Altered cerebral response to noxious heat stimulation in patients with somatoform pain disorder

Gündel, Harald; Valet, M.; Sorg, Christian; Huber, Dorothea; Zimmer, Claus; Sprenger, Till; Tölle, Thomas R.

doi:10.1016/j.pain.2007.10.003

Cited by 133 publications

(79 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For example, noxious heat led to higher blood oxygen-level dependent signalling in the insula and parahippocampal gyrus, while medial prefrontal cortex activity was reduced. 58 Reduced insula and amygdala activity was observed during emotional empathy, indicating disturbed emotional processing. 59 However, fibromyalgia, which most closely resembles somatoform pain disorders in many aspects, displays a characteristic connectivity pattern during rest, as recently shown by Cifre and colleagues.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Functional network connectivity of pain-related resting state networks in somatoform pain disorder: an exploratory fMRI study

Otti

Guendel

Henningsen

et al. 2013

J Psychiatry Neurosci

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

“…Given the high comorbidity of somatoform pain with affective disorders 61 and their influence on brain function, 58,62 depressive symptoms may have influenced our results. Several studies have indicated an important role of functional connectivity in depressive symptoms.…”

Section: Limitationsmentioning

confidence: 99%

Functional network connectivity of pain-related resting state networks in somatoform pain disorder: an exploratory fMRI study

Otti

Guendel

Henningsen

et al. 2013

J Psychiatry Neurosci

View full text Add to dashboard Cite

“…Many studies have found parahippocampal activation in response to pain (22), where it is believed to mediate the aversive drive and contribute to the negative affect inherent to pain. Interestingly, parahippocampal responses to pain are shown to be increased by anxiety in healthy volunteers (13), as well as in clinical populations suffering from anxiety-related pain disorders (23).…”

Section: Discussionmentioning

confidence: 99%

Cerebral and spinal modulation of pain by emotions

Roy

Piché

Chen

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

221

View full text Add to dashboard Cite

Emotions have powerful effects on pain perception. However, the brain mechanisms underlying these effects remain largely unknown. In this study, we combined functional cerebral imaging with psychophysiological methods to explore the neural mechanisms involved in the emotional modulation of spinal nociceptive responses (RIII-reflex) and pain perception in healthy participants. Emotions induced by pleasant or unpleasant pictures modulated the responses to painful electrical stimulations in the right insula, paracentral lobule, parahippocampal gyrus, thalamus, and amygdala. Right insula activation covaried with the modulation of pain perception, consistent with a key role of this structure in the integration of pain signals with the ongoing emotion. In contrast, activity in the thalamus, amygdala, and several prefrontal areas was associated with the modulation of spinal reflex responses. Last, connectivity analyses suggested an involvement of prefrontal, parahippocampal, and brainstem structures in the cerebral and cerebrospinal modulation of pain by emotions. This multiplicity of mechanisms underlying the emotional modulation of pain is reflective of the strong interrelations between pain and emotions, and emphasizes the powerful effects that emotions can have on pain. Descending pain-modulatory pathways originate from various cerebral structures involved in emotions (6-8) and sensorimotor functions (9). These regions are thought to affect spinal nociception through their projections to several brainstem structures, including the periaqueductal gray matter (PAG), rostroventral medulla (RVM), dorsolateral pontine tegmentum (DLPT), and nucleus cuneiformis (NCF) (10). All of these structures are thus potential cerebral sources of the descending modulation of pain by emotions. In turn, the modulation of spinal activity is expected to affect the transmission of nociceptive signals and the response of their target brain regions through the multiple ascending pathways. However, the important interconnectivity between emotional brain networks and areas implicated in the affective dimension of pain suggests that additional supraspinal mechanisms might also contribute to the emotional modulation of pain experiences. Among the potential cortical candidates, the anterior cingulate cortex (ACC) (11) and the insula (12) are well positioned to contribute to the emotional modulation of pain.Whereas the ACC appears to be involved in the motoric and motivational aspects of pain and emotions, the insula is thought to generate subjective interoceptive feelings as a result of the gradual posterior-to-anterior integration of primary interoceptive information with contextual emotional and cognitive information (12).The cerebral correlates of the emotional modulation of pain perception have been explored in two brain imaging studies. In one study, pain-related activation in the entorhinal cortex was increased by expectation-induced anticipatory anxiety of a highly painful stimulation (13). Also, the increased activation in the entorhinal...

show abstract

“…Even if cortical pain pathways are well explored, there are surprisingly few neuroimaging studies that directly address the influence of emotions on pain. Studies employing functional magnetic resonance imaging have revealed that the entorhinal cortex of the left hippocampal formation, the perigenual cingulate cortex and the mid-insula show increased activity when painful stimulation was administered after induction of negative emotions [23], and these regions amplify pain experience in chronic pain patients with depression [24,25]. Trait-like individual differences in pain-related fear might also have an impact on neural processing of pain.…”

Section: The Neurobiology Of Emotional Modulation Of Painmentioning

confidence: 99%

The relation of emotions to placebo responses

Flaten

Aslaksen

Lyby

et al. 2011

Phil. Trans. R. Soc. B

123

View full text Add to dashboard Cite

The hypothesis put forth is that expectations of treatment effects reduce negative emotions and thereby reduce symptoms, e.g. pain. Negative emotions increase pain, and it is hypothesized that placebos reduce pain by reducing negative emotions, i.e. feelings of nervousness, fear and anxiety. Placebo analgesia has been shown to be mediated via opioid activity, and relaxation increases opioid activity. The placebo acquires its relaxing effect due to verbal information that pain will be reduced, or due to associations between the placebo and the reduction in pain after effective treatment. Thus, the placebo signals that unpleasantness will be less after administration of the placebo. This involves negative reinforcement which is due to activation of a dopaminergic system that has been found to be activated during placebo analgesia and is involved in positive emotions. The nocebo effect of increased pain is, consistent with this model, because of increased fear and anxiety. The new aspect of the presented model is the hypothesis that expectations reduce negative emotions, and that negative reinforcement that involves the dopaminergic reinforcement system should be a contributor to placebo responses.

show abstract

Altered cerebral response to noxious heat stimulation in patients with somatoform pain disorder

Cited by 133 publications

References 51 publications

Functional network connectivity of pain-related resting state networks in somatoform pain disorder: an exploratory fMRI study

Functional network connectivity of pain-related resting state networks in somatoform pain disorder: an exploratory fMRI study

Cerebral and spinal modulation of pain by emotions

The relation of emotions to placebo responses

Contact Info

Product

Resources

About