Reviewer's report
Title:The severity of irritable bowel syndrome or the presence of fibromyalgia
influencing the perception of visceral and somatic stimuli
Version:1Date:24 October 2013
Reviewer: mathieu piche
Reviewer's report:
This is an interesting manuscript investigating the interaction between two
sources of chronic pain, namely visceral pain (IBS) and somatic pain (FMS). The
study was generally well conducted and the results are novel and interesting. I
have a few suggestions for the authors to improve the already well-written
manuscript.
Major comments:
1- I appreciate that the goal of the study is to compare different subgroups of
patients with IBS of different severity levels, with or without IBS. This is
accomplished in the study and well reported. However, the lack of a control
group, as acknowledged by the authors, is a serious limitation. To interpret the
results and determine if the study samples show hypersensitivity, it is necessary
to have a control group. As it stands, we don’t know if patients have visceral or
somatic hypersensitivity (as expected) and we can only say that groups are
different. I feel that the study would have much more interest and impact if a
control group of healthy volunteers (approximately 10 participants to match other
groups) were to be included.
2- The pathophysiological link between IBS and FMS is very interesting and
clinically relevant. Yet, little is known about the interactions between both
conditions. The current study provides interesting data in this regard. However,
the hypotheses are not well justified and are not based on a pathophysiological
mechanism. It would improve the manuscript if this information could be added.
This is also true for the discussion.
For instance, in both diseases, it has been shown that primary and secondary
hyperalgesia are maintained by central sensitization, through tonic nociceptive
input from peripheral afferents [1, 2]. In addition, conditioned pain modulation
(pain-inhibit-pain mechanisms - CPM) is decreased in both IBS[3-5] and
FMS[6-8]. Moreover, hyperalgesia is associated with decreased CPM in patients
with IBS[4], which may result from or contribute to central sensitization, and may
predispose to the development of other chronic pain syndromes (e.g IBS leading
to FMS). Another possibility is the contribution of psychological factors to altered
pain processing in both diseases.
On the other hand, somatic pain may inhibit visceral pain and vice-versa, through
CPM. Although CPM is reduced in IBS and FMS, it is one plausible mechanism
that may explain the decreased visceral hypersensitivity in your IBS-FMS group.
The hypothesis for graduated hypersensitivity in regard to severity should also be
provided.
3- FMS patients have not been well characterised. Do you have any measure of
severity for FMS? It would be interesting to know whether FMS patients are also
considered severe cases of FMS or whether the severity of FMS may be
somewhat attenuated by the presence of IBS (although this cannot be compared
with a group with FMS only in this study).
4- The authors confirmed their hypothesis for the effect of FMS on visceral
sensitivity in IBS but not their hypothesis for the graduated somatic sensitivity
across subgroups of IBS. The lack of a relationship between IBS severity and
somatic sensitivity should be confirmed with a correlation analysis and should be
clearly acknowledged throughout the manuscript.
5- In the discussion, a pathophysiological explanation should be provided to
discuss to results (positive and negative ones).
6- To assess sensitivity, discomfort thresholds were used. This is somewhat
difficult to relate to pain thresholds and hyperalgesia. Why discomfort and not
pain and how do you compare this to other studies?
Minor comments:
1- There seems to be a mistake in the abstract, in the last sentence of the
methods. Sensitivity cannot be measured by questionnaires.
2- References aremissing in the introduction (bottom of page 5) when stating the
common characteristics between IBS and FMS.
3- In the introduction (p.6), the details on stimulus location should be provided
when presenting the discrepancies between studies, as this is a potential factor
to be considered.
4- Please provide the method for excluding any organic disease for the diagnosis
of IBS.
5- A reference is missing for the FMS diagnosis (see Error! Bookmark not
defined)
References
1- Verne GN, Robinson ME, Vase L, Price DD. Reversal of visceral and
cutaneous hyperalgesia by local rectal anesthesia in irritable bowel syndrome
(IBS) patients. Pain 2003; 105(1-2): 223-230
2- Staud R, Nagel S, Robinson ME, Price DD. Enhanced central pain processing
of fibromyalgia patients is maintained by muscle afferent input: a randomized,
double-blind, placebo-controlled study. Pain 2009; 145(1-2): 96-104 DOI:
10.1016/j.pain.2009.05.020 PMID: 19540671
3- Wilder-Smith CH, Schindler D, Lovblad K, Redmond SM, Nirkko A. Brain
functional magnetic resonance imaging of rectal pain and activation of
endogenous inhibitory mechanisms in irritable bowel syndrome patient
subgroups and healthy controls. Gut 2004; 53(11): 1595-1601
4- Piché M, Arsenault M, Poitras P, Rainville P, Bouin M. Widespread
hypersensitivity is related to altered pain inhibition processes in irritable bowel
syndrome. Pain 2010; 148(1): 49-58
5- Piché M, Bouin M, Arsenault M, Poitras P, Rainville P. Decreased pain
inhibition in irritable bowel syndrome depends on altered descending modulation
and higher-order brain processes. Neuroscience 2011; 195: 166-175 DOI:
S0306-4522(11)00982-1 [pii];10.1016/j.neuroscience.2011.08.040 [doi]
6- Kosek E, Hansson P. Modulatory influence on somatosensory perception from
vibration and heterotopic noxious conditioning stimulation (HNCS) in fibromyalgia
patients and healthy subjects. Pain 1997; 70(1): 41-51
7- Lautenbacher S, Rollman GB. Possible deficiencies of pain modulation in
fibromyalgia. ClinJ Pain 1997; 13(3): 189-196
8- Julien N, Goffaux P, Arsenault P, Marchand S. Widespread pain in
fibromyalgia is related to a deficit of endogenous pain inhibition. Pain 2005;
114(1-2): 295-302
Level of interest: An article of importance in its field
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a statistician.
Declaration of competing interests:
I declare that I have no competing interests.
Reviewer's report
Title:The severity of irritable bowel syndrome or the presence of fibromyalgia
influencing the perception of visceral and somatic stimuli
Version:1Date:24 October 2013
Reviewer: mathieu piche
Reviewer's report:
This is an interesting manuscript investigating the interaction between two
sources of chronic pain, namely visceral pain (IBS) and somatic pain (FMS). The
study was generally well conducted and the results are novel and interesting. I
have a few suggestions for the authors to improve the already well-written
manuscript.
Major comments:
1- I appreciate that the goal of the study is to compare different subgroups of
patients with IBS of different severity levels, with or without IBS. This is
accomplished in the study and well reported. However, the lack of a control
group, as acknowledged by the authors, is a serious limitation. To interpret the
results and determine if the study samples show hypersensitivity, it is necessary
to have a control group. As it stands, we don’t know if patients have visceral or
somatic hypersensitivity (as expected) and we can only say that groups are
different. I feel that the study would have much more interest and impact if a
control group of healthy volunteers (approximately 10 participants to match other
groups) were to be included.
2- The pathophysiological link between IBS and FMS is very interesting and
clinically relevant. Yet, little is known about the interactions between both
conditions. The current study provides interesting data in this regard. However,
the hypotheses are not well justified and are not based on a pathophysiological
mechanism. It would improve the manuscript if this information could be added.
This is also true for the discussion.
For instance, in both diseases, it has been shown that primary and secondary
hyperalgesia are maintained by central sensitization, through tonic nociceptive
input from peripheral afferents [1, 2]. In addition, conditioned pain modulation
(pain-inhibit-pain mechanisms - CPM) is decreased in both IBS[3-5] and
FMS[6-8]. Moreover, hyperalgesia is associated with decreased CPM in patients
with IBS[4], which may result from or contribute to central sensitization, and may
predispose to the development of other chronic pain syndromes (e.g IBS leading
to FMS). Another possibility is the contribution of psychological factors to altered
pain processing in both diseases.
On the other hand, somatic pain may inhibit visceral pain and vice-versa, through
CPM. Although CPM is reduced in IBS and FMS, it is one plausible mechanism
that may explain the decreased visceral hypersensitivity in your IBS-FMS group.
The hypothesis for graduated hypersensitivity in regard to severity should also be
provided.
3- FMS patients have not been well characterised. Do you have any measure of
severity for FMS? It would be interesting to know whether FMS patients are also
considered severe cases of FMS or whether the severity of FMS may be
somewhat attenuated by the presence of IBS (although this cannot be compared
with a group with FMS only in this study).
4- The authors confirmed their hypothesis for the effect of FMS on visceral
sensitivity in IBS but not their hypothesis for the graduated somatic sensitivity
across subgroups of IBS. The lack of a relationship between IBS severity and
somatic sensitivity should be confirmed with a correlation analysis and should be
clearly acknowledged throughout the manuscript.
5- In the discussion, a pathophysiological explanation should be provided to
discuss to results (positive and negative ones).
6- To assess sensitivity, discomfort thresholds were used. This is somewhat
difficult to relate to pain thresholds and hyperalgesia. Why discomfort and not
pain and how do you compare this to other studies?
Minor comments:
1- There seems to be a mistake in the abstract, in the last sentence of the
methods. Sensitivity cannot be measured by questionnaires.
2- References aremissing in the introduction (bottom of page 5) when stating the
common characteristics between IBS and FMS.
3- In the introduction (p.6), the details on stimulus location should be provided
when presenting the discrepancies between studies, as this is a potential factor
to be considered.
4- Please provide the method for excluding any organic disease for the diagnosis
of IBS.
5- A reference is missing for the FMS diagnosis (see Error! Bookmark not
defined)
References
1- Verne GN, Robinson ME, Vase L, Price DD. Reversal of visceral and
cutaneous hyperalgesia by local rectal anesthesia in irritable bowel syndrome
(IBS) patients. Pain 2003; 105(1-2): 223-230
2- Staud R, Nagel S, Robinson ME, Price DD. Enhanced central pain processing
of fibromyalgia patients is maintained by muscle afferent input: a randomized,
double-blind, placebo-controlled study. Pain 2009; 145(1-2): 96-104 DOI:
10.1016/j.pain.2009.05.020 PMID: 19540671
3- Wilder-Smith CH, Schindler D, Lovblad K, Redmond SM, Nirkko A. Brain
functional magnetic resonance imaging of rectal pain and activation of
endogenous inhibitory mechanisms in irritable bowel syndrome patient
subgroups and healthy controls. Gut 2004; 53(11): 1595-1601
4- Piché M, Arsenault M, Poitras P, Rainville P, Bouin M. Widespread
hypersensitivity is related to altered pain inhibition processes in irritable bowel
syndrome. Pain 2010; 148(1): 49-58
5- Piché M, Bouin M, Arsenault M, Poitras P, Rainville P. Decreased pain
inhibition in irritable bowel syndrome depends on altered descending modulation
and higher-order brain processes. Neuroscience 2011; 195: 166-175 DOI:
S0306-4522(11)00982-1 [pii];10.1016/j.neuroscience.2011.08.040 [doi]
6- Kosek E, Hansson P. Modulatory influence on somatosensory perception from
vibration and heterotopic noxious conditioning stimulation (HNCS) in fibromyalgia
patients and healthy subjects. Pain 1997; 70(1): 41-51
7- Lautenbacher S, Rollman GB. Possible deficiencies of pain modulation in
fibromyalgia. ClinJ Pain 1997; 13(3): 189-196
8- Julien N, Goffaux P, Arsenault P, Marchand S. Widespread pain in
fibromyalgia is related to a deficit of endogenous pain inhibition. Pain 2005;
114(1-2): 295-302
Level of interest: An article of importance in its field
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a statistician.
Declaration of competing interests:
I declare that I have no competing interests.
Please review this paper.
user
Reviewer's report
Title:The severity of irritable bowel syndrome or the presence of fibromyalgia
influencing the perception of visceral and somatic stimuli
Version:1Date:24 October 2013
Reviewer: mathieu piche
Reviewer's report:
This is an interesting manuscript investigating the interaction between two
sources of chronic pain, namely visceral pain (IBS) and somatic pain (FMS). The
study was generally well conducted and the results are novel and interesting. I
have a few suggestions for the authors to improve the already well-written
manuscript.
Major comments:
1- I appreciate that the goal of the study is to compare different subgroups of
patients with IBS of different severity levels, with or without IBS. This is
accomplished in the study and well reported. However, the lack of a control
group, as acknowledged by the authors, is a serious limitation. To interpret the
results and determine if the study samples show hypersensitivity, it is necessary
to have a control group. As it stands, we don’t know if patients have visceral or
somatic hypersensitivity (as expected) and we can only say that groups are
different. I feel that the study would have much more interest and impact if a
control group of healthy volunteers (approximately 10 participants to match other
groups) were to be included.
2- The pathophysiological link between IBS and FMS is very interesting and
clinically relevant. Yet, little is known about the interactions between both
conditions. The current study provides interesting data in this regard. However,
the hypotheses are not well justified and are not based on a pathophysiological
mechanism. It would improve the manuscript if this information could be added.
This is also true for the discussion.
For instance, in both diseases, it has been shown that primary and secondary
hyperalgesia are maintained by central sensitization, through tonic nociceptive
input from peripheral afferents [1, 2]. In addition, conditioned pain modulation
(pain-inhibit-pain mechanisms - CPM) is decreased in both IBS[3-5] and
FMS[6-8]. Moreover, hyperalgesia is associated with decreased CPM in patients
with IBS[4], which may result from or contribute to central sensitization, and may
predispose to the development of other chronic pain syndromes (e.g IBS leading
to FMS). Another possibility is the contribution of psychological factors to altered
pain processing in both diseases.
On the other hand, somatic pain may inhibit visceral pain and vice-versa, through
CPM. Although CPM is reduced in IBS and FMS, it is one plausible mechanism
that may explain the decreased visceral hypersensitivity in your IBS-FMS group.
The hypothesis for graduated hypersensitivity in regard to severity should also be
provided.
3- FMS patients have not been well characterised. Do you have any measure of
severity for FMS? It would be interesting to know whether FMS patients are also
considered severe cases of FMS or whether the severity of FMS may be
somewhat attenuated by the presence of IBS (although this cannot be compared
with a group with FMS only in this study).
4- The authors confirmed their hypothesis for the effect of FMS on visceral
sensitivity in IBS but not their hypothesis for the graduated somatic sensitivity
across subgroups of IBS. The lack of a relationship between IBS severity and
somatic sensitivity should be confirmed with a correlation analysis and should be
clearly acknowledged throughout the manuscript.
5- In the discussion, a pathophysiological explanation should be provided to
discuss to results (positive and negative ones).
6- To assess sensitivity, discomfort thresholds were used. This is somewhat
difficult to relate to pain thresholds and hyperalgesia. Why discomfort and not
pain and how do you compare this to other studies?
Minor comments:
1- There seems to be a mistake in the abstract, in the last sentence of the
methods. Sensitivity cannot be measured by questionnaires.
2- References aremissing in the introduction (bottom of page 5) when stating the
common characteristics between IBS and FMS.
3- In the introduction (p.6), the details on stimulus location should be provided
when presenting the discrepancies between studies, as this is a potential factor
to be considered.
4- Please provide the method for excluding any organic disease for the diagnosis
of IBS.
5- A reference is missing for the FMS diagnosis (see Error! Bookmark not
defined)
References
1- Verne GN, Robinson ME, Vase L, Price DD. Reversal of visceral and
cutaneous hyperalgesia by local rectal anesthesia in irritable bowel syndrome
(IBS) patients. Pain 2003; 105(1-2): 223-230
2- Staud R, Nagel S, Robinson ME, Price DD. Enhanced central pain processing
of fibromyalgia patients is maintained by muscle afferent input: a randomized,
double-blind, placebo-controlled study. Pain 2009; 145(1-2): 96-104 DOI:
10.1016/j.pain.2009.05.020 PMID: 19540671
3- Wilder-Smith CH, Schindler D, Lovblad K, Redmond SM, Nirkko A. Brain
functional magnetic resonance imaging of rectal pain and activation of
endogenous inhibitory mechanisms in irritable bowel syndrome patient
subgroups and healthy controls. Gut 2004; 53(11): 1595-1601
4- Piché M, Arsenault M, Poitras P, Rainville P, Bouin M. Widespread
hypersensitivity is related to altered pain inhibition processes in irritable bowel
syndrome. Pain 2010; 148(1): 49-58
5- Piché M, Bouin M, Arsenault M, Poitras P, Rainville P. Decreased pain
inhibition in irritable bowel syndrome depends on altered descending modulation
and higher-order brain processes. Neuroscience 2011; 195: 166-175 DOI:
S0306-4522(11)00982-1 [pii];10.1016/j.neuroscience.2011.08.040 [doi]
6- Kosek E, Hansson P. Modulatory influence on somatosensory perception from
vibration and heterotopic noxious conditioning stimulation (HNCS) in fibromyalgia
patients and healthy subjects. Pain 1997; 70(1): 41-51
7- Lautenbacher S, Rollman GB. Possible deficiencies of pain modulation in
fibromyalgia. ClinJ Pain 1997; 13(3): 189-196
8- Julien N, Goffaux P, Arsenault P, Marchand S. Widespread pain in
fibromyalgia is related to a deficit of endogenous pain inhibition. Pain 2005;
114(1-2): 295-302
Level of interest: An article of importance in its field
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a statistician.
Declaration of competing interests:
I declare that I have no competing interests.
assistant