Impact of Institutional Protocol on Urinary Catheter Outcome Measures in Orthopedic Children Treated With Epidural Analgesia.

Stroke affects approximately 80 million people worldwide and remains a leading cause of death and long-term disability. Among its diverse neurological sequelae—ranging from motor and cognitive impairments to dysphagia and aphasia—central post-stroke pain (CPSP) is particularly challenging to treat and significantly impairs patients’ quality of life. While CPSP typically arises contralateral to the cerebral lesion, a subset of patients experiences mirror-image pain (MIP), characterised by hyperalgesia on the ipsilateral side. MIP has been reported in other pain conditions, including neuropathic pain, complex regional pain syndrome, and experimental models of inflammatory and peripheral nerve injury. The occurrence of MIP extends beyond the conventional understanding of unilateral pain processing, underscoring the urgent need to elucidate its underlying neural mechanisms. Despite its clinical relevance, the central and peripheral neural circuits that govern bilateral pain transmission remain largely unknown. Emerging evidence suggests that interhemispheric communication via the corpus callosum may mediate bilateral hyperalgesia. Mechanisms such as astrocyte-driven cortical signalling and circuits involving the anterior cingulate cortex (ACC) have been implicated in this process. We previously developed a long-lasting CPSP model by combining photochemically induced thrombosis (PIT) with tissue plasminogen activator (tPA), in which we observed MIP. A key previous finding was that development of MIP was abolished in lysophosphatidic acid receptor 1 (LPAR)-deficient mice. However, the neuro-pathophysiological mechanism by which LPA promotes MIP remains unknown. Our previous studies have suggested that LPA activates microglia and that a positive feedback mechanism exists whereby LPA promotes its own production. We aimed to identify potential therapeutic targets within the LPA–microglia axis. To this end, we employed advanced imaging mass spectrometry to investigate whether corpus callosum-associated propagation of inflammatory responses involving LPA is linked to microglial activation and MIP.