Remediating Brain Instabilities in a Neurology Practice
Hanno W. Kirk in 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
Neural Control of Coughing And Sneezing
Alan D. Miller, Armand L. Bianchi, Beverly P. Bishop in Neural Control of the Respiratory Muscles, 2019
The respiratory areas of the nasal mucosa are innervated primarily by the trigeminal nerve. Electrical stimulation of branches of the trigeminal nerve (anterior ethmoidal, posterior nasal, and infraorbital) can produce sneeze-like responses (fictive sneeze).41,45 Trigeminal nerve afferents project onto second-order neurons in the spinal trigeminal nucleus.25 Although stimulation of trigeminal nerve afferents has an effect on the respiratory pattern of neurons (see below), anatomical and neurophysiological evidence suggests there are no direct afferent projections to medullary areas involved in the control of breathing.24,42 Histological findings showed nasal trigeminal afferent projections within the NPBM-KF,31 suggesting that “sneeze” receptors may act in part through the pneumotaxic center/pontine respiratory group. There have been no studies of the sneeze reflex evoked by specific physiological stimuli to determine the location in the trigeminal nucleus, characteristics, and specific projections of sneeze relay neurons to the DRG or BÖT/VRG. The use of repetitive air puffs in the nasal cavity to evoke sneeze shows promise as a specific physiological stimulus.39
Comparative Anatomy of Medullary Vagal Nerve Nuclei
Sue Ritter, Robert C. Ritter, Charles D. Barnes in Neuroanatomy and Physiology of Abdominal Vagal Afferents, 2020
In most vertebrates (but apparently not including skates; see Barry6), the vagus nerve contains a few sensory fibers that innervate cutaneous areas in a fashion similar to the trigeminal nerve or spinal dorsal roots. These general somatic sensory fibers of the vagus nerve enter the spinal (descending) trigeminal tract and terminate within a portion of the spinal trigeminal nucleus.5,23,27,39 The presumption is that vagal fibers that enter the spinal trigeminal tract derive from ganglion cells that innervate skin overlying the operculum (in fishes), the tympanic membrane (in frogs) or the auricle (in mammals). Stuesse et al.39 claim, however, that vagal fibers which innervate abdominal viscera also join the spinal trigeminal tract of the frogs they studied. In contrast, in domestic cats none of the coelomic visceral fibers project to the spinal trigeminal tract.
Neck associated factors related to migraine in adolescents with painful temporomandibular disorders
Published in Acta Odontologica Scandinavica, 2021
Interestingly, compared with adolescents with only painful TMD, adolescents with both painful TMD and migraine seems to have greater associations among intensity of neck pain, a forward head posture, the number of active TrPs in the masticatory and cervical muscles, and intensity of the orofacial pain. Sensory afferent input from the regional masticatory and cervical muscle terminate in the trigeminocervical complex which is composed of the first and second cervical dorsal horns of the cervical spinal cord and the caudal part of the spinal trigeminal nucleus. Sustained and increased nociceptive input from headache and painful TMD may enhance interactions with the orofacial and neck pain intensity and the cervical and masticatory MFP and this may lead to positive feedback loop in the trigeminocervical complex. As mentioned above, a forward head posture could enhance this positive loop by increasing the cervical MFP.
Congenital alacrima
Published in Orbit, 2022
Zhenyang Zhao, Richard C. Allen
The neural regulation of lacrimal gland secretion comprises an afferent sensory arm and a parasympathetic dominant efferent arm. The afferent arm receives input from the nasal mucosa and ocular surface sensory fibers, which are composed of the polymodal nociceptors of the cornea.4 The stimulatory signal is processed in the spinal trigeminal nucleus and relayed to the superior salivary nucleus.5 The efferent arm originates from the superior salivary nucleus projecting to the pterygopalatine ganglion, initially through the greater superficial petrosal nerve, which later joins the deep petrosal nerve to form the vidian nerve before synapsing. The postganglionic fibers from the pterygopalatine ganglion provide parasympathetic innervation for the lacrimal gland.6 The same process regulates both reflex and basal tear secretion despite being different clinical concepts. This is supported by the observation that minimal basal tear secretion occurs without stimuli during sleep and under local or general anesthesia.7 Any interruptions along this pathway can lead to decreased tear production and alacrima.
Use of CGRP receptor blocker erenumab in the management of post-traumatic headache: a case series of 5 women
Published in Brain Injury, 2020
Jordan VanderEnde, Emma A. Bateman, Heather M. MacKenzie, Keith Sequeira
A growing body of scientific literature has demonstrated that excitation of nociceptors (Aδ and C-fibers) within the trigeminovascular pathway, which provides sensory innervation to the intracranial vasculature and surrounding meninges, are a cause of primary migraine headaches (11,12). In the trigeminovascular pathway, axons originating in the trigeminal ganglion innervate the dura mainly via the ophthalmic branch of the trigeminal nerve (V1) (12). CGRP is the most abundant neuropeptide in the trigeminal nerve (17). When V1 nociceptors release vasoactive neuropeptides including CGRP in response to mechanical, electrical, or inflammatory insults to the dura and meningeal vessels, it produces throbbing headache pain with associated nausea, photophobia, and phonophobia (12,17). The sensory neurons within the spinal trigeminal nucleus that receive input from these intracranial nociceptors also receive input from adjacent muscle and skin, which likely contributes to the localization of pain over the periorbital and occipital areas (12). By blocking the CGRP-related receptor, erenumab blunts the effect of CGRP on the trigeminovascular pathway and thereby disrupts the cascade of sensory afferents and vasodilation that leads to migraine headache (11,12).
Related Knowledge Centers
- Facial Nerve
- Glossopharyngeal Nerve
- Haptic Perception
- Nucleus
- Somatosensory System
- Medulla Oblongata
- Trigeminal Nerve
- Pain
- Vagus Nerve
- Cranial Nerves