Sensory dysfunction in XXXX .

@entity1 @entity1183 @entity1931 @entity8511 @entity158
Our preliminary observations on a small group of @entity8511 ( @entity8511 ) @entity1 indicated a change in the non-nociceptive, tactile sensory function in @entity8511 and provided evidence for the hypothesis of a neuropathic etiology of @entity8511 . In the present clinical study on a group of 52 @entity8511 @entity1 , we used quantitative sensory tests (QST) in addition to the blink reflex (BR) recordings in order to gain further insight into the neural mechanisms of @entity158 . Based on electrophysiologic findings, the @entity8511 @entity1 could be grouped into four different categories: (1) The results of the BR were suggestive of brainstem pathology or peripheral trigeminal neuropathy in ten (19%) @entity1 . In most of the cases, the abnormalities in the BR seemed to represent subclinical changes of the trigeminal system. (2) Increased excitability of the BR was found in the form of deficient habituation of the R2 component of the BR in 11 (21%) of the @entity1 . Two of these @entity1 also showed signs of warm @entity1931 in QST. (3) One or more of the sensory thresholds were abnormal indicating thin fiber dysfunction in altogether 35 @entity1 (76%) out of the 46 tested with QST. Thirty-three of these @entity1 showed signs of @entity1183 . (4) There were only five @entity1 with normal findings in both tests. The present findings with strong evidence for neuropathic background in @entity8511 will hopefully provide insights for new therapeutic strategies.
