Croft KE, Duff MC, Kovach CK, Anderson SW, Adolphs R, Tranel D.
1. Neuropsychologia. 2010 May;48(6):1789-801. Epub 2010 Mar 6.
Department of Neurology, Division of Behavioral Neurology and Cognitive Neuroscience, University of Iowa College of Medicine, IA, USA. kcroft@utdallas.edu
Abstract
As we learn new information about the social and moral behaviors of other people, we form and update character judgments of them, and this can profoundly influence how we regard and act towards others. In the study reported here, we capitalized on two interesting neurological patient populations where this process of complex "moral updating" may go awry: patients with bilateral damage to ventromedial prefrontal cortex (vmPFC) and patients with bilateral damage to hippocampus (HC). We predicted that vmPFC patients, who have impaired emotion processing, would exhibit reduced moral updating, and we also investigated how moral updating might be affected by severe declarative memory impairment in HC patients. The vmPFC, HC, and brain-damaged comparison (BDC) participants made moral judgments about unfamiliar persons before and after exposure to social scenarios depicting the persons engaged in morally good, bad, or neutral behaviors. In line with our prediction, the vmPFC group showed the least amount of change in moral judgments, and interestingly, the HC group showed the most amount of change. These results suggest that the vmPFC and hippocampus play critical but complementary roles in updating moral character judgments about others: the vmPFC may attribute emotional salience to moral information, whereas the hippocampus may provide necessary contextual information from which to make appropriate character judgments. 2010 Elsevier Ltd. All rights reserved.
PMCID: PMC2862792 [Available on 2011/5/1]
Tuesday, July 27, 2010
Damage to right ventromedial prefronal area abolishes judgment of harmful intent
Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. lyoung@mit.edu
Neuron. 2010 Mar 25;65(6):845-51.
Abstract
Moral judgments, whether delivered in ordinary experience or in the courtroom, depend on our ability to infer intentions. We forgive unintentional or accidental harms and condemn failed attempts to harm. Prior work demonstrates that patients with damage to the ventromedial prefrontal cortex (VMPC) deliver abnormal judgments in response to moral dilemmas and that these patients are especially impaired in triggering emotional responses to inferred or abstract events (e.g., intentions), as opposed to real or actual outcomes. We therefore predicted that VMPC patients would deliver abnormal moral judgments of harmful intentions in the absence of harmful outcomes, as in failed attempts to harm. This prediction was confirmed in the current study: VMPC patients judged attempted harms, including attempted murder, as more morally permissible relative to controls. These results highlight the critical role of the VMPC in processing harmful intent for moral judgment. (c) 2010 Elsevier Inc. All rights reserved.
Neuron. 2010 Mar 25;65(6):845-51.
Abstract
Moral judgments, whether delivered in ordinary experience or in the courtroom, depend on our ability to infer intentions. We forgive unintentional or accidental harms and condemn failed attempts to harm. Prior work demonstrates that patients with damage to the ventromedial prefrontal cortex (VMPC) deliver abnormal judgments in response to moral dilemmas and that these patients are especially impaired in triggering emotional responses to inferred or abstract events (e.g., intentions), as opposed to real or actual outcomes. We therefore predicted that VMPC patients would deliver abnormal moral judgments of harmful intentions in the absence of harmful outcomes, as in failed attempts to harm. This prediction was confirmed in the current study: VMPC patients judged attempted harms, including attempted murder, as more morally permissible relative to controls. These results highlight the critical role of the VMPC in processing harmful intent for moral judgment. (c) 2010 Elsevier Inc. All rights reserved.
Hippocampal damage abolishes stress response
Department of Psychology, Saint Louis University, St. Louis, MO 63103, USA. tbuchan7@slu.edu
Abstract
The hippocampus (HC) is necessary for learning and memory, but it also plays a role in other behaviors such as those related to stress and anxiety. In support of the latter idea, we show here that bilateral HC damage abolishes the cortisol response to psychosocial stress. We collected salivary cortisol, heart rate, and affective responses to the Trier Social Stress Test (TSST) from 7 participants with bilateral HC lesions, 12 participants with damage outside the HC, and 28 healthy normal comparison participants matched to the HC participants on age and sex. HC participants showed elevated pre-stress cortisol, but no cortisol response to the TSST. Heart rate and affective responses in the HC group were similar to those of the comparison groups. Participants with brain damage outside the HC showed stress responses that were comparable to those of the healthy comparison group. These findings support the idea that the functions of the human HC extend beyond learning and memory, and suggest that the HC is necessary for producing the cortisol response to psychosocial stress.
PMCID: PMC2692817 [Available on 2010/6/1]
Abstract
The hippocampus (HC) is necessary for learning and memory, but it also plays a role in other behaviors such as those related to stress and anxiety. In support of the latter idea, we show here that bilateral HC damage abolishes the cortisol response to psychosocial stress. We collected salivary cortisol, heart rate, and affective responses to the Trier Social Stress Test (TSST) from 7 participants with bilateral HC lesions, 12 participants with damage outside the HC, and 28 healthy normal comparison participants matched to the HC participants on age and sex. HC participants showed elevated pre-stress cortisol, but no cortisol response to the TSST. Heart rate and affective responses in the HC group were similar to those of the comparison groups. Participants with brain damage outside the HC showed stress responses that were comparable to those of the healthy comparison group. These findings support the idea that the functions of the human HC extend beyond learning and memory, and suggest that the HC is necessary for producing the cortisol response to psychosocial stress.
PMCID: PMC2692817 [Available on 2010/6/1]
Localization of Benton Facial Recognition Test and J. Lo.
Department of Neurology, Division of Behavioral Neurology and Cognitive Neuroscience, University of Iowa College of Medicine, Iowa City, IA, USA. daniel-tranel@uiowa.edu
Abstract
Two of the most successful and widely used tests developed by Arthur Benton and colleagues are the Facial Recognition Test (FRT) and Judgment of Line Orientation Test (JLO), which probe visuoperceptual and visuospatial functions typically associated with right hemisphere structures, especially parietal, occipitoparietal, and occipitotemporal structures. Taking advantage of a large database of focal lesion patients (the Iowa Neurological Patient Registry), we used a new lesion-deficit mapping technique to investigate the neuroanatomical correlates of FRT and JLO performance. For the FRT, there were 201 patients with relevant data; of these, 38 were impaired on the FRT, and failure was most strongly associated with lesions in the right posterior-inferior parietal and right ventral occipitotemporal (fusiform gyrus) areas. For the JLO, there were 181 patients with relevant data; of these, 23 were impaired on the JLO, and failure was most strongly associated with lesions in the right posterior parietal region. These findings put new empirical teeth in the localizing value of the FRT and JLO tests, and they extend and sharpen previous work that had pointed to right posterior structures as being important for FRT and JLO performance
PMCID: PMC2853018 Free PMC Article
PMID: 19051129 [PubMed - indexed for MEDLINE]
Abstract
Two of the most successful and widely used tests developed by Arthur Benton and colleagues are the Facial Recognition Test (FRT) and Judgment of Line Orientation Test (JLO), which probe visuoperceptual and visuospatial functions typically associated with right hemisphere structures, especially parietal, occipitoparietal, and occipitotemporal structures. Taking advantage of a large database of focal lesion patients (the Iowa Neurological Patient Registry), we used a new lesion-deficit mapping technique to investigate the neuroanatomical correlates of FRT and JLO performance. For the FRT, there were 201 patients with relevant data; of these, 38 were impaired on the FRT, and failure was most strongly associated with lesions in the right posterior-inferior parietal and right ventral occipitotemporal (fusiform gyrus) areas. For the JLO, there were 181 patients with relevant data; of these, 23 were impaired on the JLO, and failure was most strongly associated with lesions in the right posterior parietal region. These findings put new empirical teeth in the localizing value of the FRT and JLO tests, and they extend and sharpen previous work that had pointed to right posterior structures as being important for FRT and JLO performance
PMCID: PMC2853018 Free PMC Article
PMID: 19051129 [PubMed - indexed for MEDLINE]
Focality of clock drawing test determined by error type
Division of Behavioral Neurology and Cognitive Neuroscience, University of Iowa, IA, USA. daniel-tranel@uiowa.edu
Abstract
The Clock Drawing Test (CDT) is widely used in clinical neuropsychological practice. The CDT has been used traditionally as a "parietal lobe" test (e.g., Kaplan, 1988), but most empirical work has focused on its sensitivity and specificity for detecting and differentiating subtypes of dementia. There are surprisingly few studies of its neuroanatomical correlates. The authors investigated the neuroanatomical correlates of the CDT, using 133 patients whose lesions provided effective coverage of most of both hemispheric convexities and underlying white matter. On the CDT, 30 subjects were impaired and 87 were unimpaired (16 were "borderline"). Impairments on the CDT were associated with damage to right parietal cortices (supramarginal gyrus) and left inferior frontal-parietal opercular cortices. Visuospatial errors were predominant in patients with right hemisphere damage, whereas time setting errors were predominant in patients with left hemisphere lesions. These findings provide new empirical evidence regarding the neuroanatomical correlates of the CDT, and together with previous work, support the use of this quick and easily administered test not only as a screening measure but also as a good index of focal brain dysfunction. PsycINFO Database Record (c) 2008 APA, all rights reserved.
PMCID: PMC2834527 Free PMC Article
Abstract
The Clock Drawing Test (CDT) is widely used in clinical neuropsychological practice. The CDT has been used traditionally as a "parietal lobe" test (e.g., Kaplan, 1988), but most empirical work has focused on its sensitivity and specificity for detecting and differentiating subtypes of dementia. There are surprisingly few studies of its neuroanatomical correlates. The authors investigated the neuroanatomical correlates of the CDT, using 133 patients whose lesions provided effective coverage of most of both hemispheric convexities and underlying white matter. On the CDT, 30 subjects were impaired and 87 were unimpaired (16 were "borderline"). Impairments on the CDT were associated with damage to right parietal cortices (supramarginal gyrus) and left inferior frontal-parietal opercular cortices. Visuospatial errors were predominant in patients with right hemisphere damage, whereas time setting errors were predominant in patients with left hemisphere lesions. These findings provide new empirical evidence regarding the neuroanatomical correlates of the CDT, and together with previous work, support the use of this quick and easily administered test not only as a screening measure but also as a good index of focal brain dysfunction. PsycINFO Database Record (c) 2008 APA, all rights reserved.
PMCID: PMC2834527 Free PMC Article
Sunday, July 25, 2010
Neurology of lying-- localizaion
Spence et al. Neuroreport 2001. longer rt's and activation in VLPFC.
Langleben et al. Neuroimage 2002-- guilty knowledge test (GKT) and fMRI showed activation in SFG and ACC.
Ganis et al. Cereb Cortex 2003. right anterior prefrontal cortex was involved in well rehearsed more elaborate lies, whereas a network involving anterior prefrontal cortex involved in spontaneous lies.
Kozel et al J Neuropsychiatry and Clin Neurosci 2005- OF cortex and ACC involved in deceptio
Abe et al. (Brain 2009) noted PD patients are "honest" and have trouble lying, and that left DLPFC is dominant for inhibiting replies, esp truth telling, ie feigning ignorance.
Karim et al. Cereb Cortex-- TMS of left cortex FACILITATES lying perhaps by relieving moral conflict.
Sellal JNNP 1993- reflex epilepsy, patient had seizures when he lied. Had meningioma in right anterior clinoid. Tumor pressed on amygdala.
Hakun et al Neurocase 2008-- fMRI as lie detector-ventrolateral frontal activated even when lying was not demanded explicitly
Seth et al. Neuroimage 2006- MEEG can be used for trial by trial detection of lies.
Modell et al. J Neuropsychiatry and Clin Neurosci 1992-- pathological lying associated with decreased tracer uptake in right thalamus.
Yang et al. Br J Psych 2007. Increased white matter among pathological liars especially OF, IFG, MFG.
Fenelon et al. BMJ 1991 and other cits.-- Munchhausen's s- associated with bilateral frontotemporal atrophy, hyperperfusion of right thalamus, cerebral palsy, high signal in PVWM bihemispheric.
Grezes et al J Neurosci 2004. detecting deception activates amygdala and rostral ACC.
Harada et al. Neurosci Research 2009- moral and lie judgments activate VMPFC, lateral OF, left temporal, left temp-par junction, and right cerebellum.
Etcoff et al. Nature 2000- loss of language due to left MCA stroke was associated with increased ability to detect deception.
Stuss et al. Brain 2001- bilateral esp right OF lesions impaired ability to detect deception.
Autistics have trouble lying.
Langleben et al. Neuroimage 2002-- guilty knowledge test (GKT) and fMRI showed activation in SFG and ACC.
Ganis et al. Cereb Cortex 2003. right anterior prefrontal cortex was involved in well rehearsed more elaborate lies, whereas a network involving anterior prefrontal cortex involved in spontaneous lies.
Kozel et al J Neuropsychiatry and Clin Neurosci 2005- OF cortex and ACC involved in deceptio
Abe et al. (Brain 2009) noted PD patients are "honest" and have trouble lying, and that left DLPFC is dominant for inhibiting replies, esp truth telling, ie feigning ignorance.
Karim et al. Cereb Cortex-- TMS of left cortex FACILITATES lying perhaps by relieving moral conflict.
Sellal JNNP 1993- reflex epilepsy, patient had seizures when he lied. Had meningioma in right anterior clinoid. Tumor pressed on amygdala.
Hakun et al Neurocase 2008-- fMRI as lie detector-ventrolateral frontal activated even when lying was not demanded explicitly
Seth et al. Neuroimage 2006- MEEG can be used for trial by trial detection of lies.
Modell et al. J Neuropsychiatry and Clin Neurosci 1992-- pathological lying associated with decreased tracer uptake in right thalamus.
Yang et al. Br J Psych 2007. Increased white matter among pathological liars especially OF, IFG, MFG.
Fenelon et al. BMJ 1991 and other cits.-- Munchhausen's s- associated with bilateral frontotemporal atrophy, hyperperfusion of right thalamus, cerebral palsy, high signal in PVWM bihemispheric.
Grezes et al J Neurosci 2004. detecting deception activates amygdala and rostral ACC.
Harada et al. Neurosci Research 2009- moral and lie judgments activate VMPFC, lateral OF, left temporal, left temp-par junction, and right cerebellum.
Etcoff et al. Nature 2000- loss of language due to left MCA stroke was associated with increased ability to detect deception.
Stuss et al. Brain 2001- bilateral esp right OF lesions impaired ability to detect deception.
Autistics have trouble lying.
Saturday, July 24, 2010
Go, no go task, parcellated and localized within the VLPFC and pre SMA
Chikazoe J. Localizing performance of go/no-go tasks to prefrontal cortical subregions. Curr Opin Psych 2010; 23: 267-272.
Author divides go/no go tasks into components including working memory, stimulus-driven attention ( reorienting of attention), error monitoring, top down control processes, and response inhibition. The literature suggests the VLPFC is key to response inhibition (see Buxbaum et al, Hum Brain Mapping 2005). However, DLPFC and pre-SMA also are recruited for this task and for stop-signal and for antisaccade tasks.
Transcranial magnetic stimulation of right VLPFC disrupts response inhibition, but stimulation of left IFG, DLPFC, dorsal premotor cortex, and right angular gyrus does not. Subregions of the VLPFC play different roles. The subregions are posterior IFG, inferior frontal junction, and IFG/insula.
pIFG usually activates with go/no go stimuli. IFJ, located at border of inferior frontal sulcus and precentral sulcus, is associated with processing infrequent stimuli. Thus pIFG is the "core region" for go/no go response inhibition. The same area is involved in reorienting attention (see Corbetta M, Neuron 2008). The reorienting attention network involves pIFG, IFJ, IFG/insula, and temporal parietal junction. This is segregated from a dorsal network involving the frontal eye fields (FEF), and intraparietal sulcus that employs a top down mechanism . pIFG may activate with both networks and provide the communication between the two.
IFJ is involved in stimulus driven attention and is more involved in processing infrequent stimuli, such as infrequent go or infrequent no go on go/no go tasks. By contrast pIFG is only activated on infrequent no go.
IFG insula is activated, but is tough to differentiate from insula and IFG insula is also activated in many other tasks. Its function is not specific and it may be more related to task awareness.
Pre SMA on right is also core to response inhibition. This is true on both lesion studies and TMR studies. Pre SMA is robustly activated during go/no go whether the task is simple or complex or whether the test is oral or manual. Pre SMA is thought to be important to conflict resolution of task. The anteriror cingulate gyrus (ACC) activates for error processing. DLPFC activation may be related to top down processes and working memory.
Hemispheric asymmetry with right sided dominance is noted in most studies especially for pIFG. However the left pre SMA and VLPFC may be important. "Balance" may be disrupted with left sided lesions that can thus cause deficits on task also.
Author divides go/no go tasks into components including working memory, stimulus-driven attention ( reorienting of attention), error monitoring, top down control processes, and response inhibition. The literature suggests the VLPFC is key to response inhibition (see Buxbaum et al, Hum Brain Mapping 2005). However, DLPFC and pre-SMA also are recruited for this task and for stop-signal and for antisaccade tasks.
Transcranial magnetic stimulation of right VLPFC disrupts response inhibition, but stimulation of left IFG, DLPFC, dorsal premotor cortex, and right angular gyrus does not. Subregions of the VLPFC play different roles. The subregions are posterior IFG, inferior frontal junction, and IFG/insula.
pIFG usually activates with go/no go stimuli. IFJ, located at border of inferior frontal sulcus and precentral sulcus, is associated with processing infrequent stimuli. Thus pIFG is the "core region" for go/no go response inhibition. The same area is involved in reorienting attention (see Corbetta M, Neuron 2008). The reorienting attention network involves pIFG, IFJ, IFG/insula, and temporal parietal junction. This is segregated from a dorsal network involving the frontal eye fields (FEF), and intraparietal sulcus that employs a top down mechanism . pIFG may activate with both networks and provide the communication between the two.
IFJ is involved in stimulus driven attention and is more involved in processing infrequent stimuli, such as infrequent go or infrequent no go on go/no go tasks. By contrast pIFG is only activated on infrequent no go.
IFG insula is activated, but is tough to differentiate from insula and IFG insula is also activated in many other tasks. Its function is not specific and it may be more related to task awareness.
Pre SMA on right is also core to response inhibition. This is true on both lesion studies and TMR studies. Pre SMA is robustly activated during go/no go whether the task is simple or complex or whether the test is oral or manual. Pre SMA is thought to be important to conflict resolution of task. The anteriror cingulate gyrus (ACC) activates for error processing. DLPFC activation may be related to top down processes and working memory.
Hemispheric asymmetry with right sided dominance is noted in most studies especially for pIFG. However the left pre SMA and VLPFC may be important. "Balance" may be disrupted with left sided lesions that can thus cause deficits on task also.
Coin rotation test validation
Hill BD et al. The Neurologist. 2010; 16: 249-253
Authors validate a longstanding easy test for fine motor processing used for decades at LSU in 86 normals. Task consists of counting number of 180 degree rotations of a quarter in ten seconds by the dominant and nondominant hands. A correction for drops is used, but not that important. Task is to rotate a quarter using thumb and fingers one and two in ten seconds with an examiner using a timer and counting. If the coin is dropped, the subject gets another ten seconds. The adjusted score is the number of rotations in ten seconds minus (0.1 x rotations x drops). Traditionally, LSU has used a cut score of ten to indicate impairment. Authors believe a cut score (for both hands) of 13 is better, with increased sensitivity and some loss of specificity.
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