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Quantitative Sensory Testing (QST) - Does assessing ... - TI Pharma

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4. <strong>QST</strong> and neuropathic pain mechanisms<br />

Abstract<br />

<strong>Quantitative</strong> sensory testing (<strong>QST</strong>) allows the somatosensory profiling of patients with<br />

neuropathic pain. The ultimate goal of identifying differences in the responsiveness<br />

to sensory stimuli is the identification of differences in the mechanisms responsible<br />

for generating sensory abnormalities and their subsequent mechanism-based therapy.<br />

Recently, it was shown that distinct somatosensory patterns using a battery of <strong>QST</strong><br />

tests are present in the different clinical entities of neuropathic pain. Until now, it has<br />

not been investigated whether the responsiveness to a single <strong>QST</strong> parameter would<br />

reveal different patient subgroups. Thus, we studied patients with neuropathic pain<br />

for their responsiveness to a single <strong>QST</strong> parameter “Mechanical Pain Sensitivity”<br />

(MPS). Abnormal MPS score reflects hypersensitivity for mechanical stimulation,<br />

which occurs in ~30% of the neuropathic pain patient population. The MPS test obtains<br />

stimulus-response function to seven pinprick devices exerting forces between 8-512mN<br />

to identify abnormalities for pinprick pain. In this study we found that patients with<br />

MPS abnormalities showed two distinctive patterns of altered stimulus-response<br />

function to pinpricks. 40% of patients reported a stimulus dependent pain response<br />

whereas 60% of patients did not show such stimulus dependent behaviour and rated<br />

all pinprick intensities equally painful. Both types of responses were found within<br />

different clinical entities of neuropathic pain. Hence, we show that even a single <strong>QST</strong><br />

parameter can reveal additional, more detailed information of sensory abnormalities in<br />

neuropathic pain. Further evaluation might lead to the identification of differences in<br />

the mechanisms responsible for these distinct MPS abnormalities.

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