RT Book, Section
A1 Cohen, Stephen A.
A2 Warfield, Carol A.
A2 Bajwa, Zahid H.
SR Print(0)
ID 3412972
T1 Chapter 3. Pathophysiology of Pain
T2 Principles & Practice of Pain Medicine, 2e
YR 2004
FD 2004
PB The McGraw-Hill Companies
PP New York, NY
SN 9780071443494
LK accessanesthesiology.mhmedical.com/content.aspx?aid=3412972
RD 2024/04/19
AB Acute,  nociceptive  pain  results  from  the  complex  convergence  of  many  signals  traveling  up  and  down  the  neuraxis  and  serves  to  warn  us  of  impending  harm.  The  painful  sensations  ultimately  leave  the  periphery  and  travel  centrally,  carried  by  the  axons  of  the  primary  sensory  neurons,  the  dorsal  root  ganglia  (DRG),  which  are  relatively  quiescent  unless  specifically  stimulated  by  sensory  input.  Unlike  the  “tombs”  that  the  Belle  of  Amherst  describes,  however,  if  inflammation  or  injury  damages  the  neural  structures,  pain  sensation  (neuropathic  pain)  may  continue  long  after  the  noxious  stimuli  subside.  The  pain  response  can  then  harm  rather  than  help  the  individual.  Injured  DRG  may  become  hyperexcitable  and  display  considerable  spontaneous  electrical  activity.  Such  increased  activity  results  from  the  expression  of  a  dramatically  different  constellation  of  many  cell-specific  molecules  in  injured  cells  compared  with  normal  ones.  Ultimately,  the  operation  of  complex  neuronal  circuits  may  be  markedly  altered.  Chronic  pain  sensation  can  result  from  such  injury.