Background: Preliminary studies on epidural motor cortex stimulation (eMCS) for the treatment of drug-resistant neuropathic pain have supported the extension to novel stimulation waveforms, in particular burstDR. However, only a low level of evidence is available. The aim of this retrospective observational study was to compare the analgesic efficacy of burstDR versus tonic eMCS.
Methods: Patients suffering from unilateral, drug-resistant neuropathic pain were selected for eMCS. During the trial phase, burstDR and tonic waveforms were successively applied for three consecutive months in a double-blinded fashion and in a random order. The primary outcome criterion was the percentage of pain relief (%PR) at 3 and 6 months. The secondary outcome criterion was the proportion of patients reporting a superior %PR with the burstDR waveform.
Results: Thirteen patients were included. The averaged %PR was 75.4% ± 18.6% after burstDR eMCS and 61.1% ± 28.6% after tonic eMCS (p = 0.21). Nine patients preferred the burstDR waveform for chronic eMCS (p = 0.16), and six of them were able to decrease or withdraw their analgesic drug intake. No adverse side effect was encountered in relation to burstDR eMCS.
Conclusions: BurstDR eMCS seems at least as effective as tonic eMCS for the treatment of drug-resistant neuropathic pain and shows a similar safety profile. Although the precise mechanisms of action remain to be fully elucidated, adequate matching between the oscillatory rhythm in the motor cortex and that of the burstDR waveform may increase synaptic efficacy, thus enhancing the functional connectivity of the motor cortex with remote brain networks involved in pain modulation.
Significance Statement: In the present paper, we provide for the first time a double-blinded study comparing burstDR versus tonic eMCS for the treatment of intractable, drug-resistant neuropathic pain. Our results show that burstDR eMCS is a promising option in a population of patients especially difficult to treat, and support the ongoing move toward new stimulation waveforms able to more efficiently activate the brain networks involved in pain modulation.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/ejp.4778 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Maladaptive changes in the homeostasis of AEA-TRPV1/CB1R induces pain-related hyperactivity of nociceptors after spinal cord injury.
Cell Biosci
January 2025
State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Fudan University, Shanghai, 200438, People's Republic of China.
Background: Neuropathic pain resulting from spinal cord injury (SCI) is associated with persistent hyperactivity of primary nociceptors. Anandamide (AEA) has been reported to modulate neuronal excitability and synaptic transmission through activation of cannabinoid type-1 receptors (CB1Rs) and transient receptor potential vanilloid 1 (TRPV1). However, the role of AEA and these receptors in the hyperactivity of nociceptors after SCI remains unclear.
View Article and Find Full Text PDFCircumferential nerve wrapping with muscle autograft: a modified strategy of microvascular decompression for trigeminal neuralgia.
Neurosurg Rev
January 2025
Department of Neurosurgery, IRCCS Neuromed, Via Atinense 18, Pozzilli, IS, 86077, Italy.
Microvascular decompression is considered a first-line treatment in classical trigeminal neuralgia. Teflon is the material commonly used. The use of autologous muscle has been occasionally reported.
View Article and Find Full Text PDFUnderstanding the Physiopathology of Pain Pathways for a Practical Approach of Cancer Pain Management.
Cardiovasc Intervent Radiol
January 2025
Clinique de la Douleur., Hôpital de La Tour, Geneva, Suisse.
Pain associated with cancer is often the first symptom reported with major repercussions on patient's quality of life. Mechanical compression, release of algogenic substances by the tumor or the complications of oncologic treatment represent the major causes. Nociceptive and neuropathic pain are both induced by different mediators that give rise to a neuroinflammation creating a peripheral and central sensitization responsible of chronic pain.
View Article and Find Full Text PDFOnabotulinum toxin a treatment for posttraumatic trigeminal neuropathic pain: case series and literature review.
J Oral Facial Pain Headache
March 2024
Faculty of Dentistry, Oral & Craniofacial Science, King's College London, SE5 8AF London, UK.
This case series aimed to assess the treatment outcomes of onabotulinum toxin A (BTX-A) in patients with refractory posttraumatic trigeminal neuropathic pain (PTNP) and to conduct a narrative review of the evidence for BTX-A in PTNP. Thirteen patients were treated with BTX-A infiltrations. Patient demographic and pain characteristics, BTX-A administration, and treatment outcomes were retrospectively analyzed.
View Article and Find Full Text PDFAn accurately supervised motion-aware deep network for non-contact pain assessment of trigeminal neuralgia mouse model.
J Oral Facial Pain Headache
March 2024
Department of Oral and Maxillofacial Surgery, Peking University School of Stomatology, 100081 Beijing, China.
Pain assessment in trigeminal neuralgia (TN) mouse models is essential for exploring its pathophysiology and developing effective analgesics. However, pain assessment methods for TN mouse models have not been widely studied, resulting in a critical gap in our understanding of TN. With the rapid advancement of deep learning, numerous pain assessment methods based on deep learning have emerged.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!