Cutaneous pain

Cutaneous pain is felt in superficial structures such as the skin and subcutaneous tissues. A pin prick and a paper cut are examples of cutaneous pain. 

It is a sharp pain with a burning quality that may be easily localized. This pain may be abrupt or slow in onset. 

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Physalia nematocyst toxin (72). This phenomenon appears to be important in understanding the pathogenesis of toxin-induced cutaneous pain. Additionally, the importance of kinin-like mediators in pain production has also been hypothesized (2). 

Distinguish between cutaneous pain and deep visceral pain... 

As its name implies, deep somatic pain is generated in deep body structures, such as the periosteum, muscles, tendons, joints, and blood vessels. This type of pain is more diffuse than cutaneous pain. It may be elicited by strong pressure, ischemia, and tissue damage. 

Anandamide may reduce pain by a peripheral action, by acting on CB 1-like receptors located outside the CNS (Calignano et al. 1998). Palmitylethanolamide (PEA) is an endocannabinoid that is coreleased with anandamide and activates peripheral CB2 receptors. When the two are administered together, they show a 100-fold synergistic effect on analgesic measures. Measurements of anandamide and PEA levels in the skin show that there are sufficient amounts to create tonic activation of local cannabinoid receptors. Thus, endocannabinoids may tonically inhibit cutaneous pain. 

Capsaicin (Zostrix) is approved for the relief of pain following herpes zoster infection (postherpetic neuralgia). The drug depletes neurons of substance P, an endogenous neuropeptide that may mediate cutaneous pain. It is applied to affected skin after open lesions have healed. Local irritation is common. 

Hypercarbia depresses the excitability of the cerebral cortex and increases the cutaneous pain threshold through a central action. In patients who are hypoventilating from narcotics or anesthetics, increasing Pco may result in further CNS depression, which in turn may worsen the respiratory depression. This positive-feedback cycle can be deadly. 

Peripheral neural correlates of magnitude of cutaneous pain and hyperalgesia. / Neurophysiol 1983 50 1-26. 

The role of histamine in the transmission of cutaneous pain is far from established. 

Nociceptors are a specific subset of peripheral sensory organs, which respond to noxious stimuli. A8 mechan-oreceptors and C-polymodal nociceptors are the two main classes of cutaneous nociceptors. The sensory quality of pain evoked by activation of A8-fibres is... 

Afferent input from cutaneous and visceral nociceptors is known to converge on spinal neurons, which accounts for the referral of pain between visceral and cutaneous structures (e.g. cardiac pain gets referred to the chest and left upper arm in patients suffering from angina pectoris). Projection neurons in the spinal dorsal horn project to cell nuclei in supraspinal areas such as the thalamus, brainstem and midbrain. Of these, the synaptic junctions in the thalamus play a very important role in the integration and modulation of spinal nociceptive and non-nociceptive inputs. Nociceptive inputs are finally conducted to the cortex where the sensation of pain is perceived (Fig. 1). The mechanisms via which the cortex processes nociceptive inputs are only poorly understood. 

Epidermal nerve fiber analysis by immunocytochemical techniques using the panaxonal marker protein gene product 9.5 (PGP 9.5) allows the study of epidermal innervation by small fiber C and A5 nerve fibers (McCarthy et al. 1995 Holland et al. 1997). Studies of skin biopsies of HIV infected patients with DSP or ATN showed reduction in the number of epidermal fibers in distal areas of the lower extremities with an inverse correlation between neuropathic pain intensity and epidermal nerve fiber density (Polydefkis et al. 2002) (Fig. 4.3). There were also fewer epidermal fibers in HIV seropositive patients without clinical evidence of neuropathy, suggesting that HIV infection may be associated with the loss of cutaneous innervation even before the onset of sensory symptomatology (McCarthy et al. 1995). 

Figure 8.3 Referred pain. The mechanism of referred pain involves convergence of visceral afferent neurons and cutaneous afferent neurons with the same second-order neurons in the dorsal horn of the spinal cord. In this example, the pain of angina that originates in the heart is referred to the left arm.

Signs and Symptoms High fever coughing thick nasal discharge rapidly spreading, deep ulceration of the nasal mucosa submaxillary lymph nodes swollen and painful nodules on the skin, abdomen, and lower limbs death in 1-2 weeks. In the cutaneous form, the lymphatics are enlarged and nodular abscesses ("buds") of 0.5-2.5 cm develop, which ulcerate and discharge yellow oily pus. 

Signs and Symptoms Symptoms include pain in the lower-right abdominal area resembling appendicitis, as well as fever, headache, pharyngitis, anorexia, vomiting, and possibly watery diarrhea. May also produce arthritis, inflammation of the iris (iritis), cutaneous ulceration. Infection may also produce abscesses in the liver, bone infection (osteomyelitis), and septicemia. Carriers may be asymptomatic. May also cause infections of other sites such as wounds, joints, and the urinary tract. 

Familial lipoprotein lipase deficiency is characterized by a massive accumulation of chylomicrons and a corresponding increase in plasma triglycerides or a type I lipoprotein pattern. Presenting manifestations include repeated attacks of pancreatitis and abdominal pain, eruptive cutaneous xanthomatosis, and hepatosplenomegaly beginning in childhood. Symptom severity is proportional to dietary fat intake, and consequently to the elevation of chylomicrons. Accelerated atherosclerosis is not associated with this disease. 

Alefacept (Amevive) is a dimeric fusion protein that binds to CD2 on T cells to inhibit cutaneous T-cell activation and proliferation. It also produces a dose-dependent decrease in circulating total lymphocytes. Alefacept is approved for treatment of moderate to severe plaque psoriasis and is also effective for treatment of psoriatic arthritis. Significant response is usually achieved after about 3 months of therapy. The recommended dose is 15 mg intramuscularly once weekly for 12 weeks. Adverse effects are mild and include pharyngitis, flu-like symptoms, chills, dizziness, nausea, headache, injection site pain and inflammation, and nonspecific infection. 

Finlay, I.G., Bowszyc, J., Ramlau, C. and Gwiezdzinski,Z. (1996) The effect of topical 0.75% metronidazole gel on malodorous cutaneous ulcers. J. Pain Symptom Manag. 11, 158-162. 

Ten of 12 workers experienced acute irritant contact dermatitis of the hands after 2 days of direct contact. In the most severe case, a woman with no previous skin problems, who wore latex gloves intermittently, had painful swelling of the fingers of both hands with redness and vesicles on the palms. The affected skin later became thickened and showed a brownish discoloration. Another worker noticed small vesicles on the forehead, probably due to scratching with contaminated fingers. All cutaneous reactions cleared within 3 weeks of termination of exposure. Gas chromatograph analysis of the NMP used at the factory did not reveal any contaminating compounds. 

Adverse reactions may include death, convulsions, headache, injection site pain, increased sweating, fatigue, cutaneous vasodilation, nausea, vomiting, dizziness, agitation, dry mouth, tremors, palpitations, insomnia, dyspnea, hyperventilation, emotional lability, abnormal/blurred vision, and paresthesia. 

Interestingly, nonsteroidal anti-inflammatory drugs, such as ketoprofen 25 (Scheme 17), which are used to treat a wide range of ailments, such as inflammation, pain, and fever, also undergo photodecarboxylation. Unfortunately, many of these drugs have been shown to have cutaneous side effects, which are caused by their photodecomposition. Various research groups have demonstrated that irradiation of ketoprofen 25 yields 26 under anaerobic conditions, whereas in oxygen-saturated... 

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