Journal of Neurology

, Volume 258, Issue 12, pp 2276–2277

Vagus nerve somatosensory evoked potentials in Parkinson’s disease

Authors

    • Department of Psychiatry, Psychosomatics and PsychotherapyUniversity Clinic Wuerzburg
  • D. Weise
    • Department of NeurologyUniversity of Wuerzburg
    • Department of NeurologyUniversity of Leipzig
  • F. Metzger
    • Department of Psychiatry, Psychosomatics and PsychotherapyUniversity Clinic Wuerzburg
    • Department of Psychiatry and PsychotherapyUniversity of Tuebingen
    • German Center for Neurodegenerative DiseasesUniversity of Tuebingen
  • A. C. Ehlis
    • Department of Psychiatry, Psychosomatics and PsychotherapyUniversity Clinic Wuerzburg
    • Department of Psychiatry and PsychotherapyUniversity of Tuebingen
  • J. B. Langer
    • Department of Psychiatry, Psychosomatics and PsychotherapyUniversity Clinic Wuerzburg
  • A. Schramm
    • Department of NeurologyUniversity of Erlangen
  • A. J. Fallgatter
    • Department of Psychiatry, Psychosomatics and PsychotherapyUniversity Clinic Wuerzburg
    • Department of Psychiatry and PsychotherapyUniversity of Tuebingen
    • German Center for Neurodegenerative DiseasesUniversity of Tuebingen
  • J. Classen
    • Department of NeurologyUniversity of Wuerzburg
    • Department of NeurologyUniversity of Leipzig
Letter to the Editors

DOI: 10.1007/s00415-011-6084-z

Cite this article as:
Polak, T., Weise, D., Metzger, F. et al. J Neurol (2011) 258: 2276. doi:10.1007/s00415-011-6084-z

Dear Sirs,

Recent studies have emphasized that the pathology of Parkinson’s disease (PD) extends beyond the nigrostriatal system [1, 2]. According to the work of Braak [3], it may start in deep brain stem nuclei including the glossopharyngeal/vagus nerve complex. A method of vagus nerve somatosensory evoked potentials (VN-SEP) for the assessment of vagus nerve function has recently been developed by Fallgatter et al. [4]. In this pilot study, we tested the hypothesis that VN-SEP may be affected in PD patients.

In a prospective observational study approved by the local ethics committee and performed in accordance with the 1964 Declaration of Helsinki, 21 patients [7 females, age 66.7 ± 10.0 years (mean ± SD), range 45–79 years, mean disease duration 6.5 ± 4.1 years] with a clinical diagnosis of PD according to the British brain bank criteria [5] and 21 healthy age- and sex-matched controls (age 70.0 ± 10.2 years, range 49–81 years) were recruited after giving informed consent. All patients were on antiparkinsonian medication and had a disease stage of 2.2 ± 0.7 on the Hoehn and Yahr scale [6]. None of the participants showed signs of cognitive impairment in clinical evaluation. Stimulation was done according to published procedures [4, 7] on the inner side of the tragus (electrical square impulses of 0.1-ms duration, interstimulus interval 2 s, stimulus intensity 8 mA). Evoked potentials were recorded bipolarily from the electrode positions C3–F3, C4–F4, Fz–F3, Fz–F4 (scalp electrodes, impedances <2 kΩ, band-pass 0.1–1 kHz, analysis time 10 ms, averaging of 100 artifact-free epochs). Statistical analyses were performed by means of univariate ANOVAs for peak latencies (P1, N1, P2) and peak-to-peak amplitudes (P1-N1, N1-P2) separately. ANOVA for the VN-SEP latencies (Table 1) showed significant main effects for the within-subject factors “recording site” (CF vs. FzF, F1 = 4.484, p = 0,035) and “potential component” (P1, N1, P2, F1,2 = 198.925, p < 0.001) and for the between-subject factor “diagnosis” (patients vs. controls, F1 = 10.544, p = 0.001). No significant interactions for any of the other variables nor significant main effects, for any of the amplitude variables occurred (not shown). Post-hoc t-tests indicated longer latencies in the PD group compared to controls.
Table 1

Latencies (ms) of patients and controls

 

Patients

Controls

p

 

P1

P1

 

C3-F3

2.49 ± 0.57

2.08 ± 0.47

0.021

C4-F4

2.35 ± 0.63

2.49 ± 1.07

0.631

Fz-F3

2.60 ± 0.58

2.36 ± 0.63

0.225

Fz-F4

2.67 ± 0.96

2.19 ± 0.58

0.074

 

N1

N1

 

C3-F3

4.05 ± 0.77

3.37 ± 0.88

0.015

C4-F4

3.51 ± 1.06

3.43 ± 0.95

0.809

Fz-F3

4.33 ± 1.08

3.77 ± 1.39

0.175

Fz-F4

3.94 ± 1.30

3.68 ± 1.22

0.530

 

P2

P2

 

C3-F3

5.32 ± 1.01

4.49 ± 1.14

0.023

C4-F4

4.57 ± 1.25

4.69 ± 0.64

0.738

Fz-F3

5.21 ± 1.53

4.85 ± 1.69

0.523

Fz-F4

5.04 ± 1.24

4.76 ± 1.48

0.575

Electrode positions according to the international 10-20-system

The available evidence suggests that VN-SEP represents far field potentials of brainstem activity from vagus nuclei that can be elicited upon electrical stimulation of its auricular branch [8]. The present study disclosed significantly longer latencies in PD patients compared to controls, which may point to disease-related dysfunction of the sensory part of the vagus nerve (as part of the nucleus N. spinalis n. trigemini). Neuropathological studies have demonstrated involvement of the dorsal nucleus of the vagus nerve with sparing of other vagus nuclei [9]. Our findings, therefore, may point to a more widespread dysfunction in the vagus nerve complex than previously appreciated. Alternatively, the dorsal nucleus of the vagus nerve may be able to process somatosensory information.

Several limitations of our study have to be considered. First, the exact diagnosis of the Parkinsonian syndrome’s underlying disease would have been desirable. Likewise, drug effects cannot be ruled out. Finally, a previous study demonstrated latency prolongation in Alzheimer patients [10]. Thus, lack of formal assessment of cognitive impairment in our study may have led to inclusion of subjects with an Alzheimer comorbidity confounding the results.

In conclusion, the present study indicates that VN-SEP may be pathologically altered in PD patients. After this proof of principle has been achieved, larger studies including patients at different stages of disease, a control group without medication as well as extended neuropsychological testing will be evaluating VN-SEP as a tool capable of identifying potential pre-motor manifestations as a possible early marker in PD [11].

Conflict of interest

None.

Copyright information

© Springer-Verlag 2011