Motor cortex stimulation reduces hyperalgesia in an animal model of central pain

Lucas, Jessica M.; Ji, Yadong; Masri, Radi

doi:10.1016/j.pain.2011.02.025

Cited by 80 publications

(90 citation statements)

References 65 publications

(86 reference statements)

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“…GABAergic transmission in the ZI is complex. Cha et al reported that muscimol injection into the ZI evoked ZI neuron inactivation,52,53 but the results of Moon et al did not agree 13. It would be possible to target on complex ZI itself and posterior thalmaus.…”

Section: Discussionmentioning

confidence: 98%

Reduced GABAergic neuronal activity in zona incerta causes neuropathic pain in a rat sciatic nerve chronic constriction injury model

Moon¹,

Park²

2017

JPR

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PurposeThe zona incerta (ZI) is below the ventral tier of the thalamus and has a strong influence selectively in higher-order thalamic relays. Although neuropathic pain has been suggested to result from reduced gamma-aminobutyric acid (GABA) and GABAergic signaling in the ZI, the mechanisms remain unclear. Here, the role of GABA and GABAergic signaling was investigated in the ZI in neuropathic pain using sciatic nerve chronic constriction injury (CCI) rats.Materials and methodsSingle-unit neuronal activity was recorded, and microdialysis was performed in the ZI of CCI rats and sham-treated rats in vivo. This study also compared ZI neuronal activity after treatment with saline, the GABAA receptor agonist (muscimol), or the GABAA receptor antagonist (bicuculline).Results and conclusionCCI rats exhibited hypersensitivity to pain as evidenced by decreased hind paw withdrawal threshold and latency. CCI rats also showed reduced GABA level and decreased neuronal activity in the ZI compared with sham-treated rats. Treatment with GABAA receptor agonist, but not GABAA receptor antagonist, ameliorated pain hypersensitivity and increased the firing rate (spikes/s) of ZI neurons in CCI rats.

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Section: Discussionmentioning

confidence: 98%

Reduced GABAergic neuronal activity in zona incerta causes neuropathic pain in a rat sciatic nerve chronic constriction injury model

Moon¹,

Park²

2017

JPR

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“…The only plausible explanation that has been suggested for the effect of MCS is that it acts as a descending modulator. 12,27 More studies are required to understand the relationship between MCS and neuropathic pain. We hypothesized that MCS acts as not only a descending modulator but also an ascending modulator of pain pathways.…”

Section: Fig 5 Comparison Of the Behavioral Test Results Between Ipmentioning

confidence: 99%

“…Fonoff et al 12 and Lucas et al 27 hypothesized that MCS stimulates serotonin secretion in the periaqueductal gray (PAG) directly, or indirectly via the zona incerta (ZI). Therefore, we expected to observe changes in serotonin levels in the spinal cord.…”

Section: How Does Mcs Affect the Descending Pathway?mentioning

confidence: 99%

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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“…Bachmann et al, 2013). Intriguingly, the motor and sensory aspects of cortical reorganization after spinal cord injury seems to be tightly linked, as suggested by the beneficial effects induced by motor cortex stimulation on central pain (Lucas et al, 2011, Cha et al, 2013; Jiang et al, 2013). …”

Section: Cortical Reorganization Depends On Species (Fig 1)mentioning

confidence: 99%

Cortical reorganization after spinal cord injury: Always for good?

et al. 2014

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Plasticity constitutes the basis of behavioral changes as a result of experience. It refers to neural network shaping and re-shaping at the global level and to synaptic contacts remodeling at the local level, either during learning or memory encoding, or as a result of acute or chronic pathological conditions. ‘Plastic’ brain reorganization after central nervous system lesions has a pivotal role in the recovery and rehabilitation of sensory and motor dysfunction, but can also be “maladaptive”. Moreover, it is clear that brain reorganization it is not a “static” phenomenon but rather a very dynamic process. Spinal cord injury immediately initiates a change in brain state and starts cortical reorganization. In the long term, the impact of injury – with or without accompanying therapy – on the brain is a complex balance between supraspinal reorganization and spinal recovery. The degree of cortical reorganization after spinal cord injury is highly variable, and can range from no reorganization (i.e. “silencing”) to massive cortical remapping. This variability critically depends on the species, the age of the animal when the injury occurs, the time after the injury has occurred, and the behavioral activity and possible therapy regimes after the injury. We will briefly discuss these dependencies, trying to highlight their translational value. Overall, it is not only necessary to better understand how the brain can reorganize after injury with or without therapy, it is also necessary to clarify when and why brain reorganization can be either “good” or “bad” in terms of its clinical consequences. This information is critical in order to develop and optimize cost-effective therapies to maximize functional recovery while minimizing maladaptive states after spinal cord injury.

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Motor cortex stimulation reduces hyperalgesia in an animal model of central pain

Cited by 80 publications

References 65 publications

Reduced GABAergic neuronal activity in zona incerta causes neuropathic pain in a rat sciatic nerve chronic constriction injury model

Reduced GABAergic neuronal activity in zona incerta causes neuropathic pain in a rat sciatic nerve chronic constriction injury model

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

Cortical reorganization after spinal cord injury: Always for good?

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