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Re: Complex Regional Pain Syndrome
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Re: Complex Regional Pain Syndrome - June 14, 2005 4:48:00 AM
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Yogi
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Rick, yep, if anyone knew a treatment resolution for stage 3 CPRS they could charge a bundle, cause folks would pay whatever they had.
Anyone one able to try mirroring, please report here.
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Re: Complex Regional Pain Syndrome - June 14, 2005 5:08:00 AM
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Diane
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From: Vancouver, B.C., Canada
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Lorimer Moseley's current research is finding that pain education is a single factor that bumps up favorable longterm outcome measures (after a year) in chronic persistant pain patients by 60%, which is huge. No one has mentioned this yet, how education about pain is a tool in and of itself. Sorry I don't have a link, but I'm sure it is likely on pubmed somewhere if his paper is finished.
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Re: Complex Regional Pain Syndrome - June 14, 2005 6:16:00 AM
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JLS_PT_OCS
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Nari, don't be so quick to assume no one took notice of your mirror comment... I for one did.
Diane,
Interesting point about education. We have been toying with the idea of adding a chronic pain management education class to our repertoire of offerings. Hopefully if my "Clinical Neurodynamics" text ever arrives, that might shed some light as well.
It has been my experience with CRPS that the usual therapy measures such as forced use/WB, contrast baths, "desensitization training" etc seem cruel and to be exacerbating a painful response. I can't figure out why that's supposed to help. I don't currently have a CRPS patient to try the mirrors on, but I definitely will, as I think my current regimen of things (which if I think about it, are simply torture cast as therapy) are wrongheaded.
I don't think anyone has any actual techniques with any outcomes research behind them. Given how infrequently this occurs, it's not surprising.
But I will look more closely at the chronic pain education class, that's for sure.
Diane, do you know what kind of material was covered in the class? Or if there is some super easy powerpoint presentation I could download from somewhere that eliminates any possible work on my part? :)
J
_____________________________
Jason Silvernail DPT, OCS, CSCS
"It isn't what you're able to do that requires your courage but rather what you have come to understand and are willing to express." - Barrett Dorko,PT
**I no longer post on RehabEdge**
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Re: Complex Regional Pain Syndrome - June 14, 2005 6:20:00 AM
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Geert Jeuring
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Hello Rick, I´m not certain why the stage in this case matters. The only way to get a function back is training (specific adaptation on imposed demand). I think even after two years the tissue hasn´t lost it´s adaptive capacity. Alternative treatments can of course distract the person from the pain, and that can be used in trainingtherapy. I still think the training should be combined with analgetic measures. Although I can´t back this specific statement up with studies,but it is a process succesfull with other chronic painpatients. And none the less, it is the road less taken. In the last years I´ve often, in therapy, succesfully took the road less taken and based this decision on logic induction. It mostly resulted in Patients with more activity and was later on backed up by more recent literature.
Geert
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Re: Complex Regional Pain Syndrome - June 23, 2005 8:51:00 AM
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rickpt
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Geert,
I must disagree. Stage is everything. Although I have no clinical studies to back this opinion up, from my observations the tissues adapt to a cycle of intermittent edema, hyperhydrosis, hyperpigmentation, nail changes, allodynia, etc. Any attempt to have contact with the tissues creates flare-up. For gods sake, the anesthesiologist I work with has told me that in his history of working with this condition the leading cause of death is suicide.
How can you progressively weight bear with someone who is in tears because the sleeve of thier shirt is touching them or a slight breeze causes burning pain on the skin?
Mild edema, mild hyperhydrosis, mild skin changes, combined with severe protecting the extremity and excessive/active concentrating on the pain - these are the stages present in the acute phase. Only at this point will we have an effect on the ability to change the tissue because it has not yet entered a new stage. Only at this stage will desensitization and progressive weight bearing techniques work.
Beyond this time, as the patients' kenisiophobia increases, a new stage that is neurologically reinforced begins. Tissue changes occur in what appears to be a random pattern, i.e., present even though the patient "didn't do anything." As mentioned in the existing lterature, this reiforcement of tissue changes occur as a result of sympathetic nervous system dominance.
It is my opinion, because we will be unable to address the tissue from the outside in we must look from the inside out. We must use biofeedback, or any other modality (?) that adresses balancing parasympatheitic and sympathetic activity.
Currently, I am working with one of these patients and attempting the mirror therapy suggested (thanks Nari). Alas, mirror therapy is flaring this person up. They are not even moving the involved arm and I can witness color changes and increasing edema!
Anyone reading this, please help. In our chronic pain clinic all our patients get 1 hour education 5 days/week for 1 month adressing coping with chronic pain (thanks for the suggestion Diane - already doing it). They also have at least 1/2 hour to 45 minutes 5 days/week of biofeedback or relaxation therapy. Other than those two therapies, nothing is helping. The lightest desensitization is agonizing.
Rick
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Re: Complex Regional Pain Syndrome - June 23, 2005 9:43:00 AM
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Jon Newman
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From: Amherst, WI
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Rick,
If you have not already, consider seeing Diane's recent find of [URL=http://www.painonline.com]www.painonline.com[/URL]
While this may not give you specific treatment ideas as it pertains to a distinct thing you do to this person, it may give you ideas of what to expect or how to be around this person. I'm still reading through it and can't help but feel simultaneously grateful and helpless.
jon
_____________________________
[URL=http://www.sonymusic.com/clips/selection/30/064887/064887_03_03_30.wav]Evidence[/URL]
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Re: Complex Regional Pain Syndrome - June 23, 2005 10:03:00 AM
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Diane
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From: Vancouver, B.C., Canada
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Rick, second Jon's motion of checking out the blog he mentions above. It has filled in many gaps for me. Jason, there IS a power point presentation... Nari posted it on another forum that is not linkable from this one... (I don't know why not..)
Here is the [URL=http://www.westmeadanaesthesia.org/meetings/pain-physiology/Pain%20Physiology_files/error.htm]link to power point presentation on pain.[/URL] You have to use internet explorer to see it.
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Re: Complex Regional Pain Syndrome - July 7, 2005 7:34:00 AM
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lesain
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From: MERCEDES, BUENOS AIRES, ARGENTINA
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Nari, I use the mirror therapy and I had an excellent results, the patient tell me that she can move the affected arm since used the mirror because before she had it forgotten, the pain relief. Also I used contrast bath, Kaltenborn, weight bearing, active stretching, trigger point.
Thanks to all, since I entered to the forum I have more therapy alternatives.
Leandro
_____________________________
LEANDRO ESAIN, PT.
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Re: Complex Regional Pain Syndrome - July 7, 2005 8:19:00 AM
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Yogi
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Jason, dang, agree again, the usual CRPS treatments have seemed cruel to me, too. Especially without any evidence of efficacy. The treatments you mentioned I had read were effective for prevention, and in the first stage. Nothing was offered in the latter stages, and I think people just tried them because they didn't know about the stages.
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Re: Complex Regional Pain Syndrome - July 7, 2005 9:00:00 AM
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JLS_PT_OCS
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From: USA
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Diane-
Can't get to the presentation, but thanks for trying!
I am trying to develop one myself in the meantime...
I think for CRPS, the first stage treatments we can all agree on, it's what to do in later stages that is the trick.
J
_____________________________
Jason Silvernail DPT, OCS, CSCS
"It isn't what you're able to do that requires your courage but rather what you have come to understand and are willing to express." - Barrett Dorko,PT
**I no longer post on RehabEdge**
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Re: Complex Regional Pain Syndrome - July 7, 2005 11:22:00 AM
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Randy Dixon
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While I was driving this morning and listening to NPR I heard an interesting bit about active MRI and how they are able to show which parts of the brain are active when a patient is experiencing pain, in real time.
I didn't catch it all, between yelling at tailgaters (very effective) and trying to explain to my daughter where boogers come from, I missed some. One of the things I found interesting was that the primary practical use that the researcher found was the use of this tool as a biofeedback metric.
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Re: Complex Regional Pain Syndrome - July 7, 2005 1:32:00 PM
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nari
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I have not looked at this thread for a while - life is a bit scatty at present - and I heartily agree with what Jason and Yogi are saying; forcing anything on sensitised tissues seems quite cruel.
Leandro, keep trying with mirror therapy on chronic dysfunctional conditions, I think it has great implications for our practice.
When one thinks of the tissues as a grease fire (took a while to work out what a grease fire actually IS) or a critical state of some kind where allodynia is a raging fire, I think our best option is to trick the brain into thinking everything is OK - ie, mirrors. All that will happen in forced treatment, such as cycling and increasing WB and so on, is that the brain will continue to believe there is danger to its organism and pour on the pain...
Rick, some people just do not respond according to expectations, and that is discouraging to say the least, but I think it indicates we all need to understand more about the brain's functioning and the multitude of factors that modulate pain.
Randy - what is a booger???
Nari
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Re: Complex Regional Pain Syndrome - July 7, 2005 2:12:00 PM
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pablo w
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Leandro,
Los espejos pueden ser milagrosos.
I am in the process of summarising some relevant research on CRPS. I don't have the whole document with me at the moment, but will try to post more later.
Here is some of it:
Brain processing during mechanical hyperalgesia in complex regional pain syndrome: a functional MRI study. Mihofner, C; Forster, C; Birklein, F; Neundorfer, B; Handwerker, H. Pain 114 (2005) 93-103
12 patients with hyperalgesia to pinprick.
Von-Frey filaments used to elicit hyperalgesia, other side used as control side.
Mechanical stimulation of unaffected arm was:
non painful
primarily led to activation of S1 (primary somatosensory cortex) on the contralateral side, insula, and bilateral S2 (secondary somatosensory cortex).
Mechanical stimulation of the affected arm led to:
A significant increase in activation of S1 (contralateral)
Increase in activation of S2 (bilateral)
Associative-somatosensory cortex (contralateral)
Frontal cortices
Parts of the anterior cingulate cortex.
This indicates a complex cortical network activated during pin-prick hyperalgesia in CRPS.
The underlying neuronal matrix comprises areas not only involved in nociceptive, but also in cognitive and motor processing.
Patterns of cortical reorganisation in complex regional pain syndrome. Maihofner, C; Handwerker, H; Neundorfer, B; Birklein, F. Neurology 61(12) December 23, 2003.
Magnetoencephalography used to assess possible cortical reorganisation in S1 of patients with CRPS 1 affecting the upper limb.
12 patients
relatively short duration of symptoms (14.8 +/- 10.6 weeks), untreated (except for physical therapy and NSAIDs) at the time of investigation.
explored changes in cortical representation of digits 1 and 5 in relation to the lower lip on the unaffected vs the affected side, using a tactile stimulator.
Sensory testing revealed no symptoms associated with segmental or peripheral nerve territories. Nine patients had pinprick hyperalgesia elicited with von Frey filament (diameter 0.8mm, applying 200Nm of force)
Significant shrinkage found to the extension of the cortical hand representation for the affected side. The center of the hand shifted towards the cortical representation of the lip. This is in contrast to previous studies of healthy subjects during experimental pain or after training paradigms, in which the cortical representation expands.
Attention to the affected limb is unlikely to be the cause of reorganisation.
The best predictor for the plastic cortical changes was the degree of mechanical hyperalgesia, and also correlated well with the amount of reported pain using the McGill questionnaire.
There was no correlation with other clinical symptoms such as pain during movement, impairment of hand function, or autonomic symptoms, or duration of CRPS. The cortical reorganisation may correlate with non-segmental sensory changes reported.
Conclusion: The study showed reorganisation of S1 contralateral to the affected side, and the reorganisation appeared linked to complaints of neuropathic pain.
Cortical reorganisation is not limited to CRPS, as there is evidence that it occurs in other painful conditions (eg focal hand dystonia, chronic low back pain, phantom pain).
Tissue hypoxia in complex regional pain syndrome. Koban, M; Leis, S; Schultze-Mosgau, S; Birklein, F. Pain 104 (2003) 149-157.
19 patients meeting the criteria for CRPS 1 or 2, IASP diagnostic criteria, (1995):
1. 1. Preceding noxious event without (CRPS 1) or with nerve lesion (CRPS 2)
2. 2. Spontaneous pain or hyperalgesia not limited to a single nerve territory or disproportionate to the inciting event.
3. 3. Evidence of oedema, skin blood flow (temperature) or sudomotor abnormality in the distal part of the affected limb.
4. 4. Other diagnoses were excluded.
Patients limited to those with upper limb symptoms.
Control group consisted of healthy volunteers, and also a group of patients who underwent surgery for squamous epithelial carcinoma, in order to establish the effect of oedema on tissue oxygenation.
Measurement was capillary hamoglobin oxygenation (HbO2) using a non-invasive method. Meaurememts were taken at rest and follwoing recative hyperaemia (after inflating a cuff around the arm to suprasystolic pressure for 2 minutes).
No differences were found between sides in healthy controls.
Significant differences present between controls and patients, and between sides on patients (at rest). In the post surgery control group, there were no significant differences before and after surgery.
There was no significant correlation between temperature change and HbO2 values, or with duration of symptoms.
During application of the cuff, oxygenation dropped in all groups, and increased steeply after deflation. Following this there was no longer a significant difference between subjects’ unaffected side and controls, however there was a significant difference with the affected side.
Conclusion: Tissue hypoxia may be a significant factor in the development of chronic CRPS signs and symptoms, and appears early on. This may occur despite evidence of increased oxygenation at a more global level reported in other studies referenced.
Reflex Sympathetic Dystrophy: Early Treatment and Psychological Aspects. Geertzen, JHB; de Brujin, H; de Brujin-Kofman, AT; Arendzen, JH. Archives of Physical Medicine and Rehabilitation, Vol 75, April 1994, 442-446.
Compared the results of two prospective studies of different therapies:
1. Regional intravenous sympathetic blockade (Ismelin), and
2. local DMSO (a hydroxyl radical scavenger, applied topically)
RSD defined by having at least three of the following:
Oedema
Hyperaemia
Hyperasthesia
Hyperhidrosis
Skin atrophy
Limitation in ROM
The result of the first part of the study suggested that DMSO was more effective than regional ismelin blocks (a “tendency” to better outcomes)
The psychological branch of the study compared patients with RSD with patients who underwent ELECTIVE hand surgery (eg carpal tunnel release, tendon repair, arthrodesis). Three questionnaires were used: the Dutch Personality Questionnaire, the SCL-90, and the STAI. Patients were questioned about social life events by a rehabilitation specialist.
The conclusions from this were that there were no differences between treatment and control groups in DPQ and STAI. The SCL-90 showed a tendency to significance in “depression” and “inadequacy” (p=0.07 and 0.09 respectively). There was a significant difference in anxiety in men but not in women. Female patients were more depressed, had more feelings of inadequacy, and a high score of “psycho-neuroticism”.
3 people in the control group developed RSD.
The study quotes previous studies in which there is inconclusive evidence of any link with psychological variables and the development of RSD. Despite the lack of supporting evidence, there is a commonly held belief that patients with RSD are “neurotic”, “somatisers”, etc. One of the final remarks is that depression, emotional disturbances, anxiety, and/or life events, together with a trauma, can increase the risk of RSD and may maintain RSD.
Psychological Issues in Reflex Sympathetic Dystrophy. Covington, E. In “Reflex Sympathetic Dystrophy: A Reappraisal. Progress in Pain Research and Management, Vol 6, edited by W. Janig and M. Stanton-Hicks, IASP Press, 1996. Chapter 11, 191-215.
Most studies on the subject up to that time seemed inadequate when reviewed by other authors. One of these (Lynch, M.) concludes that “Unsupported statements by established authorities have occurred more frequently than studies designed to address these issues”.
Severe pain engenders emotional suffering, promoting behavioural changes which are subject to misinterpretation.
SMP and SIP
Some groups of patients thought to have psychogenic pain because they display excessive suffering, while another group is similarly suspect for suffering too little (in relation to studies reporting the results of MMPI on RSD patients).
There does not seem to be any “RSD personality” (Crohn’s disease, daibetes, migraine, were all attributed to personality at some stage, as were asthma and arthritis)
Studies are done on biased populations.
A prospective study of patients with Duputryene’s disease undergoing surgery (Zachariae, 1964) correctly predicted that 32 patients (from 47) would do well and did so. 17 had been classified as “unstable”, 6 as “demented” and 2 with “real mental problems”. Ten had an ambiguous prediction, and although eight had edema, pain and stiffness for three months, no cases of RSD ensued. The last five cases were predicted to be at serious risk. One developed RSD, two did quite well, and two had some prolonged edema and swelling.
Retrospective studies are difficult to interpret as no comparison with controls are possible.
RSD patients do not appear to be more distressed than patients with other chronic pain conditions.
Psychopathology does not correlate with a poor outcome.
Lets not get started on the topic of malingering, psychogenic pain, , etc.
Epidemiology of complex regional pain syndrome: a retrospective chart review of 134 patients. Allen, G; Galer, B; Schwartz, L. Pain 80 (1999) 539-544.
2.3: 1 female: male (other investigators had reported 3:1, 4.5:1, 1.6:1.
The overwhelming majority are Caucasian (? Selection bias)
The mean duration of symptoms before a pain clinic referral was 2.5 years!
Some patients had had up to 20 medical evaluations (mean 4.8)
Patients most commonly referred by surgeons (33%), only 7% by primary care doctor
Most patients had had various treatment, including physio (88%), nerve blocks (82%), TCAs (78%), opiates (70%), anticonvulsants (60%) and psychological treatments (50%).
82 % had received an average of 6 nerve blocks (one patient had 38!)
17% had a current or prior lawsuit regarding the injury
54% had workers compensation cover (but may be due to a biased sample)
restaurant workers and policemen were over-represented (twice as common as other occupations), with manual labourers next.
Only in 53% of cases where patients had a three-phase bone scan were these reported as positive.
47% of patients had been immobilised as part of their treatment (this may be a factor in the pathogenesis of CRPS) – animal studies show that immobilisation leads to the development of CRPS signs and symptoms, as well as dorsal horn alterations akin to those seen with peripheral nerve injury; a small clinical study found that signs of CRPS develop in casted orthopaedic patients following uncomplicated surgery (Butler and Galer, 1996).
The longer the duration of symptoms, the higher the likelihood that “myofascial trigger points” will be found on examination. That’s another topic!
Quantitative sensory testing, neurophysiological and psychological examinations in patients with complex regional pain syndrome and hemisensory deficits. Rommel, O; Malin, J; Zenz, M; Janig, W. Pain 93 (2001) 279-293.
33% of CRPS patients exhibit sensory impairments which extend past the painful area of the affected limb in a hemisensory distribution (Pain 80, (1999), 95).
40 (32 CRPS 1) patients underwent a bedside neurological examination. Quantitaive sensory testing was done at five locations on each side of the body.
Touch thresholds were determined with von Frey filaments. A thermal stimulator was used for cool, warm, and heat pain thresholds.
15 patients revealed a generalised sensory deficit ipsilateral to the affected limb (12 hemisensory deficit, 3 limited to the affected limb). When these generalised sensory deficits were present, they correlated with longer illness duration and more frequent allodyna/hyperalgesia than those with restricted sensory deficits.
Thresholds were generally higher on the affected side, except for cold threshold on the chest and heat distally on the affected limb.
These hemisensory impairments are hypothesised to be related to functional disturbances in processing of noxious events in the thalamus and may be a clinical correlate of subcortical brain plasticity in chronic pain.
My aplogies for the long post, and to those who have read this already. More later (from home).
Pablo
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Re: Complex Regional Pain Syndrome - July 7, 2005 3:38:00 PM
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Synergy
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From: Texas
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Randy...may I? Nari, follow this link and look at the 3rd bullet.
[URL=http://www.google.com/search?hl=en&lr=&oi=defmore&q=define:booger]What's a booger?[/URL]
I hope this helps! :)
_____________________________
Chris Adams, PT, MPT
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Re: Complex Regional Pain Syndrome - July 7, 2005 3:53:00 PM
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nari
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From: Australia
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Thanks Chris! I am forever in your debt for widening my perspective on bodily fluids...
Pablo - thanks for the lengthy and helpful post.
I particularly liked the bit on MF trigger points...might they be indicators of a kind?? And also the standard practice of immobilisation is noted (that practice should have ceased by now!)
Look forward to a sequela.
Nari
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Re: Complex Regional Pain Syndrome - July 8, 2005 1:45:00 AM
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pablo w
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From: Canberra
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Here are a few more in smaller chunks:
A controlled pilot study of the utility of mirror feedback in the treatment of complex regional pain syndrome (type 1). McCabe, CS; Haigh, RC; Ring, EFJ; Halligan, PW; Wall, PD; and Blake, DR. Rheumatology 2003, 42: 97-101.
Based on studies of another painful condition involving disturbed central processing, and the result of mirror visual feedback. It was hypothesised that the pain of CRPS is a consequence of disruption of central sensory processisng and that congruent visual feedback from the moving unaffected limb, as provided by a mirror, would restore the integrity of cortical processing, thereby relieving pain and restoring function in the affected limb.
Eight subjects with CRPS 1 of duration ranging between three weeks to three years were studied over six weeks. Al had tried a variety of treatments (physio, nerve blocks, TENS, etc).
The first control condition was exercising both limbs with no mirror. Movement exacerbated pain.
The second control condition was exercising the affected limb hidden behind a non-reflective surface. As some subjects reported immediate improvement, this was not continued as subjects were aware that the control condition was inferior to the mirror visual feedback.
The intervention was exercising the affected limb with mirror visual feedback, for 10 minutes at a time. Movement was dictated by the subjects’ pain.
The results are interesting:
Subjects with a more recent onset (less that 8 weeks) reported significant benefit using the mirror and even stopped using it as their pain had reduced to the point they didn’t feel they needed to continue with the exercise. The period of analgesia extended from a few minutes to hours over the six-week trial period. There was a reversal of vasomotor changes, as well as no pain at rest and on movement, and return to normal function.
Of the subjects with intermediate duration of symptoms (5 months, one year) one reported that the mirror immediately eased the pain on movement, with increasing periods of time of decreased stiffness, while the other had no analgesic effect but a decrease in stiffness. Both cases reported improvements in function, a reversal of vasomotor changes, and return to their normal manual occupations.
The three subjects with symptoms lasting more than two years did not observe any great change and discontinued the exercises.
Comments:
Mirror visual feedback seems to decrease pain and increase function in the acute stage of the disease, and reduce stiffness in the intermediate stages. This effect was surprising to both patients and investigators. The authors report that they were unaware of any therapeutic maneuvers or drug effects that could achieve such an immediate analgesic effect. When the intervention is stopped, initially there is an abrupt return of pain.
The results support the hypothesis that the CNS is capable of generating a feedback-dependent state that can produce pathological levels of pain. In CRPS, this might involve a mismatch between different interdependent modalities, such as disruption of normal interaction between motor intention and sensory feedback. In those with inherent vulnerability to this incongruence it can lead, in some, to referred, intractable pain following trauma, and in others can promote CRPS with a CNS origin.
Reference to studies showing increased thalamic activity in early stages, and decreased activity later.
The paper was dedicated to Professor Patrick Wall, who passed away during preparation of the manuscript.
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Re: Complex Regional Pain Syndrome - July 8, 2005 1:46:00 AM
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pablo w
Posts: 88
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From: Canberra
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Complex Regional Pain Syndrome (CRPS): Survey of Current Practices. Burton, A; Hassenbusch, S; Warneke, C; Racz, G; Stanton-Hicks, M. Pain Practice, Volume 4, Issue 2, 2004 74-83.
Despite a move towards a mechanism-based approach and guidelines for treatment, there remains controversy regarding the selection of various techniques. The impact of clinical practice guidelines remains questionable.
Surveys were sent to 453 specialists identified form the American Neuromodulation Society Member List. Response rate was 23% (105). This is considered an acceptable return rate for a mailed survey! Five were excluded as they were incomplete.
Respondents treated on average 14.9 CRPS patients per month (median 10, ranging from 1-90). They had symptoms for an average of 10 months and had seen between 1 and 10 other physicians previously.
58% reported that immediate referral to a pain specialist in cases of suspected CRPS not responding to treatment should be done, while 29% said after one month, 10% 3 months, and 3% six months.
Respondents utilise: Pharmacotherapy 85%
Nerve blocks 67%
Physiotherapy 66%
Psychological Rx 51%
Neurostimulation or intrathecal therapy
35%
Sympathectomy 19%
Pharmacotherapy: Anticonvulsants 79%
Antidepressants 73%
Opioids 50%
NSAIDs 39%
Topical agents (capsaicin, lidoderm, clonidine)
32%
Corticosteroids 10%
Bisphosphonates (Calcitonin/pamidronate)
2%
Regional anaesthesia: Sympathetic blocks 85%
Regional block 21%
Epidural block 15%
Epidural infusion 10%
Other 2%
Implantable Therapies: SCS 71%
PNS 4%
IDD 28%
59% prescribe “alternative therapies” such as medications (43%), acupuncture (42%), and others (13%). Other mentioned therapies included topical creams, magnetic devices, biofeedback, mind/body hypnosis, low frequency TENS.
In intrathecal drug delivery systems, the most common drug was morphine with
Clonidine
Bipivucaine
Hydromorphone
Fentanyl
Baclofen
Methadone
Sufentanil
Ropivacaine
Meperidine
Ziconotide
Drperidol
The emphasis of early treatment of CRPS 1 an 2 was similar, with medication, physiotherapy, and nerve blocks in descending order of frequency. By 4-6 weeks, the use of psychological therapies increases, and by 3 months the use of neural blockade tapers off, and is replaced by neuromodulation, with increasing frequency of intrathecal therapy.
In late CRPS 1, the main difference seemed to be the introduction of psychological therapies earlier on.
The respondents seem to be using guidelines thoughtfully, concluded the authors.
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Re: Complex Regional Pain Syndrome - July 8, 2005 1:46:00 AM
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pablo w
Posts: 88
Joined: November 13, 2002
From: Canberra
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Pain increases during sympathetic arousal in patients with complex regional pain syndrome. Drummond, P; Finch, P; Skipworth, S; Blockey, P. Neurology 57, October (1 of 2) 2001, 1296-1303.
24 healthy subjects, capsaicin applied to the forearm.
Vascular responses monitored, and thermal hyperalgesia rated before and after being startled, and before, during and after mental arithmetic, breath holding, forehead cooling, Valsalva maneuver, and a cold pressor test. In this group, hyperalgesia decreased after a startle, and during and after the other conditions. This demonstrates normal sympathetically mediated hypoalgesia (and/or distraction)
A CRPS group of 61 subjects was also used.
In this groep, thermal hyperalgesia increased in 70% after a startle, and after forehead cooling. Pain increased most consistently in patients with cold allodynia or punctate allodynia. It was known that injections of NA increases pain in patients with SMP.
In patients, pain increased after startle and forehead cooling. This was more marked in patients with cold allodynia. The mechanism that normally inhibits pain during sympathetic arousal is compromised in the majority of patients with CRPS. In particular, failure to recruit inhibitory spinal and supraspinal mechanisms during sympathetic arousal might contribute to pain and autonomic disturbance s in CRPS.
Stress increases sensitivity to pain.
CRPS patients may have a supersensitivity to noradrenaline.
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Re: Complex Regional Pain Syndrome - July 8, 2005 1:47:00 AM
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pablo w
Posts: 88
Joined: November 13, 2002
From: Canberra
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Abnormal contralateral pain responses from an intradermal injection of phenylephrine ina subset of patients wit complex regional pain syndrome (CRPS). Mailis-Gagnon, A; Bennett, G. Pain 111 (2004) 378-384.
Normal subjects and SIP patients experience only brief stinging pain, while both sympathectomised and non-sympathectomised patients experience an additional abnormal pain response as well a mechanical allodynia around the injection site. The response is similar to that observed with NA.
In three symapthectomised patients who had persistent symptoms, injection of phenylephrine into the contralateral (asymptomatic) limb generated an abnormal pain response in both symptomatic and asymptomatic limbs. This included mechanical
allodynia.
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Re: Complex Regional Pain Syndrome - July 8, 2005 1:48:00 AM
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pablo w
Posts: 88
Joined: November 13, 2002
From: Canberra
Status: offline
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This is my favourite, currently working with a patient along these lines.
Imagined movements cause pain and swelling in a patient with complex regional pain syndrome. Moseley, GL. Neurology 62, May (1of 2) 2004, 1644.
34 year old female, 17 months after an uncomplicated wrist fracture, presenting with CRPS symptoms. Reported pain increases during a hand-recognition task, so it was decided to investigate. Stress was unlikely to be the cause of the increased pain as even though there was an increased GSR, the patient did not report the activity to be stressful. When the hand-recognition task involved only the unaffected hand, this did not occure.
Imagined movements caused an increase in pain and swelling, even tough there was no muscle activity (ruled out with EMG) or movement of the limb.
In a chronically active and senstised nociceptive system, activation of the body schema (possibly posterior parietal cortex, which contains representations of working body schema and is active during imagined and executed hand movements) is sufficient to elicit such an output. This could evoke swelling in a limb through projections to the amygdala, the internal circuits of which are thought to be capable of associating autonomic responses with specific behaviours. Alternately, attention to the affected limb or preparing to move it, may activate descending facilitatory projections from the RVM to spinal nociceptive neurons.
Symptoms of CRPS may be mediated in part by cortical mechanisms associated with movement of the affected part.
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