Capsaicin adult treatment effects

The diverse physiological actions of capsaicin described in the previous sections have motivated numerous, equally diverse, in vivo and in vitro studies in search of biochemical correlates. The most attention, however, has been focused on the sensory system since a direct effect of capsaicin on sensory nerves has been suspected for a long time. More recent observations of capsaicin-induced sensory neuron degeneration in neonatal animals have added further impetus to determine the resultant neurochemical deficits of this lesion. It is perhaps fortunate that the small type B neurons of dorsal root ganglia which appear anatomically to succumb to capsaicin after both neonatal and adult treatment are also among the neurons for which putative neurotransmitter markers have been identified. Accordingly, these markers, two of which are the peptides somatostatin and substance P, have provided both a means to assess the neurotoxic potential of capsaicin, and to some extent relate anatomical with neurochemical investigations. For the sake of coherence the biochemical aspects of some reports cited in the previous sections are discussed here. The major conclusions in these reports will be summarized in Section 13. 

Attempts to frame the above results into a unifying scheme which would explain the behavioral effects of capsaicin is made difficult for several reasons. First, apart from investigations of thermal stimuli in the physiological range, no detailed quantitation has been conducted on the influence of capsaicin on non-nociceptive sensory stimuli. Second, it is already apparent that capsaicin when given to neonatal animals has distinctly different effects on primary afferent neurons than when given to the adult. Other routes of administration may be accommodated by one of these categories or may yield still other deficits characteristic of the treatment. The variety of behavioral results obtained need to be correlated with the neurochemical and neuroanatomical profiles that each route of capsaicin administration creates. Finally, there is the question of dose. As... 

The mechanism whereby capsaicin treatment of adult animals brings about a loss of peptides from sensory nerves is not clear. The possibilities include degeneration of those neurons, interference with terminal storage capacity, inhibition of peptide synthesis, or blockade of axonal transport. As described earlier, there is no evidence for capsaicin-induced degeneration after subcutaneous treatment of adult animals. This is supported by the observation that peptide levels partially recover in affected areas some time after treatment (Gamse et al., 19806). The results obtained after intrathecal treatment suggest a direct effect on primary afferent terminals... 

Examples of cutaneous patches are lidocaine containing patches that sometimes contain a second local anaesthetic. After applying the patch, lidocaine penetrates deep into the skin where it has a local anesthetising effect. Capsaicin containing patches are used in the treatment of peripheral neuropathic pain in non-diabetic adults. Following exposure to the patch, capsaicin penetrates the skin and interacts with the cutaneous transient receptor potential vanilloid 1 receptor (TRPVl) resulting in pain relief. 

The Capsaicin Study Group (1992) Effect of treatment with capsaicin on daily activities of patients with painful diabetic neuropathy. Diabet Care 15 159-165 Derry S, Lloyd R, Moore RA, McQuay HJ (2009) Topical capsaicin for chronic neuropathic pain in adults (Review). Cochrane Database Syst Rev, Issue 4. Art. No. CD007393 Glinski W, Glinska-Ferenz M, Pierozynska-Dubowska M (1991) Neurogtmic inflammation induced by capsaicin in patients with psoriasis. Acta Derm Venereol 71 51-54 Arnold WP, van de Kerkhof PC (1993) Topical capsaicin in pruritic psoriasis. J Am Acad Dermatol 29 438 142... 

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