High-frequency stimulation in the ventral posterolateral thalamus reverses electrophysiologic changes and hyperalgesia in a rat model of peripheral neuropathic pain

Iwata, Masashi; LeBlanc, Brian W.; Kadasi, Laith M; Zerah, Michele L.; Cosgrove, Rees; Saab, Carl Y.

doi:10.1016/j.pain.2011.07.011

Cited by 63 publications

(55 citation statements)

References 58 publications

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“…Isoflurane was used only during the mPET scan. Given that mPET measures the level of spatial radioactive distribution and the radioactivity of 18 F-FDG had already accumulated over time during the uptake period, we suggest that isoflurane could not have affected our mPET results.…”

Section: Using Mpet To Determine How Mcs Changes the Brain Networkmentioning

confidence: 97%

“…Each rat was kept in a cage for 30 minutes for adaptation before 18 F-FDG injection. The rat was lightly anesthetized using 2% isoflurane, and 18 F-FDG (2 mCi) was administered intraperitoneally.…”

Section: Immunohistochemistrymentioning

confidence: 99%

“…To study how MCS works in pain modulation, we performed mPET imaging using 18 F-FDG. We demonstrated that neuropathic pain decreased glucose metabolism in the cerebellum, striatum, and the thalamic area (Fig.…”

Section: Using Mpet To Determine How Mcs Changes the Brain Networkmentioning

confidence: 99%

“…However, mPET imaging is an indirect way of scanning whole-brain activity by measuring the radioactivity of a tracer that is selected for tracking a specific target. We selected 18 F-FDG as a glucose tracer. 18 F-FDG requires 30-60 minutes for uptake by neurons in the brain.…”

Section: Using Mpet To Determine How Mcs Changes the Brain Networkmentioning

confidence: 99%

“…We selected 18 F-FDG as a glucose tracer. 18 F-FDG requires 30-60 minutes for uptake by neurons in the brain. The rats administered 18 F-FDG were awake for 60 minutes, and we performed behavioral testing and electrical stimulation at that time.…”

Section: Using Mpet To Determine How Mcs Changes the Brain Networkmentioning

confidence: 99%

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Motor cortex stimulation and neuropathic pain: how does motor cortex stimulation affect pain-signaling pathways?

Kim

Ryu

Lee

et al. 2016

JNS

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N europathic pain is often severe, and it can afflict patients for their entire lifetime. It can be caused by direct damage to the nervous system, and by neuronal degeneration. 7,8 Patients with degenerative diseases such as Parkinson's disease or dementia may experience neuropathic pain as a complication. Many studies have found that neuropathic pain can be induced by indirect nerve damage, but the mechanisms have not yet been clearly established. 7,8,29 The symptoms of neuropathic pain differ among patients, making treatment difficult.31 Although many studies of neuropathic pain and its control have been conducted, the mechanisms behind neuropathic pain are still not clear.Motor cortex stimulation (MCS) is a treatment modality used to modulate neuropathic pain by electrical stimulation. It was introduced in 1991 by Tsubokawa et al. and has since been used in clinical practice.46,47 MCS has advantages for clinicians and patients: MCS is simpler and easier to implement for pain modulation than other surgical methods, such as direct nerve stimulation and neurectomy, and can be considered an alternative for pain control. Among the many modalities involving electrical obJective Neuropathic pain is often severe. Motor cortex stimulation (MCS) is used for alleviating neuropathic pain, but the mechanism of action is still unclear. This study aimed to understand the mechanism of action of MCS by investigating pain-signaling pathways, with the expectation that MCS would regulate both descending and ascending pathways. methods Neuropathic pain was induced in Sprague-Dawley rats. Surface electrodes for MCS were implanted in the rats. Tactile allodynia was measured by behavioral testing to determine the effect of MCS. For the pathway study, immunohistochemistry was performed to investigate changes in c-fos and serotonin expression; micro-positron emission tomography (mPET) scanning was performed to investigate changes of glucose uptake; and extracellular electrophysiological recordings were performed to demonstrate brain activity. results MCS was found to modulate c-fos and serotonin expression. In the mPET study, altered brain activity was observed in the striatum, thalamic area, and cerebellum. In the electrophysiological study, neuronal activity was increased by mechanical stimulation and suppressed by MCS. After elimination of artifacts, neuronal activity was demonstrated in the ventral posterolateral nucleus (VPL) during electrical stimulation. This neuronal activity was effectively suppressed by MCS. coNclusioNs This study demonstrated that MCS effectively attenuated neuropathic pain. MCS modulated ascending and descending pain pathways. It regulated neuropathic pain by affecting the striatum, periaqueductal gray, cerebellum, and thalamic area, which are thought to regulate the descending pathway. MCS also appeared to suppress activation of the VPL, which is part of the ascending pathway.

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Section: Using Mpet To Determine How Mcs Changes the Brain Networkmentioning

confidence: 97%

Section: Immunohistochemistrymentioning

confidence: 99%

Section: Using Mpet To Determine How Mcs Changes the Brain Networkmentioning

confidence: 99%

Section: Using Mpet To Determine How Mcs Changes the Brain Networkmentioning

confidence: 99%

Section: Using Mpet To Determine How Mcs Changes the Brain Networkmentioning

confidence: 99%

See 3 more Smart Citations

Motor cortex stimulation and neuropathic pain: how does motor cortex stimulation affect pain-signaling pathways?

Kim

Ryu

Lee

et al. 2016

JNS

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T‐type calcium channels as therapeutic targets in essential tremor and Parkinson's disease

Matthews

Puryear

Correia

et al. 2023

Ann Clin Transl Neurol

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Neuronal action potential firing patterns are key components of healthy brain function. Importantly, restoring dysregulated neuronal firing patterns has the potential to be a promising strategy in the development of novel therapeutics for disorders of the central nervous system. Here, we review the pathophysiology of essential tremor and Parkinson's disease, the two most common movement disorders, with a focus on mechanisms underlying the genesis of abnormal firing patterns in the implicated neural circuits. Aberrant burst firing of neurons in the cerebello-thalamo-cortical and basal ganglia-thalamo-cortical circuits contribute to the clinical symptoms of essential tremor and Parkinson's disease, respectively, and T-type calcium channels play a key role in regulating this activity in both the disorders. Accordingly, modulating T-type calcium channel activity has received attention as a potentially promising therapeutic approach to normalize abnormal burst firing in these diseases. In this review, we explore the evidence supporting the theory that T-type calcium channel blockers can ameliorate the pathophysiologic mechanisms underlying essential tremor and Parkinson's disease, furthering the case for clinical investigation of these compounds. We conclude with key considerations for future investigational efforts, providing a critical framework for the development of much needed agents capable of targeting the dysfunctional circuitry underlying movement disorders such as essential tremor, Parkinson's disease, and beyond.

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Altered resting activity patterns and connectivity in individuals with complex regional pain syndrome

Pietro

Lee

Henderson

2020

Human Brain Mapping

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Complex regional pain syndrome (CRPS) is a chronic neuropathic pain disorder that typically occurs in the limbs, usually the upper limb. CRPS usually develops from a peripheral event but its maintenance relies on changes within the central nervous system. While functional abnormalities in the thalamus and primary somatosensory cortex (S1) of the brain are some of the most consistently reported brain findings in CRPS, the mechanisms are yet to be explored in full, not least of all how these two regions interact and how they might relate to clinical deficits, such as the commonly reported poor tactile acuity in this condition. This study recruited 15 upper‐limb CRPS subjects and 30 healthy controls and used functional magnetic resonance imaging (fMRI) to investigate infra‐slow oscillations (ISOs) in critical pain regions of the brain in CRPS. As hypothesised, we found CRPS was associated with increases in resting signal intensity ISOs (0.03–0.06 Hz) in the thalamus contralateral to the painful limb in CRPS subjects. Interestingly, there was no such difference between groups in S1, however CRPS subjects displayed stronger thalamo‐S1 functional connectivity than controls, and this was related to pain. As predicted, CRPS subjects displayed poor tactile acuity on the painful limb which, interestingly, was also related to thalamo‐S1 functional connectivity strength. Our findings provide novel evidence of altered patterns of resting activity and connectivity in CRPS which may underlie altered thalamocortical loop dynamics and the constant perception of pain.

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High-frequency stimulation in the ventral posterolateral thalamus reverses electrophysiologic changes and hyperalgesia in a rat model of peripheral neuropathic pain

Cited by 63 publications

References 58 publications

Motor cortex stimulation and neuropathic pain: how does motor cortex stimulation affect pain-signaling pathways?

Motor cortex stimulation and neuropathic pain: how does motor cortex stimulation affect pain-signaling pathways?

T‐type calcium channels as therapeutic targets in essential tremor and Parkinson's disease

Altered resting activity patterns and connectivity in individuals with complex regional pain syndrome

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