1166
signs had an abnormal latency, although 6 of them (50%) had a significant decrease in amplitude (fig. 2 C). 5 of the 10 patients with delay of component v also had increased latency of component ill. 3 of these also had delays of wave n, but in 3 other patients this component (11) could not be identified. In no case was component I abnormal, and, in every case of abnormal latency of any component, wave v was also
delayed. Discussion
.
,
The auditory pathways from one cochlear end-organ involve the ipsilateral eighth nerve and cochlear nuclei. From these nuclei fibres pass to the olivary nuclei on both sides of the brainstem, then, via the lateral lemnisci, to, the inferior colliculi and the medial geniculate bodies. The first component of the auditory evoked response (A.E.R.) recorded by the scalp electrodes originates from activity of the eighth nerve. The later components (ll-v) arise in part from the sequential activity of the cochlear nuclei, olivary nuclei, inferior colliculi, and an area anterior to the colliculi.3 The potentials recorded are the sum of activity of many thousands of cells, and their form depends on the temporal pattern of activity of these cells. Demyelination of the tracts within the auditory pathways would be expected to delay the serial transmission of impulses to the various nuclear masses within these pathways and consequently alter the summation potentials recorded.5 The data presented here indicate that there are alterations in the form of the A.E.R. in a substantial proportion of patients with multiple sclerosis. In some cases there is considerable delay in the peak of wave v. This absolute increase in latency does not necessarily imply delays of this order in individual nerve-fibres. Clearly a lesion at a low level in such a serial system can alter all subsequent components. Thus all the patients with abnormal components n In this situation or ill had alteration of later waves. the term component v is no longer strictly correct since additional small waves (
signs had an abnormal latency, although 6 of them (50%) had a significant decrease in amplitude (fig. 2 C). 5 of the 10 patients with delay of component v also had increased latency of component ill. 3 of these also had delays of wave n, but in 3 other patients this component (11) could not be identified. In no case was component I abnormal, and, in every case of abnormal latency of any component, wave v was also
delayed. Discussion
.
,
The auditory pathways from one cochlear end-organ involve the ipsilateral eighth nerve and cochlear nuclei. From these nuclei fibres pass to the olivary nuclei on both sides of the brainstem, then, via the lateral lemnisci, to, the inferior colliculi and the medial geniculate bodies. The first component of the auditory evoked response (A.E.R.) recorded by the scalp electrodes originates from activity of the eighth nerve. The later components (ll-v) arise in part from the sequential activity of the cochlear nuclei, olivary nuclei, inferior colliculi, and an area anterior to the colliculi.3 The potentials recorded are the sum of activity of many thousands of cells, and their form depends on the temporal pattern of activity of these cells. Demyelination of the tracts within the auditory pathways would be expected to delay the serial transmission of impulses to the various nuclear masses within these pathways and consequently alter the summation potentials recorded.5 The data presented here indicate that there are alterations in the form of the A.E.R. in a substantial proportion of patients with multiple sclerosis. In some cases there is considerable delay in the peak of wave v. This absolute increase in latency does not necessarily imply delays of this order in individual nerve-fibres. Clearly a lesion at a low level in such a serial system can alter all subsequent components. Thus all the patients with abnormal components n In this situation or ill had alteration of later waves. the term component v is no longer strictly correct since additional small waves (
