Somatosensory evoked potentials in motor neuron disease

Abstract

We studied median somatosensory evoked potentials (SEPs) in an unselected series of 30 patients with sporadic motor neuron disease (MND). SEPs were affected in 17 patients (57%), with a higher incidence of abnormality in amyotrophic lateral sclerosis and bulbar palsy than in progressive muscular atrophy. In a majority of patients, simultaneous bilateral stimulation of the median nerve revealed a delay or absence of scalp-recorded central N32 and/or N60, leaving the earlier peaks intact. In the remaining cases, the N19 peak was asymmetrically prolonged. These findings suggest common involvement of somatosensory pathways in MND, either at cortical or subcortical levels, and correlate with neuropathologic reports of neuronal degeneration beyond the primary motor system.

Laser evoked potentials in amyotrophic lateral sclerosis

“…All cortical components showed a significant latency increase in ALS patients compared to controls, suggesting a conduction slowing due to an impairment of nociceptive pathways. This finding concurs with most of the studies on SEPs, showing a prolonged central conduction time [12,17,[19][20][21], though our LEP method did not allow us to discriminate a peripheral from a central delay. In ALS degeneration of subcortical structures, including the thalamus, has been reported [9], and this may subtend the delay in the afferent input to the nociceptive cortex; on the other hand no study has described peripheral involvement of nociceptive afferents.…”

“…On the other hand, recent studies report an impairment of dorsal root ganglion cells and peripheral sensory fibres, mainly of large myelinated fibres 1A, in almost 20% of ALS patients [10,11]. Nerve conduction studies and somatosensory evoked potentials (SEPs) showed abnormal slowing in the peripheral and central sensory pathways, with an elevated thermal threshold, suggesting sub-clinical abnormalities of the sensory system in ALS [12][13][14][15][16][17][18][19][20]. Furthermore, a recent study by Hamada et al, [21] showed an abnormal amplitude increase of cortical component of SEPs in ALS.…”

Impaired short‐ and long‐latency afferent inhibition in amyotrophic lateral sclerosis

“…54 In addition, abnormalities of the median nerve somatosensory evoked potentials (SEPs), such as delayed peak latency and reduced amplitude of the early components (N20, P25, N30), have been reported in previous work. [55][56][57][58][59] These abnormalities may be related to decreased SAI, as found in our patients. Moreover, Sangari et al suggested that the compensatory mechanisms at the spinal level amplify the motor neuron response to sensory inputs in ALS.…”

“…Impairment of the spinal sensory pathways has been demonstrated by diffusion tensor imaging in ALS patients, whereas the sensory nerve excitability remains intact . In addition, abnormalities of the median nerve somatosensory evoked potentials (SEPs), such as delayed peak latency and reduced amplitude of the early components (N20, P25, N30), have been reported in previous work . These abnormalities may be related to decreased SAI, as found in our patients.…”

Far‐field and cortical somatosensory evoked potentials in motor neuron disease

“…Twenty-six patients (14 males and 12 females) with MND were investigated. The criteria adopted to formulate the diagnosis and for inclusion in the study were the following: (1) family history negative for MND, (2) clinical evidence of progressive and rapid loss of muscle strength with atrophy and fasciculations dating back at least 6 months, (3) electromyographic picture of denervation in muscles of more than one limb tested and normal sensory nerve conduction, (4) patients older than 25 years (range 30-74, mean age 55 years), (5) normal radiographic investigations of the spine. According to the clinical picture, 3 forms of MND were distinguished: amyotrophic lateral sclerosis (ALS, 14 cases) with both upper and lower motor neuron involvement, progressive muscular atrophy (PMA, 6 cases) without evidence of corticospinal tract dysfunction, and progressive bulbar palsy (PBP, 6 cases).…”