Literature Abstracts Brain signature of chronic orofacial pain: A systematic review and meta-analysis on neuroimaging research of trigeminal neuropathic pain and temporomandibular joint disorders. Lin CS. PLoS One 2014;9(4):e94300. doi: 10.1371/ journal.pone.0094300. eCollection 2014.

Equal pain–unequal fear response: Enhanced susceptibility of tooth pain to fear conditioning. Meier ML, de Matos NM, Brügger M, Ettlin DA, Lukic N, Cheetham M, Jäncke L, Lutz K. Front Hum Neurosci 2014;8:526. doi: 10.3389/fnhum.2014. 00526. eCollection 2014.

Brain neuroimaging has been widely used to investigate the brain signature of chronic orofacial pain, including trigeminal neuropathic pain (TNP) and pain related to temporomandibular joint disorders (TMD). The author of this article explored the topic by performing a systematic review of the neuroimaging literature regarding the functional and structural changes in the brain of TNP and TMD pain patients. This was performed using accepted methods and resulted in a total of 22 articles being identified; 10 TNP studies and 14 TMD studies were reviewed (note, 2 had both TNP and TMD). The author assessed study quality and risk of bias by exploring each study’s criteria of patient selection, medication use by patients imaged, the use of standardized pain/psychological assessments, and the model and statistics of imaging analyses. He reported that in both groups of studies, the study quality and risk for bias was moderate to high. The major outcome of this article was the qualitative meta-analysis, and it was performed by examining the brain regions that showed significant changes in either brain functions (including the blood-oxygen-level–dependent signal, cerebral blood flow, and the magnetic resonance spectroscopy signal) or brain structure (including gray matter and white matter anatomy). The hypothesis was that the neuroimaging findings would display a common pattern as well as distinct patterns of brain signature in the disorders. This was supported by the following findings: (1) TNP and TMD patients showed consistent functional/ structural changes in the thalamus and the primary somatosensory cortex, indicating the thalamocortical pathway as the major site of plasticity. (2) The TNP patients showed more alterations at the thalamocortical pathway, and the two disorders showed distinct patterns of thalamic and insular connectivity. Additionally, functional and structural changes were frequently reported in the prefrontal cortex and the basal ganglia, suggesting the role of cognitive modulation and reward processing in chronic orofacial pain. The findings highlight the potential for brain neuroimaging as an investigative tool for understanding chronic orofacial pain. This article is important because it serves to synthesize the available knowledge in this emerging area of research. Thus by providing a readily understandable overview of this research, it adds to our understanding of the methodology and its implications. (DN)

Experimental fear conditioning in humans is widely used as a model to investigate the neural basis of fear learning and to unravel the pathogenesis of anxiety disorders. It has been observed that fear conditioning depends on stimulus salience and subject vulnerability to fear. It is further known that the prevalence of dental-related fear and phobia is exceedingly high in the population. Dental phobia is unique, as no other body part is associated with a specific phobia. Therefore, the authors hypothesize that painful dental stimuli exhibit an enhanced susceptibility to fear conditioning when compared to equal perceived stimuli applied to other body sites. They proceed with assessing this by investigating the differential susceptibility to pain-related fear by analyzing responses to an unconditioned stimulus (UCS) applied to the right maxillary canine (UCS-c) versus the right tibia (UCS-t) in 21 pain-free control subjects. For fear conditioning, UCS-c and USC-t consisted of painful electrical stimuli, matched at both application sites for equal intensity and quality perception. The authors had previously demonstrated the feasibility of isolated painful electrical stimulus of a canine tooth and this research represents an expansion of their work. UCSs were paired to simple geometric forms, which served as conditioned stimuli (CS+). Unpaired CS+ were presented for eliciting and analyzing conditioned fear responses. Outcome parameters were (1) skin conductance changes and (2) time-dependent brain activity (BOLD responses) in fear-related brain regions such as the amygdala, anterior cingulate cortex, insula, thalamus, orbitofrontal cortex, and medial prefrontal cortex. A preferential susceptibility of dental pain to fear conditioning was observed, as reflected by heightened skin conductance responses and enhanced time-dependent brain activity (BOLD responses) in the fear network. This study demonstrates fear-related neurobiological mechanisms that point toward a superior conditionability of tooth pain. The authors speculated that their results offer novel evidence that might explain the high prevalence of dental-related fears in the population. If this were true, it begs the question of why humans would have this innate ability and what evolutionary advantage it would have. (DN)

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Atrophic changes in the trigeminal nerves of patients with trigeminal neuralgia due to neurovascular compression and their association with the severity of compression and clinical outcomes. Leal PR, Barbier C, Hermier M, Souza MA, Cristino-Filho G, Sindou M. J Neurosurg 2014;120:1484–1495. doi: 10.3171/ 2014.2.JNS131288. This study was conducted (1) to prospectively evaluate atrophic changes in trigeminal nerves (TGNs) by using measurements of volume (V) and cross-sectional area (CSA) from high-resolution 3-T magnetic resonance images obtained in patients with unilateral trigeminal neuralgia (TN) and (2) to correlate these data with patient and neurovascular compression (NVC) characteristics and with clinical outcomes. Anatomical TGN parameters (V and CSA) were obtained in 50 patients (30 women and 20 men; mean age 56.42 years, range 22 to 79 years) with classic TN before treatment with microvascular decompression (MVD). Parameters were compared between the symptomatic (ipsilateral TN) and asymptomatic (contralateral TN) sides of the face. Twenty control subjects were also included. Two independent observers blinded to the side of pain separately analyzed the images. Measurements of V (from the pons to the entrance of the nerve into Meckel’s cave) and CSA (at 5 mm from the entry of the TGN into the pons) for each TGN were performed using imaging software and axial and coronal projections, respectively. These data were correlated with patient characteristics (age, duration of symptoms before MVD, side of pain, sex, and area of pain distribution), NVC characteristics (type of vessel involved in NVC, location of compression along the nerve, site of compression around the circumference of the root, and degree of compression), and clinical outcomes at the 2-year follow-up after surgery. Comparisons were made using the Bonferroni test. Interobserver variability was assessed using the Pearson correlation coefficient. The mean V of the TGN on the ipsilateral TN (60.35 ± 21.74 mm3) was significantly smaller (P < .05) than those for the contralateral TN and controls (78.62 ± 24.62 mm3 and 89.09 ± 14.72 mm3, respectively). The mean CSA of the TGN on the ipsilateral TN (4.17 ± 1.74 mm2) was significantly smaller than those for the contralateral TN and controls (5.41 ± 1.89 mm2 and 5.64 ± 0.85 mm2, respectively). The ipsilateral TN with NVC Grade III, meaning marked indentation, had a significantly smaller mean V than the ipsilateral TN with NVC Grade I, meaning mere contact, although it was not significantly smaller than that of the ipsilateral TN with NVC Grade II, meaning displacement or distortion of root. The ipsilateral TN with NVC

Grade III had a significantly smaller mean CSA than the ipsi­lateral TN with NVC Grades I and II (P < .05). The TGN on the ipsilateral TN in cured patients had a smaller mean CSA than that on the ipsilateral TN of patients with partial pain relief or treatment failure (P < .05). The same finding was almost found in relation to measurements of V, but the P value was slightly higher at .05. Results showed that TGN atrophy in patients with TN could be demonstrated by high-resolution imaging. These data suggest that atrophic changes in TGNs, which significantly correlated with the severity of compression and clinical outcomes, may help to predict long-term prognosis after vascular decompression. This information is useful in discussing treatment options and their associated outcomes for informed consent. (DN) Trigeminal neuralgia occurs and recurs in the absence of neurovascular compression. Lee A1, McCartney S, Burbidge C, Raslan AM, Burchiel KJ. J Neurosurg 2014;120:1048–1054. doi: 10.3171/ 2014.1.JNS131410. Vascular compression of the trigeminal nerve has been reported as the most common factor associated with the etiology of trigeminal neuralgia (TN). Microvascular decompression (MVD) has proven to be the most successful and durable surgical approach for this disorder. However, not all patients with TN manifest unequivocal neurovascular compression (NVC). Furthermore, patients with an initially successful MVD manifest over time a relentless rate of TN recurrence. The authors performed a retrospective review of cases of TN Type 1 (TN1) or Type 2 (TN2) involving patients 18 years or older who underwent evaluation (and surgery when indicated) at Oregon Health & Science University between July 2006 and February 2013. Surgical and imaging findings were correlated, representing the data presented in the article. The review identified a total of 257 patients with TN (219 with TN1 and 38 with TN2) who underwent high-resolution magnetic resonance imaging and angiography with 3D reconstruction of combined images by using OsiriX. Unfortunately, the criteria used to assess NVC were not stated and it was not made clear whether the reviewer(s) of the images were blinded to the clinical status. Imaging data revealed that the occurrence of TN1 and TN2 without NVC was 28.8% and 18.4%, respectively. A subgroup of 184 patients underwent surgical exploration, thus allowing the ability to have a direct correlation between what was observed by imaging with that observed during surgery. Imaging findings were highly correlated with surgical findings, with a sensitivity of 96% for TN1 and TN2 and a specificity of 90% for TN1

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and 66% for TN2. Magnetic resonance imaging detects NVC with a high degree of sensitivity. However, despite a diagnosis of TN1 or TN2, a significant number of patients have no NVC. TN clearly occurs and recurs in the absence of NVC. This research points out an important fact, namely that there has to be more to TN than NVC. (DN) Prevalence of persistent pain 3 to 5 years post primary root canal therapy and its impact on oral health-related quality of life: PEARL network findings. Vena DA, Collie D, Wu H, Gibbs JL, Broder HL, Curro FA, Thompson VP, Craig RG; PEARL Network Group. J Endod 2014 Sept 11 [Epub ahead of print]. doi: 10.1016/j.joen.2014.07.026. The frequency of persistent pain 3 to 5 years after primary root canal therapy and its impact on the patient’s perceived oral health–related quality of life was assessed within a practice-based research network. All patients of participating network practices who had received primary root canal therapy and restoration for a permanent tooth 3 to 5 years previously were invited to enroll. After the patients were retrospectively identified, they were evaluated clinically to determine the outcomes of interest—which in this report was the presence of pain associated with the tooth that was treated by root canal. Persistent pain was defined as pain occurring spontaneously or elicited by percussion, palpation, or biting. The patients also completed an oral health–related quality

of life questionnaire (Oral Health Impact Profile-14). Sixty-four network practices enrolled 1,323 patients; 13 were ineligible, 12 did not receive a final restoration, and 41 had the tooth extracted, leaving 1,257 for analysis. The time to follow-up (mean ± SD) was 3.9  ±  0.6  years. Five percent (63/1,257) of the patients reported persistent pain, whereas 24 of 63 (38%) exhibited periapical pathosis and/or root fracture (odontogenic pain). No obvious odontogenic cause for persistent pain was found for 39 of the 63 (62%) patients. Teeth treated by specialists had a greater frequency of persistent pain than teeth treated by generalists (9.3% versus 3.0%, respectively; P 

Equal pain-Unequal fear response: enhanced susceptibility of tooth pain to fear conditioning.

Experimental fear conditioning in humans is widely used as a model to investigate the neural basis of fear learning and to unravel the pathogenesis of...
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