Basal cerebral glucose distribution in long-term post-traumatic stress disorder

Molina, Mario Enrique; Isoardi, Roberto; Prado, Marcela Nathalie; Bentolila, Silvia

doi:10.1080/15622970701472094

Cited by 19 publications

(19 citation statements)

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“…Insular cortex activation has been found to be positively correlated with measures of symptom severity (Carrion et al, 2008;Hopper et al, 2007;Osuch et al, 2001) and post-scan plasma adrenocorticotropic hormone levels (Liberzon et al, 2007a). Although greater insular activation in PTSD has been confirmed by a recent voxel-wise meta-analysis (Etkin and Wager, 2007), a few studies have reported either no group differences in insular activation or relatively decreased activation in PTSD (Bremner et al, 1999a(Bremner et al, , 2004Molina et al, 2007;Moores et al, 2008;Phan et al, 2006a;Shin et al, 1999).…”

Section: Posttraumatic Stress Disordermentioning

confidence: 99%

“…Some functional neuroimaging studies have reported decreased hippocampal activation during symptomatic states (Bremner et al, 1999a) and during memory tasks that involve neutral or emotional stimuli (Astur et al, 2006;Bremner et al, 2003a, b;Moores et al, 2008;Shin et al, 2004b). One study found reduced glucose metabolic rate in the hippocampus at rest (Molina et al, 2007), and another reported that successful treatment was related to increased hippocampal activation (Peres et al, 2007). Other studies, however, have reported increased activation in the hippocampus in PTSD (Geuze et al, 2007(Geuze et al, , 2008bSachinvala et al, 2000;Semple et al, 2000;Thomaes et al, 2009;Werner et al, 2009) or a positive correlation between hippocampal activation and PTSD symptom severity (Osuch et al, 2001;Shin et al, 2004b).…”

Section: Posttraumatic Stress Disordermentioning

confidence: 99%

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The Neurocircuitry of Fear, Stress, and Anxiety Disorders

Shin

Liberzon

2009

Neuropsychopharmacol

1,710

927

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Anxiety disorders are a significant problem in the community, and recent neuroimaging research has focused on determining the brain circuits that underlie them. Research on the neurocircuitry of anxiety disorders has its roots in the study of fear circuits in animal models and the study of brain responses to emotional stimuli in healthy humans. We review this research, as well as neuroimaging studies of anxiety disorders. In general, these studies have reported relatively heightened amygdala activation in response to disorder-relevant stimuli in post-traumatic stress disorder, social phobia, and specific phobia. Activation in the insular cortex appears to be heightened in many of the anxiety disorders. Unlike other anxiety disorders, post-traumatic stress disorder is associated with diminished responsivity in the rostral anterior cingulate cortex and adjacent ventral medial prefrontal cortex. Additional research will be needed to (1) clarify the exact role of each component of the fear circuitry in the anxiety disorders, (2) determine whether functional abnormalities identified in the anxiety disorders represent acquired signs of the disorders or vulnerability factors that increase the risk of developing them, (3) link the findings of functional neuroimaging studies with those of neurochemistry studies, and (4) use functional neuroimaging to predict treatment response and assess treatment-related changes in brain function.

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Section: Posttraumatic Stress Disordermentioning

confidence: 99%

Section: Posttraumatic Stress Disordermentioning

confidence: 99%

The Neurocircuitry of Fear, Stress, and Anxiety Disorders

Shin

Liberzon

2009

Neuropsychopharmacol

1,710

927

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“…Some fMRI studies have found that the PCN is associated with imagery or recall of traumatic memories in PTSD subjects, especially those exhibiting dissociative symptoms (Lanius et al 2004(Lanius et al , 2005. Moreover, other studies have identified hypometabolism in this region at rest in PTSD subjects as compared with controls (Lange et al 2005 ;Molina et al 2010). The PCN has been related to conscious visuospatial representation and mental imagery, the so-called ' mind's eye ' (Fletcher et al 1996 ;Cavanna, 2007).…”

Section: Default Mode Networkmentioning

confidence: 99%

“…However, other structures have been consistently found to be involved in PTSD, i.e. anterior and posterior insular cortex (Osuch et al 2001 ;Liberzon et al 2003 ;Lindauer et al 2008), posterior cingulate cortex (PCC) (Bremner et al 1999 a, b ;Sachinvala et al 2000), as well as definite portions of the parietal lobe such as inferior parietal lobule (IPL)/supramarginal gyrus (Bremner et al 1999a(Bremner et al , b, 2003Shaw et al 2002) and precuneus (PCN) (Molina et al 2010). …”

Section: Introductionmentioning

confidence: 99%

Self-rating scales assessing subjective well-being and distress correlate with rCBF in PTSD-sensitive regions

et al. 2011

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Background. The aim of this study was to investigate the distribution of the regional cerebral blood flow (rCBF) in occupational-related post-traumatic stress disorder (PTSD) subjects and to seek possible correlations between brain perfusion and self-rating scales (SRS) in order to cross-check their diagnostic value and to look for their neural correlates. Method.A total of 13 traumatized underground and long-distance train drivers developing (S) and 17 not developing (NS) PTSD who had experienced a ' person under train ' accident or who had been assaulted at work underwent clinical assessment and 99m Tc-HMPAO SPECT imaging during autobiographical trauma scripts. Statistical parametric mapping was applied to analyse rCBF changes in S as compared with NS and to search for correlations between rCBF and the administered SRS scores, modelling age, months to SPECT and the ratio ' grey matter/intracranial volume ' as nuisance variables.Results. Significantly higher activity was observed during trauma script in left posterior and anterior insula, posterior cingulate, inferior parietal lobule, precuneus, caudate and putamen in PTSD subjects as compared with the trauma-exposed control group. Impact of Event Scale and World Health Organisation (10) Well-Being Index scores highly correlated with tracer uptake to a great extent in the same regions in which rCBF differences between S and NS were found.Conclusions. These findings support the involvement of insular, cingulate and parietal cortices (as well as the basal ganglia) in the pathogenesis of PTSD and in the processing of related subjective well-being and distress.

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“…The explicit neuronal mechanisms behind the PTSD pathophysiology however, are yet to be elucidated [6]. Previous functional neuroimaging studies have suggested that PTSD may exist in parallel with neurological changes in several corticolimbic regions, including the amygdala [7][8][9], the hippocampus [10][11][12][13][14], the insular [15][16][17][18][19][20] and the prefrontal cortex [21][22][23]. Such neurological alterations are viewed as being connected with the physiological and psychological abnormalities associated with PTSD including: impaired emotion; memory; visual recognition and regulation of fear responses; enhanced attention to threat-related stimuli and biased memory for adverse events [24][25][26][27][28].…”

Section: Introductionmentioning

confidence: 99%