Hsinlin Thomas Cheng

Cerebrospinal fluid (CSF) leakage can be difficult to localize and may result in unexplained intracranial hypotension with intractable positional headache. Loss of CSF cushioning can cause brain sagging, leading to compression and traction of cranial nerves within the brain cisterns and mimicking Chiari malformation. This case report describes a patient presenting with trigeminal facial pain and positional headache who was ultimately diagnosed with a thoracic spinal CSF–venous fistula. Both headache and facial pain resolved following surgical intervention. This report highlights the importance of advanced diagnostic imaging and multidisciplinary management.

Introduction: Painful trigeminal neuropathy (PTN) is a debilitating condition with persistent facial pain after a trigeminal nerve injury. It could be refractory to medication treatments and causes significant physical discomfort and psychological stress that significantly affects quality of life. This study aims to demonstrate the efficacy of trigeminal nerve blocks (TNB) for patients with PTN and to identify the parameters that affect treatment outcomes. Methods: In this retrospective chart review, we examined the medical records of 90 PTN patients who received trigeminal nerve blocks at Mass General Hospital (MGH) between March 2023 and March 2025. The trigeminal nerve blocks were performed using a variety of combinations of local anesthetics, from 2% lidocaine, 2% lidocaine plus 0.5% ropivacaine, to 4% lidocaine with 0.75% Bupivacaine. Triamcinolone was co-administered if no contraindication, including uncontrolled diabetes, hypertension, active infections, or psychological illness, existed. Results: The mean age was 50.6 years, and 71.1% of the participants were female. Seventy-three patients (81.1%) achieved ≥ 50% pain reduction. The duration of relief was: ≥ 6 weeks in 45 patients (50.0%), ≥ 8 weeks in 33 patients (36.7%), and ≥ 12 weeks in 21 patients (23.3%). Among the 33 patients with ≥ 8 weeks of relief, the effective regimens were: 2% lidocaine + triamcinolone (n=4, 12.1%), 2% lidocaine + 0.5% ropivacaine + triamcinolone (n=10, 30.3%), and 4% lidocaine + 0.75% bupivacaine + triamcinolone (n=13, 39.4%). The poor prognostic factors for treatment effects lasting shorter than 8 weeks include depression, involvement of the maxillary nerve (V2), and symptoms of facial numbness. Conclusion: The current study suggests that TNB with local anesthetics and steroids may be associated with better outcomes in patients with painful trigeminal neuropathy, based on this retrospective analysis.

Painful trigeminal neuropathy (PTN) is a very disabling but often unrecognized facial pain from various etiologies. Patients with PTN suffer from persistent, intense facial pain with significantly impaired sensory function in the trigeminal territories. This article reviews the anatomy and pathophysiology of PTN, as well as its clinical presentation and management. The peripheral inflammatory cascades, including immune cell activation, inflammatory mediator-induced nociceptor activation, and sensory hyperexcitability in the trigeminal nerve, are discussed, as are the central sensitization processes, including postsynaptic NMDA receptor activation, glial cell-mediated inflammation, and reduced inhibitory pathways in the central nervous system. A comprehensive literature review that covers multiple specialties and discusses various treatment options based on the available evidence is presented. Collectively, a practical algorithm is proposed to improve current PTN management. It provides novel guidance for managing PTN in an evidence-based, integrative, and mechanism-specific approach. In conclusion, a multidisciplinary team approach targeting both peripheral and central sensitization would be an ideal strategy for delivering optimal, mechanism-specific management in painful trigeminal neuropathy.

Purpose: Chronic orofacial pain (COP) is associated with substantial pain interference and emotional distress. Psychosocial treatments for COP are scarce, rely on talking, which is often painful for this population, and require intensive resources. There is a clear need for a novel, scalable, accessible, “talk free” intervention to reduce pain interference and emotional distress among individuals with COP. This study explored people with COP’s perceptions of a novel mind-body web-based intervention targeting pain interference and emotional distress (Face-Forward-Web) to inform its development and optimization. Patients and Methods: We conducted semi-structured focus groups (N=4 groups, 22 participants; 77% female; mean age 47 (SD = 15.9)) and used Rapid Data Analysis (RDA) to gauge perceptions of the intervention’s content structure, format, and barriers and facilitators to participation. Results: Perception of the intervention was largely positive, and participants perceived its value for increasing engagement in life activities. They emphasized the importance of tailoring the intervention to the unique characteristics of COP. They expressed that the self-paced web-based format was ideal given unpredictable pain flares and variable needs. Concurrently, they desired social connection. They perceived the content and skills as helpful and relaxing. They identified barriers and facilitators to participation, including technical considerations, reminders and incentives, and providers setting up realistic expectations for outcomes. Conclusion: This study elucidates insights that can inform psychosocial and mind-body interventions for people with COP. Findings give voice to the needs and perceptions of people with COP, guiding the development of tailored, patient-informed treatment approaches such as Face-Forward-Web.

Background: Chronic orofacial pain (COP) is common, costly, and associated with substantial pain interference and emotional distress. Psychosocial treatments for COP are scarce and limited (eg, rely on talking, which is often painful for this population; require intensive resources, limiting scalability). Here, we describe the study protocol for developing Face-Forward-Web, a “talk-free” web-based mind-body intervention for patients with COP. Objective: We aim to (1) develop Face-Forward-Web with the aid of live-video focus groups with adults with COP and (2) optimize Face-Forward-Web and our study protocol through beta testing followed by an open feasibility trial. Methods: We will accomplish these aims in 2 phases, incorporating user-centered design principles. For phase 1, we conducted semistructured focus groups (n=4 groups, 22 participants) with individuals with COP. We are using rapid data analysis followed by thematic analysis to gauge treatment needs, preferences, and perceptions of the proposed platform and skills. This information will inform session structure and content as well as development of a wireframe followed by a prototype. For phase 2, we will conduct beta testing (up to n=10) followed by a feasibility trial (up to n=20) with exit interviews to gather feedback. The primary outcomes are feasibility benchmarks such as recruitment (≥70% of the eligible participants will participate), acceptability (≥70% of the participants complete ≥4 or 5 sessions), credibility, expectancy (≥70% above the Credibility and Expectancy scale’s midpoint), and satisfaction (≥70% above the User Experience Questionnaire’s midpoint). Results: Recruitment for phase 1 began in October 2024 and concluded in January 2025. Data analysis for phase 1 will conclude in fall 2025 and for phase 2 in 2026. Results will iteratively guide the development of the intervention. Conclusions: Face-Forward-Web will be the first talk-free web-based intervention tailored to the needs of adults with COP. Results will inform a future efficacy trial. Trial Registration: ClinicalTrials.gov NCT06754917; https://clinicaltrials.gov/study/NCT06754917 International Registered Report Identifier (IRRID): DERR1-10.2196/71839

BACKGROUND Chronic orofacial pain (COP) is common, costly, and associated with substantial pain interference and emotional distress. Psychosocial treatments for COP are scarce and limited (eg, rely on talking, which is often painful for this population; require intensive resources, limiting scalability). Here, we describe the study protocol for developing Face-Forward-Web, a “talk-free” web-based mind-body intervention for patients with COP. OBJECTIVE We aim to (1) develop Face-Forward-Web with the aid of live-video focus groups with adults with COP and (2) optimize Face-Forward-Web and our study protocol through beta testing followed by an open feasibility trial. METHODS We will accomplish these aims in 2 phases, incorporating user-centered design principles. For phase 1, we conducted semistructured focus groups (n=4 groups, 22 participants) with individuals with COP. We are using rapid data analysis followed by thematic analysis to gauge treatment needs, preferences, and perceptions of the proposed platform and skills. This information will inform session structure and content as well as development of a wireframe followed by a prototype. For phase 2, we will conduct beta testing (up to n=10) followed by a feasibility trial (up to n=20) with exit interviews to gather feedback. The primary outcomes are feasibility benchmarks such as recruitment (≥70% of the eligible participants will participate), acceptability (≥70% of the participants complete ≥4 or 5 sessions), credibility, expectancy (≥70% above the Credibility and Expectancy scale’s midpoint), and satisfaction (≥70% above the User Experience Questionnaire’s midpoint). RESULTS Recruitment for phase 1 began in October 2024 and concluded in January 2025. Data analysis for phase 1 will conclude in fall 2025 and for phase 2 in 2026. Results will iteratively guide the development of the intervention. CONCLUSIONS Face-Forward-Web will be the first talk-free web-based intervention tailored to the needs of adults with COP. Results will inform a future efficacy trial. CLINICALTRIAL ClinicalTrials.gov NCT06754917; https://clinicaltrials.gov/study/NCT06754917 INTERNATIONAL REGISTERED REPORT DERR1-10.2196/71839

Purpose: Orofacial Pain (OFP) affects 15% of the general population. OFP conditions can be myofascial, also known as temporomandibular disorders (TMDs) or neuropathic. The underlying pathophysiology in several chronic OFP conditions, is unknown. Small fiber neuropathy (SFN) is a disorder of thinly myelinated A-delta and non-myelinated C-fibers and can manifest as sensory and autonomic neuropathies. SFN has been demonstrated in some OFP conditions. Our study aims to assess the presence of OFP in patients with sensory and autonomic neuropathies and assess the correlation between OFP, skin biopsy and autonomic dysfunction. Patients and Methods: This is a retrospective study (2018– 2020) of patients from the SFN registry, Massachusetts General Hospital, Boston, USA, for the presence of OFP. All patients were included. Primary outcome: Prevalence of OFP in patients with chronic neuropathies. Secondary outcomes: Correlation between OFP and skin biopsy, dysautonomia, headaches, chronic nociceptive pain, psychological conditions, and patient factors, such as mean age and BMI. Results: Charts of 450 patients with sensory and autonomic neuropathies were reviewed. 22.67% (n=102) had OFP. The mean (range) age at biopsy in patients with OFP was 48.36 (20– 81) years, female: male ratio 3.25:1. More OFP patients had negative skin biopsy results (p value< 0.05) than those with sensory neuropathies. Patients with OFP had significantly higher prevalence of psychological conditions (p value 0.000), and higher BMI > 30 (p value 0.025). Dysautonomia was significantly higher in patients with TMDs when compared to the ones without TMDs (p value 0.030). There was no significant difference in mean age, gender predilection, presence of headaches, peripheral neuropathies, and nociceptive pain between patients with and without OFP. Conclusion: OFP and sensory neuropathies can be overlapping conditions. Patients presenting with concomitant TMD and dysautonomia can be further tested for SFN. This can further help us understand a correlation if any, between idiopathic TMD/OFP conditions and SFN and further our understanding of the pathophysiology of these conditions.

BackgroundCoronavirus disease 2019 (COVID-19) causes mild symptoms to severe illness in the nervous system. Among the wide-ranged symptomology, headache is a common neurological symptom reported by COVID-19 patients. However, the prevalence, comorbidities, and ethnic susceptibilities of COVID-19-induced headaches are not well-defined. MethodsWe performed a retrospective chart review of patients who tested positive for SARS-CoV2 by reverse transcriptase -polymerase chain reaction (RT-PCR) in March and April 2020 at Massachusetts General Hospital, Boston, Massachusetts, USA. An electronic medical record review was performed to collect demographic data, major COVID-19 symptomology, and results of radiologic and laboratory tests. Data were recorded starting on the disease onset, as identified by the patient’s clinical notes. The demographical trends and prevalence of headache and comorbid symptoms were statistically analyzed. Results We identified 450 patients, 202 (44.9%) male and 248 (55.1%) female, who tested positive for COVID-19 in the study. Common symptoms included cough (66.4%), fever,(58.9%), fatigue (30.9%), and sore throat (29.6%). Forty-six percent of patients had shortness of breath, 32% had evidence of pneumonia, and 26% needed hospitalization. Gender predominance is significant in developing a sore throat, nasal congestion, hypogeusia, headache, ear pain in females, and pneumonia and inpatient hospitalization in males. Younger patients (< 50) were more likely to develop sore throat, fatigue, anosmia, hypogeusia, ear pain, myalgia /arthralgia, and headache. In contrast, older (> 50) patients were prone to develop pneumonia and required hospitalization. Compared to non-Hispanic ethnic populations, a significantly higher number of Hispanic patients reported headaches, nausea/vomiting, nasal congestion, fever, fatigue, anosmia, and myalgia/arthralgia compared to non-Hispanics, suggesting an ethnic susceptibility in COVID-19 symptomatology. Overall, patients who developed headaches were younger and more likely to have mild viral symptoms, pain, and neurological symptoms but not severe respiratory symptoms (shortness of breath and pneumonia) and hospitalization. ConclusionsOur results demonstrated gender, age, and ethnic factors in COVID symptomatology and identified that mild viral, painful, and neurological symptoms are positive predictors for headache development in COVID-19.

Purpose: Neurogenic inflammation is a major component of chronic neuropathic pain. Previously, we established the db/db mouse as an animal model of painful diabetic neuropathy (PDN) of type 2 diabetes. In the current study, we investigate the roles of interleukin (IL)-10, an anti-inflammatory cytokine, in the development of neurogenic inflammation and pain behavior in db/db mouse. Materials and Methods: We first studied IL-10 expression in lumbar dorsal root ganglion (LDRG) neurons of db/db mice using immunohistochemistry, immunoblots, and reverse transcription polymerase chain reaction during the period of pain behavior (from 8 to 16 wk of age). To determine if the reduced IL-10 expression mediates the mechanical allodynia in db/db mice, we administered recombinant mouse IL-10 or saline (control) intraperitoneally to control db/+ and db/db mice starting at 8 wk of age. IL-10 treatment was repeated every other day for 2 wk until the mice reached 10 wk of age. Results: During the period of pain behavior, reduction of IL-10 protein and gene expression was detected in LDRG of db/db mice. Treatment with recombinant IL-10, from 8 to 10 wk of age, alleviates pain behaviors in db/db mice without affecting other diabetic parameters. In parallel, IL-10 treatment reduced the upregulation of nerve growth factor (NGF), inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF)-α, and high-affinity NGF receptor (Trk A) in LDRG, as well as the numbers of iNOS-positive Langerhans cells and CD-68-positive dermal dendritic cells in the hind-foot-pad skin in db/db mice. Conclusion: Our findings suggest that the reduction in neuronal IL-10 increases inflammatory phenomena, ultimately contributing to PDN. These results suggest that the dysregulation of cytokine-mediated inflammation contributes to the development of PDN in db/db mice. Targeting this pathophysiologic mechanism could be an effective approach for treating PDN in type 2 diabetes.