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The Physiology of Pain
Published in Bernard J. Dalens, Jean-Pierre Monnet, Yves Harmand, Pediatric Regional Anesthesia, 2019
Bernard Jacques Dalens, Brigitte Storme
The connections of afferent fibers with the interneurons and tracts of the spinal cord have been established from anatomical and electrophysiological studies, which have ascertained the spinal location of ascending nociceptive information. The spinocervical tract (from the spinal cord to the lateral cervical nucleus) and dorsal columns (from the spinal cord to ipsilateral dorsal column nuclei) would probably play an important role in the transmission of pain to supraspinal areas. In their review, Dennis and Melzack19 reported at least six ascending spinal pathways involved in the transmission of pain to the brain. These studies, however, remain incomplete and cannot explain the return of sensitivity to painful stimuli about 2 to 3 months after anterolateral spinal cordotomy. Some other tracts would probably be able to convey the relevant information after the usual paths have been destroyed.
Evidence for the Presence of a Visceral Pain Pathway in the Dorsal Column of the Spinal Cord
Published in Mark J Rowe, Yoshiaki Iwamura, Somatosensory Processing: From Single Neuron to Brain Imaging, 2001
William D. Willis, Elie D. Al-Chaer, Michael J. Quast, Karin N. Westlund
Experimental work is generally consistent with clinical reports (Willis and Coggeshall, 1991). However, at least some neurons in the dorsal column nuclei can be activated by noxious stimuli (Angaut-Petit, 1975), and many of these have been shown to project to the contralateral thalamus (Ferrington et al., 1988; Cliffer et al., 1992). Because many postsynaptic dorsal column neurons respond to noxious cutaneous stimuli (Uddenberg, 1968; Angaut-Petit, 1975; Brown et al., 1983; Lu et al., 1983; however, cf. Giesler and Cliffer, 1985), nociceptive responses in the gracile nucleus have been attributed to activation of nociceptive postsynaptic dorsal column neurons (Angaut-Petit, 1975; Brown et al., 1983). However, the dorsal columns contain not only myelinated axons but also unmyelinated, peptide-containing axons, many of which originate from dorsal root ganglia (Patterson et al., 1989; 1990; Tamatani et al., 1989; Conti et al., 1990; Fabri and Conti, 1990; cf., Giuffrida and Rustioni, 1992). The function of these primary afferent fibers is unknown, but it is possible that some are nociceptive. Thus, nociceptive responses in the dorsal column nuclei could be mediated by nociceptive postsynaptic dorsal column neurons and also by the ascending collaterals of primary afferent nociceptors (Cliffer et al., 1992).
A population-based case–control study of the association between cervical spondylosis and tinnitus
Published in International Journal of Audiology, 2021
Yen-Fu Cheng, Sudha Xirasagar, Tzong-Hann Yang, Chuan-Song Wu, Nai-Wen Kuo, Herng-Ching Lin
The mechanism underlying the association is likely to be related to somatosensory pathway disruptions in cervical spondylosis. Although damage to the peripheral auditory system accounts for majority of tinnitus cases, our study affirms the potential for tinnitus to be evoked by disturbed inputs via the somatosensory pathways. Extensive studies with animal models have shown that neural stimuli originating in the auditory and somatosensory systems are integrated in the cochlea nucleus of the brainstem (CN) (Brozoski and Bauer 2005; Koehler and Shore 2013; Roberts et al. 2010; Zhang et al. 2019). In addition to the ascending auditory pathway from the auditory nerves and descending auditory pathways from the auditory centres in the midbrain and auditory cortex, the somatosensory projection of dorsal column nuclei, trigeminal and cervical ganglia also converge at this site. As a result, dysregulated synchrony across this neural ensemble along the auditory and related somatosensory pathway that converge in the cochlea nucleus can cause tinnitus-generating neural discharges, even in the absence of a permanent shift in the hearing threshold (Koehler and Shore 2013).