Pain relief by rTMS

Obadia, Nathalie; Mertens, Patrick; Guéguen, Antoine; Peyron, R.; Garcia-Larrea, Luis

doi:10.1212/01.wnl.0000325481.61471.f0

Cited by 123 publications

(87 citation statements)

References 25 publications

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“…This tendency to favor bias was made obvious in a recent study published by Andre-Obadia and colleagues 1 . In their study, the authors used a double-blind, randomized, cross-over design to investigate the analgesic effects of repetitive transcranial magnetic stimulation (rTMS), and found that posteroanterior rTMS was more effective than sham and/or lateromedial rTMS.…”

Section: The Problem: Placebo Effects Carry Consequencesmentioning

confidence: 94%

Randomized placebo-controlled cross-over designs in clinical trials: a gold standard to be reassessed

Léonard

Lafrenaye

Goffaux

2012

Current Medical Research and Opinion

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Section: The Problem: Placebo Effects Carry Consequencesmentioning

confidence: 94%

Randomized placebo-controlled cross-over designs in clinical trials: a gold standard to be reassessed

Léonard

Lafrenaye

Goffaux

2012

Current Medical Research and Opinion

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“…One year later André-Obadia et al 38 performed a doubleblinded, randomized, crossover study of high-rate rTMS against placebo in 28 patients with different subtypes of neuropathic pain. Pain relief was evaluated on daily basis over the week.…”

Section: Repetitive Transcranial Magnetic Stimulation (Rtms)mentioning

confidence: 99%

Promising treatments for neuropathic pain

Schestatsky

Vidor

Winckler

et al. 2014

Arq. Neuro-Psiquiatr.

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In the last few years the understanding of mechanisms and, consequently, the diagnosis of neuropathic pain (NP) has becoming progressively clearer in clinical practice. However, the treatment of such condition remains challenging so far. One of the reasons for such difficulty is the diversity of mechanisms involved in NP generation and its persistency. In the present review we discuss several treatment modalities for NP that are scantily applied in daily clinical practice. For that, we collected positive clinical evidence of unusual and SECS (Safe, Easy, Cheap, and Sensible) approaches for NP. The aim of this review is not to establish the "state of the art" or rigid guidelines for NP treatment. In a different way, we only want bring new possibilities of treatment to the readers and also to motivate investigators to confirm those positive preliminary but promising results for NP reliev.Keywords: neuropathic pain, treatment, unconventional, alternative, evidence-based medicine. RESUMONos últimos anos, a compreensão dos mecanismos e consequentemente do diagnóstico da dor neuropática (DN) têm se tornado cada vez mais claros na prática clínica. Entretanto, o tratamento desta condição continua sendo um desafio. Uma das razões para tal dificuldade é diversidade de mecanismos envolvidos na geração e perpetuação da DN. Na presente revisão, os autores discutem várias modalidades de tratamento para DN pouco utilizadas na prática clínica diária. Para isso, selecionamos evidências clínicas positivas de abordagens para DN consideradas não-convencionais e do tipo "SFBR" (Seguro, Fácil, Barato e Racional). O objetivo desta revisão não é estabelecer o "estado da arte" ou diretrizes rígidas para o tratamento da DN. Diferente disso, pretendemos apenas trazer aos leitores novas possibilidades de tratamento assim como motivar pesquisadores a confirmar estes resultados preliminares, mas promissores para o alívio da DN.Palavras-chave: dor neuropática, tratamento, alternativo, medicina baseada em evidência.Neuropathic pain is defined as pain caused by lesion or dysfunction of the somatosensory system 1 and is most commonly consequence from several clinical conditions, such as diabetes, chemotherapy, herpes zoster infection, chronic alcohol abuse and other idiopathic conditions, such as idiopathic small fiber neuropathy and trigeminal pain. Patients with NP usually complain of burning and tingling sensations over the skin that almost always correspond to a plausible body distribution. Antidepressants and antiepileptic drugs are the mainstay of therapy, but they usually relieve only 40-50% of the pain 2 . Since the diagnosis of NP has becoming clearer in the last few years with the advent of new neurophysiological and histological tools, it is believed that the diversity of pathophysiological mechanism might explain the refractoriness of NP to the conventional therapeutic approaches. Therefore, several lines of investigation have been developed in parallel with the sophistication of usual drugs used in NP patients. Some of these...

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“…Significant achievements of these lines of research have been the development of neurostimulation techniques for pain control, ranging from the well-known deep brain stimulation (DBS) of the posterior hypothalamus in refractory chronic cluster headache [21] to the great occipital nerve stimulation [22], the repetitive transcranial magnetic stimulation [23] and the very recently proposed transcutaneal supraorbital direct current trigeminal stimulation [24]. However, despite initial enthusiasms, and even taking into account the promising results of neurostimulation studies, it has not been possible to clarify whether the functional central ''markers'' of primary headaches pain observed could be considered as causative factors or just the, possibly reversible [25], neural correlates of the ongoing pain [26].…”

Section: Cortical Spreading Depression and Migrainementioning

confidence: 99%

Cortical spreading depression and central pain networks in trigeminal nuclei modulation: time for an integrated migraine pathogenesis perspective

et al. 2013

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The role of the cortical spreading depression (CSD)-dependent trigeminovascular activation in migraine etiopathogenesis, long considered paradigmatic, has remained substantially unproven in humans. The parallel advancement of functional neuroimaging techniques promoted the extensive exploration of the brain networks involved in pain processing in search of a possible central migraine generator. However, despite initial enthusiasms, it has not been possible to clarify whether the functional central ''markers'' of pain observed in primary headaches could be considered as causative or just the neural correlates of the ongoing pain. Nonetheless, our knowledge on the complex interactions between CSD, neurogenic inflammation, peripheral trigeminovascular input, central cortico-trigeminal nuclei direct modulation and pain processing and limbic system networks has enormously grown, allowing the reconceptualisation of migraine from a neurovascular to a pure neurolimbic pain disorder, therefore relocating it in the much broader frame of the brain and whole organism homeostatic control. In this work, the available evidences currently supporting the relevance of CSD, of peripheral trigeminovascular input and of direct cortico-trigeminal nuclei modulation in migraine pathogenesis are reviewed in the light of a possible integrated migraine etiopathogenetic perspective.

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Pain relief by rTMS

Cited by 123 publications

References 25 publications

Randomized placebo-controlled cross-over designs in clinical trials: a gold standard to be reassessed

Randomized placebo-controlled cross-over designs in clinical trials: a gold standard to be reassessed

Promising treatments for neuropathic pain

Cortical spreading depression and central pain networks in trigeminal nuclei modulation: time for an integrated migraine pathogenesis perspective

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