MANDIBULAR NERVE INVOLVEMENT IN DIABETIC POLYNEUROPATHY AND CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY

Sensory complaints in the area of the mandible and mouth often escape notice or remain undiagnosed. Using electromyographic recording of the trigeminal reflexes and motor responses, we sought trigeminal dysfunc tion in 50 patients with peripheral neuropathy, and tried to gain path ophysiological information on the mechanisms provoking trigeminal dama ge. Trigeminal reflex recordings (early and late blink reflex after su praorbital stimulation, early and late masseter inhibitory reflex afte r mental stimulation, and jaw jerk) disclosed abnormalities caused by sensory trigeminal neuropathy in 8 out of 15 patients with chronic inf lammatory demyelinating polyneuropathy (CIDP), 13 out of 23 patients w ith severe diabetic polyneuropathy, and in none of 12 patients with mi ld diabetic polyneuropathy. Six patients had abnormal motor responses in facial or masseter muscles. The response affected most frequently w as the masseter early inhibitory reflex (also called first silent peri od, SP1) after mental nerve stimulation, its latency being strongly de layed. We found these long delays not only in patients with CIDP, but also in diabetic patients with severe polyneuropathy. We conclude that peripheral polyneuropathies often cause subclinical damage to the tri geminal nerve, especially to its mandibular branch. We believe that th e nerve fibers running along the alveolar-mandibular pathway are more exposed to damage because of their cramped anatomical route in the man dibular canal and below the internal pterygoid muscle and fascia. (C) 1998 John Wiley 8 Sons, Inc.