The patient presentation to their primary care clinician for Trigeminal Neuralgia or persistent idiopathic facial pain (Atypical facial pain) often reflects a sojourn of less than adequate attempts directed at treatment for pain relief. Identification and diagnosis of these syndromes is often preceded by self-initiated modalities that may include over-the-counter medications, phytopharmaceuticals, substances of abuse, alcohol, and use of controlled substances. This is further complicated by interventions involving acupuncture, dental, chiropractic, and complementary techniques. Upon initial presentation to the primary care clinician, the patient often expresses and social discord. To address this dilemma, this article will examine the etiology, diagnosis, evaluation, presentation, the variety of treatments and available pharmacotherapies for Trigeminal Neuralgia or persistent idiopathic facial pain (Atypical facial pain). Each pharmacotherapy is to be initiated in a patient-specific, patient-focused and patient- centered personalized care plan by "going low and slow" with each opportunity to decrease both the discomfort and adverse events. The patient expectations of each intervention should be discussed thoroughly.

Purpose: To report a case of neurotrophic keratopathy (NK) in a patient with complex regional pain syndrome (CRPS) with ipsilateral facial involvement. Methods: Case report. Results: An 18-year old woman with a 5-year history of CRPS type I, a systemic disorder with a neuropathic component with associated limb and right facial involvement, presented with an insidious onset of blurred vision and pain in the right eye. Ocular examination revealed decreased corneal sensation, as measured by Cochet–Bonnet testing, associated with recurrent epithelial defects and whorl-like superficial corneal epitheliopathy. NK was suspected and confirmed by in vivo confocal microscopy (IVCM), which revealed rarefaction of the subbasal nerve plexus in the affected eye. To enhance corneal nerve health, plasma rich in growth factors drops were used. Persistence of NK prompted a superficial keratectomy with placement of an amniotic membrane graft and a course of cenegermin 0.002% (Oxervate; Dompé Farmaceutici SpA, Italy) in the postoperative period. This combination therapy resulted in successful epithelial closure and vision improvement after 8 weeks of therapy with no recurrence of disease for 11 months. Importantly, at that final visit, IVCM demonstrated growth of corneal nerves for the first time in this patient. Conclusions: This is the first case report of NK occurring in the context of CRPS, a neuropathy with ipsilateral facial pain involvement. IVCM was important in the diagnosis of NK, which responded successfully to ocular surface treatments focused on nerve health stimulation that ultimately resulted in corneal nerve growth.

Although certain risk factors can identify individuals who are most likely to develop chronic pain, few interventions to prevent chronic pain have been identified. To facilitate the identification of preventive interventions, an IMMPACT meeting was convened to discuss research design considerations for clinical trials investigating the prevention of chronic pain. We present general design considerations for prevention trials in populations that are at relatively high risk for developing chronic pain. Specific design considerations included subject identification, timing and duration of treatment, outcomes, timing of assessment, and adjusting for risk factors in the analyses. We provide a detailed examination of 4 models of chronic pain prevention (ie, chronic postsurgical pain, postherpetic neuralgia, chronic low back pain, and painful chemotherapy-induced peripheral neuropathy). The issues discussed can, in many instances, be extrapolated to other chronic pain conditions. These examples were selected because they are representative models of primary and secondary prevention, reflect persistent pain resulting from multiple insults (ie, surgery, viral infection, injury, and toxic or noxious element exposure), and are chronically painful conditions that are treated with a range of interventions. Improvements in the design of chronic pain prevention trials could improve assay sensitivity and thus accelerate the identification of efficacious interventions. Such interventions would have the potential to reduce the prevalence of chronic pain in the population. Additionally, standardization of outcomes in prevention clinical trials will facilitate meta-analyses and systematic reviews and improve detection of preventive strategies emerging from clinical trials.

There is no question that the opioid use problem in America has reached unacceptable proportions. What is in question, however, is the best way to address this problem. Unfortunately, this is a multidimensional problem that will not be solved with a simple unidimensional solution. This commentary examines the multidimensional nature of this problem and the resultant guidelines that have been proposed to address it. There is a cautionary tale of the historical dangers of applying an “obvious” solution to a problem, only to find that more investigation and an iterative approach can actually lead to the correct solution. In particular, the authors question the wisdom of implementing guidelines that have no provisions for re-examination, to assess both intended as well as unintended consequences that might occur. This is the standard for good evidence-based guideline development and implementation. To do less, even under such dire circumstances as these, is to provide less than optimum medical care.

Headache attributed to temporomandibular disorders (TMDH) is defined as a secondary headache by the International Classification of Headache Disorders 3rd edition (ICHD‐3).ObjectiveThe objective of this case‐control study is to investigate the phenotypic characteristics of chronic TMD with and without TMDH. We hypothesize that chronic TMD with TMDH is associated with increased number of bodily pain conditions, more painful sites in the head and neck region, and greater TMD pain intensity.MethodsThis is a retrospective cross‐sectional review of the medical records of consecutive patients who sought treatment at the University of North Carolina Orofacial Pain Clinic between 2013 and 2014. The inclusion criterion was a diagnosis of myalgia or arthralgia according to the Research Diagnostic Criteria for Temporomandibular Disorders. In addition, cases had a diagnosis of TMDH according to the ICHD‐3 criteria. Data on the presence and the number of self‐reported bodily pain conditions (such as fibromyalgia and low back pain), pain intensity, number of painful sites in the head and neck upon palpation, and TMD pain onset were analyzed.ResultsA total of 295 records were reviewed. Thirty‐four (29.3%) patients fulfilled inclusion criteria for cases (TMD+TMDH) and 82 (70.7%) for controls (TMD−TMDH). Cases reported greater number of bodily pain conditions than controls, with a mean of 1.97 ± 1.50 and 1.26 ± 1.28 of bodily pain conditions, respectively (P = .012, OR = 1.43 [95% CI 1.07−1.92]). In fact, 55.9% of cases reported at least 2 comorbid pain conditions compared to 37.8% controls (P = .044). Compared to controls (8.65 ± 5.32), cases (13.05 ± 4.46) exhibited greater number of painful sites upon palpation in the head and neck region (P < .0001, OR = 1.18 [95% CI 1.09−1.30]), and greater TMD pain intensity, with a mean of 6.00 ± 2.17 for cases and 5.09 ± 2.14 for controls (P = .041, OR = 1.22 [95% CI 1.01−1.47]).ConclusionIn a population of patients with chronic TMD seeking pain management, TMDH was significantly associated with an increased number of self‐reported bodily pain conditions, a greater number of painful sites in the head and neck regions, and higher TMD pain intensity.

Patients experiencing a terminal drug related event reflect a sentinel event. If this pharmacotherapy is a widely used agent, it may be viewed as a catastrophic problem. If patients are dying from illegal drug use when the medical establishment fails them by withdrawing or minimizing their medically prescribed medication, then the burden rests with their health care providers, legislation, and insurance carriers to actively participate in a collegial fashion to achieve parity. Causing a decay in functionality in previously functional patients, may occur with appropriately prescribed opioid medications addressing non-cancer pain when withdrawing or diminishing either with or without patient consent. The members of the medical profession have diminished their prescribing of opioids for their patients out of apparent fear of reprisal, state or federal government sanctions, and other concerned groups. Diminishing former dosages or deleting the opioid medication, preferably in concert with the patient, often results in inequitable patient care. Enforcing sanctioned decreases or ceasing to prescribe from their former required/established opioid medications precipitate patient discord. In absence of opioid misuse, abuse, diversion or addiction based upon medical “guidelines” and with a poor foundation of Evidence Based Medicine the CDC guidelines, it may be masked as a true guideline reflecting a decrement of clinical judgment, wisdom, and compassion. This article also discusses the role of pharmacy chains, insurance carriers, and their pharmacy benefit managers (PBMs) contribution to this multidimensional problem. There may be a potential solution, identified in this paper, if all the associated political, medical and insurance groups work cohesively to improve patient care. This article and the CDC guidelines are not focused at hospice, palliative, end of life care pain management.

In Primary Headache Disorders, Part 1, we discuss three of the primary headache disorders using the headache definitions from ICHD-III (Beta): Migraine, with and without aura; its pathophysiology and treatment are discussed. We then discuss the Trigeminal Autonomic Cephalalgias (TACs), including Cluster Headache and Hemicrania Continua, two more primary headache disorders, as well as the other TAC Headaches. We discuss pathophysiology as well as diagnosis, treatment, and pharmacotherapeutic management of these headache diatheses.

In Part 2 of Primary Headache disorders, we discuss the fourth Primary Headache Disorder, Tension Type Headache (TTHA). We are again using the ICHD-III (Beta) definitions of such headaches, taking into consideration episodic and chronic TTHA, as well as the presence or absence of pericranial muscle tenderness. We discuss the pathophysiology and pharmacotherapeutic treatment of TTHA, and the aspects of the Myofascial Pain Syndrome that enhance and help the development of TTHA. We then discuss Medication Overuse Headache (MOH), itself a Secondary headache disorder, but one that is extremely important as it assists with the chronification of both migraine and TTHA. Finally we discuss how to manage and treat those patients with MOH. Chronic migraine, which is TTHA, Migraine as well as, in many patients, MOH, is discussed along with the treatment of this multifaceted disorder.