To assess whether pseudoradicular low-back pain may be associated with subclinical sensory deficits in the distal extremity, we applied the quantitative sensory testing protocol of the German Research Network on Neuropathic Pain (DFNS) in 15 patients with pseudoradicular pain distribution. Sixteen age- and gender-matched healthy control subjects as well as 12 patients with radicular pain syndromes (L4-S1) were studied with the same protocol. Radicular pain was diagnosed using clinical criteria (pain radiation beyond the knee, motor-, sensory-, or reflex deficits, positive Laségue’s test). Z-score QST profiles revealed a selective loss of vibration detection, detection of v. Frey hair contact, and cold detection in the affected dermatomes in the radicular pain group. The contralateral dermatome was also affected, but to a lesser degree. In patients with pseudoradicular pain, the sensory profile was similar, but sensory loss was less pronounced than in the radicular pain patients. There was no significant difference between the two patient groups. Vibration detection was the most sensitive parameter with 73% abnormal values in radicular and 47% in pseudoradicular cases. These data verified the sensitivity of QST to detect sensory loss in radicular compression syndromes, and support a neuropathic component in low-back pain with radiculopathy. In contrast to some central pain syndromes this sensory loss involved predominantly large fiber functions. The subclinical sensory loss in pseudoradicular cases suggests that these patients may also have a neuropathic component of their chronic pain. The spatial incongruence of pain and sensory loss in pseudoradicular pain, however, may also indicate that the two are not causally related.
aDepartment of Anesthesiology, Heinrich-Heine-University of Düsseldorf, Düsseldorf, Germany
bInstitute of Physiology and Pathophysiology, University of Mainz, Germany
cDepartment of Neurology, University of Mainz, Germany
dDivision of Neurological Pain Research and Therapy, Department of Neurology, University of Kiel, Germany
eDepartment of Neurology, Technische Universität München, Germany
fDepartment of Neurosurgery, Heinrich-Heine-University of Düsseldorf, Düsseldorf, Germany
*Corresponding author. Address: Department of Neurology, Johannes Gutenberg-University, Langenbeckstr. 1, 55131 Mainz, Germany. Tel.: +49 6131 170; fax: +49 6131 175570.
1Authors contributed equally.
Submitted November 19, 2006; received in revised form April 18, 2007; accepted May 2, 2007.