• Sara Marconi, Cesa Scaglione, Fabio Pizza, Giovanni Rizzo, Giuseppe Plazzi, Roberto Vetrugno, Gaetano La Manna, Claudio Campieri, Sergio Stefoni, Pasquale Montagna, and Paolo Martinelli.
• Dipartimento di Scienze Neurologiche, Università di Bologna IRCCS, Institute of Neurological Sciences of Bologna, Bologna, Italy. sara-7902@libero.it
• Parkinsonism Relat. Disord. 2012 May 1; 18 (4): 362-6.

BackgroundNeurophysiological investigations disclosed spinal cord hyperexcitability in primary restless legs syndrome (p-RLS). Uremic RLS (u-RLS) is the most common secondary form, but its pathophysiological mechanisms remain unsettled. Aim of this study was to explore spinal cord excitability by evaluating group I nonreciprocal (Ib) inhibition in u-RLS patients in comparison with p-RLS patients and healthy subjects.MethodsEleven u-RLS patients undergoing long-term hemodialysis treatment, nine p-RLS patients and ten healthy subjects were studied. Soleus H reflex latency (HR-L), H(max)/M(max) ratio, and Ib inhibition were evaluated. Ib inhibition was tested measuring the amplitude changes in soleus H reflex following stimulation of the synergist gastrocnemius medialis (GM) nerve at rest. Nerve conduction studies were performed in the uremic patients.ResultsThe H(max)/M(max) ratio did not differ in the three groups. The u-RLS patients showed a normal Ib inhibition comparable with the healthy group, whereas the p-RLS group had evidence of a reduced active inhibition compared with both u-RLS patients (P = 0.04) and controls (P = 0.007), prominently at 5 ms (P = 0.007) and at 6 ms (P = 0.02) of conditioning-test interval. Neurophysiological examination disclosed abnormalities ranging from higher HR-L to clear-cut polyneuropathy in most u-RLS patients.ConclusionsUnlike p-RLS patients, u-RLS patients had normal Ib inhibition, suggesting a regular supraspinal control of Ib spinal interneurons. Subclinical peripheral nerve abnormalities were detected in most uremic patients. Peripherally disrupted sensory modulation may represent the major pathophysiological determinant of uremic RLS.Copyright © 2011 Elsevier Ltd. All rights reserved.

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