Defining and Managing Pain in Stroke and Traumatic Brain Injury Research

Abstract

Neurologic conditions such as stroke and traumatic brain injury are challenging conditions to study in humans. Animal models are necessary to uncover disease processes and develop novel therapies. When attempting to model these or other neurologic diseases, the accompanying anesthesia and analgesia create variables that are not part of the onset of the clinical disease in the human population but are critical components of the postinjury care both in humans and animals. To maximize model validity, researchers must consider whether the disease process or a novel therapy is being studied. Damage to the neurons of the brain or the spinal cord is not painful at the neural tissue itself, but alterations to nociceptive signaling along the pain pathway can induce chronic pain. In addition, trauma or surgery leading to the event is associated with damage to peripheral tissue. Inflammation is inextricably associated with tissue injury. Inflammation is known to evoke nociception in the periphery and drive long-term changes to neurons in the CNS. Analgesics and anesthetics alter these responses yet are required as part of humane animal care. Careful planning for effective drug administration consistent with the standard of care for humans and equivalent animal care is required.

To determine the differences between experience of post-operative pain after craniotomy in emergency versus elective cases.

“…19,20 Adding acetaminophen and NSAIDS as adjuncts to opioids increase patient satisfaction with pain management. 21,22,23 There are several limitations to our study, firstly it is a single center study, and we did not have enough number of patients or enough variables changing over time that may hint towards a significant change. Secondly, the study was conducted at a large tertiary care hospital in a large metropolitan city.…”

Association of concomitant headache with hypoperfusion in ischemic stroke: A multimodal CT‐based study

“… 7 , 11 , 12 Mechanisms producing pain in ischemic stroke must be different compared to other peripheral artery diseases due to the absence of pain receptors in brain tissue. 13 , 14 Studies showed lesions in the somatosensory cortex seem to predispose for headache in stroke. 11 , 15 These provided pieces of evidence for the notion that headache in stroke might be centrally driven.…”

“…Although the pathogenesis of concomitant headache during stroke is still unclear, some reasonable hypotheses have been put forward, including centrally driven lesion patterns, the necessary role of vessel wall elasticity, and susceptibility to SDs 7,11,12 . Mechanisms producing pain in ischemic stroke must be different compared to other peripheral artery diseases due to the absence of pain receptors in brain tissue 13,14 . Studies showed lesions in the somatosensory cortex seem to predispose for headache in stroke 11,15 .…”