporal cortex in patients treated with haloperidol, risperidone, amisulpride, clozapine and olanzapine. On the basis of their findings, they conclude that in the striatum and in the thalamus atypical antipsychotics induce a significantly lower D2 binding index than haloperidol does. Their results are consistent with previous studies showing only small differences between striatal and temporal cortex blockade by traditional compounds and relatively selective D2 blockade in temporal cortex caused by atypical antipsychotics (Reference Pilowsky, Mulligan and ActonPilowsky et al, 1997; Reference Bigliani, Mulligan and ActonBigliani et al, 2000).
Looking at the data from Xiberas et al (Reference Xiberas, Martinot and Mallet2001), we came to different conclusions. Using equipotent doses of antipsychotics (doses which lead to the same occupation of D2 receptors in the striatum), no differences in thalamo-striatal and temporostriatal indices between typical and atypical antipsychotics could be shown (Table 1). We suggest that atypical antipsychotics do not exert special temporal lobe or limbic selectivity. The selectivity depends more on the dose than on the type of antipsychotic (typical v. atypical). This is in agreement with Nyberg & Farde (Reference Nyberg and Farde2000) and Geddes et al (Reference Geddes, Freemantle and Harrison2000), who argue that non-equipotent doses can partly explain differences between classical and novel antipsychotics.
Drug | Binding index (%) | ||||
---|---|---|---|---|---|
Striatum | Thalamus | Temporal cortex | Temporo-striatal index | Thalamo-striatal index | |
Haloperidol 3 mg | 66.6 | 91.2 | 88.3 | 1.33 | 1.37 |
Risperidone 6 mg | 67 | 92.2 | 92.2 | 1.38 | 1.38 |
Amisulpride 1000 mg | 61.5 | 69.9 | 87.8 | 1.43 | 1.14 |
Olanzapine 20 mg | 69.6 | 91.9 | 91.8 | 1.32 | 1.32 |
Clozapine 200 mg | 45.9 | 79 | 90.1 | 1.96 | 1.72 |
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