Neurophysiologic and quantitative sensory testing in the diagnosis of trigeminal neuropathy and neuropathic pain

Abstract

This study investigated the utility of neurophysiologic examination and thermal quantitative sensory testing (QST) in the diagnosis of trigeminal neuropathy and neuropathic pain. Fifty-eight patients (14 men), 34 with sensory deficit within the inferior alveolar nerve (IAN) and 24 within the lingual nerve (LN) distribution, were included. Twenty-six patients (45%) reported neuropathic pain. Patients underwent blink reflex (BR) test and thermal QST; sensory neurography was done to the IAN patients. Results of clinical sensory testing were available from the charts of 48 patients revealing abnormal findings in 77% of the IAN and in 94% of the LN patients. The BR test was abnormal in 41%, neurography in 96%, and QST in 91% of the IAN patients. In the LN group, BR was abnormal in 33%, and QST in 100% of the patients tested. Neurophysiologic tests and QST verified the subjective sensory alteration in all but 2 IAN patients, both with old injuries, and 4 LN patients who did not undergo QST. When abnormal, thermal QST showed elevation of warm and cold detection thresholds (hypo/anesthesia), hypoalgesia was less marked, and heat allodynia was only occasionally present. Contralateral thermal hypoesthesia after unilateral injury was found in 14 patients. It was associated with the occurrence of neuropathic pain (P=0.016). Axonal Abeta afferent damage was less severe in the IAN patients with pain than in those without pain (P=0.012). Neurophysiologic tests and thermal QST provide sensitive tools for accurate diagnosis of trigeminal neuropathy and study of pathophysiological features characteristic to human neuropathic pain.

Quantitative sensory testing somatosensory profiles in patients with cervical radiculopathy are distinct from those in patients with nonspecific neck–arm pain

“…Thermal hypoaesthesia contralateral to the main pain area has been observed in patients with unilateral traumatic partial nerve injury [46] and with unilateral traumatic trigeminal neuropathy [36]. Bilateral hypoaesthesia may be mediated by peripheral nerve damage induced central plasticity [17].…”

“…One approach to assist in the interpretation of pain mechanisms underlying clinical pain presentations is the use of quantitative sensory testing (QST) [36,13,44,50,64]. To our 6 knowledge, no study has profiled patients with unilateral NSNAP comparable to our cohort, and only one study documented sensory abnormalities in patients with cervical radiculopathy [13].…”

Neuropathic pain after bilateral sagittal split osteotomy: management and prevention

“…Other reports [16,21] describe an incidence as high as 5% of neuropathic pain among patients who sustained peripheral trigeminal nerve injuries after sagittal split ramus osteotomy. Teerijoki-Oksa et al [22] prospectively followed 19 patients after BSSO surgery and found a 5% overall occurrence of neuropathic pain at 1-year follow-up, which is similar to the overall estimated incidence of neuropathic pain after traumatic and iatrogenic nerve injuries.…”

Applications of sensory and physiological measurement in oral‐facial dental pain

“…It has typical clinical features regardless of where in the body it occurs that aid in its diagnosis. For instance, neuropathic pain is often characterized as waxing and waning, and lancinating, and it may be accompanied by paresthesias, numbness, tingling, and shooting sensations 21, 22, 23, 24, 25, 26. Neuropathic pain also typically follows the distribution of one or more sensory nerves that are damaged or inflamed.…”

“…Sensory changes are sometimes also observed during clinical testing of PHN, including hyperalgesia and/or allodynia. Although some cases present with a clear history of nerve damage (e.g., due to dental procedure or other insult), the actual cause of the neuropathy often remains unknown and secondary causes such as autoimmune, malignancy, or infection could be typically considered 22, 27, 34…”