Many individuals with multiple sclerosis (MS) experience clinically significant 
pain, yet the underlying neural mechanisms for MS pain are not understood. 
Experimental autoimmune encephalomyelitis (EAE) is a well-studied disease in 
rodents that mimics many clinical and pathological features of MS, including 
central nervous system inflammation and demyelination. To determine whether EAE 
is an appropriate model for MS-related pain, nociceptive responses in both male 
and female SJL mice were measured before and after immunization with myelin 
proteolipid protein peptide 139-151 (PLP(139-151)) in complete Freund's adjuvant 
to induce 'active' EAE. To determine if changes in nociception were due to 
direct effects of encephalitogenic T cells, nociceptive responses in female SJL 
mice were measured following the transfer of activated, PLP(139-151) specific T 
cells to induce 'passive' EAE. Both forepaw and tail withdrawal latencies to a 
radiant heat stimulus were measured. In both active and passive EAE, there was 
an initial increase in tail withdrawal latency (hypoalgesia) that peaked several 
days prior to the peak in motor deficits during the acute disease phase. During 
the chronic disease phase, tail withdrawal latencies decreased and were 
significantly faster than control latencies for up to 38 days post-immunization. 
This hyperalgesia was seen in both sexes and in both active and passive EAE 
models. Forepaw withdrawal latencies remained within 1-2 s of baseline latencies 
for the entire testing period, indicating that the hypoalgesia and hyperalgesia 
were most pronounced in clinically affected body regions. These results suggest 
that both active and passive EAE are useful models of MS-related pain.