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

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

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.

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