Abnormal nociceptive processing occurs centrally and not peripherally in pain-free Parkinson disease patients: A study with laser-evoked potentials.

BACKGROUND: Several studies documented abnormal nociceptive processing in PD patients. Pain central pathways are accessible by laser-evoked potentials (LEPs). LEPs recording show a N2/P2 complex mostly generated by the anterior cingulate cortex, preceded by an earlier negative component (N1), originating from the opercular cortex. Previous work demonstrated N2/P2 amplitude reduction in PD patients and suggested a centrally-acting pathomechanism for the genesis of pain. However, since a peripheral deafferentation has been recently demonstrated in PD, it is not clear if such LEP abnormalities reflect a mechanism acting centrally or not. OBJECTIVE: To assess whether abnormalities of nociceptive inputs occur at central and/or peripheral level in pain-free PD patients with hemiparkinson using Nd:YAP LEPs. METHODS: We recorded scalp Nd:YAP-LEPs to hand stimulation in 13 pain-free patients with unilateral PD and in 13 healthy subjects. Additionally, we collected laser pain-rating in both groups. RESULTS: PD patients and normal subjects showed comparable N1, N2 and P2 latencies. The N2/P2 amplitude was significantly lower in PD patients than in controls, regardless of the clinically affected side, whereas the N1/P1 amplitude was not different. PD patients had higher pain-rating, indicative of hyperalgesia. CONCLUSIONS: These findings demonstrate that in the PD patients the abnormal processing of pain stimuli occurs at central rather than peripheral level. The co-existence of hyperalgesia and reduced amplitude of the N2/P2 complex, in spite of a normal N1/P1 component, suggests an imbalance between the medial and lateral pain systems. Such a dissociation might explain the genesis of central pain in PD.

Peroneal nerve orthodromic sensory conduction technique: normative data.

In some definite patients, a standard neurophysiological tool may not solve a complete differential diagnosis in common nerve peroneal neuropathy. In this study we have assessed a new simple procedure to study the orthodromic sensory conduction of both the superficial peroneal nerves (SPN) and deep peroneal nerves (DPN) in a heterogeneous group of 55 normal subjects. The mean sensory orthodromic conduction velocity of the SPN was 58.35 m/s. The mean sensory orthodromic conduction velocity of the mixed nerve action potential (MNAP) of the DPN was 55.27 m/s. The sensory conduction velocity, the amplitude of sensory-evoked potentials of SPN and DPN across the fibular head and the normative values are discussed. Our results confirm that these recording methods are easy to repeat and reliable in identifying peroneal neuropathy.