Introduction
Erythromelalgia is characterized by the triad of intense burning pain, marked erythema, and increased skin temperature (1,2). Patients describe a severe tingling or neuropathy-like pain (2) that usually affects the extremities: feet more frequently than hands (1,2) but also ears and face (3). Typically it is bilateral but may be unilateral, especially in secondary cases (1). Warming, exercise and dependence on legs are aggravating factors while cooling and feet elevation are relief factors (3,4). It has often an intermittent course and the typical constellation of symptoms are only apparent during the flares (1,2) that tend to occur late in the day (sometimes they continue also through the night), at specific temperatures. Frequent ice water immersion, learned by patients as an alleviating factor, can cause skin maceration, nonhealing ulcers, infection, necrosis and finally amputation (5).
The disease’s onset can be gradual. Some cases remain mild for decades; others, about one third, have a quick beginning, start spreading and becoming disabling within months (2,6). Nonetheless even the mild cases may lead to sleep interference and limit daily activities (1). Erythromelalgia patients have higher morbidity and mortality rates when compared with the general population (2).
Erythromelalgia is a rare clinical syndrome (4): the estimated incidence varies from 0.25/100,000 in Norway (7) to 1.3/100,000 in the USA (8). Women are more frequently affected than men (2.0 to 0.6 per 100 000) (8). It is classified as either primary or secondary (1): primary erythromelalgia begins spontaneously at any age; secondary erythromelalgia is associated with other diseases (e.g. auto-immune diseases) (1). Primary erythromelalgia is catego...
... middle of paper ...
..., Chen Y, Xie NC, Wang LJ. Botulinum toxin type A for the treatment of trigeminal neuralgia: results from a randomized, double-blind, placebo-controlled trial. Cephalalgia : an international journal of headache 2012:32: 443-450.
26. Simpson LL. Identification of the characteristics that underlie botulinum toxin potency: implications for designing novel drugs. Biochimie 2000:82: 943-953.
27. Guyer BM. Mechanism of Botulinum Toxin in the Relief of Chronic Pain. Current review of pain 1999:3: 427-431.
28. Aoki KR. Review of a proposed mechanism for the antinociceptive action of botulinum toxin type A. Neurotoxicology 2005:26: 785-793.
29. Zhang L, Wang WH, Li LF, Dong GX, Zhao J, Luan JY, Sun TT. Long-term remission of primary erythermalgia with R1150W polymorphism in SCN9A after chemical lumbar sympathectomy. European journal of dermatology : EJD 2010:20: 763-767.
National Institute of Arthritis and Musculoskeletal and Skin Diseases. "Hidradenitis Suppurativa: MedlinePlus." Nlm.nih.gov/. U.S. National Library of Medicine, n.d. Web. .
Raynaud syndrome is an auto-immune disorder in which blood vessels in the digits constrict. It usually strikes females between the ages of eighteen and thirty. “Between three to five percent of people are affected.” (Harvard, 2003) There is no known cause or cure. (Segala et al, 2003) Clinical features primarily deal with (but are not limited to) the digits of the fingers. Other digits that may be affected include toes, nose, and ear lobes. Exposure to cold and emotional stress triggers the vasoconstriction of the digits. It was originally described by the Catholic, French physician Maurice Raynaud in 1862. In this condition, the vasospastic response is more frequently induced by exposure to cold temperatures and is often accompanied by digital color changes. After onset, a tri-color change [blanching (white), cyanosis (blue), and reactive hyperemia (red)] occurs. “Pallor (blanching) shows vasospasm and loss of arterial blood flow, cyanosis shows the deoxygenation of static venous blood, and rubor (red) shows reactive hyperemia following return of blood flow.” (Bowling, 2003) Theories for the causes of Raynaud syndrome include: arterial wall damage, connective tissue disease (CTD), or repetitive use of vibrational tools. (Ko, 2002)
Trigeminal Autonomic Cephalalgias (TACs) are highly interesting to me: This group of unilateral, excruciating primary headaches is accompanied by ipsilateral cranial autonomic symptoms and comprises of three major forms:
It has been shown that intrathecal administriton of GABA receptor antagonists cause hyperalgesia and allodynia. Constitutive, the increase in the endogenous GABA activity in the spinal cord alleviate pain resulting from noxious and innoxious mechanical and thermal stimuli. Different GABA receptors have different roles in alleviating thermal and mechanical pain in different animal pain models. There is no study to date that has examined the involvement of GABA A and GABA B in sensory dimension of neuropathic pain resulting from compression of spinal cord. The current study tests the hypothesis that GABA A or GABA B receptors contributes to the allodynia and hyperalgesia observed after spinal cord injury. The results showed that the effect of GABA A and GABA B receptors on mechanical hyperalgesia is similar but these receptors have different effects on thermal hyperalgesia. While using baclofen as GABA B receptor agonist does not affect the thermal pain, thermal hyperalgesia resulting from spinal cord injury was greatly alleviated by different doses of GABA A agonist, muscimol. Both Baclofen and muscimol are able to reduce the mechanical and cold allodynia has been seen after spinal cord injury but the effect of baclofen is dose dependent with no effect in higher doses used in this study. While almost all doses of muscimol were used in this study reduce the amount of cold and mechanical allodynia. The other result obtained in this study is the short term effect of GABA agonist. The anitinociceptive effect of Baclofen and muscimol appear to be maxium at 15 min after injection and gradually diminished by time and their analgesic effect disappeared 3 hours after injection.
P3 – Describe the investigations that are carried out to enable the diagnosis of these physiological disorders
As stated in Chan-Tack and Bartlett’s article Botulism, “The incidence of foodborne botulism is approximately 24 cases per year. The incidence of wound botulism is 3 cases per year. The incidence of infant botulism is 71 cases per year, with a mean age of 3 months.” (2010). In addition, in merely fifteen percent of the Clostridium botulinium outbreaks are the toxin type undetermined. The first case descriptions of botulism were reported by Dr. Justinus Kerner, a German physician, in 1822. He had conducted experiments on himself and laboratory animals, which gave him this case findings (Taillac, & Kim, 2010).
A. Chronic pain signifies a developing public health issue of huge magnitudes, mainly in view of aging populations in developed countries (Russo).
Even over the short course of my clinical experience thus far, various consultants have asked my colleagues and I about the pathophysiology of AF, the causes of AF and most have been asked to describe the rhythm of the pulse of AF. Hospital doctors do not have to look far to find a patient with the often symptom less disorder, and quiz medical students on it. A study conducted in Trinity College, Dublin by Finucane et al (2011) reported that 10.8% of Irish men over the age of 80 are living with AF2. They also reported prevalence across all age groups of 3.2%. AF is highly prevalent in Ireland today, and is set to become more prevalent in the country, in keeping with our agei...
JIU-CONG, Z., LI, S.,& QING-HE, N. (2010). Botulism, where are we now?. Clinical Toxicology (15563650), 48(9), 867-879. doi: 103109/15563650.2010.535003
The most common and well described pain transmission is “gate control theory of pain”. This theory was first proposed by Melzack and Wall in 1965 whereby they used the analogy of gate to explain the inhibition of pain which exists within the dorsal horn of the spinal cord. For instance, when tissue damage occurs, substances such as prostaglandin, serotonin, histamine and bradykinin are released from the injured cell. Individual usually consume or apply pain medications such as NSAIDs whereby these medications will cause electrical nerve impulse at the end of the sensory nerve fiber via nociceptor. Nociceptor is a pain receptor that is commonly found in the skin, cornea of eye and organ of motion such as muscles and ligaments. These nerve impulses
In the United States 54 million people have a disability and only 15 percent were born with a disability (Jaeger & Bowman, 2005). If a person lives long enough, it is statistically likely that they will develop some kind of disability in their advancing years (Jaeger & Bowman, 2005). At some point in your life you could have experience a fractured bone, a minor cut, or had some type of surgery. Imagine after some minor injury that you may not even remember and then experiencing a constant pain so agonizing that no amount of pain medication can make you comfortable (Lang & Moskovitz, 2003). Some additional symptoms that you may also experience are severe burning pain, changes in bone and skin, excessive sweating, tissue swelling and extreme sensitivity to touch (Juris, 2005). These symptoms are associated with a disease that is called Reflex Sympathetic Dystrophy (RSD) but more recently termed as complex regional pain syndrome, type 1 (CRPS 1) (Juris, 2005). For simplification purposes this disease will be referred to as RSD throughout this paper.
Fibromyalgia is not a new disease that has just surfaced, it has been around for a long time, it just didn’t have a name and was not recognized for what it truly was. It was...
Wilson, J.F. (2005). Is sleep the new vital sign? Annals of Internal Medicine, 142 (10), 877-880.
Simple musculoskeletal back pain has symptoms of pain in the lumbrasacral area of the back (Jackson & Simpson, 2006). The upper thighs and knees are also known to be affected (Jackson & Simpson, 2006). This pain is usually described as a dull pain (Jackson & Simpson, 2006). Spinal nerve root pain is localised down the leg, and usually continues below the knee and into the feet (Jackson & Simpson, 2006). It has been d...
According to the 2010 paper by Dubin et. al, microneurography recordings in peripheral nerve fibers revealed that A - axon fibers are myelinated and quickly send action potentials to travel towards the central system (acute pain), while C - axon fibers are non-myelinated and send slower action potentials (extended pain) (Dubin et.al, 2010). According to Basbaum et. al 2009, when neurons were taken from dissociated DRG and cultured, both A and C fiber nociceptors had noxious heat thresholds of 43 C. Furthermore, by cloning the capsaicin receptor: when 43 C heat thresholds were exceeded by capsaicin, its respective heat receptor called TRPV1 was activated and caused subsequent depolarization of A and C fiber nociceptors, leading to painful sensation (Basbaum et. al,