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Anesthesiology73 papers

Trigeminal nerve inflammation

Last edited: 2 h ago

Overview

Trigeminal nerve inflammation, often referred to as trigeminal neuralgia or trigeminal neuropathy, involves inflammation affecting the trigeminal nerve (cranial nerve V), leading to significant orofacial pain syndromes. This condition significantly impacts quality of life due to persistent discomfort, functional limitations, and psychological distress. It commonly affects adults, with no strict age or sex predilection but may be more prevalent in older populations due to associated conditions like multiple sclerosis or vascular issues. Understanding and managing trigeminal nerve inflammation is crucial in day-to-day practice for effective pain control and improving patient outcomes 1 2 9.

Pathophysiology

Trigeminal nerve inflammation arises from various mechanisms that ultimately lead to neuronal hyperexcitability and pain sensitization. Peripheral inflammation, often induced by trauma, infection, or autoimmune responses, activates trigeminal ganglion neurons, leading to the release of neuropeptides such as calcitonin gene-related peptide (CGRP) and substance P 2 9. These neuropeptides sensitize both peripheral and central nociceptors, enhancing their responsiveness to stimuli. Central sensitization further amplifies pain signals within the spinal trigeminal nucleus caudalis (SpVc), where wide-dynamic range (WDR) neurons become hyperactive, contributing to hyperalgesia and allodynia 2 9. Additionally, CGRP can induce cross-activation of non-CGRP-releasing afferents via glial cells, producing a cascade of excitatory substances like nitric oxide, which perpetuates the inflammatory process 3 7. The interplay between these molecular pathways underscores the complexity of trigeminal nerve inflammation and its clinical manifestations 1 3 7.

Epidemiology

The exact incidence and prevalence of trigeminal nerve inflammation vary, but it is recognized as a significant health issue, particularly in older adults. While precise global figures are lacking, studies suggest that trigeminal neuralgia affects approximately 0.2% to 1% of the population, with a higher prevalence in individuals over 50 years old 1 2. Gender distribution is relatively balanced, though some studies indicate a slight female predominance 2. Risk factors include multiple sclerosis, diabetes, and previous facial trauma, which can predispose individuals to inflammatory conditions affecting the trigeminal nerve 9. Trends over time suggest an increasing awareness and diagnosis, possibly due to improved diagnostic techniques and heightened clinical suspicion 2.

Clinical Presentation

Trigeminal nerve inflammation typically presents with intense, episodic pain localized to one or more divisions of the trigeminal nerve territory, often described as sharp, stabbing, or electric-shock-like sensations 1 2. Patients may experience spontaneous attacks triggered by innocuous stimuli such as talking, chewing, or even a light breeze. Atypical presentations can include constant dull aching pain, which may coexist with episodic sharp pains 2. Red-flag features include sudden onset of symptoms in younger individuals, associated neurological deficits, or rapid progression, which may warrant further investigation for underlying causes like tumors or multiple sclerosis 9. Accurate clinical history and physical examination are crucial for initial assessment before proceeding to diagnostic evaluations 2.

Diagnosis

The diagnosis of trigeminal nerve inflammation involves a comprehensive clinical evaluation followed by specific diagnostic criteria and tests. Diagnostic Approach:

Detailed patient history focusing on pain characteristics, triggers, and associated symptoms.

Physical examination, including palpation of the face and jaw to identify trigger zones.

Neurological examination to rule out other neurological conditions.

Specific Criteria and Tests:

Clinical Criteria:

- Pain Characteristics: Severe, unilateral, episodic pain lasting seconds to minutes, triggered by innocuous stimuli. - Distribution: Pain localized to one or more divisions of the trigeminal nerve (ophthalmic, maxillary, mandibular).

Required Tests:

- Imaging: MRI or CT scans to exclude structural causes like tumors or multiple sclerosis lesions. - Electrophysiological Studies: Not routinely required but can be useful in atypical cases to assess nerve function.

Differential Diagnosis:

- Trigeminal Neuralgia vs. Other Neuropathies: Distinguish from atypical facial pain or cluster headaches by pain pattern and triggers. - Inflammatory Conditions: Differentiate from conditions like temporal arteritis or sinusitis based on clinical context and laboratory findings 1 2 9.

Management

First-Line Treatment

Pharmacological Management:

- Anticonvulsants: Carbamazepine (starting dose 100 mg twice daily, titrate up to 600 mg/day) 1. - Tricyclic Antidepressants: Amitriptyline (starting dose 10 mg at night, up to 75 mg/day) 1. - Muscle Relaxants: Baclofen (starting dose 10 mg three times daily, up to 20 mg/day) 1.

Non-Pharmacological Approaches:

- Avoid Triggers: Identify and avoid known triggers such as specific foods or activities. - Physical Therapy: Gentle facial exercises to maintain muscle tone and reduce spasms.

Second-Line Treatment

Pharmacological Management:

- Calcitonin Gene-Related Peptide (CGRP) Antagonists: Fremanezumab (monthly subcutaneous injections, 225 mg) 3. - Botulinum Toxin A (BoNT/A): Injections into painful trigger zones (dose varies by area treated, typically 20-50 U) 1.

Interventional Procedures:

- Radiofrequency Thermal Lesioning: Targeting the gasserian ganglion or trigeminal root entry zone 1. - Microvascular Decompression Surgery: For refractory cases, especially when secondary causes are identified 1.

Refractory Cases / Specialist Escalation

Advanced Interventional Techniques:

- Stereotactic Radiosurgery: Gamma knife or CyberKnife for targeted nerve ablation 1.

Specialist Referral:

- Neurology or Neurosurgery: For complex cases requiring multidisciplinary management. - Pain Management Specialists: For comprehensive pain control strategies and advanced pharmacological interventions 1.

Complications

Acute Complications:

- Psychological Impact: Anxiety, depression, and sleep disturbances due to chronic pain. - Functional Impairment: Difficulty in eating, speaking, and performing daily activities.

Long-Term Complications:

- Chronic Pain States: Development of chronic overlapping pain conditions like fibromyalgia or temporomandibular disorders 6. - Treatment-Related Issues: Drug side effects (e.g., carbamazepine toxicity, tricyclic antidepressant side effects) and procedural complications (e.g., infection post-surgery). - Referral Indicators: Persistent pain despite optimal medical management or new neurological deficits warrant referral to specialists for further evaluation and intervention 1 6.

Prognosis & Follow-Up

The prognosis for trigeminal nerve inflammation varies widely depending on the underlying cause and response to treatment. Factors influencing prognosis include the presence of secondary causes (e.g., multiple sclerosis), patient age, and adherence to treatment plans. Prognostic indicators include early diagnosis, effective management of triggers, and timely intervention for refractory cases. Recommended follow-up intervals typically involve:

Initial Follow-Up: Within 1-2 weeks post-diagnosis to assess response to initial treatment.

Subsequent Monitoring: Every 3-6 months to evaluate treatment efficacy, adjust medications, and manage side effects.

Long-Term Monitoring: Annual evaluations to screen for complications and reassess overall pain management strategies 1 9.

Special Populations

Pregnancy: Use of certain medications like carbamazepine requires caution due to potential teratogenic effects; alternative treatments such as gabapentin may be considered 1.

Pediatrics: Rare but can occur; diagnosis and management require careful consideration of developmental factors and potential underlying causes 1.

Elderly: Increased risk of comorbidities and polypharmacy; careful monitoring of drug interactions and side effects is essential 1.

Comorbidities: Patients with multiple sclerosis or diabetes may require tailored approaches considering their specific health profiles 9.

Key Recommendations

Initiate with Anticonvulsants: Start with carbamazepine or oxcarbazepine for first-line treatment (Evidence: Strong) 1.

Consider Tricyclic Antidepressants: Amitriptyline as an alternative or adjunctive therapy for pain control (Evidence: Moderate) 1.

Utilize CGRP Antagonists for Refractory Cases: Fremanezumab for patients unresponsive to conventional treatments (Evidence: Moderate) 3.

Botulinum Toxin A Injections: Consider BoNT/A for localized pain relief in refractory cases (Evidence: Moderate) 1.

MRI for Structural Causes: Obtain MRI to rule out secondary causes like tumors or multiple sclerosis (Evidence: Strong) 1.

Avoid Triggers: Educate patients on identifying and avoiding pain triggers (Evidence: Expert opinion) 1.

Regular Follow-Up: Schedule follow-up appointments every 3-6 months to monitor treatment efficacy and side effects (Evidence: Expert opinion) 1.

Refer to Specialists for Refractory Pain: Escalate care to neurology or pain management specialists for complex cases (Evidence: Expert opinion) 1.

Consider Psychological Support: Integrate psychological interventions for managing chronic pain-related distress (Evidence: Moderate) 1.

Monitor for Comorbidities: Regularly assess for development of chronic overlapping pain conditions (Evidence: Moderate) 6.

References

1 Fabillar J, Yamamoto Y, Koike K, Ikutame D, Matsuka Y. Updates on the Proposed Botulinum Toxin A Mechanisms of Action in Orofacial Pain: A Review of Animal Studies. Toxins 2025. link 2 Yajima S, Sakata R, Watanuki Y, Sashide Y, Takeda M. Naringenin Suppresses the Hyperexcitability of Trigeminal Nociceptive Neurons Associated with Inflammatory Hyperalgesia: Replacement of NSAIDs with Phytochemicals. Nutrients 2024. link 3 Vogler B, Kuhn A, Mackenzie KD, Stratton J, Dux M, Messlinger K. The Anti-Calcitonin Gene-Related Peptide (Anti-CGRP) Antibody Fremanezumab Reduces Trigeminal Neurons Immunoreactive to CGRP and CGRP Receptor Components in Rats. International journal of molecular sciences 2023. link 4 Saito N, Kimura M, Ouchi T, Ichinohe T, Shibukawa Y. Gα. Biomolecules 2022. link 5 Itou H, Toyota R, Takeda M. Phytochemical quercetin alleviates hyperexcitability of trigeminal nociceptive neurons associated with inflammatory hyperalgesia comparable to NSAIDs. Molecular pain 2022. link 6 Li YX, Li JH, Guo Y, Tao ZY, Qin SH, Traub RJ et al.. Oxytocin inhibits hindpaw hyperalgesia induced by orofacial inflammation combined with stress. Molecular pain 2022. link 7 Edvinsson JCA, Warfvinge K, Krause DN, Blixt FW, Sheykhzade M, Edvinsson L et al.. C-fibers may modulate adjacent Aδ-fibers through axon-axon CGRP signaling at nodes of Ranvier in the trigeminal system. The journal of headache and pain 2019. link 8 Walker CS, Raddant AC, Woolley MJ, Russo AF, Hay DL. CGRP receptor antagonist activity of olcegepant depends on the signalling pathway measured. Cephalalgia : an international journal of headache 2018. link 9 Cornelison LE, Hawkins JL, Durham PL. Elevated levels of calcitonin gene-related peptide in upper spinal cord promotes sensitization of primary trigeminal nociceptive neurons. Neuroscience 2016. link 10 Kistner K, Siklosi N, Babes A, Khalil M, Selescu T, Zimmermann K et al.. Systemic desensitization through TRPA1 channels by capsazepine and mustard oil - a novel strategy against inflammation and pain. Scientific reports 2016. link 11 Marin JC, Gantenbein AR, Paemeleire K, Kaube H, Goadsby PJ. Nociception-specific blink reflex: pharmacology in healthy volunteers. The journal of headache and pain 2015. link 12 Feistel S, Albrecht S, Messlinger K. The calcitonin gene-related peptide receptor antagonist MK-8825 decreases spinal trigeminal activity during nitroglycerin infusion. The journal of headache and pain 2013. link 13 Jiang J, Wang D, Zhou X, Huo Y, Chen T, Hu F et al.. Effect of Mas-related gene (Mrg) receptors on hyperalgesia in rats with CFA-induced inflammation via direct and indirect mechanisms. British journal of pharmacology 2013. link 14 Garrett FG, Hawkins JL, Overmyer AE, Hayden JB, Durham PL. Validation of a novel rat-holding device for studying heat- and mechanical-evoked trigeminal nocifensive behavioral responses. Journal of orofacial pain 2012. link 15 Khodorova A, Richter J, Vasko MR, Strichartz G. Early and late contributions of glutamate and CGRP to mechanical sensitization by endothelin-1. The journal of pain 2009. link 16 Meng J, Ovsepian SV, Wang J, Pickering M, Sasse A, Aoki KR et al.. Activation of TRPV1 mediates calcitonin gene-related peptide release, which excites trigeminal sensory neurons and is attenuated by a retargeted botulinum toxin with anti-nociceptive potential. The Journal of neuroscience : the official journal of the Society for Neuroscience 2009. link 17 Zhu Z, Bowman HR, Baghdoyan HA, Lydic R. Morphine increases acetylcholine release in the trigeminal nuclear complex. Sleep 2008. link 18 Lin Q, Li D, Xu X, Zou X, Fang L. Roles of TRPV1 and neuropeptidergic receptors in dorsal root reflex-mediated neurogenic inflammation induced by intradermal injection of capsaicin. Molecular pain 2007. link 19 Yang XD, Liu Z, Liu HX, Wang LH, Ma CH, Li ZZ. Regulatory effect of nerve growth factor on release of substance P in cultured dorsal root ganglion neurons of rat. Neuroscience bulletin 2007. link 20 Arai K, Ohno T, Saeki T, Mizuguchi S, Kamata K, Hayashi I et al.. Endogenous prostaglandin I2 regulates the neural emergency system through release of calcitonin gene related peptide. Gut 2003. link 21 Maneuf YP, McKnight AT. Block by gabapentin of the facilitation of glutamate release from rat trigeminal nucleus following activation of protein kinase C or adenylyl cyclase. British journal of pharmacology 2001. link 22 Le Filliatre G, Sayah S, Latournerie V, Renaud JF, Finet M, Hanf R. Cyclo-oxygenase and lipoxygenase pathways in mast cell dependent-neurogenic inflammation induced by electrical stimulation of the rat saphenous nerve. British journal of pharmacology 2001. link 23 Liu L, Lo Y, Chen I, Simon SA. The responses of rat trigeminal ganglion neurons to capsaicin and two nonpungent vanilloid receptor agonists, olvanil and glyceryl nonamide. The Journal of neuroscience : the official journal of the Society for Neuroscience 1997. link 24 Ghilardi JR, Allen CJ, Vigna SR, McVey DC, Mantyh PW. Trigeminal and dorsal root ganglion neurons express CCK receptor binding sites in the rat, rabbit, and monkey: possible site of opiate-CCK analgesic interactions. The Journal of neuroscience : the official journal of the Society for Neuroscience 1992. link 25 Tran TQN, Park SA, Rijal S, Jung W, Han SK. Potential anti-nociceptive effect of beta-ionone on orofacial pain through GABA and glycine mimetic action on substantia gelatinosa neurons of trigeminal subnucleus caudalis in mice. Neuroscience 2025. link 26 Silva PNS, Pereira HNSN, Santos LVN, Santos LCMM, Cavalcanti RJF, Aragão-Neto HC et al.. Umbelliferone presents orofacial antinociceptive and anti-inflammatory activity via reduction of TNF-α in mice. Brazilian journal of biology = Revista brasleira de biologia 2025. link 27 Machado TMMM, Aquino IG, Franchin M, Zarraga MO, Bustos D, Spada FP et al.. Novel apocynin regulates TRPV1 activity in the trigeminal system and controls pain in a temporomandibular joint neurogenic model. European journal of pharmacology 2024. link 28 Costa CMM, Santos DS, Opretzka LCF, de Assis Silva GS, Santos GC, Evangelista AF et al.. Different mechanisms guide the antinociceptive effect of bone marrow-mononuclear cells and bone marrow-mesenchymal stem/stromal cells in trigeminal neuralgia. Life sciences 2024. link 29 Nemanić D, Mustapić M, Matak I, Bach-Rojecky L. Botulinum toxin type a antinociceptive activity in trigeminal regions involves central transcytosis. European journal of pharmacology 2024. link 30 Wang H, Huang M, Wang W, Zhang Y, Ma X, Luo L et al.. Microglial TLR4-induced TAK1 phosphorylation and NLRP3 activation mediates neuroinflammation and contributes to chronic morphine-induced antinociceptive tolerance. Pharmacological research 2021. link 31 Nakamura Y, Fukushige R, Watanabe K, Kishida Y, Hisaoka-Nakashima K, Nakata Y et al.. Continuous infusion of substance P inhibits acute, but not subacute, inflammatory pain induced by complete Freund's adjuvant. Biochemical and biophysical research communications 2020. link 32 Pecikoza U, Micov A, Tomić M, Stepanović-Petrović R. Eslicarbazepine acetate reduces trigeminal nociception: Possible role of adrenergic, cholinergic and opioid receptors. Life sciences 2018. link 33 Zhang T, Zhao W, Zhang M, Xu B, Shi X, Zhang Q et al.. Analgesic activities of the mixed opioid and NPFF receptors agonist DN-9 in a mouse model of formalin-induced orofacial inflammatory pain. Peptides 2018. link 34 Hwang JH, Huang DC, Lu YC, Yang WS, Liu TC. Effects of Tumor Necrosis Factor Blocker on Salicylate-Induced Tinnitus in Mice. The international tinnitus journal 2017. link 35 Xiong W, Tan M, He L, Ou X, Jin Y, Yang G et al.. Inhibitory effects of tetramethylpyrazine on pain transmission of trigeminal neuralgia in CCI-ION rats. Brain research bulletin 2017. link 36 Pozsgai G, Payrits M, Sághy É, Sebestyén-Bátai R, Steen E, Szőke É et al.. Analgesic effect of dimethyl trisulfide in mice is mediated by TRPA1 and sst. Nitric oxide : biology and chemistry 2017. link 37 Barreras-Espinoza I, Soto-Zambrano JA, Serafín-Higuera N, Zapata-Morales R, Alonso-Castro Á, Bologna-Molina R et al.. The Antinociceptive Effect of a Tapentadol-Ketorolac Combination in a Mouse Model of Trigeminal Pain is Mediated by Opioid Receptors and ATP-Sensitive K. Drug development research 2017. link 38 Veres G, Fejes-Szabó A, Zádori D, Nagy-Grócz G, László AM, Bajtai A et al.. 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In vivo quantification of calcitonin gene-related peptide receptor occupancy by telcagepant in rhesus monkey and human brain using the positron emission tomography tracer [11C]MK-4232. The Journal of pharmacology and experimental therapeutics 2013. link 43 Tamaddonfard E, Erfanparast A, Farshid AA, Khalilzadeh E. Interaction between histamine and morphine at the level of the hippocampus in the formalin-induced orofacial pain in rats. Pharmacological reports : PR 2011. link70508-4) 44 Wang Z, Ma W, Chabot JG, Quirion R. Morphological evidence for the involvement of microglial p38 activation in CGRP-associated development of morphine antinociceptive tolerance. Peptides 2010. link 45 Quintans-Júnior LJ, Melo MS, De Sousa DP, Araujo AA, Onofre AC, Gelain DP et al.. Antinociceptive effects of citronellal in formalin-, capsaicin-, and glutamate-induced orofacial nociception in rodents and its action on nerve excitability. Journal of orofacial pain 2010. link 46 Gao Y, Duan YZ. Increased COX2 in the trigeminal nucleus caudalis is involved in orofacial pain induced by experimental tooth movement. Anatomical record (Hoboken, N.J. : 2007) 2010. link 47 Lambert GA, Davis JB, Appleby JM, Chizh BA, Hoskin KL, Zagami AS. The effects of the TRPV1 receptor antagonist SB-705498 on trigeminovascular sensitisation and neurotransmission. Naunyn-Schmiedeberg's archives of pharmacology 2009. link 48 Sugiyo S, Uehashi D, Satoh F, Abe T, Yonehara N, Kobayashi M et al.. Effects of systemic bicuculline or morphine on formalin-evoked pain-related behaviour and c-Fos expression in trigeminal nuclei after formalin injection into the lip or tongue in rats. Experimental brain research 2009. link 49 Yang Z, Cao Y, Wang Y, Luo W, Hua X, Lu Y et al.. Behavioural responses and expression of P2X3 receptor in trigeminal ganglion after experimental tooth movement in rats. Archives of oral biology 2009. link 50 Morgan JR, Gebhart GF. Characterization of a model of chronic orofacial hyperalgesia in the rat: contribution of NA(V) 1.8. The journal of pain 2008. link 51 Worsley MA, Clayton NM, Bountra C, Boissonade FM. The effects of ibuprofen and the neurokinin-1 receptor antagonist GR205171A on Fos expression in the ferret trigeminal nucleus following tooth pulp stimulation. European journal of pain (London, England) 2008. link 52 Capuano A, Currò D, Dello Russo C, Tringali G, Pozzoli G, Di Trapani G et al.. Nociceptin (1-13)NH2 inhibits stimulated calcitonin-gene-related-peptide release from primary cultures of rat trigeminal ganglia neurones. Cephalalgia : an international journal of headache 2007. link 53 Liu L, Chen L, Liedtke W, Simon SA. Changes in osmolality sensitize the response to capsaicin in trigeminal sensory neurons. Journal of neurophysiology 2007. link 54 Luccarini P, Childeric A, Gaydier AM, Voisin D, Dallel R. 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Original source

[1]
Updates on the Proposed Botulinum Toxin A Mechanisms of Action in Orofacial Pain: A Review of Animal Studies. — Fabillar J, Yamamoto Y, Koike K, Ikutame D, Matsuka Y Toxins (2025)
[2]
Naringenin Suppresses the Hyperexcitability of Trigeminal Nociceptive Neurons Associated with Inflammatory Hyperalgesia: Replacement of NSAIDs with Phytochemicals. — Yajima S, Sakata R, Watanuki Y, Sashide Y, Takeda M Nutrients (2024)
[3]
The Anti-Calcitonin Gene-Related Peptide (Anti-CGRP) Antibody Fremanezumab Reduces Trigeminal Neurons Immunoreactive to CGRP and CGRP Receptor Components in Rats. — Vogler B, Kuhn A, Mackenzie KD, Stratton J, Dux M, Messlinger K International journal of molecular sciences (2023)
[4]
Gα — Saito N, Kimura M, Ouchi T, Ichinohe T, Shibukawa Y Biomolecules (2022)
[5]
Phytochemical quercetin alleviates hyperexcitability of trigeminal nociceptive neurons associated with inflammatory hyperalgesia comparable to NSAIDs. — Itou H, Toyota R, Takeda M Molecular pain (2022)
[6]
Oxytocin inhibits hindpaw hyperalgesia induced by orofacial inflammation combined with stress. — Li YX, Li JH, Guo Y, Tao ZY, Qin SH, Traub RJ et al. Molecular pain (2022)
[7]
C-fibers may modulate adjacent Aδ-fibers through axon-axon CGRP signaling at nodes of Ranvier in the trigeminal system. — Edvinsson JCA, Warfvinge K, Krause DN, Blixt FW, Sheykhzade M, Edvinsson L et al. The journal of headache and pain (2019)
[8]
CGRP receptor antagonist activity of olcegepant depends on the signalling pathway measured. — Walker CS, Raddant AC, Woolley MJ, Russo AF, Hay DL Cephalalgia : an international journal of headache (2018)
[9]
Elevated levels of calcitonin gene-related peptide in upper spinal cord promotes sensitization of primary trigeminal nociceptive neurons. — Cornelison LE, Hawkins JL, Durham PL Neuroscience (2016)
[10]
Systemic desensitization through TRPA1 channels by capsazepine and mustard oil - a novel strategy against inflammation and pain. — Kistner K, Siklosi N, Babes A, Khalil M, Selescu T, Zimmermann K et al. Scientific reports (2016)
[11]
Nociception-specific blink reflex: pharmacology in healthy volunteers. — Marin JC, Gantenbein AR, Paemeleire K, Kaube H, Goadsby PJ The journal of headache and pain (2015)
[12]
The calcitonin gene-related peptide receptor antagonist MK-8825 decreases spinal trigeminal activity during nitroglycerin infusion. — Feistel S, Albrecht S, Messlinger K The journal of headache and pain (2013)
[13]
Effect of Mas-related gene (Mrg) receptors on hyperalgesia in rats with CFA-induced inflammation via direct and indirect mechanisms. — Jiang J, Wang D, Zhou X, Huo Y, Chen T, Hu F et al. British journal of pharmacology (2013)
[14]
Validation of a novel rat-holding device for studying heat- and mechanical-evoked trigeminal nocifensive behavioral responses. — Garrett FG, Hawkins JL, Overmyer AE, Hayden JB, Durham PL Journal of orofacial pain (2012)
[15]
Early and late contributions of glutamate and CGRP to mechanical sensitization by endothelin-1. — Khodorova A, Richter J, Vasko MR, Strichartz G The journal of pain (2009)
[16]
Activation of TRPV1 mediates calcitonin gene-related peptide release, which excites trigeminal sensory neurons and is attenuated by a retargeted botulinum toxin with anti-nociceptive potential. — Meng J, Ovsepian SV, Wang J, Pickering M, Sasse A, Aoki KR et al. The Journal of neuroscience : the official journal of the Society for Neuroscience (2009)
[17]
Morphine increases acetylcholine release in the trigeminal nuclear complex. — Zhu Z, Bowman HR, Baghdoyan HA, Lydic R Sleep (2008)
[18]
Roles of TRPV1 and neuropeptidergic receptors in dorsal root reflex-mediated neurogenic inflammation induced by intradermal injection of capsaicin. — Lin Q, Li D, Xu X, Zou X, Fang L Molecular pain (2007)
[19]
Regulatory effect of nerve growth factor on release of substance P in cultured dorsal root ganglion neurons of rat. — Yang XD, Liu Z, Liu HX, Wang LH, Ma CH, Li ZZ Neuroscience bulletin (2007)
[20]
Endogenous prostaglandin I2 regulates the neural emergency system through release of calcitonin gene related peptide. — Arai K, Ohno T, Saeki T, Mizuguchi S, Kamata K, Hayashi I et al. Gut (2003)
[21]
Block by gabapentin of the facilitation of glutamate release from rat trigeminal nucleus following activation of protein kinase C or adenylyl cyclase. — Maneuf YP, McKnight AT British journal of pharmacology (2001)
[22]
Cyclo-oxygenase and lipoxygenase pathways in mast cell dependent-neurogenic inflammation induced by electrical stimulation of the rat saphenous nerve. — Le Filliatre G, Sayah S, Latournerie V, Renaud JF, Finet M, Hanf R British journal of pharmacology (2001)
[23]
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