1.2.2 STUDIES IN MULTIPLE SCLEROSIS
1.2.2.3 Brainstem auditory evoked potentials
Robinson and Rudge (1975) produced a first preliminary report of brainstem auditory evoked potentials (BAEPs) in MS. In 30 patients, 27 definite and three with probable diagnosis of MS, they examined potentials occurring within 10 ms of a binaural click stimulus. Of these, wave V
(believed by them to be generated in the region of the in ferior colliculus) was the best defined so that it was chosen to classify records. Abnormalities were recorded in 22 cases (73%), 12 of whom had no brainstem deficits.
Amplitude attenuation was encountered more often than latency increase (16 and 10 cases, respectively) and was the only abnormality in the asymptomatic cases. In a fol lowing study, Robinson and Rudge (1977) examined 88
patients with definite MS. In 57 cases (65%) the amplitude and latency of the wave V were beyond the 95% confidence limits constructed for the normal population. Abnormalities occurred in 82% and 76% of patients who had definite or probable clinical evidence of a brainstem lesion and in 51% of those whose brainstem functions otherwise appeared nor mal. Recording of middle latency components (between 10 and
60 msec) added an additional 12% of abnormalities to the whole group of patients. Similar results were obtained by Stockard et al. (1977), using monaural stimulation. In this study, normal limits were based on the evaluation of the I-III, I-V and III-V inter-component latency separations as
well as the amplitude of wave V, although delays were con sidered a more reliable sign of abnormality than waveform attenuation. Abnormalities were found in 65/100 patients and in 45 consisted of components with increased latency with or without reduced amplitude. When patients were divided into definite, probable and possible diagnostic categories, the incidence of abnormal BAEPs was 93%, 77% and 35% respectively. Only the definite cases had unequivo cal clinical evidence of a brainstem lesion. In a more com prehensive study, Robinson and Rudge (1980) compared BAEPs between definite or uncertain MS cases, patients with iso lated neurological syndromes compatible with demyelination, patients with a single acute non-diagnosed episode and sub jects with brainstem or disseminated disorder different from demyelination. The latter included vascular, compres sive, inflammatory or degenerative disease and Arnold- Chiari malformation. Early and middle latency components were analysed. Abnormal responses were recorded in 56/96 MS cases, in 9/18 patients with progressive spastic
paraparesis, in 4/4 patients with bilateral retrobulbar neuritis, in 9/27 patients with an isolated non-diagnosed neurological episode and in 26/100 patients with disorders different from demyelination. Changes of the middle latency responses were detected only in the MS group, in whom these increased the total yield of abnormalities. Thus, recording of middle latency components added significant power to the test. Among MS cases, abnormal BAEPs were strongly as
sociated with clinical signs of a brainstem lesion. A high incidence of abnormal responses (70% or more) was detected in patients showing brainstem dysfunctions, despite the fact that in some of them the diagnosis of MS was uncer tain. By contrast, in patients not showing brainstem disor ders the incidence of abnormal responses decreased by about 50% from definite to probable or possible cases.
A serial study on 27 MS cases was carried out in order to investigate the relationship between BAEP abnormalities and clinical changes (Robinson and Rudge, 1978). During a follow up period ranging from nine to 30 months, 16
patients experienced relapses and remissions, not always involving the brainstem, while 11 showed a stable clinical course. In 10 of the latter group, amplitude and latency of the BAEPs were remarkably constant between consecutive
recordings and in only one did the latency become abnormal. By contrast, BAEPs showed "fluctuations", i.e. deteriora tion, improvement or normalisation, in 8/16 patients with unstable clinical course. The changes were usually unre lated to the timing or type of symptoms and in only one case was an abnormality detected in coincidence with a
relapse involving the brainstem. The authors suggested that the instability of the BAEPs could be due to a general ef fect of activity of the disease on conduction in
Kjaer (1980a) pointed out that the incidence of abnor mal BAEPs increased with illness duration and degree of disability, as one would expect. In this series of 121 definite or suspected MS cases, patients with duration of symptoms of about 20 years had a significantly higher in cidence of abnormalities than those who had been ill for about two years. Also, among definite cases, the occurrence of abnormalities was almost twice as frequent in patients with moderate or severe disability as compared with those with mild clinical involvement.
Recent studies focused on the clinical and MRI corre lates of BAEP abnormalities. In one investigation (Baum et al., 1988), BAEPs were abnormal in 19/43 (44%) definite MS cases and were significantly correlated with the presence of brainstem dysfunctions. Areas of altered signal in the medulla, pons and mid-brain were detected in 60.5% of patients. In 71% of cases showing both BAEP and MRI abnor malities, the level of the MRI lesion corresponded to that suggested by the BAEP findings. Thus, there was a close correlation between BAEP and MRI findings. The conclusions of van der Poel et al. (1988) were different. They studied 40 patients, of whom 28 were classified as definite MS and 12 had an isolated brainstem syndrome compatible with
demyelination. BAEPs were abnormal in 21/28 definite MS cases (75%) but in only one patient with an isolated brainstem lesion. Wave V was affected in every abnormal waveform. MRI was performed in 20 cases only and showed a
variety of lesions in the medulla, pons and mid-brain in 9/9 MS cases and 5/11 (45%) patients with an isolated brainstem lesion. Although areas of increased signal at pontine level were detected in all patients with abnormal BAEPs, there was no clear pattern of correlation between alteration of single BAEP components and location of MRI lesions. Often, MRI and BAEP abnormalities were not commen surate with each other in the sense that large MRI lesions were sometimes associated with minimal or no BAEP abnor malities and, less frequently, BAEPs were found abnormal in the absence of an associated MRI lesion. Since this inves tigation was carried out with the same scanner as the one currently in use, there was considered to be a little prospect for further correlation studies.