Vagus nerve somatosensory evoked potentials in Parkinson’s disease

Polak, Thomas; Weise, David; Metzger, Florian; Ehlis, Ann‐Christine; Langer, J.; Schramm, Axel; Fallgatter, Andreas J.; Claßen, Joseph

doi:10.1007/s00415-011-6084-z

Cited by 18 publications

(21 citation statements)

References 10 publications

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“…Moreover, clinical studies have shown that the dorsal motor nucleus of the vagus nerve is disrupted at an early disease stage [32] by a-syn and Lewy body pathology in Parkinson's disease [33]. This finding was followed by the discovery that there was a close relationship between peripheral vagus nerve impairment and inhibition of the dopamine system in brain structures [34].…”

Section: Discussionmentioning

confidence: 99%

Intranasal administration of alpha-synuclein aggregates: a Parkinson's disease model with behavioral and neurochemical correlates

Gruden

Давыдова

Narkevich

et al. 2014

Behavioural Brain Research

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Parkinson's disease (PD) is a neurodegenerative disorder in which both alpha-synuclein (α-syn) and dopamine (DA) have a critical role. Our previous studies instigated a novel PD model based on nasal inoculation with α-syn aggregates which expressed parkinsonian-like behavioral and immunological features. The current study in mice substantiated the robustness of the amyloid nasal vector model by examining behavioral consequences with respect to DA-ergic neurochemical corollaries. In vitro generated α-syn oligomers and fibrils were characterized using atomic force microscopy and the thioflavin T binding assay. These toxic oligomers or fibrils administered alone (0.48 mg/kg) or their 50:50 combination (total dose of 0.48 mg/kg) were given intranasally for 14 days and "open-field" behavior was tested on days 0, 15 and 28 of the protocol. Behavioral deficits at the end of the 14-day dosing regime and on day 28 (i.e., 14 days after treatment completion) induced rigidity, hypokinesia and immobility. This was accompanied by elevated nigral but not striatal DA, DOPAC and HVA concentrations in response to dual administration of α-syn oligomers plus fibrils but not the oligomers by themselves. α-Syn fibrils intensified not only the hypokinesia and immobility 14 days post treatment, but also reduced vertical rearing and enhanced DA levels in the substantia nigra. Only nigral DA turnover (DOPAC/DA but not HVA/DA ratio) was augmented in response to fibril treatment but there were no changes in the striatum. Compilation of these novel behavioral and neurochemical findings substantiate the validity of the α-syn nasal vector model for investigating parkinsonian-like symptoms.

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Section: Discussionmentioning

confidence: 99%

Intranasal administration of alpha-synuclein aggregates: a Parkinson's disease model with behavioral and neurochemical correlates

Gruden

Давыдова

Narkevich

et al. 2014

Behavioural Brain Research

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“…However, eletrophysiological stimulation of the sensory auricular branches of the vagal nerve do not demonstrate variation in the vagus nerve somatosensory evoked potentials (Fallgatter et al 2003) of PD (Polak et al 2011) and AD patients (Polak et al 2007) thus indicating a more widespread dysfunction of the vagus nerve complex in PD than previously described (Polak et al 2011). Therefore, such findings are not underlying the pathology associated with unilaterality.…”

mentioning

confidence: 82%

The significance of neuronal lateralisation in Parkinson’s disease

Riederer

Sian-Hülsmann

2012

J Neural Transm

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The destruction of the dopaminergic neurons in the substantia nigra (SN) and consequent depletion of striatal dopamine elicits the main movement deficits related to Parkinson's disease (PD). In the early stages of the illness, the motor symptoms are often exhibited asymmetrically. Thus, the onset of PD features starts on either the right or left side. The side of onset appears to determine the prognosis of the disorder and other features, such as right-side tremor dominance has a better prognosis in contrast to left-side dominant bradykinesia-rigidity. In addition, left-side onset of motor features is associated with cognitive decline. Therefore, an intricate relation appears to exist between the side of disease onset and progression/severity and other non-motor symptoms. Unilateral PD in turn corresponds to neuronal nigrostriatal degeneration in the contralateral hemisphere. Indeed positron emission tomography has demonstrated a positive correlation between symptom asymmetry and brain function (Hoorn et al. Parkinsonism Relat Disord 17:58-60, 2011), which corresponds to a unilateral pattern of degeneration. This phenomenon appears to be exclusive to PD. Additionally, the variation in motor symptom(s) dominance exhibited in the disorder conforms to the notion that PD is a spectrum disease with many sub-groups. Thus, clinical and post mortem studies on "lateralisation" may serve as a vital tool in understanding the mechanism(s) eliciting the characteristic destruction of the SN neurons. Additionally, it may be employed as a predictive indicator for the symptomology and prognosis of the illness thus allowing selective treatment strategies targeted at the pronounced hemispheric degeneration.

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“…Thus, prolongation of VSEP latencies as compared with healthy controls may be because of brainstem involvement demonstrated in half of the cases. Prolongation of VSEP latencies without statistically significant change of amplitudes as compared with controls reflects the situation of VSEP analysis in neurodegenerative diseases such as Alzheimer's dementia and Parkinson's disease [1,2] with nonfocal brainstem affection involving specific brainstem nuclei [5,6]. In contrast to neurodegenerative diseases, this is the first study showing a hint for a direct connection between neurological and radiological results and VSEP latencies.…”

Section: Discussionmentioning

confidence: 65%

“…The principle of VSEP is based on the electrical stimulation of the auricular branch of the vagus nerve (ABVN [3]) showing afferences not only to trigeminal nuclei, but also to the solitary tract nucleus as a central afference of the main vagus trunk [4]. VSEP can be detected as short-range far-field potentials all over the scalp and show prolonged latencies in Alzheimer's dementia and Parkinson's disease [1,2]. However, the conclusion of VSEP being generated at brainstem level resulting from these studies is based upon the assumption of degeneration of specific brainstem nuclei in those neurodegenerative diseases [5,6] partially overlapping with vagus afferences [7].…”

Section: Introductionmentioning

confidence: 99%

“…Vagus somatosensory-evoked potentials (VSEP) were proposed for clinical practice as a possible means for the early and differential diagnosis for neurodegenerative diseases and the functional assessment of specific brainstem nuclei in those diseases [1,2]. The principle of VSEP is based on the electrical stimulation of the auricular branch of the vagus nerve (ABVN [3]) showing afferences not only to trigeminal nuclei, but also to the solitary tract nucleus as a central afference of the main vagus trunk [4].…”

Section: Introductionmentioning

confidence: 99%

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Vagus somatosensory-evoked potentials are prolonged in patients with multiple sclerosis with brainstem involvement

Polak

Zeller²,

Fallgatter³

et al. 2013

NeuroReport

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Vagus somatosensory-evoked potentials (VSEP) were proposed as a neurophysiological indicator of brainstem dysfunction based on prolonged latencies found in Alzheimer's dementia and Parkinson's disease. We now aimed at a further confirmation of this view independent from neurodegenerative diseases and hypothesized that VSEP in multiple sclerosis with brainstem affection show prolonged latencies, too. In 15 patients with multiple sclerosis according to McDonald and 15 healthy controls after stimulation of the auricular branch of the vagus nerve at the tragus (electrical square impulses, impulse width 0.1 ms, interstimulus interval 2 s, intensity 8 mA), evoked potentials were recorded from electrode positions C3-F3, C4-F4, Fz-F3 and Fz-F4. Analysis of variance showed a significant main effect of the factor diagnosis on latency P1 (F(1,24)=7.067, P=0.001), no significant effect for latencies N1 and P2 nor for the amplitudes. A subgroup of patients with signs of brainstem affection showed a trend for longer P1 latencies (F(1,11)=5916, P=0.033) as compared with the group without. We take this result as further hint for VSEP to be generated at brainstem level which needs confirmation in larger-scale studies and other brainstem-affecting diseases. The method could be suitable for the demonstration of the involvement of differential brainstem nuclei in various neurodegenerative diseases.

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Vagus nerve somatosensory evoked potentials in Parkinson’s disease

Cited by 18 publications

References 10 publications

Intranasal administration of alpha-synuclein aggregates: a Parkinson's disease model with behavioral and neurochemical correlates

Intranasal administration of alpha-synuclein aggregates: a Parkinson's disease model with behavioral and neurochemical correlates

The significance of neuronal lateralisation in Parkinson’s disease

Vagus somatosensory-evoked potentials are prolonged in patients with multiple sclerosis with brainstem involvement

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