I have a scientific paper of 2 case reports that I would like to present as a poster.
Case 1 report and clinical presentation
For onset, patient reports started one month ago. For location, he reports right-sided. For quality, he reports shooting. For severity, he reports pain level 10-11/10 (only lasts a split second). For the duration, he reports intermittent weekly. For symptom triggers, he reports no known trigger/insidious. For aggravating factors, he reports chewing (eating salty food). For alleviating factors, he reports none. For associated symptoms, he reports no jaw clicking, no jaw popping, and no jaw locking. For prior treatment, he reports a soft diet and extraction of deciduous lower right 1st molar. For prior opinion, he reports to the dentist and oral surgeon. For symptom status, he reports pain being worse than when it started. These symptoms are acute and begin with no clear triggering events. Previous consultations include an evaluation with his dentist. Symptoms are right-sided only and aggravated by jaw use and function. The patient is aware of teeth clenching and grinding. The patient reported right-sided facial pain that is described as electrical shocks that last a few seconds. The pain is on the right side of the lower jaw and shoots up. This started when he was chewing food. It happens when he eats a certain type of food. Mostly salty food, He had a tooth extracted on the lower right side. He thinks it was a baby tooth. Shortly after the tooth was extracted, he did not have pain for 10 days. He remembers eating or sucking on lemon drops and the shock came back. He thought maybe the extracted socket was infected and was seen in the ER. He was given antibiotics at the ER. He then saw his dentist and was told the extraction site was healing fine. His pain started a month ago while he was chewing, he saw his dentist and he had his ‘baby tooth ‘ pulled by an oral surgeon. The pain disappeared until the 11th of February. He saw a different OS today and he did thermal testing, bite test, and percussion and it did not trigger the pain. He describes the pain as zapping pain, shock-like and it is triggered by brushing his teeth or swishing his mouth with certain salty food, the pain lasts for a split second and has a refractory period of a few minutes.
Medical history
The patient reported that he had episodes of high blood pressure that resolved with proper diet and exercise. For medication, the patient reported taking 600 mg ibuprofen twice/day for his pain which did not help.
Past diagnostic imaging
Panoramic image that showed extracted deciduous lower right 1st molar, and retained deciduous lower left 1st molar.
Examination
General Appearance oriented to time, place, and person, well-nourished, well-developed, no acute distress (had multiple episodes of pain that made him jump out of place and guard his muscles). Skin: Rash no rash/lesion. During the visit had multiple episodes of pain that made him jump out of his place and guard his muscles, triggered by light touch of the area, swishing with mouthwash or water, and moving his jaw. These symptoms are indicative of trigeminal nerve hyperactivity.
Trigeminal nerve block injection, 1 cc of 0.5% Bupivacaine was injected in the right inferior alveolar nerve. Prior to injection, informed consent was obtained. Procedure risks were explained, and questions were reviewed and answered. The patient’s pre-injection pain score was a 10 on a 0-10 scale.
The patient was seated comfortably in the examination room. The painful area was identified. A 27-gauge, 2 inch was inserted. There was no blood on aspiration. The above medication solution was then gradually injected without difficulty. The needle was withdrawn after injection. The patient tolerated the procedure well without immediate complications. The patient was observed for an adequate time post-operatively. The patient’s post-injection pain score was a 0 on a 0-10 scale. The patient was advised to contact the office if any questions arose and to return in 1 week for follow-up care.
Diagnostic imaging:
Inferior alveolar nerve block arrested the pain episodes. The patient will report back to me if the pain recurs following cessation of the local anesthetic effect. I discussed this with pt.: TN is typified by attacks that can stop for a period and then return, but the condition can be progressive. The attacks often worsen over time, with fewer and shorter pain-free periods before they recur.
The patient was provided education about the anatomy and pathophysiology of the trigeminal system as it pertains to the specific diagnoses outlined as well as education on treatment options and prognosis. I prescribed gabapentin 100mg tid to be increased to 200 mg tid after 5 days. An MRI of the brain, with and without contrast with TN protocol was ordered.
Due to the young age of the patient (y.o) compared to the usual presentation of TN which is in older patients (60-70 y.o) and to the frequency of pain attacks that ranged from X-X/day. An MRI of the brain was ordered, with and without contrast cerebellopontine angle.
Results revealed a 2.2 cm X 1.4 cm diffusion-restricting mass (epidermoid cyst) in the right cerebellopontine. The mass demonstrated slight signal abnormality on the highly T2-weighted images and an increase in flair signal as opposed to normal CSF fluid. The mass impinging on the pons, brainstem, and the right trigeminal nerve.
Diagnosis and management
Secondary trigeminal neuralgia due to intracranial epidermoid cyst. On follow-up. I reviewed the brain imaging with the patient. This included a T3 Brain MRI to rule out secondary cause for trigeminal neuralgia. Criteria for completing imaging was met including no recent previous imaging, the nature and pain severity, and the result may change treatment strategy. requested the MRI interpretation and it was faxed to us. The report revealed that there is a 2.2×1.4 epidermoid cyst in the right cerebellopontine angle, the mass is located on the pons, brainstem, and right trigeminal nerve.
Since the patient was in severe pain and was not able to finish a sentence without having a jolt of pain, I performed an inferior alveolar nerve block which took care of the pain. I prescribed 150 mg oxcarbazepine twice a day to be increased to 300 mg after 3 days. I have submitted an online referral to neurosurgery. I have also referred him to the UMN ER and contacted the neurosurgeon resident in charge regarding the case. I contacted the patient an hour later and he reported he was still pain-free.
Case 2 report and clinical presentation
The patient is here due to pain on the right side of her face. She has had this pain since 2014. She has had 3 root canals and still has the pain. The pain is worsening. The pain is in the temporal area, eye, and tissue around the tooth. Had a cone beam done recently. Pain is 6 usually, but some days it is 8-9 on a 0-10 scale. The pain is daily. notes symptoms beginning 1 year ago. She notes at that time maxillary right-sided tooth pain. She notes a “shooting” pain in her eye and temple. Her dentist did an RCT on tooth #4 three months ago without a change in her symptoms. Teeth #2 and 3 were treated endodontically in 2014 and 2016. Her dentist adjusted the tooth occlusion and adjusted interproximally. Pressure to the tooth feels better. Pain is daily but not constant. She has pain, which is sharp, lasting several seconds, and lingers in an achy pain that will last minutes to hours. She’s unsure of triggers. Pain doesn’t typically wake her from sleep. She is using OTC Advil 400 mg which offers minimum improvement. She denies numbness, vision changes, or balance issues. She denies jaw pain. She has not seen her physician. She notes 8/10 anxiety and sees her therapist weekly. She’s aware of clenching and grinding her teeth.
The patient reports ear pain but reports no difficulty hearing; right. She reports no sinus problems; the cone beam showed a difference from the left side to the right was more cloudy and smaller. She reports anxiety but reports no depression. She reports no fever and no significant weight gain. She reports no dry eyes and no visual change. She reports no sore throat, no snoring, no mouth ulcers, and no teeth problems. She reports no chest pain and no palpitations. She reports no cough, no shortness of breath, and no sleep apnea. She reports no abdominal pain, no nausea, and no vomiting. She reports no incontinence. She reports no muscle weakness. She reports no rashes. She reports no weakness, no numbness, no seizures, and no dizziness. She reports no fatigue. She reports no swollen glands and no excessive bleeding. She reports no hives.
Past and current medical history
Past diagnostic imaging
Cone Beam CT scan, Full bitewings, and periapical X-rays that were within normal limits.
Examination
General Appearance well-nourished, well-developed, oriented to time, place, and person, and no acute distress. Extra and intraoral examination was within normal limits. The patient had a normal affect and was appropriate to the situation. She did follow directions and participated in the evaluation thoroughly. During the appointment she had 2-3 pain episodes, however, I was unable to trigger her pain. No sensory changes. No teeth were tender to percussion. No periapical tenderness or swelling. During the exam, she was clenching her teeth.
Review of Systems:
The patient reports ear pain but reports no difficulty hearing; right. She reports no sinus problems; the cone beam showed a difference from the left side to the right-right was more cloudy and smaller. She reports anxiety but reports no depression. She reports no fever and no significant weight gain. She reports no dry eyes and no visual change. She reports no sore throat, no snoring, no mouth ulcers, and no teeth problems. She reports no chest pain and no palpitations. She reports no cough, no shortness of breath, and no sleep apnea. She reports no abdominal pain, no nausea, and no vomiting. She reports no incontinence. She reports no muscle weakness. She reports no rashes. She reports no weakness, no numbness, no seizures, and no dizziness. She reports no fatigue. She reports no swollen glands and no excessive bleeding. She reports no hives.
Diagnostic imaging
MRI of the brain was done with contrast 3T. Technique: Postcontrast sagittal T1 SPGR, sagittal T2 flair, and axial T1 spin-echo flair. The contrast used is Gadoterate meglumine 14 mL. No sedation was used. There is a punctate focus of enhancement with associated T2/flair signal abnormality in the right paramedian frontal lobe. The additional enhancing lesion in the left paramedian parietal lobe, 2 punctate foci of enhancement with associated T2/T2 flair signal abnormality. In conjunction with previous non-contrast MRIs of the brain, these findings are highly suspicious for demyelinating disease.
Diagnosis and management
A diagnosis of atypical facial pain and right V1/2 atypical neuralgic pain was reached during the first assessment. Medications were offered to the patient as an option to address her initial symptoms which the patient declined.
Diagnostic imaging and lab work:
An MRI of the brain + brain stem, w/o contrast-side: bilateral mri type: closed 3.0 T high field to rule out intracranial mass or demyelinating disease. A fluoroscopic guided lumbar puncture to obtain cerebrospinal fluid for laboratory analysis was ordered. The patient was also referred to a neurologist.
IgG CSF
4.56 (H)
<=3.40 mg/dL
Lymphocytes,CSF
96 (H)
40- 80 %
MONOCYTES,CSF
3 (L)
15 – 45 %
IgG INDEX
1.55 (H)
0.30 – 0.60
IgG synthesis
12.50 (H)
<=8.00 mg/day
Oligoclonal BANDS
Present
(A) Absent
IgG index and IgG synthesis interpretation, CSF/serum rate are both increased. abnormal study consistent with a demyelinating disease process.
Discussion
Definition
According to the beta version of the 3rd edition of the International Classification of Headache Disorders (ICHD-3 Beta), Trigeminal neuralgia (TN) is a chronic pain condition characterized by abrupt recurrent unilateral brief electric shock-like pains. In other words, the pain comes from the trigeminal nerve, which starts near the top of the ear and splits in three, toward the eye, cheek, and jaw. This chronic pain responding to a normally innocuous stimulus, such as light touch or warmth, and is perceived as painful (a phenomenon referred to as allodynia), may develop without apparent cause or be a result of another diagnosed disorder. In addition, there is a chance to have persistent background facial pain of moderate intensity.
Classification
TN is additionally subcategorized into classical, secondary, or idiopathic, depending on the fundamental cause (figure 1). The classical type (CTN), the most common and accounts for 75% of cases, is identified when there is a demonstration of morphologic changes in the trigeminal nerve root from vascular compression, ipsilateral to the side of the pain. It was demonstrated either during surgery or on MR imaging with appropriate trigeminal sequences.
The secondary type (STN) is due to an identifiable underlying neurologic disease (except trigeminal neurovascular compression), accounting for approximately 15% of cases.
The fundamental neurological disease includes cerebellopontine angle tumor, arteriovenous malformation, and multiple sclerosis. Specifically, approximately two percent of people with multiple sclerosis have symptoms similar to those of TN. Approximately 10% of cases are diagnosed as the idiopathic type, whenever there is no apparent cause for TN. Lambru G, et al. Pract Neurol 2021;21:392–402. doi:10.1136/practneurol-2020-002782
Figure 1 International Classification of Headache Disorders Edition 3 subclassification of trigeminal neuralgia.
Diagnostic criteria for TN According to (ICHD-3 Beta)
13.1.1 Classical trigeminal neuralgia (Tic douloureux)
A. At least three attacks of unilateral facial pain fulfilling criteria B and C
B. Occurring in one or more divisions of the trigeminal nerve, with no radiation beyond the trigeminal distribution
C. Pain has at least three of the following four characteristics:
1. recurring in paroxysmal attacks lasting from a fraction of a second to 2 minutes
2. severe intensity
3. electric shock-like, shooting, stabbing or sharp in quality
4. precipitated by innocuous stimuli to the affected side of the face
D. No clinically evident neurological deficit
E. Not better accounted for by another ICHD-3 diagnosis.
Etiology
The predominant pathophysiological mechanism of TN is demyelination of trigeminal sensory fibers within either the nerve root or, less commonly, the brainstem. Presumably, demyelination leads into the generation of ectopic impulses and ephaptic crosstalk. In a large proportion of the patients, demyelination is caused by a neurovascular conflict with structural changes such as the trigeminal root compression. However, only half of the CTN patients have morphological changes. There are also other unknown etiological factors. As STN, this is defined as TN secondary to an underlying disease. It can be caused by multiple sclerosis or a space-occupying lesion affecting the trigeminal nerve. PMID: 28076964
Triggers:
Typical triggers inducing pain include: eating, erinking, smiling, brushing teeth, and talking (J Oral Maxillofac Surg 79:2370−2371, 2021)
Classification:
Typical and Atypical
Idiopathic TN1 and TN2 In the classification scheme we propose, a diagnosis that was previously referred to as classic or typical TN is referred to as TN1. As described earlier, this is an idiopathic sharp, shooting, electrical shock-like, episodic pain lasting several seconds, with pain-free intervals between attacks. This diagnosis is fairly straightforward and most neurosurgeons are familiar with this clinical entity. We propose that TN2 describes idiopathic trigeminal facial pain that is aching, throbbing, or burning for more than 50% of the time and is constant in nature (constant background pain being the most significant attribute). There may be a minor component of sharp, episodic pain. In the absence of a demonstrable structural pathological entity, we theorize that if left untreated, TN1 progresses toward TN2 and signifies further neural injury. In cases of facial pain with the features of TN2, the likelihood of detecting a structural entity, such as a tumor or a vascular malformation in the posterior fossa is higher. With this in mind, the neurosurgeon should obtain imaging studies in these patients before a definitive diagnosis of TN2 is made. Neuropathic and Deafferentation TN Pain in the distribution of the trigeminal nerve in patients with a history of injury to the trigeminal system identifies a specific subset of cases. The patients in these cases are suffering from a form of neuropathic pain involving the trigeminal system, as opposed to the idiopathic forms of TN
(TN1 and TN2). This group of patients is divided into two subsets. The first, trigeminal neuropathic pain, includes patients who have suffered an unintentional injury to the trigeminal system as a result of facial trauma; oral surgery; ear, nose, and throat surgery; skull base surgery; posterior fossa surgery; or stroke. The second, trigeminal deafferentation pain, includes patients who received an intentional injury to their trigeminal system, such as neurectomy, gangliolysis, rhizotomy, nucleotomy, tractotomy, or other denervating
procedures. Trigeminal neuropathic pain mostly constitutes an unremitting throbbing or burning in the affected area, whereas trigeminal deafferentation pain is described as burning, crawling, itching, or tearing. Anesthesia Dolorosa, an extreme condition, is described as excruciating pain perceived in an insensate region of the face.
Symptomatic and Postherpetic TN
Two separate criteria easily identified in the patient’s history are worthy of inclusion. One, symptomatic TN, describes the association of TN with MS. In patients with TN who are younger than 40 years of age, particularly those with evidence of sensorimotor dysfunction, a diagnosis of MS should be considered. Approximately 1% of patients with TN have MS; conversely, the incidence of TN in the population of patients with MS is between 1 and 3%. The
Pathological origin in these cases appears to be demyelination, either in the trigeminal nerve or within the descending tract of the trigeminal system in the brainstem. Pain is characteristically either episodic or constant in nature. The other, postherpetic TN, describes trigeminal pain resulting from an outbreak of facial herpes zoster. This condition usually affects the first division and is marked by the development of allodynia superimposed on a burning dysesthesia. Trophic changes may be noted.
Atypical Facial Pain
A final criterion in our classification scheme is atypical facial pain. We propose that this term be limited to patients reporting facial pain in the context of a somatoform pain
disorder. These patients usually experience bilateral facial pain, which spreads outside a trigeminal distribution, along with multiple pain complaints in other body regions, including diagnostic clusterings such as fibromyalgia or chronic fatigue syndrome. Patients must be evaluated using psychological testing prior to confirmation of this diagnosis. (PMID: 15913279).
Epidermoid cyst
Epidermoid cysts are slow-growing masses that compress neurovascular tissue with painless (1) or only minimal clinical symptoms. The most common locations of intracranial epidermoids are the CPA (40-50%)(3,7). Intracranial tumors infrequently lead to TN (< 1%(6). However, specifically tumors resulting in TN are acoustic neuromas and epidermoid cysts, usually located in the posterior fossa (5) and meningioma, schwannomas, and pituitary adenoma, located in central fossa (6) and demyelination disorders such as multiple sclerosis (7). Epidermoid-related TN presents in younger age and longer duration of symptoms than those with a classic typed TN (vascular compression-related or idiopathic) (2,3,6,7). In previous case series of epidermoid-related TN, 17, 18, 48 years old (6,7), the mean age at diagnosis of epidermoid cyst was 37.8-38.8 years, and the mean duration from onset of symptoms to diagnosis was 3.1-11.5 years (2,3).
MS
Multiple sclerosis (MS) is a chronic inflammatory disease-causing demyelination and axonal degeneration in the central nervous system. The common symptoms of MS include fatigue, vision problems, muscle spasms, stiffness and weakness, problems with thinking, learning, and planning, as well as depression and anxiety (9). Neuropathic pain is a common symptom in patients with MS (8).
CRITERIA OF MS.
Nowadays multiple sclerosis (MS) is diagnosed by applying multiple kinds of tests and assessments. Not any single examination can be a diagnostic test to confirm MS. In order to make an MS diagnosis, these are indicators as follows:
Find evidence of damage in at least two separate areas of the central nervous system (CNS), which includes the brain, spinal cord and optic nerves AND
evidence that the damage occurred at different points in time AND
Rule out all other possible diagnoses.
The McDonald Criteria, published in 2017 by the International Panel on the Diagnosis of Multiple Sclerosis, include specific guidelines for using MRI and cerebrospinal fluid analysis to speed the diagnostic process. In other words, a patient, who experienced at least two clinical attacks and has clear-cut evidence of damage in at least two distinct brain areas, can be definitively diagnosed with MS. The MRI can show a second area of damage in a person who has experienced only one relapse of MS-like symptoms — referred to as clinically-isolated syndrome (CIS). The MRI can also be used to confirm that damage has occurred at two different points in time. The presence of oligoclonal bands in cerebrospinal fluid analysis can be used instead of dissemination in time to confirm the MS diagnosis in some circumstances.
Lhermitte's sign (also known as Lhermitte's phenomenon, or the barber chair phenomenon) describes an electric shock-like sensation that occurs on flexion of the neck, which radiates down the spine, frequently into the legs, arms, and sometimes to the trunk. Lhermitte's sign is not specific to MS. It is a symptom that can occur with any abnormality of the cervical spinal cord, usually involving active inflammation or impingement on a disc. It potentially shows in vitamin B12 deficiency, cervical spondylosis, and any other conditions (Khare S, Seth D., 2015).
Role of the dentist in trigeminal neuralgia
Since trigeminal neuralgia pain occurs frequently in the V2, V3 distribution, dentists are frequently the first provider to visit for such pain.
Figure 1: Panoramic x-ray of case-1
Figure 2: MRI case-1
Figure 3: Schematic diagram showing the location of the epidermoid cyst (orange color) in case one.
Figure 4: A schematic diagram illustrating the three divisions of the trigeminal nerve.
