Loading [Contrib]/a11y/accessibility-menu.js
1.
Sutter B, Teragawa S, Radke J. Trigeminal Neuralgia Patients Treated with Disclusion Time Reduction (DTR): A Retrospective Cohort Study. Adv Dent Tech. Published online August 12, 2020:90-105.
Download all (11)
  • Figure 1. Left image is post MVD incision where a Teflon strip is placed between the nerve and offending blood vessel. Right image is gamma knife surgery where the nerve is irradiated.
  • Figure 2. The T-Scan Novus handle and BioEMG III are used to capture data that cannot be recorded by any other means. These synchronized technologies allow the user to record occlusal data in real-time with the muscles’ response to the occlusal function. The patient occludes into MIP with the sensor placed between their teeth and maintains intercuspation for 1-3 seconds, before performing a lateral excursive movement in one direction only (right or left).
  • Figure 3. A pre-operative bite force data scan. This patient reported unilateral pain on the left side. 69.3% of total bite force (green) is on the left affected side (green line) and the remaining 30.7% is on the right (red line).
  • Figure 4. A pre-ICAGD right excursive Disclusion Time/ muscle activity data scan. This patient reported unilateral pain on the right side. The right Disclusion Time is 0.61 seconds on the right side because the posterior right teeth are frictionally engaged (elevation of the blue line between C and D) indicating a prolonged right group function precedes that anterior guidance becoming effective. Note that the muscle elevation is 214 µv in the right anterior temporalis (Blue Arrow).
  • Figure 5. Teeth with paper marks pre ICAGD.
  • Figure 6. Post ICAGD all posterior left and right lateral excursive marks have been removed.
  • Figure 7. A post-ICAGD bite force data scan. This is the same patient as in Figure 3 after the bite correction. Note 54.5% of total bite force is on the left side and the remaining 45.5% is on the right. The ideal distribution occlusal force is 50% right-to-left +/- 5%.
  • Figure 8. A post-ICAGD right excursive Disclusion Time/muscle activity data scan on the same patient (Figure 4) showing the Disclusion Time was reduced to 0.12 seconds. At C the red line rises quickly to 100%, as the other colored lines drop to 0% force, indicating complete canine guidance control resulted from eliminating the friction in the posterior quadrants. Note the muscle activity is reduced in all muscles, most notably the right anterior temporalis which dropped post-ICAGD from 214µv to 3.7µv (blue arrow). That is 56 times less temporalis muscle activity than pre-ICAGD.
  • A 1. PHQ-15 form is self-reported by the patient checking the appropriate box in each row. The values assigned to score it are: Bothered not at all = 0, Bothered a little = 1, Bothered a lot = 2. Total score is the sum of all scores.
  • A 2. Symptom Frequency Form is self-reported by the patient by checking the appropriate box in each row. The values assigned to score it are: Never = 0, Occasionally = 1, Often = 2, All the time = 3. Total score is the sum of all scores.
  • A 3. Pain Intensity Form is self-reported by the patient checking the appropriate box in each row. The values assigned to score it are: None = 0, Slight = 1, Moderate = 2, Severe = 3, Intolerable = 4. Total score is the sum of all scores.

Abstract

Objective: Treating and managing Trigeminal Neuralgia (TN) remains a significant challenge. TN is thought to be either idiopathic in nature or related to vascular nerve compression. The purpose of this study was to treat patients diagnosed with TN utilizing the T-Scan to guide measured occlusal corrections in bite force and timing. The null hypothesis was that occlusal corrections would not significantly improve TN symptoms.

Methods and Materials: Twenty-five patients diagnosed with TN completed questionnaires that evaluated pain frequency, severity, any functional restrictions and somatization with a PHQ-15 scale, before undergoing the ICAGD coronoplasty. The questionnaires were repeated 1 month and 3 months post-ICAGD therapy. Pre and post ICAGD Disclusion Times (DT) and sEMG temporalis and masseter levels underwent the Student’s t-Test. The pain scales, symptom questionnaires, and the PHQ-15 scores were subjected to the Wilcoxon Signed-Rank Rest.  = 0.05.

Results: The pre-ICAGD group means of TN pain and frequency were significantly reduced after ICAGD (p < 0.00001). Many other chronic symptoms were also reduced in severity and frequency, while improvements in functional restrictions (p < 0.0004) and PHQ-15 scores (p < 0.0012) were observed at 1-month and 3-months post ICAGD.

Conclusions: In this small group of TN subjects, occlusal factors were the major contributor to their TN condition as all occlusally treated subjects reported reductions in symptom frequency, severity, functional restrictions and their levels of muscle activity decreased following DTR therapy. TN may have an overlooked occlusal etiology in long Disclusion Time. ICAGD should be considered a pain treatment option in patients diagnosed with TN.

INTRODUCTION

Trigeminal Neuralgia (TN) is a well-known orofacial pain condition that remains the most common of the cranial neuralgias.1 It is also referred to as “The Suicide Disease” and Tic-Douloureux. TN is clinically diagnosed from symptom presentation, which is followed by an MRI to confirm the diagnosis. TN affects 4-5 persons per 100,000 each year, mainly affecting patients of 50 years and older, but anyone can be diagnosed with TN.2 TN presents with a characteristic trigger zone that elicits intense shooting pain. The response, often referred to as an “attack” or “flare up,” is uncharacteristically intense compared to the stimulus. Activities such as brushing teeth, shaving, eating, or a cold wind blowing on the face have been known to set off a TN attack.1

According to Burket’s Oral Medicine, “A diagnosis of TN is usually based upon a history of shooting pain along a branch of the trigeminal nerve, precipitated by touching a trigger zone. A TN diagnosis can be made from an examination that demonstrates the shooting pain.”1 The exact cause of TN remains debatable, but approximately 10% of the cases present with a verifiable pathosis, such as vascular malformation or tumor. The most commonly accepted TN etiology is vascular compression and demyelination of the trigeminal nerve root. Unfortunately, no other description has been offered, with 90% of all cases being deemed idiopathic.1

Historically in 1910, Cushing first described a “cranial nerve vascular compression syndrome,”3 where a sixth cranial nerve palsy resulted from increased intracranial pressure in the posterior arteries that stretched the nerve. Dandy extrapolated this concept to cranial nerve 5. He published the surgical results of treating the trigeminal nerve sensory root of two TN patients,4 and subsequently operated on 215 TN patients, cataloguing each case’s causative etiology.5 Tumors accounted for 5.6%, arterial nerve compression for 30.7%, venous nerve compression for 14%, but in 40% of the patients “no gross findings were observed” (the largest single category). Gardner et al. attempted to verify Dandy’s observations, but the authors found vascular compression was present in less than 50% of his patients.6–10

In a 1993 manuscript entitled Vascular Compression is the cause of Trigeminal Neuralgia,11 Janetta wrote: “It is a central truth of science and medicine that ideas that precede the technology to prove or disprove them, lie fallow,” claiming the initial findings of the TN pioneers lacked magnification capabilities, where the nerve roots could not be completely examined.11 Jannetta advocated that neurovascular compression was the primary etiology of TN, despite reporting on 10 microvascular decompression (MVD) studies12–21 where incomplete relief, or TN symptom recurrence was observed in 4-32% cases, and negative MVD findings observed (no compression found) in 2-16% of these same subject groups. Confounding things further, multiple MRI studies analyzing both TN patients and non-TN control patients found neurovascular compression present in the non-TN control group, while some TN affected subjects presented without neurovascular compression.22–26 These same studies concluded that successfully using MRI findings to guide both surgical and non-surgical treatments for TN, ranged downward from 100 - 47%. Furthermore, two of these studies reported neurovascular compression (NVC) was present on the non-TN (unaffected) side of the face in 43%-76% of the patients, with false positives (NVC but no TN pain or diagnosis) being reported 15-56% of the time.22–26

Cadaver studies performed on people known to not have had TN, where 50 trigeminal nerve roots were examined, determined that 60% of these non-TN patients had unilateral direct vascular contact with the nerve tissue, and 20% had bilateral.27 Interestingly, some of the cadavers had contact force sufficient to cause an indentation of the nerve tissue.27 A second cadaver study reported in 7-12% NVC was observed in patients with no history of TN.28 Lastly, it has been demonstrated that TN can occur and reoccur in the absence of neurovascular compression,29 and that an estimated 99.94% of individuals with a neurovascular compression do not exhibit TN.29

Current TN treatment modalities include medications (usually the first attempt), with Micro-Vascular Decompression (MVD), and gamma knife surgery,30,31 as surgical options which have demonstrated some success at treating TN, but not the extent one would expect if neurovascular compression was the only etiology. Figure 1. Moreover, these treatments carrying significant adverse effects patients must weigh before undergoing therapy. As an alternative to surgical intervention, Botulinum Toxin-A (BTX-A) is also being used for TN treatment32 as well as with other chronic pain patients and conditions33–35 (myofascial pain dysfunction,36 painful diabetic polyneuropathy, post herpetic neuralgia (PHN), complex regional pain syndrome, and neuropathic low back pain.37 The contractility of the targeted muscles is reduced as the administration of Botox therapeutically blocks the pre-synaptic cholinergic nerve terminals. There is additional speculation that Botox might have an anti-nociceptive affect that has yet to be proved out definitively.38,39

Figure 1
Figure 1.Left image is post MVD incision where a Teflon strip is placed between the nerve and offending blood vessel. Right image is gamma knife surgery where the nerve is irradiated.

Given that the data does not clearly support neurovascular compression as being the sole etiology of TN, medicine and dentistry must hold other potential etiologies as equally possible. Dental Occlusion, which has never been proposed in the TN literature to be a possible TN etiologic contributor, was previously found in a case report to be a significant factor in both chronic orofacial pain and TN symptoms.30 Both pain conditions were resultant from bite force and bite timing abnormalities, that were resolved with the Immediate Complete Anterior Guidance Development (ICAGD) measured occlusal adjustment procedure.40 ICAGD reduces the frictional contacts of the posterior teeth that occur during lateral excursive movements, to establish measurable immediate posterior disclusion of the molars and premolars in < 0.5 seconds per excursion.40–48 The metric that determines how well ICAGD has been performed is the Disclusion Time (DT), which is the elapsed time (in seconds) between the start of a lateral excursion and the time-moment complete working side and non-working side molar and premolar disclusion is reached. The reason short DT is critically important, is because DT below 0.5 seconds have repeatedly been shown to markedly lessen excursive function elevated muscle hyperactivity.40–48 Over the past 30 years, this process known as Disclusion Time Reduction (DTR) via the ICAGD computer-guided coronoplasty, has successfully treated occluso-muscular TMD symptoms in multiple published studies, that were performed by different researchers who all used the same ICAGD process, and obtained similar therapeutic results.40–48

Objectives

Therefore, the objectives of this cohort study were to perform the ICAGD coronoplasty on a small group of confirmed TN patients whom presented with long Disclusion Times, high excursive muscle activity levels, and/or a bite force imbalance, all of which could promote TN episodes. The results of this Pilot Study will either corroborate or contradict the prior case report’s observed TN symptom reductions that followed the measured occlusal adjustment therapy.

METHODS & MATERIALS

Twenty-nine patients previously diagnosed by a primary care physician with Trigeminal Neuralgia (TN) that was confirmed by a neurologist, were evaluated in a dental practice that offers specialized Disclusion Time Reduction TMD services. All patients had prior magnetic resonance imaging (MRI), which confirmed neurovascular compression of the trigeminal nerve. Nine of the 29 prospective candidates had been treated with an accepted TN treatment; six had undergone MVD surgery, and three were treated with Gamma Knife surgery. However, neither the surgical NVC corrections, nor the irradiation of CN V’s ganglia were effective, as those nine patients never saw their pain leave, or their pain returned “full force” shortly following the procedures. Two other potential subjects were eliminated for not meeting the inclusion criteria (below), and two more patients did not complete their course of ICAGD, leaving a total of 25 study participants. An IRB exemption was requested and obtained for a retrospective cohort study #BIRB/94Z/2019.

Inclusion Criteria

  • A TN diagnosis from a neurologist with MRI indicating existing neurovascular compression of Cranial Nerve V

  • The existence of ongoing TN symptomatic episodes

  • 28 teeth with symmetrically missing teeth (if one molar was missing on the left side, then one had to be missing on the right side)

  • Near normal occlusal relations with molars and premolars in contact during the right and left excursions

  • Angles Class I and Class III occlusal relations, with guiding anterior teeth that were either in contact, or near to contact

  • Patients that had been previously treated with MVD and/or Gamma Knife surgery but did not receive TN symptom resolution

  • Patients older than 18 years of age

Exclusion Criteria

  • Severe Class II and Class III malocclusions and anterior open bite where anterior guidance contact could not be achieved

  • A previous history of TMJ trauma

  • The presence of unstable Temporomandibular Joint internal derangements verified by CBCT and/or Joint Vibration Analysis (JVA).

  • Patients that had been previously treated with MVD and/or Gamma Knife surgery that received TN symptom resolution

  • Patients who had undergone prior TMD therapy, including prior occlusal adjustment treatment.

  • Patients younger than 18 years of age

Informed consent was obtained for undergoing the ICAGD coronoplasty, and for collecting pain symptom severity and frequency data from questionnaires. The study protocol required the participants to fill out questionnaires that detailed TN symptoms, chronic muscular symptoms, pain intensity and frequency, functional restrictions, and a 15 item Patient Health Questionnaire (PHQ-15), which is a validated psychiatric instrument used to detect a Somatic Symptom Disorder (SSD).49–51 The PHQ-15 detects the presence of somatization, and has been recommended for use by the DC/TMD for patient assessment in dental practices treating TMD.52 Oral health histories were also obtained where the whole participant group reported experiencing a large number of TN symptoms as well as TMD symptoms with moderate to severe frequencies and intensities. The TN symptom every participant shared was a trigger zone in the CN-V2 or CN-V3 region that when touched could set off electric or stabbing pain as well as facial pain. The TMD symptoms seemed more random and no correlation could be made from any one symptom to the TN trigger zone symptom.

All participants underwent a pre-ICAGD right and left excursive Disclusion Time/muscle hyperactivity evaluation with the synchronized T-Scan 9/BioEMG III technologies (Tekscan Inc., S. Boston, MA USA; Bioresearch Assoc., Inc. Milwaukee, WI, USA) (Figure 2). The subjects closed firmly into their Maximum Intercuspation Position (MIP), held their teeth together for 1-3 seconds, and then completed a single direction right (or left) excursion until only their anterior teeth were in contact. They repeated the recording in the opposite direction to generate 2 separate pre- ICAGD excursive recordings. This specific recording method insured high quality Disclusion Time and EMG data was obtained from all subjects.40

Figure 2
Figure 2.The T-Scan Novus handle and BioEMG III are used to capture data that cannot be recorded by any other means. These synchronized technologies allow the user to record occlusal data in real-time with the muscles’ response to the occlusal function. The patient occludes into MIP with the sensor placed between their teeth and maintains intercuspation for 1-3 seconds, before performing a lateral excursive movement in one direction only (right or left).

Additionally, the subjects had their pre-ICAGD right side-to-left side Bite Force imbalance reported in percentages (Figure 3), and their pre-ICAGD Disclusion Times reported in seconds (Figure 4), both to be compared to their post ICAGD values.

Figure 3
Figure 3.A pre-operative bite force data scan. This patient reported unilateral pain on the left side. 69.3% of total bite force (green) is on the left affected side (green line) and the remaining 30.7% is on the right (red line).
Figure 4
Figure 4.A pre-ICAGD right excursive Disclusion Time/ muscle activity data scan. This patient reported unilateral pain on the right side. The right Disclusion Time is 0.61 seconds on the right side because the posterior right teeth are frictionally engaged (elevation of the blue line between C and D) indicating a prolonged right group function precedes that anterior guidance becoming effective. Note that the muscle elevation is 214 µv in the right anterior temporalis (Blue Arrow).

Description of the ICAGD Occlusal Adjustment Procedure

The teeth were dried on 1 side of the arch (operator’s selection), after which each subject closed into their Maximum Intercuspal Position (MIP) with 21 micron-thick articulating paper (Accufilm, Parkell, Inc. Farmingdale, NY, USA) interposed between their teeth, and to then move their mandible into a right excursion out to edges of their right canine teeth, then slide back into MIP, and then move out to edges of their left canine teeth. With this movement the teeth made excursive track lines that marked the long Disclusion Time contacts on the frictionally involved teeth for adjustment (Figure 5).

Figure 5
Figure 5.Teeth with paper marks pre ICAGD.

The pre-ICAGD T-Scan/BioEMG recordings guided the author to the proper areas of the occlusal surfaces that required excursive adjustments. All working and non-working posterior lateral interferences that represented the prolonged frictional contacts were removed completely, while the centric stop contacts were left intact except to lessen their broad surface area into small surface area contacts, located on supporting cusps and in central fossae. This process was repeated on the initial side of treatment until complete visual disclusion had been obtained (Figure 6). The same process of marking the teeth excursively and removing all working and non-working posterior lateral interferences was then performed on the 2nd side of the arch, until complete visual disclusion had been obtained on the 2nd side.

Figure 6
Figure 6.Post ICAGD all posterior left and right lateral excursive marks have been removed.

ICAGD was considered completed.

  1. all lateral posterior excursive interferences had been visually removed,

  2. disclusion of all posterior teeth in the right and left excursions afforded the patient noticeably easier lateral movements than pre-ICAGD,

  3. the remaining pattern of habitual closure contacts were located solely on cusp tips, in fossae, and on marginal ridges,

  4. any patient self-closure into MIP rapidly rising forces detected by the T-Scan, were refined to achieve measurable bilateral simultaneous force rises of moderate contact force (Figure 7).

  5. the Disclusion Times had been measurably reduced to < 0.5 seconds in each excursion

Figure 7
Figure 7.A post-ICAGD bite force data scan. This is the same patient as in Figure 3 after the bite correction. Note 54.5% of total bite force is on the left side and the remaining 45.5% is on the right. The ideal distribution occlusal force is 50% right-to-left +/- 5%.

At this same treatment appointment, new post ICAGD excursive recordings were obtained in the same manner as pre-ICAGD, to verify the Disclusion Time durations were correct. Any remaining prolonged excursive contacts were adjusted until each excursion’s Disclusion Time was less than 0.5 seconds (Figure 8).

Figure 8
Figure 8.A post-ICAGD right excursive Disclusion Time/muscle activity data scan on the same patient (Figure 4) showing the Disclusion Time was reduced to 0.12 seconds. At C the red line rises quickly to 100%, as the other colored lines drop to 0% force, indicating complete canine guidance control resulted from eliminating the friction in the posterior quadrants. Note the muscle activity is reduced in all muscles, most notably the right anterior temporalis which dropped post-ICAGD from 214µv to 3.7µv (blue arrow). That is 56 times less temporalis muscle activity than pre-ICAGD.

Patients were seen at Day 1, at 1-month, and at 3-months to undergo refinements to the above procedure, to fine tune the MIP occlusal contacts, improve the Disclusion Times if needed, and to allow time for the muscles to heal from the rendered occlusal refinements. At each of these follow-up visits, the patients filled out new questionnaires regarding their symptoms, pain intensity and frequency, functional restrictions and their PHQ-15 somatization resultant from undergoing ICAGD. All subjects’ self-assessment data were subjected to the non-parametric Wilcoxon Signed-Rank Test. The Disclusion Time values and EMG levels pre and post ICAGD were subjected to the Students paired t-test (Alpha = 0.05). This concluded both the treatment and data collection phases of the study.

RESULTS

The mean age of the TN subjects was 43.8 +/- 14.87 (84% (21) female and 16% (4) male). There was some randomness to the group in that consecutive patients were treated as they presented to the practice. This resulted in an unequal distribution of the sex and age demographics, which had no observable effects on the Results.

The TN trigger zone ultimately resolved in all participants to the point that the electric shocks/stabbing pain ceased. A few patients reported the trigger zones moved from V2 to V3 (or vice versa), or moved from a position that was external to the mouth to internal. Three patients reported this finding, 2 were next to the left maxillary second premolar and 1 was to the right mandibular premolar. These were transient and resolved in a few weeks to months. Patients also reported unsolicted improvements in follow up appointments such as: “I can brush my teeth without pain”, “I can walk down the frozen food isle at the store with no scarves on.” “I went running outside even when it is cold without being covered up”, and “I can shave my face without fear of getting shocked.”

The study participants reported higher pre-ICAGD self-assessment means and medians for their TN pain level intensity, pain frequency, their functional restrictions, and significantly higher PHQ-15 scores compared to their post-ICAGD responses (Table 1).

Table 1.The participants’ pre-ICAGD Pain scores, Frequency of Pain scores and Functional Restriction scores showed significant reductions at each time-point. All of the self-assessment scores diminished dramatically and reached a minimum by the 3rd month. A maximum pain score was 48, a maximum frequency score was 36 and a maximum restriction score was 27.
Pre-Tx Pain Totals 1 Month Post-Tx Pain 3 Months Post-Tx Pain Pre-Tx Symptom Frequency 1 Month Post-Tx Frequency 3 Months Post-Tx Frequency Pre-Tx Functional Restriction 1 Month Post-Tx Restriction 3 Months Post-Tx Restriction
Median 28 12 6 21 11 6 12 4 2
Mean 27.9 13.6 6.30 22.4 11.4 5.58 11.9 5.40 2.90
SD 8.13 7.39 4.25 6.64 6.36 3.91 6.21 4.48 2.23
p = Pre-Tx to 1 month 0.00001 Pre-Tx to 3 months 0.00001 1 month to 3 months 0.00001 Pre-Tx to 1 month 0.00001 Pre-Tx to 3 months 0.00001 1 month to 3 months 0.00001 Pre-Tx to 1 month 0.00004 Pre-Tx to 3 months 0.00001 1 month to 3 months 0.00039
Pain Levels: 0 = none, 1 = slight, 2 = moderate, 3 = severe, 4 = intolerable Symptom Frequencies: 0 = never, 1 = occasionally, 2 = often, 3 = always Functional Restrictions: 0 = none, 1 = slight, 2 = moderate, 3 = severe

Wilcoxon Signed-Rank Test, Tx = Treatment, SD = Standard Deviation

  • There were dramatic statistically significant reductions in the TN pain severity and episode frequency means at 1-month after ICAGD (36 +/- 14.3 days; p < 0.00001), with statistically significant further pain severity and frequency improvements observed at 3-months (88 +/- 13.6 days; p < 0.00001). Table 1.

  • There were statistically significant improvements in mean functional restriction scores at 3-months post-ICAGD (p < 0.0004).

  • There were statistically significant reductions in the group’s PHQ-15 mean scores at 1-month and 3-months post ICAGD (p < 0.0012). Table 2.

  • The self-reported TN and other symptom improvements were obtained solely because there were statistically significant time-duration changes made to the pre-ICAGD Disclusion Times by the ICAGD coronoplasty (p = 0.0001). Table 3.

  • There were statistically significant reductions in the group muscle activity level (EMG) means for all 4 muscles post-ICAGD compared to pre-ICAGD, that coincided with shortening the Disclusion Times (p = 0.00001). Table 4.

Table 2.Group PHQ-15 means at Pre-treatment, 1-month, and 3-months post-ICAGD.
Changes in PHQ-15 Scores Mean +/- SD PHQ-15 Interpretations
Pre-Tx PHQ-15 scores 13.2 +/- 4.84 DSM-IV/DSM-5 Interpretation = Somatoform Disorder
PHQ-15 Pre-Tx to 1 Month post-Tx 0.00001*
1 month Post-Tx PHQ-15 scores 7.2 +/- 3.79 DSM-IV/DSM-5 Interpretation = Other Neurotic Disorders
PHQ-15 Pre-Tx to 3 Months Post-Tx 0.00001*
3 months Post-Tx PHQ-15 scores 4.5 +/- 2.89 DSM-IV Interpretation = No Psychiatric Disorders
PHQ-15 1 Month to 3 Months Post-Tx 0.00118*

* Wilcoxon Signed-Rank Test, Tx = treatment

Table 3.The mean initial Disclusion Times were prolonged before ICAGD was applied. A dramatic reduction in the Disclusion Times was accomplished with ICAGD.
Disclusion Time Pre-Tx Right Side Disclusion Time Post-Tx Right Side Disclusion Time Pre-Tx Left Side Disclusion Time Post-Tx Left Side
Means 2.19 0.36 1.79 0.32
Standard Deviations 0.93 0.15 1.31 0.12
Wilcoxon Signed-Rank Test - p < 0.00001 0.00001
Student's Paired t-test - p < 0.00000 0.000003

Tx = treatment

Table 4.The mean EMG levels decreased markedly post-ICAGD compared to pre-ICAGD, dramatically reducing the amount of effort required by the muscles to move the mandible in lateral excursions.
EMG Pre and Post Treatment TA-R TA-R TA-L TA-L MM-R MM-R MM-L MM-L
Pre-Tx Post-Tx Pre=Tx Post-Tx Pre=Tx Post-Tx Pre=Tx Post-Tx
Mean 62.8 13.8 60.3 17.4 28.6 15.8 26.4 11.6
SD 59.26 13.02 58.04 20.79 17.50 10.33 15.37 8.83
Student's paired t test p = 0.0000006 0.000001 0.000004 0.0000002
Wilcoxon Signed-Rank Test p < 0.00001 0.00001 0.00001 0.00001

All data sets tested and found to be approximately normally distributed

The pre-ICAGD group mean PHQ-15 score =13.2 +/- 4.84, with a range of 6 - 23, suggesting that the 18 of the 25 subjects that scored higher than 10 likely exhibited a faux in retrospect SSD condition prior to receiving ICAGD treatment. The remaining 7 subjects scored a faux in retrospect “Other neurotic Disorder.” (Table 2). However, only one month after initial ICAGD treatment, the subject group’s PHQ-15 mean score statistically significantly dropped = 7.2 +/- 3.79 (p = 0.00001), which mean score (between 5 and 10) suggests a lesser neurotic symptom. At three months post ICAGD the subjects’ group PHQ-15 mean score dropped further to 4.5 +/- 2.89, which was significantly lower than the one month mean (p = 0.00118). At the three-month follow-up only one subject still scored a 12, but with numerous physical conditions complaints outside of the orofacial area. Six subjects scored between 5 and 10 and fully 18 subjects scored below 5.

DISCUSSION

The outcome of this computer-guided occlusal adjustment Trigeminal Neuralgia study contradicts all of the previous articles where it has been concluded that the physical symptoms of TN are secondary to Cranial Nerve V compression from its surrounding vasculature.31,32 This is the 2nd publication to show reducing the Disclusion Times of TN patients’ lateral excursions can rapidly and definitively lessen the frequency and intensity of TN bouts. However, this is the 1st research publication to show that Disclusion Time Reduction (DTR) with the ICAGD coronoplasty can successfully treat a group of chronic TN sufferers. The Results of this study would suggest that TN is actually subset of TM Disorders, because this study’s findings corroborate the successful TMD muscular symptom outcomes of many prior published DTR/ICAGD studies that have been in the literature since the early 1990s all the way up to 2020.40–48,53

The findings of this study also bring into question that NVC is the sole etiology for TN symptoms, while supporting other investigators who have determined in autopsy that neurovascular compression can occur in patients with no history of TN.54 Kalia suggested in 2014, “surely there are undiscovered factors in the TN story” and “perhaps the challenge is to find yet another cause of TN.”55 The fact that a number of the subjects had noticeable TN improvement or resolution from ICAGD, despite attempting multiple prior surgical treatments, adds significant credibility that the occlusion was etiologic for their TN conditions. And although ICAGD is an irreversible procedure that sacrifices about 120-180 microns of enamel (out of an existing 2000-2500 microns per tooth) to calm down the muscle hyperactivity and improve the neurophysiology, ICAGD has a long track record in studies of producing successful Occluso-muscular Dysfunction (OMD) symptom resolutions without requiring splints or orthotics, and without marked post treatment complications.40–48,53 From a contextual point of view ICAGD is a conservative treatment, especially when compared to MVD or Gamma Knife surgery (Figure 1). Therefore, it would be prudent that occlusal force imbalances and long Disclusion Times be ruled out as being causative for TN, before encouraging MVD or gamma knife surgery as a treatment option.

The reduction in muscle hyper-activity that was observed in this study must be considered as a contributory component of patients reporting symptom improvement, which corroborates the findings of prior ICAGD and DTR studies, in which when muscle hyperactivity was reduced, sustained relief followed without subjects requiring multiple retreatments.40–48,53 In that way, DTR treatment is self- limiting, and demonstrated long-term symptom control.56 And while there is great evidence showing Botulinum Toxin (BTX-A) is efficacious in treating TN,32,57–60 the BTX-A refractory period is short (3-6 months), requiring re-dosing the patient repeatedly to re-control the symptoms.

There are over 40 different diagnoses that fall under the TMD umbrella, where routinely there is a component of muscular pain. Muscle compensation is the body’s first adaptive mechanism to all structural shortcomings. Although Botulinum Toxin (BTX-A) has been used with Trigeminal Neuralgia patients32,57–60 to therapeutically block the pre-synaptic cholinergic nerve terminals and reduce muscle contractility, the results of this study suggest that the pathophysiologic mechanisms of TN must be reconsidered. In this subject group, elevated masticatory muscle activity levels were statistically reduced through computer-guided occlusal alterations, that also reduced TN pain frequency and intensity, while simultaneously improving muscle function. This was accomplished in the absence of any BTX-A administration, which supports the position that there is muscular component to idiopathic TN, which to date has been largely overlooked. TN in this subject group likely consisted of a muscular structural problem with shooting nerve pain as a secondary symptom, because a structural correction/alteration (occlusal adjustment to the excursive friction) relieved the muscle and/or nerve pain. BTX-A represents a symptomatic treatment, rather than a corrective therapy to the underlying malocclusion problem.

Of note is that in this TN/ICAGD study, the PHQ-15 scores statistically improved, corroborating a prior emotional assessment DTR study that showed the emotional states of TMD sufferers were improved after undergoing ICAGD.61 As occurred in that study of 83 emotionally affected TMD sufferers whose depression score improved rapidly after ICAGD,61 the TN subject group in this study also rapidly emotionally responded once their chronic TN pain was removed by ICAGD. For the 25 subjects in this TN study, the PHQ-15 pre-ICAGD scores indicated 18 subjects exhibited a possible somatoform disorder, and the remaining 7 subjects exhibited a "neurotic disorder." As the T-Scan-guided occlusal adjustments were performed, and the subjects’ painful symptoms were reduced, their PHQ-15 scores receded. At 1-month post ICAGD, only 4 subjects exhibited scores indicative of a somatoform disorder, 12 scored as other neurotic disorder, and the remaining 9 subjects’ PHQ-15 scores indicated they had fully recovered from their previous emotional disorder.

At three months, only one of the 25 subjects’ PHQ-15 scores was marginally suggestive of a possible somatoform disorder. However, that subject retained painful physical symptoms that (based upon the response of the other 24 subjects to the ICAGD treatment), did not appear to be related to the masticatory system. Six other subjects’ scores reduced to the level of other neurotic disorder, and the eighteen remaining subjects’ PHQ-15 scores indicated they had fully recovered emotionally. Considering that only occlusal adjustments were performed and no psychological counselling was a part of the treatment, it appears that the initial PHQ-15 scores were representing both false positive SSD or other neurotic disorder diagnoses based upon the significant secondary emotional distress present. As has been previously noted,61 the emotional recovery can take several months for a patient recovering from severe chronic physical pains.

This study’s outcome demonstrates the high risk of obtaining false positive diagnoses when testing for SSD, prior to the elimination of any existing physically painful conditions. The absolute requirement of establishing an absence of physically painful conditions before establishing SSD diagnosis is well understood by psychiatry,62–64 but seems often misunderstood by dentistry. While it cannot be concluded from this study that the T-Scan guided occlusal adjustments cured any SSD or other neurologic disorders, the well-known fact that chronic pain from any physical source predictably causes emotional distress, is not even debatable. This study’s results exemplify why an emotional evaluation cannot result in a valid psychiatric diagnosis, in the presence of physically driven chronic pain. Use of the PHQ-15 should follow the verification that all physical factors have been accounted for there, such that no physical etiology for symptoms is present. This is an important requirement that must precede any accurate diagnosis of emotionally driven symptoms.

Most of the TN literature contains substantial variation in agreement to the neurovascular compression explanation of TN. Obtaining an accurate diagnosis of neurovascular compression TN, is complicated because the anatomic appearances of neurovascular compression must be confirmed by MRI. However, multiple publications indicate that MRI may not be able to accurately detect if a structural nerve problem exists,22–26 which limits MRI from being an effective TN diagnostic image. Clinicians could be aided in making accurate TN diagnoses by requiring that TN patients fill out a TMD signs and symptoms questionnaire (See Appendix). If there are additional chronic muscular symptoms present along with the intense TN electric shock, the TN patient may be suffering from (OMD), which is one form of TMD. This was clearly the scenario for the 25 TN patients in this cohort study.

LIMITATIONS

Despite the very small P values reporting a high-level statistical significance in the TN symptom improvements, the Disclusion Time changes, and in the emotional PHQ-15 improvements observed, there were a number of limitations to the study design. First, there was a small sample size of 25 subjects, so large-scale TN symptom improvement extrapolations should not be made. A second limitation was that subjects were their own controls and not statistically compared to a separate TN subject control group. This should be done in a future study where ½ the TN patients receive a mock ICAGD procedure and the other ½ receive true ICAGD. As this specific study attempted to determine a measured treatment effect (changes TN symptoms after ICAGD), using the subjects as their own controls was necessary. To compensate for this limitation, many self-report questionnaires were used to determine pre to post ICAGD TN symptom improvements.

CONCLUSIONS

Twenty-five Trigeminal Neuralgia subjects experienced reductions in TN episodic frequency and pain severity, while functionally improving with much lower the levels of muscle activity following having their Disclusion Times shortened with the ICAGD coronoplasty. The subjects’ PHQ-15 scores also significantly reduced as their chronic pain levels were reduced. This points to the occlusion as being the primary causative agent for the symptoms in this group of TN patients, despite that the occlusion has been overlooked in the TN literature as being a potential TN etiologic component. Disclusion Time Reduction using ICAGD should be considered as an alternative treatment option for those patients diagnosed with painful Trigeminal Neuralgia. A second conclusion from this research is that emotional responses can be secondary to actual physically painful conditions and that the emotional factors can return to normal after the physical conditions have been corrected and the physical pain is relieved.


Statement of possible conflicts of interest

Dr. Ben Sutter claims no conflict of interest. Dr. Susan Teragawa claims no conflict of interest. John Radke is the Chairman of the Board of Directors of BioResearch Associates, Inc., the manufacturer of the BioEMG III. He receives no commission or other monetary incentive from the sales of the T-Scan or the BioEMG III.

Statement of funding

No funding from any source was provided for this study.

Accepted: August 10, 2020 CDT

References

1.
Greenberg M. Burket’s Oral Medicine: Diagnosis and Treatment. 10th ed. B.C. Decker; 2003.
Google Scholar
2.
Katusic S, Williams D, Beard C, Bergstralh E, Kurland L. Epidemiology and Clinical Features of Idiopathic Trigeminal Neuralgia and Glossopharyngeal Neuralgia: Similarities and Differences, Rochester, Minnesota, 1945-1984. Neuroepidemiology. 1991;10(5-6):276-281.
Google Scholar
3.
Cushing H. Strangulation of the nerve abducens by lateral branches of the basilar artery in cases of brain tumor: with an explanation of some obscure palsies on the basis of arterial constriction. Brain. 1910;33(3):204-235. doi:10.1093/brain/33.3.204
Google Scholar
4.
Dandy WE. Section of the sensory root of the trigeminal nerve at the pons: preliminary report of the operative procedure. Bull Johns Hopkins Hosp. 1925;36:105-106.
Google Scholar
5.
Dandy WE. Concerning the cause of trigeminal neuralgia. Am J Surg. 1934;24(2):447-455. doi:10.1016/s0002-9610(34)90403-7
Google Scholar
6.
Gardner WJ. Concerning the mechanism of trigeminal neuralgia and hemifacial spasm. J Neurosurg. 1952;19:947-958.
Google Scholar
7.
Gardner WJ. Trigeminal Neuralgia. Clin Neurosurg. 1968;15:1-55. doi:10.1093/neurosurgery/15.cn_suppl_1.1
Google Scholar
8.
Gardner WJ, Miklos MV. Response of trigeminal neuralgia to “decompression” of sensory root: discussion of cause of trigeminal neuralgia. JAMA. 1959;170(15):1773-1776. doi:10.1001/jama.1959.03010150017004
Google Scholar
9.
Gardner WJ, Pinto JP. The Taarnhjo operation: relief of trigeminal neuralgia without numbness. Clev Clin Q. 1953;20(2):364-367. doi:10.3949/ccjm.20.2.364
Google Scholar
10.
Gardner WJ, Todd EM, Pinto JP. Roentgenographic findings in trigeminal neuralgia. AJR. 1956;76:346-350.
Google Scholar
11.
Jannetta PJ. Vascular Compression is the Cause of Trigeminal Neuralgia. APS Journal. 1993;2(4):217-227. doi:10.1016/s1058-9139(05)80246-3
Google Scholar
12.
Ferguson GG, Breet DC, Peerless SJ, Barr HWK, Girvin JP. Trigeminal neuralgia: a comparison of the results of percutaneous rhizotomy and microvascular decompression. Can J Neurol Sci. 1981;8(3):207-214. doi:10.1017/s0317167100043225
Google Scholar
13.
Mori K, Morimoto M, Kurisada M, et al. Analysis of microvascular decompression for the treatment of trigeminal neuralgia and hemifacial spasm. Arch Jpn Chir. 1986;55:768-776.
Google Scholar
14.
Burchiel KJ, Steege TD, Howe JF, Loeser JD. Comparison of percutaneous radiofrequency gangliolysis and microvascular decompression for the surgical management of tic douloureux. Neurosurgery. 1981;9(2):111-119. doi:10.1227/00006123-198108000-00001
Google Scholar
15.
Wilson CB, Yorke C, Prioleau G. Microsurgical vascular decompression for trigeminal neuralgia and hemifacial spasm. West J Med. 1980;132:481-484.
Google Scholar
16.
Loveren H, Tew JM, Keller JT, Nurre MA. A 10-year experience in the treatment of trigeminal neuralgia. J Neurosurg. 1982;57(6):757-764. doi:10.3171/jns.1982.57.6.0757
Google Scholar
17.
Piatt JH Jr, Wilkins RH. Treatment of tic douloureux and hemifacial spasm by posterior fossa exploration: therapeutic implications of various neurovascular relationships. Neurosurgery. 1984;14:462-471.
Google Scholar
18.
Sindou M, Keravel Y, Abdennedi B, Szapiro J. Traitement neurochirurgical de la nevralgie trigeminale: abord direct ou methode percutanee? Neurochirurgie. 1987;33:89-111.
Google Scholar
19.
Bederson JB, Wilson CB. Evaluation of microvascular decompression and partial sensory rhizotomy in 252 cases of trigeminal neuralgia. J Neurosurg. 1987;71:359-367.
Google Scholar
20.
Apfelbaum RI. Surgical management of disorders of the lower cranial nerves. In: Schmidek H, Sweet WH, eds. Operative Neurosurgical Techniques. Grune & Stratton; 1988:1063-1081.
Google Scholar
21.
Jannetta PJ. Neurovascular compression in cranial nerve and systemic disease. Ann Surg. 1980;192(4):518-525. doi:10.1097/00000658-198010000-00010
Google ScholarPubMed CentralPubMed
22.
Masur H, Papke K, Bongartz G, Vollbrecht K. The significance of three-dimensional MR-defined neurovascular compression for the pathogenesis of trigeminal neuralgia. J Neurol. 1995;242(2):93-98. doi:10.1007/bf00887823
Google Scholar
23.
Kuroiwa T, Matsumoto S, Kato A, et al. MR imaging of idiopathic trigeminal neuralgia: correlation with non-surgical therapy. Radiat Med. 1996;14(5):235-239.
Google Scholar
24.
Matsumoto S, Kishikawa T, Kudo S, Matsuo Y, Totoki T, Harano K. Magnetic resonance imaging of idiopathic trigeminal neuralgia. Nihon Igaku Hoshasen Gakkai Zasshi. 1991;51(1):91-93.
Google Scholar
25.
Fukuda H, Ishikawa M, Okumura R. Demonstration of neurovascular compression in trigeminal neuralgia and hemifacial spasm with magnetic resonance imaging: comparison with surgical findings in 60 consecutive cases. Surg Neurol. 2003;59(2):93-100. doi:10.1016/s0090-3019(02)00993-x
Google Scholar
26.
Miller JP, Acar F, Hamilton BE, Burchiel KJ. Radiographic evaluation of trigeminal neurovascular compression in patients with and without trigeminal neuralgia. J Neurosurg. 2009;110(4):627-632. doi:10.3171/2008.6.17620
Google Scholar
27.
Hardy DG, Rhoton AL Jr. Microsurgical relationship of the superior cerebellar artery and the trigeminal nerve. J Neurosurg. 1978;49(5):669-678. doi:10.3171/jns.1978.49.5.0669
Google Scholar
28.
Adams CBT. Microvascular compression: an alternative view and hypothesis. J Neurosurg. 1989;70(1):1-12. doi:10.3171/jns.1989.70.1.0001
Google Scholar
29.
Lee A, McCartney S, Burbidge C, Raslan AM, Burchiel KJ. Trigeminal Neuralgia occurs and recurs in the absence of neurovascular compression. J Neurosurg. 2014;120(5):1048-1054. doi:10.3171/2014.1.jns131410
Google Scholar
30.
Sutter BA. Complex Medical Diagnoses with an Underlying Dental Etiology; Case Reviews. In: Kerstein RB, ed. Handbook of Research on Clinical Applications of Computerized Occlusal Analysis in Dental Medicine. IGI Global; 2019:1243-1315.
Google Scholar
31.
Al-Quliti KW. Update on neuropathic pain treatment for trigeminal neuralgia. The pharmacological and surgical options. Neurosciences (Riyadh). 2015;20(2):107-114. doi:10.17712/nsj.2015.2.20140501
Google ScholarPubMed CentralPubMed
32.
Obermann M. Recent advances in understanding/managing trigeminal neuralgia. F1000Res. 2019;8(F1000 Faculty Rev):505. doi:10.12688/f1000research.16092.1
Google ScholarPubMed CentralPubMed
33.
Ataran R, Bahramian A, Jamali Z, et al. The Role of Botulinum Toxin A in Treatment of Temporomandibular Joint Disorders: A Review. J Dent (Shiraz). 2017;18(3):157-164.
Google Scholar
34.
Song PC, Schwartz J, Blitzer A. The emerging role of botulinum toxin in the treatment of temporomandibular disorders. Oral Dis. 2007;13(3):253-260. doi:10.1111/j.1601-0825.2007.01352.x
Google Scholar
35.
Freund B, Schwartz M. The use of botulinum toxin for the treatment of temporomandibular disorder. Oral Health. 1998;88(2):32-37.
Google Scholar
36.
Fallah HM, Currimbhoy S. Use of botulinum toxin A for treatment of myofascial pain and dysfunction. J Oral Maxillofac Surg. 2012;70(5):1243-1245. doi:10.1016/j.joms.2012.01.015
Google Scholar
37.
Argoff C. The emerging use of botulinum toxins for the treatment of neuropathic pain. Pain Med. 2010;11(12):1750-1752. doi:10.1111/j.1526-4637.2010.00997.x
Google Scholar
38.
Piovesan EJ, Teive HG, Kowacs PA, Della Coletta MV, Werneck LC, Silberstein SD. An open study of botulinum-A toxin treatment of trigeminal neuralgia. Neurology. 2005;65(8):1306-1308. doi:10.1212/01.wnl.0000180940.98815.74
Google Scholar
39.
Brenner SB, Voller T, Sycha B, et al. An open study of botulinum-A toxin treatment of trigeminal neuralgia. Neurology. 2006;66(9):1458-1459. doi:10.1212/01.wnl.0000224704.05779.92
Google Scholar
40.
Kerstein RB. Disclusion Time reduction therapy with immediate complete anterior guidance development: the technique. Quint Int. 1992;23:735-747.
Google Scholar
41.
Kerstein RB, Radke J. Masseter and temporalis excursive hyperactivity decreased by measured anterior guidance development. Cranio. 2012;30(4):243-254. doi:10.1179/crn.2012.038
Google Scholar
42.
Kerstein RB, Radke J. Average Chewing Pattern improvements following Disclusion Time Reduction. Cranio. 2017;35(3):135-151. doi:10.1080/08869634.2016.1190526
Google Scholar
43.
Kerstein RB, Chapman R, Klein M. A comparison of ICAGD (Immediate Complete Anterior Guidance Development) to “mock ICAGD” for symptom reductions in chronic myofascial pain dysfunction patients. J Craniomandib Pract. 1997;15(1):21-37. doi:10.1080/08869634.1997.11745990
Google Scholar
44.
Thumati P, Sutter BA, Kerstein RB, Yiannios N, Radke J. Beck Depression Inventory changes in muscular TMD subjects after measured occlusal treatment. Adv Dent Tech. 2018;1(1):1-13.
Google Scholar
45.
Kerstein RB, Wright NR. An electromyographic and computer analysis of patients suffering from chronic myofascial pain dysfunction syndrome, pre and post - treatment with immediate complete anterior guidance development. J Prosthet Dent. 1991;66(5):677-686. doi:10.1016/0022-3913(91)90453-4
Google Scholar
46.
Thumati P, Manwani R, Mahantshetty M. The effect of reduced Disclusion Time in the treatment of myofascial pain dysfunction syndrome using immediate complete anterior guidance development protocol monitored by digital analysis of occlusion. Cranio. 2014;32(4):289-299. doi:10.1179/2151090314y.0000000004
Google Scholar
47.
Thumati P, Thumati RP. The effect of disocclusion time-reduction therapy to treat chronic myofascial pain: A single group interventional study with 3-year follow-up of 100 cases. J Ind Prostho Soc. 2016;16(3):234-241. doi:10.4103/0972-4052.176529
Google ScholarPubMed CentralPubMed
48.
Yiannios N, Kerstein RB, Radke J. Treatment of frictional dental hypersensitivity (FDH) with computer-guided occlusal adjustments. Cranio. 2016;35(6):347-357. doi:10.1080/08869634.2016.1251692
Google Scholar
49.
van Ravesteijn H, Wittkampf K, Lucassen P, et al. Detecting somatoform disorders in primary care with the PHQ-15. Ann Fam Med. 2009;7(3):232-238. doi:10.1370/afm.985
Google ScholarPubMed CentralPubMed
50.
Interian A, Allen LA, Gara MA, Escobar JI, Díaz-Martínez AM. Somatic complaints in primary care: further examining the validity of the Patient Health Questionnaire (PHQ-15). Psychosomatics. 2006;47(5):392-398. doi:10.1176/appi.psy.47.5.392
Google Scholar
51.
Kroenke K, Spitzer RL, Williams JBW. The PHQ-15: validity of a new measure for evaluating the severity of somatic symptoms. Psychosom Med. 2002;64(2):258-266. doi:10.1097/00006842-200203000-00008
Google Scholar
52.
Schiffman E et al. Diagnostic Criteria for Temporomandibular Disorders (DC/TMD) for Clinical and Research Applications: Recommendations of the International RDC/TMD Consortium Network and Orofacial Pain Special Interest Group. J Oral Facial Pain Headache Winter. 2014;28(1):6-27.
Google Scholar
53.
Thumati P, Poovani S, Bharathi B, Mounika A, Kerstein RB. Radke J.A Disclusion Time Reduction Randomized Controlled Occlusal Adjustment Trial. Adv Dent Tech. 2020;2(2):1-23. https:/​/​adtt.scholasticahq.com/​article/​12683-a-disclusion-time-reduction-randomized-controlled-occlusal-adjustment-trial
Google Scholar
54.
Adams CBT. Microvascular compression: an alternative view and hypothesis. J Neurosurg. 1989;70(1):1-12. doi:10.3171/jns.1989.70.1.0001
Google Scholar
55.
Kalia KK. Letter to the editor. Challenging vascular compression as a cause of trigeminal neuralgia. J Neurosurg. 2014;121(4):1004. doi:10.3171/2014.5.jns14971
Google Scholar
56.
Kerstein RB. Treatment of myofascial pain dysfunction syndrome with occlusal therapy to reduce lengthy Disclusion Time – a recall evaluation. Cranio. 1995;13(2):105-115. doi:10.1080/08869634.1995.11678053
Google Scholar
57.
Castillo-Álvarez F, Hernando de la Bárcena I, Marzo-Sola ME. Botulinum toxin in trigeminal neuralgia. Toxina botulínica en la neuralgia del trigémino. Med Clin (Barc). 2017;148(1):28-32. doi:10.1016/j.medcli.2016.07.032
Google Scholar
58.
Ostrowski H, Roszak J, Komisarek O. Botulinum toxin type A as an alternative way to treat trigeminal neuralgia: a systematic review. Neurol Neurochir Pol. 2019;53(5):327-334. doi:10.5603/pjnns.a2019.0030
Google Scholar
59.
Morra ME, Elgebaly A, Elmaraezy A, et al. Therapeutic efficacy and safety of Botulinum Toxin A Therapy in Trigeminal Neuralgia: a systematic review and meta-analysis of randomized controlled trials. J Headache Pain. 2016;17(1):63. doi:10.1186/s10194-016-0651-8
Google ScholarPubMed CentralPubMed
60.
Kowacs PA, Utiumi MAT, Nascimento FA, Piovesan EJ, Teive HAG. OnabotulinumtoxinA for trigeminal neuralgia: a review of the available data. Arq Neuropsiquiatr. 2015;73(10):877-884. doi:10.1590/0004-282x20150109
Google Scholar
61.
Thumati P, Sutter B, Kerstein RB, Yiannios N, Radke J. Changes in the Beck Depression Inventory -II Scores of TMD Subjects after Measured Occlusal Treatment. Adv Dent Tech. 2018;1(1):1-13. https:/​/​adtt.scholasticahq.com/​article/​5019-changes-in-the-beck-depression-inventory-ii-scores-of-tmd-subjects-after-measured-occlusal-treatment
Google Scholar
62.
Wolfe F, Walitt BT, Katz RS, Häuser W. Symptoms, the nature of fibromyalgia, and diagnostic and statistical manual 5 (DSM-5) defined mental illness in patients with rheumatoid arthritis and fibromyalgia. PLoS ONE. 2014;9(2):e88740. doi:10.1371/journal.pone.0088740
Google ScholarPubMed CentralPubMed
63.
Cho KJ, Lee NS, Lee YS, et al. The Changes of Psychometric Profiles after Medical Treatment of Lower Urinary Tract Symptoms Suggestive of Benign Prostatic Hyperplasia. Clin Psychopharmacol Neurosci. 2015;13(3):269-274. doi:10.9758/cpn.2015.13.3.269
Google ScholarPubMed CentralPubMed
64.
Heidari Z, Keshteli AH, Feizi A, Afshar H, Adibi P. Somatic Complaints Are Significantly Associated with Chronic Uninvestigated Dyspepsia and Its Symptoms: A Large Cross-sectional Population Based Study. J Neurogastroenterol Motil. 2017;23(1):80-91. doi:10.5056/jnm16020
Google ScholarPubMed CentralPubMed

Appendix - Forms Used

A 1. PHQ-15 form is self-reported by the patient checking the appropriate box in each row. The values assigned to score it are: Bothered not at all = 0, Bothered a little = 1, Bothered a lot = 2. Total score is the sum of all scores.
A 2. Symptom Frequency Form is self-reported by the patient by checking the appropriate box in each row. The values assigned to score it are: Never = 0, Occasionally = 1, Often = 2, All the time = 3. Total score is the sum of all scores.
A 3. Pain Intensity Form is self-reported by the patient checking the appropriate box in each row. The values assigned to score it are: None = 0, Slight = 1, Moderate = 2, Severe = 3, Intolerable = 4. Total score is the sum of all scores.