Abstract
Chronic pain syndromes present a subversion of both functional and structural nociceptive networks. We used transcranial magnetic stimulation (TMS) to evaluate changes in cortical excitability and plasticity in patients with chronic migraine (CM) treated with botulinum neurotoxin type A (BoNT/A). We enrolled 11 patients with episodic migraine (EM) and 11 affected by CM. Baseline characteristics for both groups were recorded using single- and paired-pulse TMS protocols. The same TMS protocol was repeated in CM patients after four cycles of BoNT/A completed in one year. At baseline, compared with EM patients, patients with CM had a lower threshold in both hemispheres (right hemisphere: 46% ± 7.8 vs. 52% ± 4.28, p = 0.03; left hemisphere: 52% ± 4.28 vs. 53.54% ± 6.58, p = 0.02). In EM, paired-pulse stimulation elicited a physiologically shaped response, whereas in CM, physiological intracortical inhibition (ICI) between 1 and 3 ms intervals was absent at baseline. On the contrary, increasing intracortical facilitation (ICF) was observed for all interstimulus intervals (ISIs). In CM, cortical excitability was partially reduced after BoNT/A treatment, along with a significant decrease observed in MIDAS score (from 20.7 to 9.8; p = 0.008). The lower motor threshold in CM reflects a higher cortical hyperexcitability. The lack of physiological ICI in CM could indicate sensitisation of the trigeminovascular system. Although reduced, this type of response is still observable after treatment, despite a marked clinical improvement. Our study suggests a long-term alteration of cortical plasticity due to chronic pain.
Highlights
Acute pain lasts for only a limited amount of time and is produced by tissue injury and the concurrent activation of local nociceptive transducers
Five chronic migraine (CM) patients were excluded because they were treated with antiepileptic drugs or benzodiazepines or because of contraindications for transcranial magnetic stimulation (TMS); four additional CM patients denied their consent to botulinum neurotoxin type A (BoNT/A) treatment or the TMS protocol
Our study demonstrates that patients suffering from CM present an altered response to paired-pulse TMS (pp-TMS), confirming the hypothesis of an alteration of cortical plasticity due to chronic pain
Summary
Acute pain lasts for only a limited amount of time and is produced by tissue injury and the concurrent activation of local nociceptive transducers. Pain is defined as chronic if it lasts for a long period of time and does not respond completely to therapy. Chronic pain may be initiated by local injury or disease, but it usually persists for a longer period of time and tends to be maintained by factors not directly linked to the original event [1]. Neuroimaging and non-invasive brain stimulation techniques allow the identification of a complex network of brain structures that contribute to the pain experience and their specific roles in each dimension of the whole phenomenon. Most of these brain areas are multimodal, responding to both noxious and salient non-noxious stimuli. The thalamus, insula, several brainstem structures, and other interconnected brain areas take part in this network as well
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