Bilateral Sensory Abnormalities in Patients with Unilateral Neuropathic Pain; A Quantitative Sensory Testing (QST) Study

Abstract

In patients who experience unilateral chronic pain, abnormal sensory perception at the non-painful side has been reported. Contralateral sensory changes in these patients have been given little attention, possibly because they are regarded as clinically irrelevant. Still, bilateral sensory changes in these patients could become clinically relevant if they challenge the correct identification of their sensory dysfunction in terms of hyperalgesia and allodynia. Therefore, we have used the standardized quantitative sensory testing (QST) protocol of the German Research Network on Neuropathic Pain (DFNS) to investigate somatosensory function at the painful side and the corresponding non-painful side in unilateral neuropathic pain patients using gender- and age-matched healthy volunteers as a reference cohort. Sensory abnormalities were observed across all QST parameters at the painful side, but also, to a lesser extent, at the contralateral, non-painful side. Similar relative distributions regarding sensory loss/gain for non-nociceptive and nociceptive stimuli were found for both sides. Once a sensory abnormality for a QST parameter at the affected side was observed, the prevalence of an abnormality for the same parameter at the non-affected side was as high as 57% (for Pressure Pain Threshold). Our results show that bilateral sensory dysfunction in patients with unilateral neuropathic pain is more rule than exception. Therefore, this phenomenon should be taken into account for appropriate diagnostic evaluation in clinical practice. This is particularly true for mechanical stimuli where the 95% Confidence Interval for the prevalence of sensory abnormalities at the non-painful side ranges between 33% and 50%.

Assessment and manifestation of central sensitisation across different chronic pain conditions

“…There is ample preclinical (Tal and Bennett, 1994;Malan et al, 2000), human experimental (Shenker et al, 2008), and clinical (Konopka et al, 2012) evidence that for neuropathic-like conditions the signs and symptoms (sensory abnormalities) can extend into regions beyond those directly innervated by the injured nerve. This emphasises that there may be no non-affected control site in a chronic pain patient.…”

“…Use of the standardised QST protocol of the German Research Network on Neuropathic Pain has revealed abnormality for some sensory parameters at the non-affected side that was as high as 57%; this indicates that bilateral sensory dysfunction in patients with unilateral neuropathic pain is more the rule than the exception (Konopka et al, 2012) and often very minimal sensory differences exist between affected and non-affected areas (Geber et al, 2011). Studies of thermal sensory function at the affected and non-affected side of acute and chronic complex regional pain syndrome patients have shown bilateral sensory changes as well (Huge et al, 2008).…”

Altered Central Sensitization and Pain Modulation in the CNS in Chronic Joint Pain

“…Clinically, bilateral presentation of pain symptoms occurred in about 5-15 % of patients with complex regional pain syndrome [93,94]. There is abundant clinical evidence that the signs and symptoms extend into regions beyond those directly innervated by the injured nerve in neuropathic conditions [95,96]. Patients with second-degree burns can develop sensory abnormalities involving the contralateral, uninjured side of the body [97].…”

Antinociceptive action of botulinum toxin type A in carrageenan-induced mirror pain

“…Contralateral mirror-imaging has been experimentally demonstrated in a variety of injuries in laboratory animals: inflammatory cutaneous and joint (reviewed in Shenker et al 2003), inflammatory and non-inflammatory muscle Radhakrishnan et al 2003) and neuropathic (reviewed in Koltzenburg et al 1999). Altered contralateral sensory perception after unilateral injury or in chronic pain syndromes is reported as well in clinics (Huge et al 2008;de la Llave-Rincón et al 2009;Fernández-de-las-Peñas et al 2009;Konopka et al 2012;Werner et al 2013). However, the frequency of this disorder in humans is not known.…”