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The trigeminal root entry zone (TREZ) is the transitional zone of central and peripheral tissue compartments in the trigeminal root. Microvascular compression on the TREZ is the main etiology of most idiopathic trigeminal neuralgia (TN) patients. However, the pathogenesis of TN is still uncertain. To investigate the glial plasticity changes in oligodendrocytes, Schwann cells, astrocytes and microglia/macrophages in the TREZ in TN, immunohistochemical staining and Western blot methods were performed in rats with TN induced by compression injury. The results showed that mechanical compression injury in the trigeminal nerve of the TN rats induced glial plasticity in the TREZ, which dynamically changed the glial interface of the CNS–PNS transitional zone. Additionally, glial fibrillary acidic protein (GFAP)-immunoreactive astrocyte processes significantly proliferated and extended distally from the central region to the peripheral side of the TREZ after nerve compression injury in the TN group. Moreover, the expression of p75 in Schwann cells was upregulated on the peripheral side of the TREZ, and activated Iba-1-immunoreactive microglia/macrophages were observed on both sides of the TREZ. A significantly higher number of Schwann cells, astrocytes and microglia/macrophages were found in the TN group than in the sham operation group (p < 0.05). In conclusion, mechanical compression injury in the TN rats activated various glial cells, including oligodendrocytes, astrocytes, Schwann cells and microglia/macrophages, in the CNS–PNS transitional zone of TREZ. Changes in glial cell plasticity in the TREZ after compression injury might be involved in TN pathogenesis.

Purpose To evaluate changes in ocular surface and central corneal sub-basal nerve fiber layer (SBNFL) after topical cyclosporin therapy in chronic glaucoma patients on long-term topical antiglaucoma therapy. Methods A prospective comparative study of ocular surface evaluation of chronic glaucoma patients on long-term topical therapy treated concurrently with a topical cyclosporine 0.05% twice daily for 6 months and controls was done. The study parameters evaluated at recruitment and at the 6-month follow-up included details of topical antiglaucoma medications, visual acuity, intraocular pressure, ocular surface evaluation parameters (TBUT, Schirmers I, ocular surface staining scores and ocular surface disease (OSD) index score (OSDI)), central corneal sensation (Cochet Bonnett aesthesiometer), and central confocal microscopy to study the SBNFL density (SBNFLD). Results Thirty-two eyes of 16 patients with chronic glaucoma and 30 eyes of 15 normal subjects as controls were studied. Mean TBUT, pre/post CsA treatment was 8.67±3.01/12.24±1.83 s ( P =0.007). Mean conjunctival/corneal staining scores pre/post CsA treatment were 3.38±1.93/1.50±0.718 ( P =0.00) /5.19±1.82/1.81±0.78 ( P =0.098), respectively. Mean OSDI pre/post CsA treatment scores were 30.63±14.61/14.76±6.06 ( P =0.007). Mean corneal sensations scores pre/post CsA treatment were 4.64±0.46/4.94±0.39 ( P =0.002). Central corneal SBNFLD pre and post CsA treatment was 8811.35±2985.29/10335.13±4092.064  μ m/mm 2 ( P =0.0001). Conclusions Schirmer’s test, ocular surface staining scores, OSDI, corneal sensations, and corneal SBNFLD showed a statistically significant improvement following a 6-month concurrent topical CsA therapy.

Abstract INTRODUCTION: Burst stimulation is a new paradigm that eliminates paresthesias typically observed with traditional tonic stimulation. We used a rodent model of episodic migraine to compare the efficacy of tonic and burst stimulation in treating trigeminal allodynia. METHODS: Twelve Sprague-Dawley rats with spontaneous trigeminal allodynia1 were implanted with miniaturized paddle leads over the occipital nerves, and the leads connected to a pulse generator located dorsally. Rats were randomly assigned to receive 4 frequencies: tonic 60 Hz, tonic 500 Hz, burst 40 Hz, and burst 50 Hz. Tonic 500 Hz and burst 50 Hz were the most effective parameters on short-term trials conducted previously. Tonic 60 Hz and burst 40 Hz are the most common parameters in clinical use. After establishing baseline hypersensitivity, the stimulation was turned ON for 10 days, followed by OFF for 10 days. Daily periorbital sensitivity was assessed using von Frey filaments (VFF). Rats were characterized as hypersensitive or as responders when VFF thresholds were 4 g or 6 g, respectively. Analysis of variance tests were used for analysis. RESULTS: Overall, both tonic and burst ONS significantly improved VFF thresholds compared with baseline (P < .005). Tonic stimulations had a superior response (P = .022) on day 1, but the burst stimulations produced superior efficacy from day 3. On 3, 4, 6, and 9 of ON days, there were statistically superior reduction of allodynia observed for burst stimulations. After the stimulation was turned OFF on day 10, tonic stimulations lost efficacy sooner, whereas burst stimulations had a trend in maintaining superior efficacy for an additional day (day 11, P = .053). CONCLUSION: Tonic stimulation had superior take-off efficacy, but there was a latent positive response associated with burst stimulation that made it superior to tonic stimulation. In addition, burst stimulations exhibited a better therapeutic carryover effect that lasted for a day after stimulation was OFF. Human trials of burst stimulation for headache disorders are warranted to clinically validate our results.

Headache and facial pain – in particular, temporomandibular disorders (TMDs) – are very prevalent conditions in the general population. TMDs are defined as a collection of symptoms and signs involving masticatory muscles, the temporomandibular joints (TMJs), or both. The pain reported by TMD patients is typically located in the muscles of mastication, in the preauricular area, or in the TMJs. In many cases, headaches and facial pain will occur in the same patient. Much of the research relative to the relationship of these disorders focuses on statistics of association and prevalence data. This review will provide a brief description of the types and classifications of orofacial pains (OFPs), as well as point to relevant research describing the commonalities and potential comorbid nature of these maladies. Finally, several recent papers describing morphologic changes to the brain in headache and TMD individuals will be discussed in an effort to stimulate further research into the potential common pathophysiologic mechanism that may explain the comorbid nature of these disorders.

The trigeminal sensory system consists of the trigeminal nerve, the trigeminal ganglion, and the trigeminal sensory nuclei (the mesencephalic nucleus, the principal nucleus, the spinal trigeminal nucleus, and several smaller nuclei). Various sensory signals carried by the trigeminal nerve from the orofacial area travel into the trigeminal sensory system, where they are processed into integrated sensory information that is relayed to higher sensory brain areas. Thus, knowledge of the trigeminal sensory system is essential for comprehending orofacial pain. This review elucidates the individual nuclei that comprise the trigeminal sensory system and their synaptic transmission. Additionally, it discusses four types of orofacial pain and their relationship to the system. Consequently, this review aims to enhance the understanding of the mechanisms underlying orofacial pain.

The initial phase in the development of a migraine is still poorly understood. Here, we describe a previously unknown signaling pathway between stressed neurons and trigeminal afferents during cortical spreading depression (CSD), the putative cause of migraine aura and headache. CSD caused neuronal Pannexin1 (Panx1) megachannel opening and caspase-1 activation followed by high-mobility group box 1 (HMGB1) release from neurons and nuclear factor κB activation in astrocytes. Suppression of this cascade abolished CSD-induced trigeminovascular activation, dural mast cell degranulation, and headache. CSD-induced neuronal megachannel opening may promote sustained activation of trigeminal afferents via parenchymal inflammatory cascades reaching glia limitans. This pathway may function to alarm an organism with headache when neurons are stressed.

This study aims to achieve the complete removal of trigeminal schwannoma (TS) while preserving cranial nerve function. We focused on the outcomes of different surgical approaches and address the contributions of different operative techniques. Forty-two TS cases, treated surgically in Qilu Hospital during a 12-year period, were reviewed and analyzed. There were 18 males and 24 females who were classified into four groups: type A (11 cases, 26%), type B (10 cases, 24%), type C (17 cases, 40%), and type D (4 cases, 10%). Various surgical approaches were applied accordingly. Surgical outcome and cranial nerve function were the criteria used to judge different surgical groups. The conventional approach was performed in 20 cases; the skull base approach was performed in 22 cases. Total and near-total resection was achieved in 80% of conventional cases and in 100% of skull base cases ( χ 2 = 4.86, P < 0.05). Total resection was achieved in 81.5% of non-cavernous involvement cases and in 40% of cavernous involvement cases ( χ 2 = 7.47, P < 0.05). Cranial nerve deficits were improved or unchanged after the operation in most cases; there was no significant difference between the conventional (76.9%) and skull base (87.5%) groups ( χ 2 = 0.56, P > 0.05). The selection of operative approach should be based on the developmental patterns of the tumor. In comparison to the conventional approach, the skull base approach provides better exposure of the tumors and increases the frequency of total and near-total/partial resections. Cavernous sinus involvement was the major impediment to total removal of the trigeminal schwannomas. Treatment always aims for total tumor resection; preservation or improvement of cranial nerve function can be achieved in most cases.

Migraine is the most common neurological disorder, and much has been learned about its mechanisms in recent years. However, the origin of painful impulses in the trigeminal nerve is still uncertain. Despite the attention paid recently to the role of central sensitisation in migraine pathophysiology, in our view, neuronal hyperexcitability depends on activation of peripheral nociceptors. Although the onset of a migraine attack might take place in deep-brain structures, some evidence indicates that the headache phase depends on nociceptive input from perivascular sensory nerve terminals. The input from arteries is probably more important than the input from veins. Several studies provide evidence for input from extracranial, dural, and pial arteries but, likewise, there is also evidence against all three of these locations. On balance, afferents are most probably excited in all three territories or the importance of individual territories varies from patient to patient. We suggest that migraine can be explained to patients as a disorder of the brain, and that the headache originates in the sensory fibres that convey pain signals from intracranial and extracranial blood vessels.

BackgroundPhotophobia is a potentially debilitating symptom often found in dry eye disease (DE), migraine and traumatic brain injury (TBI).MethodsWe conducted a review of the literature via a PubMed search of English language articles with a focus on how photophobia may relate to a shared pathophysiology across DE, migraine and TBI.ResultsDE, migraine and TBI are common conditions in the general population, are often comorbid, and share photophobia as a symptom. Across the three conditions, neural dysregulation of peripheral and central nervous system components is implicated in photophobia in various animal models and in humans. Enhanced activity of the neuropeptide calcitonin gene-related peptide (CGRP) is closely linked to photophobia. Current therapies for photophobia include glasses which shield the eyes from specific wavelengths, botulinum toxin, and inhibition of CGRP and its receptor. Many individuals have persistent photophobia despite the use of these therapies, and thus, development of new therapies is needed.ConclusionsThe presence of photophobia in DE, migraine and TBI suggests shared trigeminothalamic pathophysiologic mechanisms, as explained by central neuroplasticity and hypersensitivity mediated by neuropeptide CGRP. Treatment strategies which target neural pathways (ie, oral neuromodulators, transcutaneous nerve stimulation) should be considered in patients with persistent photophobia, specifically in individuals with DE whose symptoms are not controlled with traditional therapies.

Abstract BACKGROUND Trigeminal nerve atrophy and neurovascular compression (NVC) are frequently observed in classical trigeminal neuralgia (CTN). OBJECTIVE To determine whether nerve characteristics contribute to Gamma Knife (Elekta AB, Stockholm, Sweden) surgery (GKS) outcomes in unilateral CTN without previous surgery. METHODS From 2006 to 2012, 67 patients with unilateral CTN without previous surgery received GKS with a maximal dose of 90 Gy delivered to the trigeminal nerve juxta brainstem. Two evaluators, blinded to the side of pain, analyzed the magnetic resonance images before GKS to obtain the parameters, including nerve cross-sectional area (CSA), vessel type of NVC, and site of NVC along the nerve. Correlations of the parameters with pain relief (Barrow Neurological Institute [BNI] grades I-IIIb) and recurrence (BNI grades VI-V) were made by using Cox regression and Kaplan–Meier analyses. RESULTS The median CSA of the symptomatic nerves was significantly smaller than that of the asymptomatic nerves (4.95 vs 5.9 mm2, P < .001). After adjustment for age and sex, larger nerve CSA was associated with lower initial pain relief (hazard ratio 0.81, P = .03) and lower pain recurrence after initial response (hazard ratio 0.58, P = .02). Patients with nerve atrophy (CSA of ≤ 4.4 mm2 after receiver operating characteristic curve analysis) had a lower 5-yr probability of maintaining pain relief after initial response than those without nerve atrophy (65% vs 86%, P = .04). CONCLUSION Trigeminal nerve atrophy may predict pain recurrence in patients with initial post-GKS relief of CTN. Arterial and proximal NVC are not predictive of GKS outcomes. Future studies are required to determine optimal treatments for long-term pain relief in patients with CTN and trigeminal nerve atrophy.