Very Fast Oscillations Evoked by Median Nerve Stimulation in the Human Thalamus and Subthalamic Nucleus

2004 ◽  
Vol 92 (6) ◽  
pp. 3171-3182 ◽  
Author(s):  
Ritsuko Hanajima ◽  
Robert Chen ◽  
Peter Ashby ◽  
Andres M. Lozano ◽  
William D. Hutchison ◽  
...  
Keyword(s):  
Median Nerve ◽  
Subthalamic Nucleus ◽  
Nerve Stimulation ◽  
Medial Lemniscus ◽  
Median Nerve Stimulation ◽  
Human Thalamus ◽  
Sensory Evoked Potentials ◽  
Sensory Evoked ◽  
Fast Oscillations ◽  
Low Amplitude

Very fast oscillations (VFOs; 500–1,500 Hz) are associated with sensory-evoked potentials (SEPs), but their origin is unknown. To characterize the origins of VFOs, we studied 35 patients with deep brain stimulation (DBS) electrodes [15 with thalamic and 20 with the subthalamic nucleus (STN) electrodes]. We recorded median nerve stimulation–evoked SEPs from the thalamus and STN with microelectrodes during stereotactic surgery and from the contacts of the DBS electrodes postoperatively. We also examined the firing of individual neurons in thalamus in relation to the VFOs. In the thalamus, VFOs with frequencies around 1,000 Hz were superimposed on slow potentials. Both slow and fast SEP components showed phase reversals in the somatosensory thalamus [ventralis caudalis (Vc)]. Median nerve poststimulus time histograms showed that single thalamic neurons fired at preferred times at intervals between 0.8 to 1.2 ms that were synchronous with the VFOs, although the neurons fired only once or a few times per trial. In the STN, low-amplitude SEPs with VFOs were observed at a latency similar to the thalamic SEPs. The VFOs from STN probably represent volume conduction, possibly from the medial lemniscus. We conclude that the thalamic VFOs are generated within Vc and that they induce time-locked firing in a network of neurons.

scholarly journals The Oscillatory Effects of Rhythmic Median Nerve Stimulation

2020 ◽  
Author(s):  
Mairi S. Houlgreave ◽  
Barbara Morera Maiquez ◽  
Matthew J. Brookes ◽  
Stephen R. Jackson
Keyword(s):  
Evoked Potentials ◽  
Median Nerve ◽  
Somatosensory Cortex ◽  
Nerve Stimulation ◽  
Afferent Input ◽  
List Type ◽  
Beta Band ◽  
Median Nerve Stimulation ◽  
Sensory Evoked Potentials ◽  
Sensory Evoked

AbstractEntrainment of brain oscillations can be achieved using rhythmic non-invasive brain stimulation, and stimulation of the motor cortex at a frequency associated with sensorimotor inhibition can impair motor responses. Despite the potential therapeutic applications, these techniques do not lend themselves to use outside a clinical setting. Here, the aim was to investigate whether rhythmic median nerve stimulation (MNS) could be used to entrain oscillations related to sensorimotor inhibition. MEG data were recorded from 20 participants during 400 trials, where for each trial 10 pulses of MNS were delivered either rhythmically or arrhythmically at 12 or 20Hz. Our results demonstrate a frequency specific increase in relative amplitude in the contralateral somatosensory cortex during rhythmic but not arrhythmic stimulation. This was coupled with an increase in inter-trial phase coherence at the same frequency, suggesting that the oscillations synchronised with the pulses of MNS. While the results show that 20Hz rhythmic peripheral nerve stimulation can produce entrainment, the response to 12Hz stimulation was largely due to the presence of rhythmic sensory evoked potentials. Regardless rhythmic MNS resulted in synchronous firing of neuronal populations within the contralateral somatosensory cortex meaning these neurons were occupied in processing of the afferent input. Therefore, MNS could prove therapeutically useful in disorders associated with hyperexcitability within the sensorimotor cortices.HighlightsRhythmic median nerve stimulation at 12Hz causes rhythmic sensory evoked potentials.Rhythmic median nerve stimulation at 20Hz causes entrainment of beta-band neural oscillations.

scholarly journals Median Nerve Stimulation Facilitates the Identification of Somatotopy of the Subthalamic Nucleus in Parkinson’s Disease Patients under Inhalational Anesthesia

Biomedicines ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 74
Author(s):  
Yu-Chen Chen ◽  
Chang-Chih Kuo ◽  
Shin-Yuan Chen ◽  
Tsung-Ying Chen ◽  
Yan-Hong Pan ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Median Nerve ◽  
Subthalamic Nucleus ◽  
Nerve Stimulation ◽  
Electrode Placement ◽  
Beta Band ◽  
Inhalational Anesthesia ◽  
Median Nerve Stimulation ◽  
Power Spectral

Deep brain stimulation (DBS) improves Parkinson’s disease (PD) symptoms by suppressing neuropathological oscillations. These oscillations are also modulated by inhalational anesthetics used during DBS surgery in some patients, influencing electrode placement accuracy. We sought to evaluate a method that could avoid these effects. We recorded subthalamic nucleus (STN) neuronal firings in 11 PD patients undergoing DBS under inhalational anesthesia. Microelectrode recording (MER) during DBS was collected under median nerve stimulation (MNS) delivered at 5, 20, and 90 Hz frequencies and without MNS. We analyzed the spike firing rate and neuronal activity with power spectral density (PSD), and assessed correlations between the neuronal oscillation parameters and clinical motor outcomes. No patient experienced adverse effects during or after DBS surgery. PSD analysis revealed that peripheral 20 Hz MNS produced significant differences in the dorsal and ventral subthalamic nucleus (STN) between the beta band oscillation (16.9 ± 7.0% versus 13.5 ± 4.8%, respectively) and gamma band oscillation (56.0 ± 13.7% versus 66.3 ± 9.4%, respectively) (p < 0.05). Moreover, 20-Hz MNS entrained neural oscillation over the dorsal STN, which correlated positively with motor disabilities. MNS allowed localization of the sensorimotor STN and identified neural characteristics under inhalational anesthesia. This paradigm may help identify an alternative method to facilitate STN identification and DBS surgery under inhalational anesthesia.

Recovery of peripheral and central responses to median nerve stimulation

1988 ◽  
Vol 69 (6) ◽  
pp. 585-588 ◽  
Author(s):  
Ricardo C. Reisin ◽  
Douglas S. Goodin ◽  
Michael J. Aminoff ◽  
Mary M. Mantle
Keyword(s):  
Median Nerve ◽  
Nerve Stimulation ◽  
Median Nerve Stimulation

scholarly journals Median nerve stimulation induces analgesia via orexin-initiated endocannabinoid disinhibition in the periaqueductal gray

2018 ◽  
Vol 115 (45) ◽  
pp. E10720-E10729 ◽  
Author(s):  
Yi-Hung Chen ◽  
Hsin-Jung Lee ◽  
Ming Tatt Lee ◽  
Ya-Ting Wu ◽  
Yen-Hsien Lee ◽  
...  
Keyword(s):  
Pain Management ◽  
Median Nerve ◽  
Nerve Stimulation ◽  
Antinociceptive Effect ◽  
Low Frequency ◽  
Periaqueductal Gray ◽  
Orexin A ◽  
Median Nerve Stimulation ◽  
Opioid Receptor Antagonists ◽  
Nociceptive Responses

Adequate pain management remains an unmet medical need. We previously revealed an opioid-independent analgesic mechanism mediated by orexin 1 receptor (OX1R)-initiated 2-arachidonoylglycerol (2-AG) signaling in the ventrolateral periaqueductal gray (vlPAG). Here, we found that low-frequency median nerve stimulation (MNS) through acupuncture needles at the PC6 (Neiguan) acupoint (MNS-PC6) induced an antinociceptive effect that engaged this mechanism. In mice, MNS-PC6 reduced acute thermal nociceptive responses and neuropathy-induced mechanical allodynia, increased the number of c-Fos–immunoreactive hypothalamic orexin neurons, and led to higher orexin A and lower GABA levels in the vlPAG. Such responses were not seen in mice with PC6 needle insertion only or electrical stimulation of the lateral deltoid, a nonmedian nerve-innervated location. Directly stimulating the surgically exposed median nerve also increased vlPAG orexin A levels. MNS-PC6–induced antinociception (MNS-PC6-IA) was prevented by proximal block of the median nerve with lidocaine as well as by systemic or intravlPAG injection of an antagonist of OX1Rs or cannabinoid 1 receptors (CB1Rs) but not by opioid receptor antagonists. Systemic blockade of OX1Rs or CB1Rs also restored vlPAG GABA levels after MNS-PC6. A cannabinoid (2-AG)-dependent mechanism was also implicated by the observations that MNS-PC6-IA was prevented by intravlPAG inhibition of 2-AG synthesis and was attenuated inCnr1−/−mice. These findings suggest that PC6-targeting low-frequency MNS activates hypothalamic orexin neurons, releasing orexins to induce analgesia through a CB1R-dependent cascade mediated by OX1R-initiated 2-AG retrograde disinhibition in the vlPAG. The opioid-independent characteristic of MNS-PC6–induced analgesia may provide a strategy for pain management in opioid-tolerant patients.

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