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Remediating Brain Instabilities in a Neurology Practice
Published in Hanno W. Kirk, Restoring the Brain, 2020
We cannot talk about the entity of “headache” in a chapter dedicated to the practice of clinical neurofeedback in a neurology specialty without expanding on this most common of complaints in medicine. The central pathophysiology of headache syndromes has a shared mechanism with arousal disorders38 and with myofascial head and neck pain disorders,39 accounting for frequent comorbidities. Headache invariably shows up in refractory extracranial disorders (e.g. autoimmune disease and chronic fatigue syndrome). Regardless of the association, chronic headache syndromes reflect an imminent or prevailing central dysregulation by whatever disease entity, effecting a consistent firing of afferents to the trigeminal complex (this largest of the cranial nerves serving a major sensory function to all anatomic structures above the shoulders, as well as providing motor efferents to the muscles of mastication). The spinal trigeminal nucleus, in particular, receives pain (and temperature) sensation from the head and facial structures and descends to the third cervical level, receiving nociceptive cervical afferents.40
Ascending Projections of the Solitary Tract Nucleus
Published in I. Robin A. Barraco, Nucleus of the Solitary Tract, 2019
G. J. Ter Horst, C. Streefland
The trigeminal and facial nuclei innervations from the NTS, which originate in the rostral and intermediate — gustatory — parts,11,14 terminate in the dorsal, jaw-closer parts of the motor trigeminal nucleus and in the dorsomedial part of the spinal trigeminal and facial nuclei.10,11 Such trigeminal projections are not found in monkeys,19 but this may be attributed to the limitations of the autoradiographic tract tracing method with respect to the identification of small projections in fiber-rich regions like the medulla oblongata.
Diagnosis and Management of Facial Pain
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Rajiv K. Bhalla, Timothy J. Woolford
The majority of painful stimuli from the face are transmitted to the spinal tract of the brain stem via afferents in the trigeminal nerve. Pain afferents from the VIIIth, IXth and Xth cranial nerves also relay in the spinal tract. Facial pain from deep structures tends to be a dull, poorly localized ache because the afferent nerves innervating them are unmyelinated. Facial skin is supplied by myelinated nerves that produce a sharper pain. Various neurophysiological models have been proposed to explain the nociceptive inputs causing tension headache and migraine, and suggest pathogenesis similar to that of fibromyalgia and irritable bowel syndrome, conditions that frequently coexist. Experimental studies suggest that increased excitability of the central nervous system generated by repetitive and sustained pericranial myofascial input may be partly responsible, along with widespread changes in brain function and connectivity.1,2 By extrapolation, facial pain is likely to be caused by central sensitization of the trigeminal nucleus by myofascial, vascular or supraspinal input, with exacerbations or provocation of pain induced by supraspinal inhibition of the trigeminal nucleus by psychological influences.3 To add to this, surgery, trauma and inflammation may promote nociceptive stimulation of the trigeminal caudal nucleus and initiate pain.
Intratracheal instillation of respirable particulate matter elicits neuroendocrine activation
Published in Inhalation Toxicology, 2023
Devin I. Alewel, Andres R. Henriquez, Mette C. Schladweiler, Rachel Grindstaff, Anna A. Fisher, Samantha J. Snow, Thomas W. Jackson, Urmila P. Kodavanti
Neural and neuroendocrine system regulation of the innate immune response to stress has been well established (Sternberg, 2006; Walsh et al. 2021). In the nose, projections of the trigeminal nerve perceive irritant and noxious stimuli and communicate with the mesencephalic trigeminal nucleus of the central nervous system (CNS) (Harkema et al. 2006). Moreover, the lungs are densely innervated with diverse mechano- and chemo-sensitive receptors extending from the vagus nerve that monitor irritation reflexes induced by pollutants depositing into the tracheobronchial and pulmonary airways (Mazzone and Undem 2016). Pulmonary injury stimulates vagal neurons and transfers stimuli through the jugular and nodose ganglions, which project to brain regions such as the hypothalamus for systemic feedback, often in the form of neuroendocrine activation and adrenal hormone release (Gackière et al. 2011; Mazzone and Undem 2016; Snow et al. 2018; Kodavanti 2019).
Back and neck pain: A comparison between acute and chronic pain–related Temporomandibular Disorders
Published in Canadian Journal of Pain, 2022
Jack Botros, Mervyn Gornitsky, Firoozeh Samim, Zovinar der Khatchadourian, Ana Miriam Velly
Our findings suggest that central dysregulation mechanisms37,38 are implicated in the process of pain-related TMD chronification involving peripheral and central sensitization mechanisms. Central pain is characterized as being diffuse or multifocal and thus is associated with comorbid pain conditions.19,39 Another suggested mechanism is trigeminocervical convergence.40–42 The neurons in the trigeminal nucleus caudalis that extend to C2 and the lateral cervical nucleus are stimulated by trigeminal activation, causing symptoms in both the trigeminal and cervical regions. This mechanism could be activated as pain-related TMDs becomes chronic, leading to the observed association between chronic pain–related TMDs and neck pain but not back pain. Moreover, the association of chronic disability with neck pain calls attention to the importance of including disability as a factor defining chronic pain–related TMDs in addition to pain duration, which agrees with the latest IASP recommendations.25 This accurate distinction will aid clinicians in developing the most suitable and effective management protocols, which may involve a multidisciplinary team to address comorbidities associated with pain persistence or disability.
Post-concussion Syndrome Light Sensitivity: A Case Report and Review of the Literature
Published in Neuro-Ophthalmology, 2022
Mohammad Abusamak, Hamzeh Mohammad Alrawashdeh
Trigeminal ganglion neurons are both autonomic and sensory. The trigeminovascular reflex regulates the dilatation of innervated vessels by mediators, such as calcitonin gene-related peptide (CGRP) and nitric oxide, which are released after being activated by nociceptive sensory stimuli. The activation of superior salivatory and Edinger-Westphal nuclei by collaterals from the caudal trigeminal nucleus is known as the trigeminal-autonomic reflex, which is considered a multi-synaptic reflex. Parasympathetic activity in the pterygopalatine ganglion is activated by superior salivatory signals that dilate blood vessels and mediate lacrimation via the ciliary ganglion, in contrast to pupillary constriction, which is mediated by Edinger-Westphal output. These two reflexes explain the injection of conjunctival vessels and excessive tearing along with peri-orbital pain in patients with migraine or cluster headaches, which mostly occur with photophobia.1