BACKGROUND: Neurophysiological 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. METHODS: Eleven 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. RESULTS: The 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. CONCLUSIONS: Unlike 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.

Marconi, S., Scaglione, C., Pizza, F., Rizzo, G., Plazzi, G., Vetrugno, R., et al. (2012). Group I nonreciprocal inhibition in restless legs syndrome secondary to chronic renal failure. PARKINSONISM & RELATED DISORDERS, 18(4), 362-366 [10.1016/j.parkreldis.2011.12.002].

Group I nonreciprocal inhibition in restless legs syndrome secondary to chronic renal failure.

PIZZA, FABIO;RIZZO, GIOVANNI;PLAZZI, GIUSEPPE;LA MANNA, GAETANO;CAMPIERI, CLAUDIO;STEFONI, SERGIO;
2012

Abstract

BACKGROUND: Neurophysiological 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. METHODS: Eleven 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. RESULTS: The 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. CONCLUSIONS: Unlike 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.
2012
Marconi, S., Scaglione, C., Pizza, F., Rizzo, G., Plazzi, G., Vetrugno, R., et al. (2012). Group I nonreciprocal inhibition in restless legs syndrome secondary to chronic renal failure. PARKINSONISM & RELATED DISORDERS, 18(4), 362-366 [10.1016/j.parkreldis.2011.12.002].
Marconi, S; Scaglione, C; Pizza, F; Rizzo, G; Plazzi, G; Vetrugno, R; La Manna, G; Campieri, C; Stefoni, S; Montagna, P; Martinelli, P
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11585/113488
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