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Lower Limb
Published in Bobby Krishnachetty, Abdul Syed, Harriet Scott, Applied Anatomy for the FRCA, 2020
Bobby Krishnachetty, Abdul Syed, Harriet Scott
Due to the innervation of the hip, there is incomplete analgesia as the joint is also supplied by obturator and sciatic nerves, which are not blocked. Furthermore, site of incision of hip surgery will not be covered as cutaneous innervation is from superior cluneal nerves, lateral cutaneous nerve of thigh and iliohypogastric nerves. Therefore, it cannot be used as the sole anaesthetic technique and may be inadequate for analgesia on its own (Table 6.7).
Comparative Anatomy of Medullary Vagal Nerve Nuclei
Published in Sue Ritter, Robert C. Ritter, Charles D. Barnes, Neuroanatomy and Physiology of Abdominal Vagal Afferents, 2020
Somatic Sensorb — The vagus nerve provides cutaneous innervation to a small area of the skin in the vicinity of the caudal gill slits, operculum or outer ear. The fibers innervating this somatic sensory modality are believed to terminate in the spinal trigeminal nucleus.
SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
The ulnar nerve also provides sensory innervation to the fifth digit, the medial half of the fourth digit, and the corresponding part of the palm: Palmar branch of ulnar nerve: Supplies cutaneous innervation to the anterior skin and nails.Dorsal cutaneous branch of ulnar nerve: Supplies cutaneous innervation to the dorsal medial hand and the dorsum of the medial 1.5 fingers.
Capsaicin 8% dermal patch in clinical practice: an expert opinion
Published in Expert Opinion on Pharmacotherapy, 2020
Cesare Bonezzi, Amedeo Costantini, Giorgio Cruccu, Diego M.M. Fornasari, Vittorio Guardamagna, Vincenzo Palmieri, Enrico Polati, Pierangelo Zini, Anthony H Dickenson
Furthermore, topical exposure to capsaicin causes sensations of heat, burning, stinging or itching, since activation of TRPV1 results in sensory neuronal depolarization, and can induce local sensitization to receptor activation by heat, acidosis and endogenous agonists. However, high concentrations of capsaicin or repeated applications can lead to a persistent local effect on cutaneous nociceptors, constituted by reduced spontaneous activity and a loss of responsiveness to a wide range of sensory stimuli [5]. At concentrations higher than those required to activate TRPV1, capsaicin can also cause mitochondria dysfunction by directly inhibiting electron chain transport. At the same time, the peripheral fibers in the affected zone pull back from their cutaneous innervation territories rendering them less likely to be activated by peripheral stimuli. Thus, the peripheral fibers with their nociceptors and associated ion channels are no longer amenable to activation by stimuli applied to the treated area, and central sensitization is thereby attenuated. This retraction is due to several effects that include temporary loss of membrane potential, inability to transport neurotrophic factors and reversible retraction of epidermal and dermal nociceptive fiber terminals, which all block the transmission of nociceptive stimuli for a prolonged period [5,32]. This condition is temporary and reversible, and terminals are usually reconstituted within 3 months after the administration of capsaicin. Remarkably, due to the high selectivity of capsaicin for the TRPV1 receptor and the selective expression of TRPV1 in nociceptive sensory nerves, other skin sensory nerve endings may remain intact and functional, with no loss of tactile and vibratory sensations [33].
Ethical questions arising from Otfrid Foerster’s use of the Sherrington method to map human dermatomes
Published in Journal of the History of the Neurosciences, 2022
Brian Freeman, John Carmody, Damian Grace
The experimental technique Foerster used had been developed in the years 1893–1897 to map segmental tactile fields or dermatomes in animals by the British histopathologist and neurophysiologist Charles Scott Sherrington (1857–1952; Liddell 1952).2The obituary includes an 11-page bibliography of Sherrington’s works compiled by the American neurophysiologist, neurosurgeon, and medical historian John Farquhar Fulton (1899–1960), who had studied under Sherrington in Oxford, England, in 1923–1925 and 1928–1930. Sherrington (1893) appreciated that there is a significant cutaneous overlap of the sensory nerves from adjacent dorsal roots and that cutting a single root (dorsal rhizotomy) would never permit the accurate determination of the extent of its cutaneous innervation in the living animal. He therefore divided “a short series of the spinal nerves immediately above and immediately below the one to be investigated” (Sherrington 1898) and, about eight hours postoperatively, plotted the area of the skin that retained “æsthesia” or tactile sensibility—that is, the dermatome corresponding to the intact dorsal root; the animals were then sacrificed to determine precisely which roots had been sectioned. Later, Sherrington summarized in extraordinary detail his methods for plotting cutaneous fields in monkeys and the precautions that were necessary for accurate mapping, concluding “I recognize that the problem here attempted has been one imperfectly accessible by inquiry upon animals. It awaits fuller solution in the opportunities afforded by human disease where the attention of an instructed human subject can be enlisted and interrogated verbally” (Sherrington 1901; italics added).
Great toe drop following knee ligament reconstruction: A case report
Published in Physiotherapy Theory and Practice, 2020
David A Boyce, Chantal Prewitt
Dermatome distributions can vary greatly. The most common dermatome distribution of the L5 nerve root is that of the lateral and anterior lower leg, dorsum of the foot, and great toe region. The cutaneous innervation from the SFN virtually overlaps the L5 dermatome by supplying the same area of the lower leg and foot, whereas the DFN supplies the skin between the first and second toe dorsally (Jenkins, 2008). This patient did not demonstrate any sensory loss upon physical examination; however, closer inspection by the examiner may have resulted in sensory loss findings.