Pain pathoetiology after TBI: neural and nonneural mechanisms.
Individuals recovering from traumatic brain injury (TBI) frequently experience acute and chronic pain. Their pain experience is the net effect of many interacting and very complex physiologic, biochemical, and psychological mechanisms involving both the peripheral and central nervous system. This article reviews the basics of neural mechanisms and pathways of pain after TBI, and discusses clinical implications. Numerous intracranial and extracranial tissues must be considered in the evaluation of pain after TBI, with the specific mechanism of trauma influencing the anatomic distribution of injuries. The differential diagnosis usually falls into one of the following pathoetiologic classifications: primary or secondary musculoskeletal, vascular, visceral, and neural pain syndromes.
Walker
William C
WC
Department of Physical Medicine and Rehabilitation, Medical College of Virginia at Virginia Commonwealth University , Richmond, Va 23298, USA. wcwalker@mail2.vcu.edu.
D000208:Acute Disease; D001930:Brain Injuries / Q000150:complications* / Q000503:physiopathology*; D002908:Chronic Disease; D020773:Headache Disorders / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D009434:Neural Pathways / Q000503:physiopathology; D009619:Nociceptors / Q000503:physiopathology; D010146:Pain / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology*