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Drooling, Aspiration, and Oesophageal Problems
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Botulinum toxin injections are useful. They block release of acetylcholine from parasympathetic secretomotor nerves in the salivary glands. Onabotulinum toxin A (Botox) is the most common type used. Most clinicians inject equal amounts into the submandibular and parotid glands under ultrasound guidance. Maximal effect is at 2–6 weeks, with a median duration of response of 4 months. Transient post-injection dysphagia can occur; therefore, caution is advised for an orally fed child with a pre-existing swallowing impairment.
The salivary glands
Published in Neeraj Sethi, R. James A. England, Neil de Zoysa, Head, Neck and Thyroid Surgery, 2020
The auriculotemporal nerve (a branch of V3) provides sensory innervation to the parotid gland. This division of the trigeminal nerve exits the skull through the foramen ovale. The auriculotemporal nerve also carries parasympathetic secretomotor fibres to the parotid. They originate in the otic ganglion in the infratemporal fossa. The preganglionic parasympathetic fibres to the otic ganglion come from the glossopharyngeal nerve (CN IX) [2].
Pineal Gland
Published in Paul V. Malven, Mammalian Neuroendocrinology, 2019
The gross morphology of the pineal gland ranges from a spherical shape in ruminant ungulates to a cylindrical structure containing deep and superficial portions in rodent species (Rollag et al., 1985). The pineal tissue consists of non-neuronal parenchymal cells, the pinealocytes, that share some antigenic characteristics with retinal cells but not neuroglia (Korf et al., 1986). The pineal gland contains a few neuroglial cells but lacks neuronal perikarya. Although there is a tissue connection between the pineal gland and adjacent epithalamus, there do not appear to be any axons passing through this connecting neural tissue. However, there are numerous axonal terminals in the pineal gland; they are derived from postganglionic axons that originate outside the CNS in the superior cervical ganglion (SCG). The SCG is the rostral-most ganglion of the sympathetic chain, and it contains the perikarya of postganglionic sympathetic neurons. The perikarya in the SCG are activated by preganglionic axons originating in the CNS. Postganglionic axons enter the pineal gland from outside the CNS and innervate pinealocytes. Norepinephrine (NE) is the neurotransmitter released at these secretomotor terminals (see Figure 1-1). The ultrastructure of these terminals is similar to synaptic contacts between neurons.
Autonomic symptoms and associated factors in patients with chronic heart failure
Published in Acta Cardiologica, 2023
Hellen Da Silva, Sofie Pardaens, Marc Vanderheyden, Johan De Sutter, Heleen Demeyer, Michel De Pauw, Laurent Demulier, Jan Stautemas, Patrick Calders
The Composite Autonomic Symptom Score 31 (COMPASS 31) is a short-form questionnaire used to assess the distribution, severity, and frequency of autonomic symptoms. This questionnaire is a validated, easy-to-administer tool to assess autonomic symptoms, which has already been used in different chronic populations [8,17]. The questionnaire contains 31 questions, divided into six subdomains: (i) orthostatic intolerance (four questions); (ii) vasomotor (three questions); (iii) secretomotor (four questions); (iv) gastrointestinal (12 questions); (v) bladder (three questions) and (vi) pupillomotor function (five questions). The total score provides a continuum score from 0 to 100 points with a higher score representing more autonomic symptoms and with a maximum weighted score for orthostatic intolerance of 40, vasomotor of 5, secretomotor of 15, gastrointestinal of 25, bladder of 10, and pupillomotor function of 5 [17,18].
Lacrimal gland botulinum toxin injection for epiphora management
Published in Orbit, 2022
Johnathan Jeffers, Katherine Lucarelli, Sruti Akella, Pete Setabutr, Ted H. Wojno, Vinay Aakalu
Botulinum toxin was first purified in 1897, with seven different serotypes eventually identified.15,16 The toxin works by inhibiting the presynaptic release of acetylcholine at the neuromuscular junction and by autonomic nerve fibers. This ultimately results in a decreased concentration of post-synaptic acetylcholine receptors and subsequent muscle weakening.17 In the field of ophthalmology, botulinum toxin is commonly used to treat strabismus, blepharospasm, and hemifacial spasm. The use of botulinum toxin injection in medical treatments first started in 1970s, with the use of Botulinum Toxin A in animal trials.18 Dr. Allen Scott, an ophthalmologist was one of the first medical professionals to utilize the toxin as a medical treatment.19 The use of botulinum toxin for injection has been proven to be a safe procedure after over 40 years of use. Initial utilization of the purified toxin in ophthalmology included intramuscular injections for cases of strabismus.18 Frueh, Felt, Wojno, and Musch first described the use of botulinum toxin, previously known as oculinum for treatment of benign blepharospasm in 1984.20 There is also interest in using botulinum toxin to treat epiphora by injecting the lacrimal gland.21–23 Here, the inactivation of acetylcholine release from postganglionic parasympathetic secretomotor fibers lead to decreased tearing.16
Emerging therapies in the management of Irritable Bowel Syndrome (IBS)
Published in Expert Opinion on Emerging Drugs, 2022
Jill E. Elwing, Hadi Atassi, Benjamin D. Rogers, Gregory S. Sayuk
The pathogenesis of IBS is best understood in the context of a biopsychosocial model, recognizing the contributions of environmental exposures, psychological factors, and bowel-specific mechanisms to the development of IBS symptoms [9]. At the center of IBS pathophysiology are alterations in the brain-gut axis, a network of bi-directional communications between the central nervous system (CNS) and the bowel. Development of central sensitization leads not only to abdominal symptoms, but often comorbid non-GI somatic symptoms, in the IBS patient [10]. Further, visceral hypersensitivity and alterations in the secretomotor function of the gut have mechanistic relevance in some cases of IBS. The complexity of IBS pathophysiology, coupled with the reliance on symptoms to establish a diagnosis, leads to the recognition of IBS as a heterogeneous condition [11]. This presents unique opportunities for the development of therapies that address multiple different mechanisms, yet at the same time poses challenges to the development of therapies that are effective in a substantial portion of IBS sufferers.