Pain Perception in Schizophrenia: Evidence of a Specific Pain Response Profile

Lévesque, M.; Potvin, Stéphane; Marchand, Serge; Stip, Émmanuel; Grignon, Sylvain; Lalonde, Pierre; Lipp, Olivier; Goffaux, Philippe

doi:10.1111/j.1526-4637.2012.01505.x

Cited by 46 publications

(39 citation statements)

References 44 publications

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“…Additionally, de la Fuente‐Sandoval et al ()) observed that drug‐naïve SCZ patients had a higher pain tolerance and a reduced activation in brain regions related to affective‐cognitive aspects of pain processing (insula and cingulate cortex) to thermal painful stimuli than HC. This pain insensitivity in SCZ patients was normally explained by a supra‐spinal mechanism involving bottom‐up and/or top‐down modulations in previous studies (de la Fuente‐Sandoval et al, ; Levesque et al, ; Potvin et al, ). For example, Levesque et al () observed that SCZ patients had a decreased sensitivity to prolonged pain, which was not accompanied by any difference in the nociceptive flexion reflex response.…”

Section: Discussionmentioning

confidence: 71%

“…This pain insensitivity in SCZ patients was normally explained by a supra‐spinal mechanism involving bottom‐up and/or top‐down modulations in previous studies (de la Fuente‐Sandoval et al, ; Levesque et al, ; Potvin et al, ). For example, Levesque et al () observed that SCZ patients had a decreased sensitivity to prolonged pain, which was not accompanied by any difference in the nociceptive flexion reflex response. To achieve better understandings of the supra‐spinal mechanism, we performed seed‐based RSFC analyses for thalamus and PAG, which are key nodes in the ascending and descending pain modulation pathways respectively.…”

Section: Discussionmentioning

confidence: 71%

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A modality‐specific dysfunction of pain processing in schizophrenia

Zhou

Liang

et al. 2019

Human Brain Mapping

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Clinical observations showed that schizophrenia (SCZ) patients reported little or no pain under various conditions that are commonly associated with intense painful sensations, leading to a higher risk of morbidity and mortality. However, this phenomenon has received little attention and its underlying neural mechanisms remain unclear. Here, we conducted two experiments combining psychophysics, electroencephalography (EEG), and functional magnetic resonance imaging (fMRI) techniques to investigate neural mechanisms of pain insensitivity in SCZ patients. Specifically, we adopted a stimulus–response paradigm with brief stimuli of different sensory modalities (i.e., nociceptive, non‐nociceptive somatosensory, and auditory) to test whether pain insensitivity in SCZ patients is supra‐modal or modality‐specific, and used EEG and fMRI techniques to clarify its neural mechanisms. We observed that perceived intensities to nociceptive stimuli were significantly smaller in SCZ patients than healthy controls, whereas perceived intensities to non‐nociceptive somatosensory and auditory stimuli were not significantly different. The behavioral results were confirmed by stimulus‐evoked brain responses sampled by EEG and fMRI techniques, thus verifying the modality‐specific nature of the modulation of nociceptive information processing in SCZ patients. Additionally, significant group differences were observed in the spectral power of alpha oscillations in prestimulus EEG and the seed‐based functional connectivity in resting‐state fMRI (seeds: the thalamus and periaqueductal gray that are key nodes in ascending and descending pain pathways respectively), suggesting a possible contribution of cortical–subcortical dysfunction to the phenomenon. Overall, our study provides insight into the neural mechanisms of pain insensitivity in SCZ and highlights a need for systematic assessments of their pain‐related diseases.

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Section: Discussionmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 71%

A modality‐specific dysfunction of pain processing in schizophrenia

Zhou

Liang

et al. 2019

Human Brain Mapping

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“…Alterations in PUFA levels, therefore, could have wide-ranging effects both on neural functioning, inflammation, and any connections between the two. Abnormal pain reporting in schizophrenia has long been noted (Bonnot et al, 2009; Levesque et al, 2012), and eicosanoids could also be relevant in that domain. Interestingly, low levels of PUFAs in schizophrenia patients have been associated with negative symptoms (Bentsen et al, 2011; Bentsen et al, 2012), positive symptoms (Sumiyoshi et al, 2008), and poor cognition (Condray et al, 2008; Condray and Yao, 2011), indicating that they may be associated with pathology.…”

Section: Mechanismsmentioning

confidence: 99%

Inflammation and the two-hit hypothesis of schizophrenia

Feigenson

Kusnecov

Silverstein

2014

Neuroscience & Biobehavioral Reviews

234

174

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The high societal and individual cost of schizophrenia necessitates finding better, more effective treatment, diagnosis, and prevention strategies. One of the obstacles in this endeavor is the diverse set of etiologies that comprises schizophrenia. A substantial body of evidence has grown over the last few decades to suggest that schizophrenia is a heterogeneous syndrome with overlapping symptoms and etiologies. At the same time, an increasing number of clinical, epidemiological, and experimental studies have shown links between schizophrenia and inflammatory conditions. In this review, we analyze the literature on inflammation and schizophrenia, with a particular focus on comorbidity, biomarkers, and environmental insults. We then identify several mechanisms by which inflammation could influence the development of schizophrenia via the two-hit hypothesis. Lastly, we note the relevance of these findings to clinical applications in the diagnosis, prevention, and treatment of schizophrenia.

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“…In line with a previous metaanalysis [43], we examined the funnel plot of the composite outcome searching for extreme outliers and removed from the database and all analyses one extreme publication bias outlier [39]. Across the resultant sample of 17 studies, we first conducted a composite analysis pooling aggregated pain measure data on pain threshold, pain tolerance and sensory threshold together from all studies to establish an overall difference in pain sensitivity.…”

Section: Meta-analysismentioning

confidence: 99%

Decreased pain sensitivity among people with schizophrenia

Stubbs

Thompson

Acaster³

et al. 2015

Pain

105

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Schizophrenia patients report reduced pain sensitivity in clinical studies, but experimental studies are required to establish pain sensitivity as a potential endophenotype. We conducted a systematic review of electronic databases from database inception until 15/04/2015, including experimental studies investigating pain among schizophrenia-spectrum disorder patients versus healthy controls.A random effect meta-analysis yielding Hedges' g ±95% confidence intervals (CIs) as the effect size measure (ES) was conducted. Primary outcome was a pooled composite of pain threshold, pain tolerance, and sensory threshold; secondary outcomes included these parameters individually, plus physiological pain response, and pain intensity/unpleasantness. Across 17 studies, schizophreniaspectrum disorder patients (n=387, age=30.7±6.9 years, female=31.9%, illness duration=7.0±5.7 years) were compared with controls (n=483, age=29.5±7.4 years, female=31.0%). Patients had elevated pain threshold/pain tolerance/sensory threshold versus controls (ES=0.493, 95% CI=0.145-0.839, p=0.005; studies=17). Results were similar in antipsychotic-free individuals (ES=0.599, 95% CI=0.291-0.907, p<0.0001; studies=8), with trend-level significance in antipsychotic-treated individuals (ES=0.428, p=0.085; studies=11 spectrum disorders. How this alteration links to other dimensions of schizophrenia and physical comorbidity-related help-seeking behaviour/morbidity/mortality requires further study. schizophrenia, pain, experimental pain, physical health, pain assessment, pain management 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 Dr. Correll has been a consultant and/or advisor to or has received honoraria from AbbVie, Actavis, Alkermes, Bristol-Myers Squibb, Eli Lilly, Genentech, Gerson Lehrman Group, IntraCellular Therapies, Janssen/J&J, Lundbeck, MedAvante, Medscape, Otsuka, Pfizer, ProPhase, Reviva, Roche, Sunovion , 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 3 Abstract Schizophrenia patients report reduced pain sensitivity in clinical studies, but experimental studies are required to establish pain sensitivity as a potential endophenotype. We conducted a systematic review of electronic databases from database inception until 15/04/2015, including experimental studies investigating pain among schizophrenia-spectrum disorder patients versus healthy controls. Key words:A random effect meta-analys...

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Pain Perception in Schizophrenia: Evidence of a Specific Pain Response Profile

Abstract: Results indicate that schizophrenic subjects present a specific experimental pain response profile, characterized by elevated sensitivity to acute pain but reduced sensitivity to prolonged pain.

Cited by 46 publications

References 44 publications

A modality‐specific dysfunction of pain processing in schizophrenia

A modality‐specific dysfunction of pain processing in schizophrenia

Inflammation and the two-hit hypothesis of schizophrenia

Decreased pain sensitivity among people with schizophrenia

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