Tactile discrimination, but not tactile stimulation alone, reduces chronic limb pain

Lorimer Moseley G(a)(b); Zalucki Nadia M(c)(d); Wiech Katja(b)
(a) Pain Imaging Neuroscience Group, Department of Physiology, Anatomy & Genetics, Le Gros Clark Building, University of Oxford, South Parks Road, Oxford OXI 3QX, United Kingdom
(b) FMRIB Centre, University of Oxford, United Kingdom
(c) School of Physiotherapy, The University of Sydney, Australia
(d) Department of Physiotherapy, Launceston General Hospital, Launceston, Australia

Abstract

Chronic pain is often associated with reduced tactile acuity. A relationship exists between pain intensity, tactile acuity and cortical reorganisation. When pain resolves, tactile function improves and cortical organisation normalises. Tactile acuity can be improved in healthy controls when tactile stimulation is associated with a behavioural objective. We hypothesised that, in patients with chronic limb pain and decreased tactile acuity, discriminating between tactile stimuli would decrease pain and increase tactile acuity, but tactile stimulation alone would not. Thirteen patients with complex regional pain syndrome (CRPS) of one limb underwent a waiting period and then ∼2 weeks of tactile stimulation under two conditions: stimulation alone or discrimination between stimuli according to their diameter and location. There was no change in pain (100 mm VAS) or two-point discrimination (TPD) during a no-treatment waiting period, nor during the stimulation phase (p > 0.32 for both). Pain and TPD were lower after the discrimination phase [mean (95% CI) effect size for pain VAS = 27 mm (14-40 mm) and for TPD = 5.7 mm (2.9-8.5 mm),p < 0.015 for both]. These gains were maintained at three-month follow-up. We conclude that tactile stimulation can decrease pain and increase tactile acuity when patients are required to discriminate between the type and location of tactile stimuli.

See full article at Pain 137,3 600-608

Comments

  1. Hi Lorrimer
    hopefully dried out from the Edinburgh soaking and recovered from ironing mishaps!!
    On the tactile sensory alterations in the above caseload I’m wondering if we can extrapolate to a broader patient group.
    1. Is there merit in trying to differentiate tactile, 2 point discrimination, vibration sensitivity or any other sensory teasting modality as part of a diiagnostic clinical work-up. I ask because I just tested some patients clinically where there functional defecits could be catagorised as proprioceptive deficiencies. I then tested passive limb re-position sense and 256htz vibration sensitivity. Both markers were surprisingly distorted which led me to re-introduce joint reposition replication into the ACL program – not something I would normally bother with.

    2 Do you think there may be sub-classes of sensory modalities we should look at in association with movement impairment syndromes?

    3. Tantalisingly – maybe sensory modality testing could be a marker for selection of treatment strategies which are peripheral or cenrtally focused. It appears we “get lucky” alot of the time with the peripheral strategy but I’m always looking to tip the odds.

    Love the site and where your comming from – even just for preservation of clinician sanity!

    Cheers

    David

    [Reply]

    Lorimer Reply:

    Hi David. I have now decided to never iron anything ever again.

    Re Point 1. “Is there merit in trying to differentiate tactile, 2 point discrimination, vibration sensitivity or any other sensory teasting modality as part of a diagnostic clinical work-up?”
    I do it routinely with chronic pain patients. I have no data aside from what I presented but the (anecdotal) feel of it is that it is informative.

    2 “Do you think there may be sub-classes of sensory modalities we should look at in association with movement impairment syndromes?”
    I don’t know, do you?

    3. “Tantalisingly – maybe sensory modality testing could be a marker for selection of treatment strategies which are peripheral or cenrtally focused. It appears we “get lucky” alot of the time with the peripheral strategy but I’m always looking to tip the odds.”
    – Perhaps. I am not sure – certainly increased TPD must involve compromised receptive fields in S1, but that may be consequent to peripheral probs (testable with detection thresholds), spinal or thalamic (don’t know how to differentiate these clinically, do you?)

    “Love the site and where your comming from – even just for preservation of clinician sanity!” – Thanks a million David.

    [Reply]

  2. Greetings Lorrimer – thanks for the feedback
    Don’t worry, I’m not thinking of of formulating guidelines on the basis of these musings – just generating some ideas that could be easily tested and / or refuted in the clinic.

    I’m thinking whether any sensory discrepancy is a reflection of cortical mapping alterations or whether some modalities are more specific ie why did you choose TPD?
    Back in the days of teaching with David Butler and Louis Gifford we use to advocate 256htz vibration sensiivity testing as an early indicator of “sub-clinical neuropathy” prior to NCT defecits.
    I now see it’s associated with proprioceptive deficits – perhaps moving to a more central mechanism?

    We getting into the business of differentiating central versus peripheral mechanisms here I guess – the clinical hot potato (dare I say it as an Irishman).

    David

    [Reply]

  3. CHECK OUT pain 146 (2009) 5-6 sensory profiles in neuropathic pain

    [Reply]

  4. Lorimer
    an interesting follow up on the case I described above.
    Knee re-position sense and 256Htz vibration cutaenous sensory acuity both significantly improved with re-positioning training for 2 weeks.(as distinct from 10 weeks of usual ACL stuff)
    I see some interesting discussion in … J Physiol 581.3 (2007) pp 971–980 971 Impairment of human proprioception by high-frequency cutaneous vibration, N. S.Weerakkody, D. A. Mahns, J. L. Taylor and S. C. Gandevia

    Quote
    “The emerging view, supported by a combination of
    psychophysical and microneurographical data (e.g.Collins
    et al. 2000, 2005; Edin, 2004), is that cutaneous feedback
    provides proprioceptive information that is integrated
    with that from muscle spindles to provide judgement of
    joint position and movement. Our result implies that
    there is convergence between skin (PC) and proprioceptive
    projections along the somatosensory pathway. This
    could be between skin and muscle afferents or among
    the cutaneous inputs to proprioception. One possible
    location where this may occur is the dorsal column nuclei
    as it contains prominent inputs from vibration-sensitive
    receptors (e.g. Bystrzycka et al. 1977; Douglas et al. 1978;
    Ferrington & Rowe, 1982; Connor et al. 1984; see also
    Hummelsheim et al. 1985). Suppression at the thalamic or
    cortical level is also possible, although there is no definite
    data for humans.”

    Gandevia’s angle was on proprioceptive interference using high frequency vibration. I wonder if it’s a step too far to think about sensory impairment as a useful measure of proprioceptive interference/compromise – particularly in the light of postulated convergence of pathways?

    The reason I suggest this is that not many joint are as easy to do joint re-position replication measurement as the knee or shoulder.

    How have you surmounted this for the spine research you’ve done?

    David

    [Reply]

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