Electrophysiological evidence for a defect in the processing of temporal sound patterns in multiple sclerosis

Abstract

Objectives: To assess the processing of spectrotemporal sound patterns in multiple sclerosis by using auditory evoked potentials (AEPs) to complex harmonic tones. Methods: 22 patients with definite multiple sclerosis but mild disability and no auditory complaints were compared with 15 normal controls. Short latency AEPs were recorded using standard methods. Long latency AEPs were recorded to synthesised musical instrument tones, at onset every two seconds, at abrupt frequency changes every two seconds, and at the end of a two second period of 16/s frequency changes. The subjects were inattentive but awake, reading irrelevant material. Results: Short latency AEPs were abnormal in only 4 of 22 patients, whereas long latency AEPs were abnormal to one or more stimuli in 17 of 22. No significant latency prolongation was seen in response to onset and infrequent frequency changes (P1, N1, P2) but the potentials at the end of 16/s frequency modulations, particularly the P2 peaking approximately 200 ms after the next expected change, were significantly delayed. Conclusion:The delayed responses appear to be a mild disorder in the processing of change in temporal sound patterns. The delay may be conceived of as extra time taken to compare the incoming sound with the contents of a temporally ordered sensory memory store (the long auditory store or echoic memory), which generates a response when the next expected frequency change fails to occur. The defect cannot be ascribed to lesions of the afferent pathways and so may be due to disseminated brain lesions visible or invisible on magnetic resonance imaging.A large proportion of patients with established multiple sclerosis (MS) have lesions of central auditory pathways, which can be shown by using short latency auditory evoked potentials (AEPs).1 Abnormalities are also often observed in long latency event related potentials (ERPs). These, however, cannot usually be ascribed to afferent pathway lesions but presumably to localised or diffuse lesions within the brain.2 Most patients in the advanced stages of MS exhibit some degree of cognitive impairment.3 Minor cognitive deficits have also been noted in the early stages, for example, in the performance of verbal memory and abstract reasoning tasks. 4 In a group of mildly affected MS patients whose clinical symptoms were entirely attributable to disease of the spinal cord, the P3 component of the ERP was yet found to be significantly altered as compared with control subjects during performance of auditory and visual working memory tasks. 5 An earlier ERP component reflecting short term memory processes is the mismatch negativity. 6 This potential is elicited automatically (that is, not requiring the conscious attention of the subject) by discrete sounds that differ in some respect from the preceding sequence of sounds. The mismatch negativity appears to depend on retention of the sounds in a sensory memory store, the long auditory store or echoic memory, which decays over a period of a few seconds. 7 The chief distinction betwe...

Central auditory evaluation in multiple sclerosis: case report

“…However some researchers have found abnormalities in the LAEPs of patients with MS 4,9,10 . In such cases, one might infer that the disease had not affected the auditory areas related to the generation of such potential.…”

“…Abnormal evoked responses to different types of stimuli provide clues for the location of plaques or lesions, confirm clinically ambiguous lesions and confirm the organic basis of symptoms. A large proportion of patients with established MS also show lesions of the central auditory pathways, which can be identified by brainstem auditory evoked potentials (BAEPs), middle-latency auditory evoked potentials (MLAEPs) and late auditory evoked potentials (LAEPs), as well as by using neuroimaging procedures [2][3][4] . Unfortunately, many professionals are not cognizant of the auditory deficits that may be associated with this pathology.…”

Regulation of conduction time along axons

“…Abnormal timing and synchrony in the auditory brainstem haven been suggested to contribute to auditory neuropathy (Oertel, 2005; Zeng et al, 2005), a form of hearing impairment with normal cochlear conduction but disordered neural conduction (Starr et al, 1996; Starr et al, 2000). Likewise, patients with demyelinating diseases like MS display loss of hearing acuity and impaired temporal processing in the auditory brainstem (Noffsinger et al, 1972; Levine et al, 1993; Rappaport et al, 1994; Jones et al, 2002). At a cellular level, dysmyelination has been shown to cause increase in spike jitter and failures (Kim et al, 2013).…”

Effects of Age and Type of Stimulus on the Cortical Auditory Evoked Potential in Healthy Malaysian Children

“…To record the CAEP, scalp electrodes are placed on specific locations of the head and stimuli such as tone bursts or speech syllables are presented repetitively to evoke electrical potentials along the central auditory pathway. As reported elsewhere, CAEP has been found to be sensitive in identifying hearing loss and disorders affecting the central auditory pathway including tumors, multiple sclerosis, and brain injury [5][6][7]. Abnormal CAEP waveforms have also been reported in children with syndromic features, attention deficit hyperactivity disorder, autism, learning disabilities, auditory processing disorder, auditory neuropathy, and epilepsy [8][9][10][11][12][13][14][15].…”