scholarly journals Thalamic Relay Nucleus Stimulation as a Preventive Method against Recurrent Tendency following Thalamotomy for Intractable Pain

1976 ◽  
Vol 16pt2 (3) ◽  
pp. 247-254
Author(s):  
TAKASHI TSUBOKAWA ◽  
AKIO KOTANI ◽  
HIROSHI NISHIMOTO ◽  
YOICHI KATAYAMA ◽  
NOBUO MORIYASU
Keyword(s):  
Intractable Pain ◽  
Thalamic Relay ◽  
Preventive Method ◽  
Relay Nucleus

Thalamic relay nucleus stimulation for relief of intractable pain. Clinical results and β-endorphin immunoreactivity in the cerebrospinal fluid

Pain ◽  
1984 ◽  
Vol 18 (2) ◽  
pp. 115-126 ◽  
Author(s):  
Takashi Tsubokawa ◽  
Takamitsu Yamamoto ◽  
Yoichi Katayama ◽  
Teruyasu Hirayama ◽  
Haruo Sibuya
Keyword(s):  
Cerebrospinal Fluid ◽  
Clinical Results ◽  
Intractable Pain ◽  
Thalamic Relay ◽  
Relay Nucleus

Clonazepam suppresses GABAB-mediated inhibition in thalamic relay neurons through effects in nucleus reticularis

1994 ◽  
Vol 71 (6) ◽  
pp. 2576-2581 ◽  
Author(s):  
J. R. Huguenard ◽  
D. A. Prince
Keyword(s):  
Gamma Aminobutyric Acid ◽  
Postsynaptic Inhibition ◽  
Nucleus Reticularis ◽  
Thalamic Relay ◽  
Relay Nucleus ◽  
A Site ◽  
Thalamic Relay Neurons ◽  
Gabaa Antagonist ◽  
Relay Neurons

1. Experiments were carried out using patch-clamp techniques in rat thalamic slices, maintained in vitro, to examine the effects of the benzodiazepine compound, clonazepam (CZP), on intrathalamic inhibition. Bath-applied CZP reduced the gamma-aminobutyric acid-B (GABAB) component of inhibitory postsynaptic potentials and currents (IPSPs and IPSCs, respectively) evoked in rat thalamic somatosensory relay neurons by stimulation of nucleus reticularis thalami (nRt), without consistently affecting the GABAA IPSP. Secondary IPSPs, which occur as a result of intrathalamic oscillations, were dramatically reduced. 2. Voltage-clamp experiments combined with local or bath perfusion of the GABAA antagonist bicuculline methiodide (BMI), demonstrated that nRt is a site of GABAA-mediated postsynaptic inhibition that affects inhibitory output onto relay neurons. BMI enhanced both GABAA and GABAB postsynaptic inhibition in relay neurons when applied to nRt. Focal applications in the ventrobasal relay nucleus near the recording electrode blocked the GABAA-mediated IPSP but had no effects on GABAB inhibitory potentials. 3. Results suggest that CZP acts to facilitate recurrent inhibition in nRt and decrease its inhibitory output onto relay neurons. Intra-nRt GABAA-mediated inhibition thus has an important role in controlling thalamic excitability and in the anti-absence actions of CZP.

Chronic motor cortex stimulation in patients with thalamic pain

1993 ◽  
Vol 78 (3) ◽  
pp. 393-401 ◽  
Author(s):  
Takashi Tsubokawa ◽  
Yoichi Katayama ◽  
Takamitsu Yamamoto ◽  
Teruyasu Hirayama ◽  
Seigou Koyama
Keyword(s):  
Sensory Neurons ◽  
Pain Control ◽  
Precentral Gyrus ◽  
Content Type ◽  
Nociceptive Neurons ◽  
Thalamic Relay ◽  
Relay Nucleus ◽  
Pain Inhibition ◽  
Thalamic Pain ◽  
Stimulation Of

✓ Analysis of the authors' experience over the last 10 years has indicated that excellent pain control has rarely been obtained by thalamic relay nucleus stimulation in patients with thalamic pain. In the present study, 11 patients with thalamic pain were treated by chronic stimulation of the precentral gyrus. In eight patients (73%), the stimulation system was internalized since excellent pain control was achieved during a 1-week test period of precentral gyrus stimulation. In contrast, no clear effect was noted or the original pain was even exacerbated by postcentral gyrus stimulation. The effect of precentral stimulation was unchanged in five patients (45%) for follow-up periods of more than 2 years. In the remaining three patients, the effect decreased gradually over several months. This outcome was significantly better than that obtained in an earlier series tested by the authors with thalamic relay nucleus stimulation (p < 0.05). The pain inhibition usually occurred at intensities below the threshold for production of muscle contraction (pulse duration 0.1 to 0.5 msec, intensity 3 to 8 V). When good pain inhibition was achieved, the patients reported a slight tingling or mild vibration sensation during stimulation projected in the same area of distribution as their pain. The authors discuss the possibility that, in deafferentation pain, sensory neurons below the level of deafferentation cannot exert their normal inhibitory influences toward deafferented nociceptive neurons because of the development of aberrant connections. Thus, while stimulation of the first- to third-order sensory neurons at the level of the thalamic relay nucleus or below cannot bring about good pain inhibition in patients with thalamic pain, activation of hypothetical fourth-order sensory neurons through precentral stimulation may be able to inhibit deafferented nociceptive neurons within the cortex. None of the patients developed either observable or electroencephalographic seizure activity.

Vagal-Evoked Activity in the Parafascicular Nucleus of the Primate Thalamus

2005 ◽  
Vol 94 (4) ◽  
pp. 2976-2982 ◽  
Author(s):  
Shin-Ichi Ito ◽  
A. D. Craig
Keyword(s):  
Vagus Nerve Stimulation ◽  
Macaque Monkey ◽  
Physiological Effects ◽  
Afferent Activity ◽  
Parafascicular Nucleus ◽  
Thalamic Relay ◽  
Relay Nucleus ◽  
Intralaminar Nucleus ◽  
Vagal Afferent ◽  
Evoked Activity

The physiological effects of ascending vagal afferent activity in the primate forebrain have not been established, and because vagus nerve stimulation (VNS) is useful clinically for treatment of epilepsy and depression, these actions need to be identified. We used a roving microelectrode to record vagal-evoked potentials in the thalamus of the macaque monkey. In addition to the anticipated activation in the gustatory/visceral thalamic relay nucleus, we found an unexpectedly larger and earlier response focus with multi-unit discharges in the adjacent parafascicular nucleus. These data reveal a potent vagal input to this intralaminar nucleus, which is normally considered to be involved in motor control. This finding indicates that a role for this vagal activation site in the anti-epileptic effects of VNS needs to be considered.

scholarly journals Dynamic Transitions of Epilepsy Waveforms Induced by Astrocyte Dysfunction and Electrical Stimulation

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Honghui Zhang ◽  
Zhuan Shen ◽  
Qiangui Zhao ◽  
Luyao Yan ◽  
Lin Du ◽  
...  
Keyword(s):  
Experimental Studies ◽  
Low Frequency ◽  
Single Pulse ◽  
Neuronal Population ◽  
Absence Epilepsy ◽  
Neuronal Populations ◽  
Stimulation Mode ◽  
Thalamic Relay ◽  
Relay Nucleus ◽  
Feedforward Inhibition

Experimental studies have shown that astrocytes participate in epilepsy through inducing the release of glutamate. Meanwhile, considering the disinhibition circuit among inhibitory neuronal populations with different time scales and the feedforward inhibition connection from thalamic relay nucleus to cortical inhibitory neuronal population, here, we propose a modified thalamocortical field model to systematically investigate the mechanism of epilepsy. Firstly, our results show that rich firing activities can be induced by astrocyte dysfunction, including high or low saturated state, high- or low-frequency clonic, spike-wave discharge (SWD), and tonic. More importantly, with the enhancement of feedforward inhibition connection, SWD and tonic oscillations will disappear. In other words, all these pathological waveforms can be suppressed or eliminated. Then, we explore the control effects after different external stimulations applying to thalamic neuronal population. We find that single-pulse stimulation can not only suppress but also induce pathological firing patterns, such as SWD, tonic, and clonic oscillations. And we further verify that deep brain stimulation can control absence epilepsy by regulating the amplitude and pulse width of stimulation. In addition, based on our modified model, 3 : 2 coordinated reset stimulation strategies with different intensities are compared and a more effective and safer stimulation mode is proposed. Our conclusions are expected to give more theoretical insights into the treatment of epilepsy.

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