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NEUROLOGY 2004;62:1951-1957
© 2004 American Academy of Neurology

Sensory regeneration following intraoperatively verified trigeminal nerve injury

S. K. Jääskeläinen, MD PhD, T. Teerijoki-Oksa, DDS, A. Virtanen, MSSc, O. Tenovuo, MD PhD and H. Forssell, DDS PhD

From the Departments of Clinical Neurophysiology (Dr. Jääskeläinen), Oral and Maxillofacial Surgery (Drs. Teerijoki-Oksa and Forssell), and Neurology (Dr. Tenovuo), Turku University Hospital; and Research and Development Centre (Dr. Virtanen), Social Insurance Institution, Turku, Finland.

Address correspondence and reprint requests to Dr. Satu K. Jääskeläinen, Dept. of Clinical Neurophysiology, Turku University Hospital, PO Box 52, FI-20521 Turku, Finland; e-mail: satu.jaaskelainen{at}tyks.fi

Objective: To follow recovery of sensory function mediated by both myelinated and unmyelinated axons in relation to the type of inferior alveolar nerve (IAN) injury.

Methods: The authors assessed the function of afferent Aß-, A{delta}-, and C-fibers of the IAN using neurophysiologic (mental nerve blink reflex, sensory nerve conduction [NCS] of the IAN) and quantitative sensory tests (QST; cold, warm, heat pain, and tactile modalities). The tests were done 2 weeks, 1, 3, 6, and 12 months postoperatively and compared to the preoperative baseline in 20 patients undergoing mandibular bilateral sagittal split osteotomy. Nineteen patients underwent intraoperative monitoring.

Results: In primarily demyelinating injuries (21/40 nerves), the sensory alteration and all tests normalized on the group level within the first 3 months. After partial axonal lesions (15/40 nerves), neurophysiologic and thermal QST results remained abnormal at 1-year control in a high proportion of the IAN distributions (up to 67%). At 1 year, the tactile QST was abnormal in 40%, but the NCS in 87% of the symptomatic IAN distributions. Neuropathic pain occurred in 5% of the patients, only after severe axonal damage.

Conclusions: Sensory nerve conduction and thermal quantitative sensory testing showed incomplete sensory regeneration at 1 year after axonal trigeminal nerve damage. Clinical examination with tactile quantitative sensory testing was less reliable in the follow-up of sensory recovery. Sensory Aß-, A{delta}-, and C-fibers recovered function at similar rates. The trigeminal nerve does not differ from other peripheral nerves as regards susceptibility to neuropathic pain.

Received July 2, 2003. Accepted in final form January 31, 2004.




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[Abstract] [Full Text] [PDF]