Often misread by neurologists as mere spasticity, the heightened flexor response has been noted in the surveys, but not reported in the literature until now.
Clifford Woolf, one of the Harvard/MGH brain trust on pain, has consistently produced reliable and significant data which expand our knowledge of pain. He and his group should have been awarded the Nobel for recognizing that sensitization in nerve injury pain represents reduplication at each successive synapse in the ascending pathway, right up to the thalamus, and that this was mediated by acidifying cytokines such as the leukotrienes.
Then again, pain does not seem to concern the Nobel committee. A Nobel was awarded for identifying Nitric Oxide (NO) as a gaseous neurotransmitter, but its role in pain and neuroinflammation has caused no particular stir. Inflammation in cancer/heart disease does get the award juices going, however, and since neuroinflammation is hot in the cell signalling arena, Woolf may yet get his due for the early identification of leukotrienes and neuroninflammtion in nerve injury pain.
Now Dr. Woolf has studied a truly minute aspect of central pain, the flexor reflex in hypersensitized cord. The surveys have included occasional but very consistent reports that patients who suffered cord injury leading to central pain noticed the appearance of the flexor reflex, sometimes also called the “withdrawal reflex”. It is a reflexive withdrawal from light touch, which normal individuals do not display.
This author had an interesting discusson on this topic in central pain with the author of one of the major texts on neurology, who felt the heightened flexor reflex was an unmasking of the fetal spinal protective reflexes, the residual of which can be seen in newborns. These reflexes disappear in predictable sequence and timing, which is a very reliable method of dating the actual age of any newborn. Traditionally, a mature newborn had wrinkles at least 2/3 of the way along the foot. Measurement of withdrawal reflexes allows a much more soophisticated and refined calculation of the gestational age of any newborn. These reflexes disappear in the first few weeks or months of life.
Woolf’s noting of flexor withdrawal heightening makes the whole topic more interesting, because Bryan Hains has shown that the sodium ion responsible for central pain is a FETAL ion channel, ie. NaV 1.3. This channel is not present to any degree in those who do not have central pain. Now we see what some feel is a fetal protective reflex being established as part of central pain for many with cord injury.
Simply stated, if you have central pain and are not entirely paralyzed, either spastic or flaccid paralysis, an UNEXPECTED light touch against something will cause a withdrawal of that extremity. This is unexpected and involuntary. It is essentially a flexor movement. Now someone as intelligent as Woolf has determined that this probably comes from the plasticity changes in the central nervous system which accompanies central pain. Woolf used a model of PNI for his study, but the basic principles extend to CP. See Anesthesiology. 2007 Apr;106(4):864-7