Patients with trigeminal nerve damage report moderate-to-severe levels of pain and unpleasantness with evidence for varied site-dependent somatosensory disturbances. This is based on the results of a comprehensive set of psychophysical and electrophysiological investigations published in The Clinical Journal of Pain.
The goal of the current study was to investigate the somatosensory changes related to trigeminal nerve damage using psychophysical and electrophysiological tools.
The study cohort included 37 patients (24 women, mean age 44.6 years) attending Department of Dentistry and Oral Health, Aarhus University, Denmark and Faculty of Odontology, Malmö University, Sweden; and Skåne University Hospital, Lund, Sweden. Most patients were diagnosed with painful posttraumatic trigeminal neuropathy (n=30), and a minority had nonpainful posttraumatic trigeminal neuropathy (n=7).
Psychophysical tests like quantitative sensory testing and qualitative sensory testing and the electrophysiological “nociceptive-specific” blink reflex were performed.
The scores from the Pain Catastrophizing Scale (PCS), Beck Depression Inventory-II (BDI-II), State-Trait Anxiety Inventory (STAI) measuring state anxiety (STAI-S) and STAI-T measuring trait anxiety, the 8-item Jaw Function Limitation Scale (JFLS-8), 4-item and 15-item Patient Health Questionnaire (PHQ-4 and PHQ-15), Oral Behaviors Checklist (OBC), and 49-item Oral Health Impact Profile (OHIP-49) were compared between the patients and a group of 20 healthy controls (10 women and 10 men, mean age 37.7 ±11.4 years).
The main quantitative sensory testing finding observed was an abnormal somatosensory function in ≥1 parameter in 94.7% of patients with damage to the nerve branches innervating the extraoral region and 88.9% of patients with damage to the nerve branches innervating the intraoral region.
Among 19 patients in whom extraoral QST was performed, at least 1 parameter with loss or gain of somatosensory function was evident in 13 patients (68.4%) on the unaffected side and in 18 patients (94.7%) on the affected side. Among 18 intraorally assessed subjects, in 15 patients (83.3%) there was at least 1 parameter with loss or gain of somatosensory function on the unaffected side and in 16 patients (88.9%) on the affected side.
Qualitative sensory testing identified a side-to-side difference in the tactile and pinprick stimulation in >77% of the patients. An abnormal “nociceptive-specific” blink reflex response was dependent on the trigeminal branch stimulated; abnormal findings were observed in > 71% of patients for V2 branch and > 42% for the V3 branch stimulation. No correlations were seen between any of the QST and “nociceptive-specific” blink reflex parameters.
Compared to the healthy participants, patients showed higher scores for pain catastrophizing (10.7±9.4 vs 17.4±13.0, P <.001), symptoms of depression (3.2±3.0 vs 10.2±9.1, P =.029) and anxiety (STAI-S: 30.1±7.1 vs 37.9±13.5; STAI-T: 33.5±6.2 vs 39.9±12.7, P =.038), limited jaw function (0.1±0.5 vs 15.5±15.5, P <.001), more somatic symptoms, and significantly impaired oral health-related quality of life.
The researchers acknowledged several study limitations, including difficult and low recruitment with potential variation in data collection, use of healthy reference data instead of age- and sex-matched controls, and lack of testing extra-trigeminal sites owing to concern for patient fatigue from multiple investigations.
“The present study comprehensively quantifies and profiles the pathophysiological characteristics of trigeminal nerve damage and attests to the need of using clinical history, psychophysical, and electrophysiological investigations for diagnosis of trigeminal nerve damage,” concluded the researchers.
Disclosure: Several study authors declared affiliations with the pharmaceutical industry. Please see the original reference for a full list of authors’ disclosures.
Pillai RS, Pigg M, List T, et al. Assessment of somatosensory and psychosocial function of patients with trigeminal nerve damage. Clin J Pain. 2020;36(5):321‐335. doi:10.1097/AJP.0000000000000806
This article originally appeared on Neurology Advisor