Baris Isak1, Hatice Tankisi2, Birger Johnsen1, Kirsten Pugdahl1, Nanna Brix Finnerup3, Anders Fuglsang-Frederiksen1. 1. Department of Clinical Neurophysiology, Aarhus University Hospital, Aarhus, Denmark. 2. Department of Clinical Neurophysiology, Aarhus University Hospital, Aarhus, Denmark. Electronic address: hatitank@rm.dk. 3. Danish Pain Research Centre, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Abstract
OBJECTIVE: Mild involvement of sensory nerves has been reported in previous studies in ALS patients. In this study, we assessed sensory pathways in ALS patients using laser evoked potentials (LEPs) and somatosensory evoked potentials (SSEPs). METHODS: We recruited 18 ALS patients and 31 healthy subjects. Neodymium-doped yttrium aluminium perovskite (Nd:YAP)-laser was used to evoke LEPs in upper (UE) and lower (LE) extremities. N1 and N2P2 potentials were obtained from contralateral insular cortex (T3 or T4) and vertex (Cz), respectively. Median SSEPs were recorded from C3' or C4' and tibial SSEPs from Cz'. RESULTS: Compared to controls, ALS patients had longer N2 and P2 latencies, and smaller N2P2 amplitudes in both UE- and LE-LEPs (p<0.05), and longer latencies for median and tibial SSEPs (p<0.05). LEPs and SSEPs were abnormal in 72.2% and 56.6% patients, respectively. CONCLUSIONS: Cortical potentials showed that A-beta or A-delta sensory fibres, or both, were impaired in more than half of the ALS patients. SIGNIFICANCE: The findings support that ALS is a multi-systemic disorder involving, although to a lesser degree, other systems than the motor.
OBJECTIVE: Mild involvement of sensory nerves has been reported in previous studies in ALSpatients. In this study, we assessed sensory pathways in ALSpatients using laser evoked potentials (LEPs) and somatosensory evoked potentials (SSEPs). METHODS: We recruited 18 ALSpatients and 31 healthy subjects. Neodymium-doped yttrium aluminium perovskite (Nd:YAP)-laser was used to evoke LEPs in upper (UE) and lower (LE) extremities. N1 and N2P2 potentials were obtained from contralateral insular cortex (T3 or T4) and vertex (Cz), respectively. Median SSEPs were recorded from C3' or C4' and tibial SSEPs from Cz'. RESULTS: Compared to controls, ALSpatients had longer N2 and P2 latencies, and smaller N2P2 amplitudes in both UE- and LE-LEPs (p<0.05), and longer latencies for median and tibial SSEPs (p<0.05). LEPs and SSEPs were abnormal in 72.2% and 56.6% patients, respectively. CONCLUSIONS: Cortical potentials showed that A-beta or A-delta sensory fibres, or both, were impaired in more than half of the ALSpatients. SIGNIFICANCE: The findings support that ALS is a multi-systemic disorder involving, although to a lesser degree, other systems than the motor.