Post by Max on Jun 30, 2005 7:11:23 GMT -5
Significant fall in metabolism after 4 months (Ro)accutane exposure in all scanned human acne-subjects
A mean -21% fall in metabolism the orbitofrontal cortex in human subjects exposed to (Ro)accutane was observed. Brain functioning in adults was measured with [(18)F]fluorodeoxyglucose positron emission tomography before and after 4 months of treatment with isotretinoin (N=13) or an antibiotic (N=15). Isotretinoin but not antibiotic treatment was associated with decreased brain metabolism in the orbitofrontal cortex (-21% change versus 2% change for antibiotic), a brain area known to mediate symptoms of depression [1].
Picture 1. Bremner JD et al. Functional brain imaging alterations in acne patients treated with isotretinoin. (2005) Am J Psychiatry. May;162(5):983-91.
The function of the orbitofrontal cortex
The function of the orbitofrontal cortex (OFC) is not fully known. However, alterations in behavior could with high certainity be expected in subjects with altered OFC function. By imaging techniques the orbitofrontal cortex has been associated with mood, but also with learning, response to rewards and decision-making [2]. These associations may except for effects on mood also to certain extent predict human behavior. Further yet not suggested behavioral functions may exist. Further yet not described physiological functions of the OFC are highly likely to exist.
Review of the OFC in Elliott et al (2004):
"Several previous studies have suggested that the orbitofrontal cortex and amygdala interact closely in associative learning paradigms (Baxter et al., 2000; Kalivas and Nakamura, 1999 and Schoenbaum et al., 1998). It has been suggested (Baxter et al., 2000 and Schoenbaum et al., 1998) that the connection between OFC and amygdala is critical for response selection on the basis of incentive value. However, the present results suggest that the responses of these regions can be functionally dissociated. While amygdala responses to reward were significantly modulated by movement, OFC responses were not. Recent results from functional neuroimaging (Breiter et al., 2001; Elliott et al., 2003 and O'Doherty et al., 2001), as well as animal electrophysiology (Schultz, 2000) and lesion studies (Mobini et al., 2002), suggest that a critical function of the OFC is assigning relative reward value. The rewards in the movement and the no-movement conditions of the present study are of equal value. It has also been argued that the OFC plays a role in analytic reward detection and expectation of reward (Schultz, 2000). Again both the experience of rewards and the expectation of rewards are matched in the movement and no-movement conditions, and a lack of differential OFC activity is therefore plausible. It is important to note that both animal studies reviewed above, and neuropsychological studies of patients with OFC damage (Bechara et al., 1994; Bechara et al., 1996 and Rolls et al., 1994), suggest that OFC plays a role in behavioural modification in the face of changing reward values. The present study is not incompatible with this hypothesis. Reward values here remain constant and therefore no behavioural modification is required. It is plausible that amygdala and striatum mediate already established reward-eliciting behaviours, while medial OFC monitors ongoing reward experience, ready to modify behaviour (via top-down connections to the amygdala and striatum) if necessary" [2].
A mean -21% fall in metabolism the orbitofrontal cortex in human subjects exposed to (Ro)accutane was observed. Brain functioning in adults was measured with [(18)F]fluorodeoxyglucose positron emission tomography before and after 4 months of treatment with isotretinoin (N=13) or an antibiotic (N=15). Isotretinoin but not antibiotic treatment was associated with decreased brain metabolism in the orbitofrontal cortex (-21% change versus 2% change for antibiotic), a brain area known to mediate symptoms of depression [1].
Picture 1. Bremner JD et al. Functional brain imaging alterations in acne patients treated with isotretinoin. (2005) Am J Psychiatry. May;162(5):983-91.
The function of the orbitofrontal cortex
The function of the orbitofrontal cortex (OFC) is not fully known. However, alterations in behavior could with high certainity be expected in subjects with altered OFC function. By imaging techniques the orbitofrontal cortex has been associated with mood, but also with learning, response to rewards and decision-making [2]. These associations may except for effects on mood also to certain extent predict human behavior. Further yet not suggested behavioral functions may exist. Further yet not described physiological functions of the OFC are highly likely to exist.
Review of the OFC in Elliott et al (2004):
"Several previous studies have suggested that the orbitofrontal cortex and amygdala interact closely in associative learning paradigms (Baxter et al., 2000; Kalivas and Nakamura, 1999 and Schoenbaum et al., 1998). It has been suggested (Baxter et al., 2000 and Schoenbaum et al., 1998) that the connection between OFC and amygdala is critical for response selection on the basis of incentive value. However, the present results suggest that the responses of these regions can be functionally dissociated. While amygdala responses to reward were significantly modulated by movement, OFC responses were not. Recent results from functional neuroimaging (Breiter et al., 2001; Elliott et al., 2003 and O'Doherty et al., 2001), as well as animal electrophysiology (Schultz, 2000) and lesion studies (Mobini et al., 2002), suggest that a critical function of the OFC is assigning relative reward value. The rewards in the movement and the no-movement conditions of the present study are of equal value. It has also been argued that the OFC plays a role in analytic reward detection and expectation of reward (Schultz, 2000). Again both the experience of rewards and the expectation of rewards are matched in the movement and no-movement conditions, and a lack of differential OFC activity is therefore plausible. It is important to note that both animal studies reviewed above, and neuropsychological studies of patients with OFC damage (Bechara et al., 1994; Bechara et al., 1996 and Rolls et al., 1994), suggest that OFC plays a role in behavioural modification in the face of changing reward values. The present study is not incompatible with this hypothesis. Reward values here remain constant and therefore no behavioural modification is required. It is plausible that amygdala and striatum mediate already established reward-eliciting behaviours, while medial OFC monitors ongoing reward experience, ready to modify behaviour (via top-down connections to the amygdala and striatum) if necessary" [2].
