Central Post-Stroke Pain: An Integrative Review of Somatotopic Damage, Clinical Symptoms, and Neurophysiological Measures

Abstract

Introduction: The physiopathology of central post-stroke pain (CPSP) is poorly understood, which may contribute to the limitations of diagnostic and therapeutic advancements. Thus, the current systematic review was conducted to examine, from an integrated perspective, the cortical neurophysiological changes observed via transcranial magnetic stimulation (TMS), focusing on the structural damage, and clinical symptoms in patients with CPSP.Methods: The literature review included the databases EMBASE, PubMed, and ScienceDirect using the following search terms by MeSH or Entree descriptors: [(“Cerebral Stroke”) AND (“Pain” OR “Transcranial Magnetic Stimulation”) AND (“Transcranial Magnetic Stimulation”)] (through September 29, 2020). A total of 297 articles related to CPSP were identified. Of these, only four quantitatively recorded cortical measurements.Results: We found four studies with different methodologies and results of the TMS measures. According to the National Institutes of Health (NIH) guidelines, two studies had low methodological quality and the other two studies had satisfactory methodological quality. The four studies compared the motor threshold (MT) of the stroke-affected hemisphere with the unaffected hemisphere or with healthy controls. Two studies assessed other cortical excitability measures, such as cortical silent period (CSP), short-interval intracortical inhibition (SICI), and intracortical facilitation (ICF). The main limitations in the interpretation of the results were the heterogeneity in parameter measurements, unknown cortical excitability measures as potential prognostic markers, the lack of a control group without pain, and the absence of consistent and validated diagnosis criteria.Conclusion: Despite the limited number of studies that prevented us from conducting a meta-analysis, the dataset of this systematic review provides evidence to improve the understanding of CPSP physiopathology. Additionally, these studies support the construction of a framework for diagnosis and will help improve the methodological quality of future research in somatosensory sequelae following stroke. Furthermore, they offer a way to integrate dysfunctional neuroplasticity markers that are indirectly assessed by neurophysiological measures with their correlated clinical symptoms.

Corticomotor excitability is altered in central neuropathic pain compared with non-neuropathic pain or pain-free patients

“…Our results support that these are genuine findings in CNP and suggest these are not uniquely related to corticospinal motor injury or non-specific effects of chronic pain in general (e.g., sleep abnormalities, mood, fatigue) or to psychotropic analgesic medication use. Among the CE measures, MEP is one of the most studied parameters in cortical clinical neurophysiology [5].…”

“…These data suggest that the motor cortex could serve as an entry gate allowing for modulation of neuronal activity when targeted by neuromodulatory interventions but equally allowing for a read-out of part of the global excitability status of extra-motor areas by means of CE measurements. Despite the potential to probe the corticomotor system to gain mechanistic insights into the development of CNP, the available data is based on a small number of patients, either lacking a control group or using healthy individuals as comparators [5].…”

Post-Intensive Care Syndrome in Patients Suffering From Acute Subarachnoid Hemorrhage: Results From an Outpatient Post-ICU Aftercare Clinic

“…When pain is related to the stroke, amitriptyline, lamotrigine, and GABA receptor agonist are advised as first-line pharmacotherapeutic options [ 61 ]. Also, non-pharmacotherapeutic interventional therapies such as motor cortex stimulation or transcranial magnetic stimulation have been shown to provide relief in difficult-to-treat patients [ 62 ].…”

Avellis syndrome with ipsilateral prosopalgia, glossopharyngeal neuralgia, and central post-stroke pain: A case report and literature review

“…The infarcted site in this case is MO. Studies [ 16 , 19 ] have shown that lateral MO infarction is more likely to cause burning pain on the contralateral body, which may be caused by the stimulation to the lateral spinothalamic tract. The anatomic sequence of lateral spinothalamic tract from the lateral to the middle is sacral, lumbar, thoracic, and cervical, so patients with lateral MO infarction are prone to paresthesia of the lower limb at the onset and then upper limb paresthesia becomes obvious, [ 20 ] which is consistent with this case.…”