The characteristics of chronic central pain after traumatic brain injury

Abstract

Central pain following traumatic brain injury (TBI) has not been studied in depth. Our purpose was to conduct a systematic study of patients with TBI suffering from chronic central pain, and to describe the characteristics of the central pain. Groups were TBI patients with (TBIP) and without central pain (TBINP) and healthy controls. TBI patients with other pain mechanisms were excluded from the study. Participants underwent quantitative somatosensory testing in the painful and pain-free body regions. Thresholds for warmth, cold, heat-pain, touch and graphesthesia were measured and pathologically evoked pain (allodynia, hyperpathia and wind-up pain) evaluated. Chronic pain was mapped and characterized. Chronic pain developed at a relatively late onset (6.6+/-9 months) was almost exclusively unilateral and reported as pricking, throbbing and burning. Although both TBIP and TBINP exhibited a significant reduction in thermal and tactile sensations compared to controls, thermal sensations in the painful regions of TBIP were significantly more impaired than pain-free regions in the same patients (p<0.01) and in TBINP (p<0.01). Painful regions also exhibited very high rates of allodynia, hyperpathia and exaggerated wind-up. The characteristics of the chronic pain resembled those of other central pain patients although TBIP displayed several unique features. The sensory profile indicated that damage to the pain and temperature systems is a necessary but not sufficient condition for the development of chronic central pain following TBI. Neuronal hyperexcitability may be a contributing factor to the chronic pain.

Trigeminal Pain Molecules, Allodynia, and Photosensitivity Are Pharmacologically and Genetically Modulated in a Model of Traumatic Brain Injury

“…Periorbital allodynia was correlated with persistent increases in CGRP post-CCI in mice 8,9 and has been a useful outcome reported for patients with PTH and migraine. [5][6][7] A trained technician performed von Frey (North Coast Medical Inc., Gilroy, CA) testing blinded to experimental conditions. Testing was performed during the morning daylight portion of their circadian cycle (9 am to 12 pm), as described previously.…”

“…8 Mechanical allodynia (cutaneous hypersensitivity to a mechanical stimulus that is otherwise innocuous under normal conditions) is a painful response in humans, common in patients with migraine, and has been reported in patients with PTH. [5][6][7] Allodynia in the trigeminal (periorbital) zone after cortical injury in mice and rats indicates that trigeminal pain neurons have become sensitized postinjury. 6,8,9 The phenomenon known as peripheral sensitization of neurons in the trigeminal ganglia originates at the level of the afferent terminal innervating the meningeal vasculature (i.e., the meningeal nociceptor) and involves activation of the trigeminovascular system during a migraine attack.…”

“…2 Mechanical allodynia (cutaneous hypersensitivity to a mechanical stimulus that is otherwise innocuous under normal conditions) is a pain response common in patients with migraine and has also been reported in patients with PTH. [5][6][7] Trigeminal allodynia and photophobia have been studied in animal models of TBI and migraine.…”

Stress repair mechanism activity explains inflammation and apoptosis

“…The simultaneous, synergistic activation of both components induces "positive feedback" so that peak SRM activity occurs several hours after injury [129]. The constantly fluctuating activities of the three synergistic pathways enable the SRM to focus its powerful effects and generate an infinite variety of manifestations [281,284,[502][503][504]536,[559][560][561][562][563].…”

Abstracts

“…Il est à noter qu'aucune diffé-rence significative n'a été observée dans les deux groupes concernant le froid et la douleur. Ce résultat a été répliqué dans plusieurs études [2,3,8,13]. L'interprétation de ces résultats reste difficile.…”