question: Why does a pimple hurt less after being popped even though it is now an open wound?
comment: You relieve the pressure under the skin when you pop it. The pimple is caused by a blockage of your pores which causes a buildup of pressure. The increased pressure causes inflammation locally putting pressure on the nerves in your skin. When you pop it, you relieve pressure allowing the fluid to drain. Make sure to clean your skin regularly to prevent infections of your pimple craters!
passages: Generally, the spread of infection is determined by barriers such as muscle, bone and fasciae. Pus moves by the path of least resistance, e.g. the fluid will more readily dissect apart loosely connected tissue planes, such the fascial spaces, than erode through bone or muscles. In the head and neck, potential spaces are primarily defined by the complex attachment of muscles, especially mylohyoid, buccinator, masseter, medial pterygoid, superior constrictor and orbicularis oris.
   When FIC is performed with the loss of resistance technique, the injection site for FIC is found by drawing an imaginary line between the pubic tubercle to the anterior superior iliac spine. The injection site is 1 cm. below the lateral one third and the medial two thirds of this line. Two losses of resistances are felt as the fascia lata and the fascia iliaca is penetrated by a semi-blunt cannula. Aspiration (drawing back the cannula) is performed, after which a local analgesic is injected while compressing on the skin distally to increase cranial distribution.
   Modern understanding of the fascial spaces of the head and neck developed from the landmark research of Grodinsky and Holyoke in the 1930s. They injected a dye into cadavers to simulate pus. Their hypothesis was that infection in the head and neck mainly spread by hydrostatic pressure. This is now accepted to be true for most infections in the head and neck, with the exception of actinomycosis which tends to burrow into the skin, and mycotuberculoid infections which tend to spread via the lymphatics.
   Three types of surgery have been done to decompress the pudendal nerve: transperineal, transgluteal, and transichiorectal. A follow-up of patients of this surgery after 4 years found that 50% felt their pain had improved to various extents, although control patients were not followed up for comparison. If surgery does bring relief of symptoms, patients will mostly experience it within 4 weeks of surgery.
   Unlike classical venous malformations, pain in FAVA is multifactorial and clinical response to slcerotherapy of the venous component can be less effective. While intralesional steroid injections and nerve block may offer temporary or partial pain relief, the source of pain is often the solid intramuscular lesion. Surgical resection and image-guided percutaneous cryoablation may offer an effective control of pain in FAVA lesions.
   For patients who desire definitive close, surgery is the only option. Prior to determining candidacy for surgical closure, the etiology of the perforation must be determined. Often this requires a biopsy of the perforation to rule out autoimmune causes. If a known cause such as cocaine is the offending agent, it must be ensured that the patient is not still using the irritant.
   The pain in Dercum's disease is often reported to be refractory to analgesics and to non-steroidal anti-inflammatory drugs (NSAIDs). However, this has been contradicted by the findings of Herbst et al. They reported that the pain diminished in 89% of patients (n=89) when treated with NSAIDs and in 97% of patients when treated with narcotic analgesics (n=37). The dosage required and the duration of the pain relief are not precisely stated in the article.
  
  Lidocaine
   A study of five often-recommended treatments for skin pain (Maalox, 2% lidocaine gel, baby shampoo, milk, or water) concluded that:
  
  ...there was no significant difference in pain relief provided by five different treatment regimens. Time after exposure appeared to be the best predictor for decrease in pain...
   Further, recent research has found that ketamine, a sedative, is capable of blocking referred pain. The study was conducted on patients suffering from fibromyalgia, a disease characterized by joint and muscle pain and fatigue. These patients were looked at specifically due to their increased sensitivity to nociceptive stimuli. Furthermore, referred pain appears in a different pattern in fibromyalgic patients than non-fibromyalgic patients. Often this difference manifests as a difference in terms of the area that the referred pain is found (distal vs. proximal) as compared to the local pain. The area is also much more exaggerated owing to the increased sensitivity.
   Pressure wounds are often the result of local ischemia from the increased pressure. Increased pressure also plays a roles in many diabetic foot ulcerations as changes due to the disease causes the foot to suffer limited joint mobility and creates pressure points on the bottom of the foot. Effective measures to treat this includes a surgical procedure called the gastrocnemius recession in which the calf muscle is lengthened to decrease the fulcrum created by this muscle and resulting in a decrease in plantar forefoot pressure.
  
  Section::::Treatment.:Growth factors and hormones.
   A 2007 Cochrane Review stated that the evidence comparing NPWT to alternative care was flawed and required more study, but the evidence did support improved healing and called for more, better quality research to be conducted. A 2010 systematic review found "consistent evidence of the benefit of NPWT" in the treatment of diabetic ulcers of the feet. Results for bedsores were conflicting and research on mixed wounds was of poor quality, but promising. The review did not find evidence of increased significant complications. The review concluded "There is now sufficient evidence to show that NPWT is safe, and will accelerate healing, to justify its use in the treatment of diabetes-associated chronic leg wounds. There is also evidence, though of poor quality, to suggest that healing of other wounds may also be accelerated."
   Section::::Surgical technique.:Dangers.:Numbness (paresthesia).
  
  Post-operatively, local areas of numbness (paresthesia) might occur in the contoured portion(s) of the gluteal region, and might perdure for a long time after the surgery. Hence, the patient is advised to facilitate the re-sensitizing of the numb area(s) with applications of gentle massage, to prevent the development of a neuroma complication, and to alleviate pain. Nonetheless, depending upon the tissue-healing capabilities of the patient, he or she can recover in full at 2-years post-operative.
  
  Section::::Surgical technique.:Outcome.
   Repeated topical applications of capsaicin, are followed by a prolonged period of reduced skin sensibility referred to as desensitization, or nociceptor inactivation. Capsaicin not only depletes substance P but also results in a reversible degeneration of epidermal nerve fibers. Nevertheless, benefits appear modest with standard (low) strength preparations, and topical capsaicin can itself induce pain.
  
  Section::::Treatments.:Surgical Interventions.
  
  In some cases a nerve block can be used to treat.
   Further research determined that a large majority of μ-opioid-expressing neurons also expressed CCK receptors. Microinjection in the RVM with either a CCK-saporin or a dermorphin-saporin conjugate eliminated neurons expressing either receptor. Injection of the CCK-saporin conjugate also reversed allodynia and hyperalgesia in a nerve injury model, producing the same results as the dermorphin-saporin conjugate. This destruction of neurons was relatively specific, as less than 10% of neurons in the RVM were destroyed. This suggests that the targeted neurons are the ones responsible for maintaining chronic neuropathic pain states, and that the observed effect was not due to diffuse destruction of RVM neurons.
   What they found was that many herpetic areas representing the peripheral distribution of single roots or individual sections of the cord, corresponded closely with areas of referred pain from diseases of different internal organs. This led Head to conclude that irradiation of abnormal afferent impulses produces a state of excessive irritability in the grey matter of the dorsal horn at the level which they enter it. As a result of this, impulses from the skin that pass through it are exaggerated or disordered so that a stimulus that would not usually provoke a painful reaction does so.
   The mechanism by which lidocaine reduces pain in Dercum's disease is unclear. It may block impulse conduction in peripheral nerves, and thereby disconnect abnormal nervous impulse circuits. Nonetheless, it might also depress cerebral activity that could lead to increased pain thresholds. Iwane et al. performed an EEG during the administration of intravenous lidocaine. The EEG showed slow waves appearing 7 minutes after the start of the infusion and disappearing within 20 minutes after the end of the infusion. On the other hand, the pain relief effect was the greatest at about 20 minutes after the end of the infusion.
   In other words, after a peripheral nerve lesion, aberrant sprouting occurs in the dorsal horn which can explain that a non-noxious stimulus is perceived as being noxious. This is one of the explanatory models of the different mechanisms of central sensitization. Recent studies demonstrated the positive effects of the method, while applying it to CRPS's patients with allodynia. They suggest Somatosensory Rehabilitation as a good method to follow for this condition as well, no matter for how long the patient suffered from CRPS condition.
  
  Section::::Teaching.
   NGF plays a critical role in the regulation of both innate and acquired immunity. In the process of inflammation, NGF is released in high concentrations by mast cells, and induces axonal outgrowth in nearby nociceptive neurons. This leads to increased pain perception in areas under inflammation. In acquired immunity, NGF is produced by the Thymus as well as CD4+ T cell clones, inducing a cascade of maturation of T cells under infection.
  
  Section::::Function.:Ovulation.
   The Aβ fibres are from cutaneous mechanoreceptors and respond to touch stimuli; the Aδ and C fibres are nociceptor afferents which respond to painful stimuli. The touch fibres have a larger diameter than the pain fibres, which means that they transmit their action potentials much faster than the smaller diameter fibres.
  
  Section::::Gate Control Theory.
  
  Section::::Gate Control Theory.:Melzack and Wall.
  
  The Gate Control Theory of Pain, first proposed in the 1960s by Melzack and Wall, states that the concurrent activation of tactile afferent nerve fibers inhibits activation of nociceptive afferent fibres.
   In principle, an adequate intensity of stimulation is necessary to achieve pain relief with TENS. An analysis of treatment fidelity (meaning that the delivery of TENS in a trial was in accordance with current clinical advice, such as using "a strong but comfortable sensation" and suitable, frequent treatment durations) showed that higher fidelity trials tended to have a positive outcome.
   In severe or untreated cases, the tympanic membrane may perforate, allowing the pus in the middle-ear space to drain into the ear canal. If there is enough, this drainage may be obvious. Even though the perforation of the tympanic membrane suggests a highly painful and traumatic process, it is almost always associated with a dramatic relief of pressure and pain. In a simple case of acute otitis media in an otherwise healthy person, the body's defenses are likely to resolve the infection and the ear drum nearly always heals.
   In 1955, DC Sinclair and G Weddell developed peripheral pattern theory, based on a 1934 suggestion by John Paul Nafe. They proposed that all skin fiber endings (with the exception of those innervating hair cells) are identical, and that pain is produced by intense stimulation of these fibers. Another 20th-century theory was gate control theory, introduced by Ronald Melzack and Patrick Wall in the 1965 "Science" article "Pain Mechanisms: A New Theory". The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord, and that the more large fiber activity relative to thin fiber activity at the inhibitory cell, the less pain is felt.
   The principal buffers for increased volumes include CSF and, to a lesser extent, blood volume. These buffers respond to increases in volume of the remaining intracranial constituents. For example, an increase in lesion volume (e.g., epidural hematoma) will be compensated by the downward displacement of CSF and venous blood.
  
  The Monro–Kellie hypothesis is named after Edinburgh doctors Alexander Monro and George Kellie.
  
  Section::::Diagnosis.
   For example, the rhamphoid cusp "y" = "x" has a singularity of order 2 at the origin. After blowing up at its singular point it becomes the ordinary cusp "y" = "x", which still has multiplicity 2.
  
  In the previous example it was fairly clear that the singularity improved since the degree of one of the monomials defining it got smaller. This does not happen in general. 
   According to Bernard, experts do not agree on the identity of this cone and therefore it seemed better to separate it into two varieties, according to their habitat. Bernard thus mentions two Conus pulcher varieties: "C. pulcher" f. "papilionaceus" (Lightfoot, 1786) and "C. pulcher" f. "prometheus" (Lightfoot, 1786)
  
  Section::::Description.
  