Mandibular nerve involvement in diabetic polyneuropathy and chronic inflammatory demyelinating polyneuropathy

✍ Scribed by G. Cruccu; R. Agostino; M. Inghilleri; P. Innocenti; A. Romaniello; M. Manfredi

• Publisher: John Wiley and Sons
• Year: 1998
• Tongue: English
• Weight: 147 KB
• Volume: 21
• Category: Article
• ISSN: 0148-639X
• DOI: 10.1002/(sici)1097-4598(199812)21:12<1673::aid-mus8>3.0.co;2-a

✦ Synopsis

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 dysfunction in 50 patients with peripheral neuropathy, and tried to gain pathophysiological information on the mechanisms provoking trigeminal damage. Trigeminal reflex recordings (early and late blink reflex after supraorbital stimulation, early and late masseter inhibitory reflex after mental stimulation, and jaw jerk) disclosed abnormalities caused by sensory trigeminal neuropathy in 8 out of 15 patients with chronic inflammatory demyelinating polyneuropathy (CIDP), 13 out of 23 patients with severe diabetic polyneuropathy, and in none of 12 patients with mild diabetic polyneuropathy. Six patients had abnormal motor responses in facial or masseter muscles. The response affected most frequently was the masseter early inhibitory reflex (also called first silent period, SP1) after mental nerve stimulation, its latency being strongly delayed. 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 trigeminal nerve, especially to its mandibular branch. We believe that the nerve fibers running along the alveolar-mandibular pathway are more exposed to damage because of their cramped anatomical route in the mandibular canal and below the internal pterygoid muscle and fascia.