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	<title>Comments for Neuroconscience</title>
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	<link>http://neuroconscience.com</link>
	<description>Researching Brain Plasticity, Cognitive Neuroscience, and Cognitive Science</description>
	<lastBuildDate>Thu, 23 Feb 2012 06:20:19 +0000</lastBuildDate>
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		<title>Comment on Insula and Anterior Cingulate: the ‘everything’ network or systemic neurovascular confound? by thoughts on thoughts &#187; Blog Archive &#187; BOLD confounds</title>
		<link>http://neuroconscience.com/2012/02/18/insula-and-anterior-cingulate-the-everything-network-or-systemic-neurovascular-confound/#comment-1334</link>
		<dc:creator><![CDATA[thoughts on thoughts &#187; Blog Archive &#187; BOLD confounds]]></dc:creator>
		<pubDate>Thu, 23 Feb 2012 06:20:19 +0000</pubDate>
		<guid isPermaLink="false">http://neuroconscience.com/?p=665#comment-1334</guid>
		<description><![CDATA[[...] Micah at neuroconscience blog has a posting on possible BOLD signal problems. (here) [...]]]></description>
		<content:encoded><![CDATA[<p>[...] Micah at neuroconscience blog has a posting on possible BOLD signal problems. (here) [...]</p>
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		<title>Comment on Snorkeling ’the shallows’: what&#8217;s the cognitive trade-off in internet behavior? by Michael</title>
		<link>http://neuroconscience.com/2010/06/08/snorkeling-%e2%80%99the-shallows%e2%80%99-whats-the-cognitive-trade-off-in-internet-behavior/#comment-1333</link>
		<dc:creator><![CDATA[Michael]]></dc:creator>
		<pubDate>Thu, 23 Feb 2012 02:44:21 +0000</pubDate>
		<guid isPermaLink="false">http://neuroconscience.wordpress.com/?p=335#comment-1333</guid>
		<description><![CDATA[Quite unbelievable.  Most of the responses above are different versions of: &quot;I think what I think already, and that&#039;s good enough for me.&quot; For some reason Steven Pinker stopped thinking a long time ago and many of the other responses that echo his response to Carr&#039;s book a versions of the same. Even people who seem to have read Carr&#039;s book clearly have not read it.  Perhaps they are too busy trying to click on links when they see underlined text?]]></description>
		<content:encoded><![CDATA[<p>Quite unbelievable.  Most of the responses above are different versions of: &#8220;I think what I think already, and that&#8217;s good enough for me.&#8221; For some reason Steven Pinker stopped thinking a long time ago and many of the other responses that echo his response to Carr&#8217;s book a versions of the same. Even people who seem to have read Carr&#8217;s book clearly have not read it.  Perhaps they are too busy trying to click on links when they see underlined text?</p>
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		<title>Comment on Insula and Anterior Cingulate: the ‘everything’ network or systemic neurovascular confound? by Micah</title>
		<link>http://neuroconscience.com/2012/02/18/insula-and-anterior-cingulate-the-everything-network-or-systemic-neurovascular-confound/#comment-1330</link>
		<dc:creator><![CDATA[Micah]]></dc:creator>
		<pubDate>Wed, 22 Feb 2012 08:14:37 +0000</pubDate>
		<guid isPermaLink="false">http://neuroconscience.com/?p=665#comment-1330</guid>
		<description><![CDATA[As many of you had questions or comments regarding the best way to deal with respiratory related issues, I spoke briefly with Torben at yesterday&#039;s lab meeting. Removal of respiratory noise is fairly simple, but the real problem is with end-tidal C02. According to Torben, most noise experts agree that regression techniques only partially remove the artifact, and that an unknown amount is left behind even following signal regression. This may be due to slow vascular saturation effects that build up and remain irrespective of shear breath frequency.  A very tricky problem indeed.]]></description>
		<content:encoded><![CDATA[<p>As many of you had questions or comments regarding the best way to deal with respiratory related issues, I spoke briefly with Torben at yesterday&#8217;s lab meeting. Removal of respiratory noise is fairly simple, but the real problem is with end-tidal C02. According to Torben, most noise experts agree that regression techniques only partially remove the artifact, and that an unknown amount is left behind even following signal regression. This may be due to slow vascular saturation effects that build up and remain irrespective of shear breath frequency.  A very tricky problem indeed.</p>
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		<title>Comment on Insula and Anterior Cingulate: the ‘everything’ network or systemic neurovascular confound? by Tim Jacob</title>
		<link>http://neuroconscience.com/2012/02/18/insula-and-anterior-cingulate-the-everything-network-or-systemic-neurovascular-confound/#comment-1326</link>
		<dc:creator><![CDATA[Tim Jacob]]></dc:creator>
		<pubDate>Tue, 21 Feb 2012 16:33:12 +0000</pubDate>
		<guid isPermaLink="false">http://neuroconscience.com/?p=665#comment-1326</guid>
		<description><![CDATA[Where in the brain is smell?
No two papers on brain imaging and olfaction agree on anything. PET studies found greater right orbitofrontal cortex (OFC) activation with odour versus no odour (Small et al,1997). Some fMRI studies also report a right-sided asymmetry (O’Doherty et al, 2000; Sobel et al, 1998; Yousem et al, 1999). O’Doherty et al (2000), showed 6/8 had stronger right OFC activation than left. Using banana and vanillin as stimuli, found right OFC activation in 4/5 subjects and left OFC activation in 3/5. In contrast Zald and Pardo, (2000) found greater left activation with hydrogen sulphide. Left activation was also found by Royet et al (2000) using PET in response to pleasant and unpleasant olfactory stimuli. To add further confusion, Fulbright et al (1998), using fMRI, did not find any OFC activation when comparing pleasant and unpleasant odours – then, a subsequent study by Rolls et al (2003) found that pleasant odours activated the medio-rostral OFC whereas no activity was observed in the OFC for unpleasant odours. Both unpleasant and pleasant odours activated the anterior cingulate cortex and anterior insula (Rolls et al., 2003) but it is a medial activation and doesn’t appear to show marked lateralization with the exception that unpleasant odours activated a region of the right OFC. Levy et al (1997) using fMRI found that odour activated the OFC, cingulate gyrus, piriform and entorhinal cortices, hippocampus and amygdala. PET studies found vanillin activated the amygdala, piriform cortices bilaterally and parts of the anterior insula cortex – and caused frontal and right parietal deactivation in women (though not in men). Women exhibited less activation than men in Levy et al (1997) in contradiction to EEG studies in which women showed higher amplitude evoked responses and also to other fMRI studies (Yousem et al., 1999). PET studies showed no such gender differences (Bengtsson et al, 2001). The OFC has been implicated in hedonic differentiation with the activation in the right medial OFC being greater for pleasant than unpleasant odours but the left lateral OFC showed greater responsiveness to unpleasant than pleasant odours (Anderson et al, 2003). The bilateral middle orbitofrontal cortex (OFC), left lateral OFC, right insula, and bilateral anterior/middle cingulate gyri were most frequently activated by odor stimulation (Katata et al, 2009), but, in contrast to Anderson et al, the left middle OFC and right lateral OFC were significantly more often activated in the participants who perceived the odour stimulation as unpleasant, while the right anterior cingulate gyrus was more often activated in those who perceived the odour as pleasant.

In the last few years I have looked at EEG and lateralisation of olfactory brain activation, following the lead of Davidson (1995). However, with the hegemony of brain imaging, and with the confusion outlined above, I haven’t had the confidence to publish opposing results.


References
1.	Anderson, A.K., Christoff, K., Stappen, I., Panitz, D., Ghahremani, D.G., Glover, G., Gabrieli, J.D.E., Sobel, N. 2003.  Dissociated neural representations of intensity and valence in human olfaction. Nature Neuroscience 6 (2) , pp. 196-202

2.	Bengtsson, S., Berglund, H., Gulyas, B., Cohen, E., Savic, I. 2001. Brain activation during odor perception in males and females. NeuroReport 12 (9) , pp. 2027-2033

3.	Davidson, R.J., Sutton, S.K. 1995. Affective neuroscience: The emergence of a discipline. Current Opinion in Neurobiology 5 (2) , pp. 217-224

4.	Fulbright, R.K., Skudlarski, P., Lacadie, C.M., Warrenburg, S., Bowers, A.A., Gore, J.C., Wexler, B.E. 1998. Functional MR imaging of regional brain responses to pleasant and unpleasant odors. American Journal of Neuroradiology 19 (9) , pp. 1721-1726

5.	Katata, K., Sakai, N., Doi, K., Kawamitsu, H., Fujii, M., Sugimura, K., Nibu, K.-I. 2009. Functional MRI of regional brain responses to &#039;pleasant&#039; and &#039;unpleasant&#039; odors.Acta Oto-Laryngologica 129 (SUPPL. 562) , pp. 85-90

6.	Levy, L.M., Henkin, R.I., Hutter, A., Lin, C.S., Martins, D., Schellinger, D. 1997 .Functional MRI of human olfaction. Journal of Computer Assisted Tomography 21 (6) , pp. 849-856

7.	O&#039;Doherty, J., Rolls, E.T., Francis, S., Bowtell, R., McGlone, F., Kobal, G., Renner, B., Ahne, G. 2000. Sensory-specific satiety-related olfactory activation of the human orbitofrontal cortex. NeuroReport 11 (4) , pp. 893-897

8.	Rolls, E.T., Kringelbach, M.L., De Araujo, I.E.T. 2003. Different representations of pleasant and unpleasant odours in the human brain. European Journal of Neuroscience 18 (3) , pp. 695-703


9.	Royet, J.-P., Zald, D., Versace, R., Costes, N., Lavenne, F., Koenig, O., Gervais, R. 2000. Emotional responses to pleasant and unpleasant olfactory, visual, and auditory stimuli: A positron emission tomography study. Journal of Neuroscience 20 (20) , pp. 7752-7759

10.	Small, D.M., Jones-Gotman, M., Zatorre, R.J., Petrides, M., Evans, A.C. 1997. Flavor processing: More than the sum of its parts. NeuroReport 8 (18) , pp. 3913-3917

11.	Sobel, N., Prabhakaran, V., Desmond, J.E., Glover, G.H., Goode, R.L., Sullivan, E.V., Gabriell, J.D.E. 1998. Sniffing and smelling: Separate subsystems in the human olfactory cortex. Nature 392 (6673) , pp. 282-286

12.	Yousem, D.M., Maldjian, J.A., Siddiqi, F., Hummel, T., Alsop, D.C., Geckle, R.J., Bilker, W.B., Doty, R.L. 1999. Gender effects on odor-stimulated functional magnetic resonance imaging. Brain Research 818 (2) , pp. 480-487

13.	Zald, D.H., Pardo, J.V. 2000. Functional neuroimaging of the olfactory system in humans. International Journal of Psychophysiology 36 (2), pp. 165-181]]></description>
		<content:encoded><![CDATA[<p>Where in the brain is smell?<br />
No two papers on brain imaging and olfaction agree on anything. PET studies found greater right orbitofrontal cortex (OFC) activation with odour versus no odour (Small et al,1997). Some fMRI studies also report a right-sided asymmetry (O’Doherty et al, 2000; Sobel et al, 1998; Yousem et al, 1999). O’Doherty et al (2000), showed 6/8 had stronger right OFC activation than left. Using banana and vanillin as stimuli, found right OFC activation in 4/5 subjects and left OFC activation in 3/5. In contrast Zald and Pardo, (2000) found greater left activation with hydrogen sulphide. Left activation was also found by Royet et al (2000) using PET in response to pleasant and unpleasant olfactory stimuli. To add further confusion, Fulbright et al (1998), using fMRI, did not find any OFC activation when comparing pleasant and unpleasant odours – then, a subsequent study by Rolls et al (2003) found that pleasant odours activated the medio-rostral OFC whereas no activity was observed in the OFC for unpleasant odours. Both unpleasant and pleasant odours activated the anterior cingulate cortex and anterior insula (Rolls et al., 2003) but it is a medial activation and doesn’t appear to show marked lateralization with the exception that unpleasant odours activated a region of the right OFC. Levy et al (1997) using fMRI found that odour activated the OFC, cingulate gyrus, piriform and entorhinal cortices, hippocampus and amygdala. PET studies found vanillin activated the amygdala, piriform cortices bilaterally and parts of the anterior insula cortex – and caused frontal and right parietal deactivation in women (though not in men). Women exhibited less activation than men in Levy et al (1997) in contradiction to EEG studies in which women showed higher amplitude evoked responses and also to other fMRI studies (Yousem et al., 1999). PET studies showed no such gender differences (Bengtsson et al, 2001). The OFC has been implicated in hedonic differentiation with the activation in the right medial OFC being greater for pleasant than unpleasant odours but the left lateral OFC showed greater responsiveness to unpleasant than pleasant odours (Anderson et al, 2003). The bilateral middle orbitofrontal cortex (OFC), left lateral OFC, right insula, and bilateral anterior/middle cingulate gyri were most frequently activated by odor stimulation (Katata et al, 2009), but, in contrast to Anderson et al, the left middle OFC and right lateral OFC were significantly more often activated in the participants who perceived the odour stimulation as unpleasant, while the right anterior cingulate gyrus was more often activated in those who perceived the odour as pleasant.</p>
<p>In the last few years I have looked at EEG and lateralisation of olfactory brain activation, following the lead of Davidson (1995). However, with the hegemony of brain imaging, and with the confusion outlined above, I haven’t had the confidence to publish opposing results.</p>
<p>References<br />
1.	Anderson, A.K., Christoff, K., Stappen, I., Panitz, D., Ghahremani, D.G., Glover, G., Gabrieli, J.D.E., Sobel, N. 2003.  Dissociated neural representations of intensity and valence in human olfaction. Nature Neuroscience 6 (2) , pp. 196-202</p>
<p>2.	Bengtsson, S., Berglund, H., Gulyas, B., Cohen, E., Savic, I. 2001. Brain activation during odor perception in males and females. NeuroReport 12 (9) , pp. 2027-2033</p>
<p>3.	Davidson, R.J., Sutton, S.K. 1995. Affective neuroscience: The emergence of a discipline. Current Opinion in Neurobiology 5 (2) , pp. 217-224</p>
<p>4.	Fulbright, R.K., Skudlarski, P., Lacadie, C.M., Warrenburg, S., Bowers, A.A., Gore, J.C., Wexler, B.E. 1998. Functional MR imaging of regional brain responses to pleasant and unpleasant odors. American Journal of Neuroradiology 19 (9) , pp. 1721-1726</p>
<p>5.	Katata, K., Sakai, N., Doi, K., Kawamitsu, H., Fujii, M., Sugimura, K., Nibu, K.-I. 2009. Functional MRI of regional brain responses to &#8216;pleasant&#8217; and &#8216;unpleasant&#8217; odors.Acta Oto-Laryngologica 129 (SUPPL. 562) , pp. 85-90</p>
<p>6.	Levy, L.M., Henkin, R.I., Hutter, A., Lin, C.S., Martins, D., Schellinger, D. 1997 .Functional MRI of human olfaction. Journal of Computer Assisted Tomography 21 (6) , pp. 849-856</p>
<p>7.	O&#8217;Doherty, J., Rolls, E.T., Francis, S., Bowtell, R., McGlone, F., Kobal, G., Renner, B., Ahne, G. 2000. Sensory-specific satiety-related olfactory activation of the human orbitofrontal cortex. NeuroReport 11 (4) , pp. 893-897</p>
<p>8.	Rolls, E.T., Kringelbach, M.L., De Araujo, I.E.T. 2003. Different representations of pleasant and unpleasant odours in the human brain. European Journal of Neuroscience 18 (3) , pp. 695-703</p>
<p>9.	Royet, J.-P., Zald, D., Versace, R., Costes, N., Lavenne, F., Koenig, O., Gervais, R. 2000. Emotional responses to pleasant and unpleasant olfactory, visual, and auditory stimuli: A positron emission tomography study. Journal of Neuroscience 20 (20) , pp. 7752-7759</p>
<p>10.	Small, D.M., Jones-Gotman, M., Zatorre, R.J., Petrides, M., Evans, A.C. 1997. Flavor processing: More than the sum of its parts. NeuroReport 8 (18) , pp. 3913-3917</p>
<p>11.	Sobel, N., Prabhakaran, V., Desmond, J.E., Glover, G.H., Goode, R.L., Sullivan, E.V., Gabriell, J.D.E. 1998. Sniffing and smelling: Separate subsystems in the human olfactory cortex. Nature 392 (6673) , pp. 282-286</p>
<p>12.	Yousem, D.M., Maldjian, J.A., Siddiqi, F., Hummel, T., Alsop, D.C., Geckle, R.J., Bilker, W.B., Doty, R.L. 1999. Gender effects on odor-stimulated functional magnetic resonance imaging. Brain Research 818 (2) , pp. 480-487</p>
<p>13.	Zald, D.H., Pardo, J.V. 2000. Functional neuroimaging of the olfactory system in humans. International Journal of Psychophysiology 36 (2), pp. 165-181</p>
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		<title>Comment on Insula and Anterior Cingulate: the ‘everything’ network or systemic neurovascular confound? by Micah</title>
		<link>http://neuroconscience.com/2012/02/18/insula-and-anterior-cingulate-the-everything-network-or-systemic-neurovascular-confound/#comment-1325</link>
		<dc:creator><![CDATA[Micah]]></dc:creator>
		<pubDate>Tue, 21 Feb 2012 08:45:40 +0000</pubDate>
		<guid isPermaLink="false">http://neuroconscience.com/?p=665#comment-1325</guid>
		<description><![CDATA[Thanks, and I agree! In my last study we collected both respiration and pulse using equipment that came with our Seimens Trio. It was very easy and gave me peace of mind knowing that I could compare breath fluctuation and regress it out of my data if needed. I think some of the negative reaction to my post is that people are jumping to defend strong-within subjects design. Again, I agree totally. My own work is with groups (for example meditation) and I wanted to drive home the point that I&#039;m quite worried datasets like mine may be plagued by baseline breathing artifacts. It&#039;s a pretty simple worry if you think about it. One group trains breath awareness and control during challenge, the other doesn&#039;t. Then you challenge that group in fMRI and they alter breathing rates during that particular condition, shifting to a more meditative frequency. Now you&#039;ll be sure to see lots of ACC and Insula showing up in that condition- but it&#039;s not the neural correlates of meditation!]]></description>
		<content:encoded><![CDATA[<p>Thanks, and I agree! In my last study we collected both respiration and pulse using equipment that came with our Seimens Trio. It was very easy and gave me peace of mind knowing that I could compare breath fluctuation and regress it out of my data if needed. I think some of the negative reaction to my post is that people are jumping to defend strong-within subjects design. Again, I agree totally. My own work is with groups (for example meditation) and I wanted to drive home the point that I&#8217;m quite worried datasets like mine may be plagued by baseline breathing artifacts. It&#8217;s a pretty simple worry if you think about it. One group trains breath awareness and control during challenge, the other doesn&#8217;t. Then you challenge that group in fMRI and they alter breathing rates during that particular condition, shifting to a more meditative frequency. Now you&#8217;ll be sure to see lots of ACC and Insula showing up in that condition- but it&#8217;s not the neural correlates of meditation!</p>
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	<item>
		<title>Comment on Insula and Anterior Cingulate: the ‘everything’ network or systemic neurovascular confound? by Micah</title>
		<link>http://neuroconscience.com/2012/02/18/insula-and-anterior-cingulate-the-everything-network-or-systemic-neurovascular-confound/#comment-1324</link>
		<dc:creator><![CDATA[Micah]]></dc:creator>
		<pubDate>Tue, 21 Feb 2012 08:39:49 +0000</pubDate>
		<guid isPermaLink="false">http://neuroconscience.com/?p=665#comment-1324</guid>
		<description><![CDATA[I’m familiar with the body of both Glover and Biswal’s work. I’m not sure what I said that caused you to think I was so ignorant of the history of vascular problems in MRI. I’m no methodologist, my primary work is in cognitive control, but my methods teacher happens to have a focus in respiration and noise filtering in MRI. I don’t really agree with your assertion that we should have seen this explosion earlier. If you look at the figure (which is obviously not of scientific quality, but for illustration purposes) you can see that the ACC spike started much earlier than the past two years.

Further my exact criticism is that these issues, while probably not so much an issue for a well controlled within-subjects design, could severely impact both event-related and resting states using between subject design. I know in my own data, and my colleagues data, the anterior insula is one region that seems to pop in all of our data. Given that it’s clearly more susceptible to C02 artifacts, I don’t think we should hand wave away this issue.

And you are correct; a lot of work has been done linking resting state to neural activity. I’m not one to claim resting state is all bullshit. But you have to admit that these problems are magnified immensely when one is dealing with groups of people sitting at rest for 5+ minute periods.]]></description>
		<content:encoded><![CDATA[<p>I’m familiar with the body of both Glover and Biswal’s work. I’m not sure what I said that caused you to think I was so ignorant of the history of vascular problems in MRI. I’m no methodologist, my primary work is in cognitive control, but my methods teacher happens to have a focus in respiration and noise filtering in MRI. I don’t really agree with your assertion that we should have seen this explosion earlier. If you look at the figure (which is obviously not of scientific quality, but for illustration purposes) you can see that the ACC spike started much earlier than the past two years.</p>
<p>Further my exact criticism is that these issues, while probably not so much an issue for a well controlled within-subjects design, could severely impact both event-related and resting states using between subject design. I know in my own data, and my colleagues data, the anterior insula is one region that seems to pop in all of our data. Given that it’s clearly more susceptible to C02 artifacts, I don’t think we should hand wave away this issue.</p>
<p>And you are correct; a lot of work has been done linking resting state to neural activity. I’m not one to claim resting state is all bullshit. But you have to admit that these problems are magnified immensely when one is dealing with groups of people sitting at rest for 5+ minute periods.</p>
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		<title>Comment on Insula and Anterior Cingulate: the ‘everything’ network or systemic neurovascular confound? by Dan</title>
		<link>http://neuroconscience.com/2012/02/18/insula-and-anterior-cingulate-the-everything-network-or-systemic-neurovascular-confound/#comment-1322</link>
		<dc:creator><![CDATA[Dan]]></dc:creator>
		<pubDate>Tue, 21 Feb 2012 03:25:52 +0000</pubDate>
		<guid isPermaLink="false">http://neuroconscience.com/?p=665#comment-1322</guid>
		<description><![CDATA[While not downplaying some of these issues, you really don&#039;t know much about the history &amp; existing knowledge in these areas. fMRI is, obviously, most sensitive to areas with larger vasculature &amp; draining veins. Go back to the early to mid 1990&#039;s articles and this is a good portion of what they focus on. You reference Chang &amp; Glover, but Glover is a respected name in the field &amp; he&#039;s been studying cardiac &amp; respiration noise &amp; artifacts for a long time (for example search RETROICOR 1999) artifacts for a long time. Biswal is the first person to publish on resting connectivity (1996) It seems the core of Di... Biswal&#039;s Ceb Cortex paper you site is that they&#039;re using an easy-to-collect calibration method (just the standard deviation of a resting scan) rather than more complex methods like induced hypercapnia. The results are similar to the many hypercapnia studies. Check the references to the Di paper.

As for your specific concerns regarding the insula &amp; ACC, remember that some of these draining vein vascular artifacts are less on modern 3T scanners than on 1.5T scanners. If your sinister methodoligical  confound was correct, we should have expected the late 90&#039;s to be the explosion of research in these areas &amp; around other heavily vascularized areas.

There are many sloppy studies out there that might be more sensitive to these issues, but good task designs &amp; cognitive subtraction goes a long way. There&#039;s a lot of good work showing the resting connectivity has a real neural component, but the challenge of distinguishing neural connectivity differences from vascular or motion differences across populations is still a wide open and acknowledged research concern. 

There are reasons for the insula/ACC fad... and I agree it&#039;s a bit of a fad, but all the research can&#039;t be explained away as a simple vascular confound.]]></description>
		<content:encoded><![CDATA[<p>While not downplaying some of these issues, you really don&#8217;t know much about the history &amp; existing knowledge in these areas. fMRI is, obviously, most sensitive to areas with larger vasculature &amp; draining veins. Go back to the early to mid 1990&#8242;s articles and this is a good portion of what they focus on. You reference Chang &amp; Glover, but Glover is a respected name in the field &amp; he&#8217;s been studying cardiac &amp; respiration noise &amp; artifacts for a long time (for example search RETROICOR 1999) artifacts for a long time. Biswal is the first person to publish on resting connectivity (1996) It seems the core of Di&#8230; Biswal&#8217;s Ceb Cortex paper you site is that they&#8217;re using an easy-to-collect calibration method (just the standard deviation of a resting scan) rather than more complex methods like induced hypercapnia. The results are similar to the many hypercapnia studies. Check the references to the Di paper.</p>
<p>As for your specific concerns regarding the insula &amp; ACC, remember that some of these draining vein vascular artifacts are less on modern 3T scanners than on 1.5T scanners. If your sinister methodoligical  confound was correct, we should have expected the late 90&#8242;s to be the explosion of research in these areas &amp; around other heavily vascularized areas.</p>
<p>There are many sloppy studies out there that might be more sensitive to these issues, but good task designs &amp; cognitive subtraction goes a long way. There&#8217;s a lot of good work showing the resting connectivity has a real neural component, but the challenge of distinguishing neural connectivity differences from vascular or motion differences across populations is still a wide open and acknowledged research concern. </p>
<p>There are reasons for the insula/ACC fad&#8230; and I agree it&#8217;s a bit of a fad, but all the research can&#8217;t be explained away as a simple vascular confound.</p>
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		<title>Comment on Insula and Anterior Cingulate: the ‘everything’ network or systemic neurovascular confound? by practiCalfMRI</title>
		<link>http://neuroconscience.com/2012/02/18/insula-and-anterior-cingulate-the-everything-network-or-systemic-neurovascular-confound/#comment-1321</link>
		<dc:creator><![CDATA[practiCalfMRI]]></dc:creator>
		<pubDate>Tue, 21 Feb 2012 01:41:44 +0000</pubDate>
		<guid isPermaLink="false">http://neuroconscience.com/?p=665#comment-1321</guid>
		<description><![CDATA[My inverted logic: If you can measure it during an fMRI experiment without significantly altering the experiment, measure it! I think this applies to both heart rate (where variation also causes issues - see Chang &amp; Glover) and breathing. (BIOPAC will sell you an awesome system for about $10K, or &lt;20 hrs of scan time on most scanners...) To me the onus is on people to show why they *didn&#039;t* measure HR/resp.

And finally: http://tinyurl.com/753z87c

It won&#039;t make you depressed, but it will make you even more cautious!]]></description>
		<content:encoded><![CDATA[<p>My inverted logic: If you can measure it during an fMRI experiment without significantly altering the experiment, measure it! I think this applies to both heart rate (where variation also causes issues &#8211; see Chang &amp; Glover) and breathing. (BIOPAC will sell you an awesome system for about $10K, or &lt;20 hrs of scan time on most scanners&#8230;) To me the onus is on people to show why they *didn&#039;t* measure HR/resp.</p>
<p>And finally: <a href="http://tinyurl.com/753z87c" rel="nofollow">http://tinyurl.com/753z87c</a></p>
<p>It won&#039;t make you depressed, but it will make you even more cautious!</p>
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		<title>Comment on Insula and Anterior Cingulate: the ‘everything’ network or systemic neurovascular confound? by Micah</title>
		<link>http://neuroconscience.com/2012/02/18/insula-and-anterior-cingulate-the-everything-network-or-systemic-neurovascular-confound/#comment-1320</link>
		<dc:creator><![CDATA[Micah]]></dc:creator>
		<pubDate>Mon, 20 Feb 2012 23:19:13 +0000</pubDate>
		<guid isPermaLink="false">http://neuroconscience.com/?p=665#comment-1320</guid>
		<description><![CDATA[Thanks for your interesting comment. Funny that you reference that van Orden paper, the thing literally just came across my desk two days ago. It looks very interesting and I hope to get around to reading it soon. My quick response to you is that, while there are (arguable) explanatory benefits to the lesion method over pure correlation, the lesion method is itself problematic in many ways. The two main problems, I&#039;m sure your aware, are that lesions are rarely focal in nature. Even in the case of a focal lesion, the fact that one could only ever hope to find a handful of individuals limits the generalizability of the findings.  Particularly if you, like I do, believe that the mature brain is defined by radical individual differences in both structure and function.]]></description>
		<content:encoded><![CDATA[<p>Thanks for your interesting comment. Funny that you reference that van Orden paper, the thing literally just came across my desk two days ago. It looks very interesting and I hope to get around to reading it soon. My quick response to you is that, while there are (arguable) explanatory benefits to the lesion method over pure correlation, the lesion method is itself problematic in many ways. The two main problems, I&#8217;m sure your aware, are that lesions are rarely focal in nature. Even in the case of a focal lesion, the fact that one could only ever hope to find a handful of individuals limits the generalizability of the findings.  Particularly if you, like I do, believe that the mature brain is defined by radical individual differences in both structure and function.</p>
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		<title>Comment on Insula and Anterior Cingulate: the ‘everything’ network or systemic neurovascular confound? by vw</title>
		<link>http://neuroconscience.com/2012/02/18/insula-and-anterior-cingulate-the-everything-network-or-systemic-neurovascular-confound/#comment-1319</link>
		<dc:creator><![CDATA[vw]]></dc:creator>
		<pubDate>Mon, 20 Feb 2012 19:53:45 +0000</pubDate>
		<guid isPermaLink="false">http://neuroconscience.com/?p=665#comment-1319</guid>
		<description><![CDATA[Indeed, it can&#039;t hurt. I have to say though, your discussion of respiration really did scare me a bit. It&#039;s something we always hear about and figure we should account for, some day, when there&#039;s time. But I think I want to start collecting it now. If only to, as you suggest, compare conditions and ensure respiration is not a confound. And if we can squeeze more power out of a study by correcting for respiration, that&#039;s always welcome.]]></description>
		<content:encoded><![CDATA[<p>Indeed, it can&#8217;t hurt. I have to say though, your discussion of respiration really did scare me a bit. It&#8217;s something we always hear about and figure we should account for, some day, when there&#8217;s time. But I think I want to start collecting it now. If only to, as you suggest, compare conditions and ensure respiration is not a confound. And if we can squeeze more power out of a study by correcting for respiration, that&#8217;s always welcome.</p>
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