Discussions By Condition: Skin conditions

Unbearable skin sensitivity to touch

Posted In: Skin conditions 11 Replies
  • Posted By: Anonymous
  • March 7, 2007
  • 10:25 PM

I'm 19 years old now. This is something that I've had for several years, and it has gotten progressively worse. Basically, when I'm not moving or doing something, I become conscious of the skin on my neck and anything touching it will make me go crazy. It's not that it burns or stings or itches, it's just uncomfortable. It's worst when I sleep, and in the past it would be the collar of a shirt that would irritate it. So I stopped wearing a shirt to sleep. Now air blowing on it will make me feel uncomfortable, so I have to sleep with a hand covering my neck so that I will feel I have control over what touches it. When I was a child, wearing a collared shirt would drive me insane. It's really hard to describe and I've never heard of anyone else with this problem.

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  • I too have skin sensitivity. It is comes and goes, usually in the same general location (my right thigh up to my lower crotch area. Sometimes it lasts days and my upper leg joint gets achy. There is no rash or anything visible.Any ideas?
    Anonymous 42789 Replies Flag this Response
  • I have this, too. It seems to have gotten worse as I get older. I never really noticed these problems when I was young. But as I got a bit older, into my teens, I could no longer wear turtle neck shirts. I then started to become very conscious about the sensitivity of my neck in my early 20's. These neck sensitivity thing comes and goes away. After I had my hair cut short in my mid-20's, it's gotten worse. I think it has something to do with my short hair touching my neck. But again, it comes and goes away. I'm in my late 20's now and it's becoming a problem for me lately. This discomfort is causing me a stiff neck and other problems while trying to not move my neck too much so that nothing would touch it...it is hard to explain. But from all this, I do think it's more of a mental thing than a physiological problem. I noticed that this problem happens to only the left side of my neck. However, if I start to intentionally think about or start to notice the right side of my neck, I could feel the same discomfort. I think to stop the discomfort is to train the brain to stop thinking about the sensitivity of the neck. It's very hard, but I think that's what's happening.
    Anonymous 42789 Replies Flag this Response
  • I too have sensitivity to my neck, but only on the right side and only when some one else touches it, if I touch it no problem, someone else I feel like there is a chainsaw behind my head. I have to cut my own hair because it's so uncomfortable for someone else to do it. The last time I got a haircut I was shaking and sweating and the woman kept asking me if I was alright, I was I just couldn't control it. So now I do it myself rather then explain every time. If anyone figures out what it is let me know! justin2@maine.rr.com
    Anonymous 42789 Replies Flag this Response
  • i was googling neck sensitivity when i found this. i have this problem to. i wont notice for months then suddenly my neck is super hypersensitive. when i was a kid they told me it was because i subconsciously hated myself...what idiots. im a very positive person. anyway, i too have to keep a hand on it sometimes
    Anonymous 42789 Replies
    • September 30, 2009
    • 07:08 PM
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  • thats how i describe it too" that creepy feeling you get when watching a horror movie"email me and lets talk about itbryanandmikki@gmail.com
    Anonymous 42789 Replies
    • September 30, 2009
    • 07:10 PM
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  • Presently i am 18 y/o and this skin's hypersensitivity started just a year later. it was accompanied by asthma when i first experienced this "allergy". I don't really know if it is an allergy because i don't even know its cause.I get so itchy all over my body... but the worst part there is that i cant scratch the itchy parts because the more i scratch it, the more it will become itchy.when i comb my hair, my head becomes itchy because the traces of the comb on my scalp become rashes.According to one of the doctors i have consulted, it's just because of my skin's hypersensitivity.To get a relief from itch, i am taking cetirizine tablet and the itch somehow disappears.but the patch redness of my skin when being touch a bit harder is still there...:(This skin condition gives me sleepless nights and uneasy feeling...I am hoping for a reply of somebody who has the same conditionor anybody who knows the cure.If not the cure,the cause.Thank you very muchmail me at:jemcayetano@ymail.com
    Anonymous 42789 Replies
    • October 30, 2009
    • 05:49 AM
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  • please help me. i completely related to the first post. i spend most days trying to not wear shirts and trying to keep my hair off of my neck. if someone finds out any clue to what this is , i beg you to respond.
    Anonymous 42789 Replies Flag this Response
  • I know this sounds odd but I too experienced the same thing but in spots about 3 of them on my left side torso ~1 in diameter and one on my neck- it made me miserable. I went to a chiropractor for a different reason and just mentioned it in passing to him and after a few minor adjustments relieved a lot of the irritation. My sensitivity I guess the best way to describe it was under the skin, an itch I couldn't itch but the slight touch of a shirt would irritate it. I was embarrassed and miserable. The adjustments stopped it though it had to do with the nerve flow in my spinal chord. hope this helps someone, I looked a long time for an answer and never really found anything till this.
    Anonymous 42789 Replies Flag this Response
  • please help me. i completely related to the first post. i spend most days trying to not wear shirts and trying to keep my hair off of my neck. if someone finds out any clue to what this is , i beg you to respond.I can also relate to the first post and to this one. I am 60 years old now and have had this problem for as long as i can remember,It seems to be completely random as to when it happens and i suffer with it for a few days and then it dissappears again. I cannot bear anything to touch my neck, and even a wind can set it off. During the day it is mainly ok but its at night that it really plays up, as soon as i relax and try to sleep it gives a real twitch and i have to get up again or else it just gets more and more intense. Keeping moving seems to lessen the intensity of it. The sensation is very hard to describe, its not pain or itching but it certainly is unbearable. If anyone would like to contact me further my email is.... philip_wilkin@hotmail.com
    Anonymous 42789 Replies
    • September 3, 2010
    • 11:22 AM
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  • http://juniorprof.wordpress.com/2008/07/05/what-is-hyperalgesia-what-is-allodynia/What is hyperalgesia? What is allodynia?Posted on July 5, 2008 by juniorprof| 27 CommentsTwo of the most commonly used terms in the pain research and medicine world are hyperalgesia and allodynia. The word hyperalgesia means an increased response to a painful stimulus. The word allodynia means a painful response to a normally innocuous stimulus.Here is an example of hyperalgesia: if your arm was pricked by a pin and you said that it gave you 3 out of 10 pain this would be your baseline response. If an experimenter then gave you some injection (let’s say capsaicin — the pungent ingredient in hot peppers) and then 30 minutes later pricked you with the pin again and you reported 6 out of 10 pain this would be hyperalgesia. For hyperalgesia to occur it is important for the stimulus to be painful to begin with. Remember that hyperalgesia is always an increased pain response to a noxious stimulus.Here is an example of allodynia: if an experimenter brushed your arm with a cotton bud (like a q-tip) you would almost certainly say that the stimulus was not painful — 0 out of 10. If the experimenter then injected your arm with capsaicin and brushed your arm again 30 minutes later you would likely report that it was painful — let’s say 4 out of 10 pain. This is an allodynia, a painful response to an innocuous stimulus. In order for allodynia to occur the stimulus MUST NOT normally be painful.So now that we know what these word mean it is time to understand why they occur. First of all, there are a variety of pain conditions where one of these conditions is present but not the other. This is because they are mechanistically different. Sensory neurons that innervate your skin and visceral organs roughly fall into three categories: 1) Rapidly adapting mechanotransducers. These are neurons that respond to touch and non-noxious temperatures, they conduct action potentials (or nerve impulses) rapidly and they make a subset of nerve fibers called A-beta fibers. 2) Proprioceptive neurons. These are neurons that tell you about the position of your muscles, they also conduct action potentials rapidly and they comprise the other subset of nerve fibers called A-beta fibers. 3) Nociceptors. These are pain sensing neurons that respond to painful mechanical or thermal stimulation. They also comprise the class of neurons that respond to chemical irritants (like capsaicin). They are lightly or unmyelinated so they conduct action potentials more slowly than A-beta fibers. They also generally fail to adapt to stimulation so they keep firing until the stimulus is removed or escaped from. These neurons fall into two classes, A-delta (the lightly myelinated ones) or C-fibers (the unmyelinated ones). Neurons of all of these classes send a projection into the dorsal horn of the spinal cord where processing of incoming sensory information first occurs (all you neuroscientists forget about A-betas and the dorsal funiculus, they send a projection to lamina III as well where they synapse on interneurons that send projections back into lamina I/II). This processing center in the dorsal horn of the spinal cord is commonly referred to as “the gate” — a term that was spawned from Melzack and Wall’s famous gate theory of pain control. These signals are then sent onto the brain where sensory perception occurs.The physiological basis of hyperalgesia and allodynia lies in the distinction between the type of fibers that carry the information evoked by the stimulus in the periphery.HYPERALGESIA:Remember that hyperalgesia always involves a noxious stimulus, it just becomes more painful when hyperalgesia is present. The noxious stimulus activates nociceptors in the periphery that then send the signal onto the spinal cord. Hyperalgesia involves an amplification of the pain signal. This amplification can occur in the periphery (e.g. the nociceptor is sensitized by an irritant, by inflammation or by disease) or in the spinal cord (via an amplification of synaptic transmission between the nociceptor and the dorsal horn neuron that sends the signal to the brain) or in both locations. There are some cases where the amplification is thought to occur in higher brain centers as well. This can happen, for instance, after a stroke. We will talk more about mechanisms of amplification and there promise for therapy in a later post.ALLODYNIA:Allodynia involves a noxious response to an innocuous stimulus (think putting on a shirt with a severe sunburn). Because the stimulus is innocuous, and generally of the mechanical variety, it could be carried by rapidly adapting mechanotransducers or by sensitized nociceptors. These two possibilities have been the focus of decades of research both in humans and in animals. While there is evidence that the information can be carried by sensitized nociceptors this is quite controversial. Our current understanding of allodynia suggests that nociceptor mechanical thresholds do not change enough for them to carry information concerning light touch, brush or gentle vibration in conditions where allodynia is present. Rather, it appears that rapidly adapting mechanotransducers (or A-beta fibers) continue to be the sole carrier of this information in conditions where allodynia is present. The change that causes allodynia occurs in the spinal cord. Through an unknown process, A-beta-fibers gain access to the nociceptive channel. In normal conditions A-beta-fibers cannot activate dorsal horn neurons that respond only to painful stimulation. In allodynic conditons, these same neurons begin to receive input from A-beta-fibers. This allows for A-beta-mediated information to gain access to the nociceptive channel thereby stimulating the perception of pain in the brain. Because allodynia can occur rapidly it is unlikely that this change is mediated by a physical change in the connections of neurons in the dorsal horn (although this may occur over the longer term). Rather, it appears that there are changes in the neurochemistry of the “gate” such that inhibitory neurotransmission can switch to excitation. Because GABA (the primary inhibitory neurotransmitter in the brain) can switch from inhibition to excitation (or vice-a-versa) in certain conditions (like epilepsy and during early neural development) much current focus is on the role of GABA in allodynia.In chronic pain conditions both allodynia and hyperalgesia are major problems for these patients. Small movements, putting on or wearing clothes and even sitting or laying down can become very painful due to allodynia. Patients are often able to avoid hyperalgesia but hyperalgesia can be so intense that it causes an aversion to even the most mundane of activities for fear of triggering an attack. In the chronic pain patient both of these conditions are extremely difficult to treat. Allodynia is notoriously resistant to opiate and NSAID analgesics especially in conditions involving a peripheral neuropathy caused by injury or disease (like diabetes).To wrap up:Hyperalgesia is an increased response to a noxious stimulus. It is caused by sensitization of peripheral nociceptors and/or by sensitization of central neurons that carry nociceptive information.Allodynia is a painful response to a non-painful stimuli. It is caused by a change in the dorsal horn of the spinal cord that gives non-noxious sensory information access to the nociceptive system causing innocuous stimuli to be perceived as painful.
    Anonymous 42789 Replies
    • January 9, 2011
    • 04:28 PM
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  • AllodyniaFrom Wikipedia, the free encyclopediaJump to: navigation, search Allodynia, meaning "other pain", is a pain due to a stimulus which does not normally provoke pain and can be either thermal or mechanical. It is pain from a stimulus that does not normally lead to the sensation of pain, and often occurs after injury to a site. Allodynia is different from hyperalgesia, an extreme reaction to a stimulus which is normally painful.Contents• 1 Types• 2 Causes• 3 Pathophysiology o 3.1 Cellular levelo 3.2 Molecular level• 4 Treatment o 4.1 Endogenous body mechanisms for reducing paino 4.2 Drugs• 5 References TypesThere are different kinds or types of allodynia:• Mechanical allodynia (also known as tactile allodynia) o Static mechanical allodynia – pain in response to light touch/pressureo Dynamic mechanical allodynia – pain in response to brushing• Thermal (hot or cold) allodynia – pain from normally mild skin temperatures in the affected area CausesAllodynia is a clinical feature of many painful conditions, such as neuropathies, complex regional pain syndrome, postherpetic neuralgia, fibromyalgia, and migraine. Allodynia may also be caused by some populations of stem cells used to treat nerve damage including spinal cord injury. One of the etiology of static mechanical allodynia is A-beta fibers lesions: Static mechanical allodynia is a paradoxical painful hypoaesthesia. Pathophysiology Cellular levelThe cell types involved in nociception and mechanical sensation are the cells responsible for allodynia. In healthy individuals, nociceptors sense information about cell stress or damage and temperature at the skin and transmit it to the spinal cord. The cell bodies of these neurons lie in dorsal root ganglia, important structures located on both sides of the spinal cord. The axons then pass through the dorsal horn to make connections with secondary neurons. The secondary neurons cross over to the other (contralateral) side of the spinal cord and reach nuclei of the thalamus. From there, the information is carried through one or more neurons to the somatosensory cortex of the brain. Mechanoreceptors follow the same general pathway. However, they do not cross over at the level of the spinal cord, but at the lower medulla instead. In addition, they are grouped in tracts that are spatially distinct from the nociceptive tracts.Despite this anatomical separation, mechanoreceptors can influence the output of nociceptors by making connections with the same interneurons, the activation of which can reduce or completely eliminate the sensation of pain. Another way to modulate the transmission of pain information is via descending fibers from the brain. These fibers act through different interneurons to block the transmission of information from the nociceptors to secondary neurons.Both of these mechanisms for pain modulation have been implicated in the pathology of allodynia. Several studies suggest that injury to the spinal cord might lead to loss and re-organization of the nociceptors, mechanoreceptors and interneurons, leading to the transmission of pain information by mechanoreceptors A different study reports the appearance of descending fibers at the injury site. All of these changes ultimately affect the circuitry inside the spinal cord, and the altered balance of signals probably leads to the intense sensation of pain associated with allodynia.Different cell types have also been linked to allodynia. For example, there are reports that microglia in the thalamus might contribute to allodynia by changing the properties of the secondary nociceptors. The same effect is achieved in the spinal cord by the recruitment of immune system cells such as monocytes/macrophages and T lymphocytes. Molecular levelThere is a strong body of evidence that the so called sensitization of the central nervous system contributes to the appearance of allodynia. Sensitization refers to the increased response of neurons following repetitive stimulation. In addition to repeated activity, the increased levels of certain compounds lead to sensitization, as well. The work of many researchers has led to the elucidation of pathways that can result in neuronal sensitization both in the thalamus and dorsal horns. Both pathways depend on the production of chemokines and other molecules important in the inflammatory response.A very important molecule in the thalamus appears to be cysteine-cysteine chemokine ligand 21 (CCL21). The concentration of this chemokine is increased in the ventral posterolateral nucleus of the thalamus where secondary nociceptive neurons make connections with other neurons. The source of CCL21 is not exactly known, but two possibilities exist. First, it might be made in primary nociceptive neurons and transported up to the thalamus. Most likely, neurons intrinsic to the ventral posterolateral nucleus make at least some of it. In any case, CCL21 binds to C-C chemokine receptor type 7 and chemokine receptor CXCR3 receptors on microglia in the thalamus. The physiologic response to the binding is probably the production of prostaglandin E2 (PGE2) by cyclooxygenase 2 (COX-2). Activated microglia making PGE2 can then sensitize nociceptive neurons as manifested by their lowered threshold to pain.The mechanism responsible for sensitization of the central nervous system at the level of the spinal cord is different from the one in the thalamus. Tumor necrosis factor-alpha (TNF-alpha) and its receptor are the molecules that seem to be responsible for the sensitization of neurons in the dorsal horns of the spinal cord. Macrophages and lymphocytes infiltrate the spinal cord, for example, because of injury, and release TNF-alpha and other pro-inflammatory molecules. TNF-alpha then binds to the TNF receptors expressed on nociceptors, activating the MAPK/NF-kappa B pathways. This leads to the production of more TNF-alpha, its release, and binding to the receptors on the cells that released it (autocrine signalling). This mechanism also explains the perpetuation of sensitization and thus allodynia. TNF-alpha might also increase the number of AMPA receptors, and decrease the numbers of GABA receptors on the membrane of nociceptors, both of which could change the nociceptors in a way that allows for their easier activation. Another outcome of the increased TNF-alpha is the release of PGE2, with a mechanism and effect similar to the ones in the thalamus. Treatment Endogenous body mechanisms for reducing painAs already mentioned, there are descending neurons that modulate the perception of pain. Many of these neurons originate in nuclei in the brainstem and pass through the periaqueductal gray (PAG) area of the midbrain.The body possesses an additional mechanism to control pain: the release of endogenous opioids, especially at the level of the PAG. There are neurons that release enkephalins, endorphins, and dynorphins at the PAG, and in this way modulate its ability to modulate pain perception. Other neurons can release their endogenous opioids at the source of the pain, as well. If this occurs, the transmission of pain information from the nociceptors to the secondary neurons is blocked, and no pain is felt. Unfortunately, these endogenous mechanisms are often damaged and nonfunctional in people suffering from allodynia, so the application of pharmaceuticals is needed. DrugsNumerous compounds alleviate the pain from allodynia. Some are specific for certain types of allodynia while others are general. They include:Dynamic mechanical allodynia - compounds targeting different ion channels; opioids• Mexiletine• Lidocaine (IV/topical)• Tramadol• Morphine (IV)• Alfentanil (IV)• Ketamine (IV)• Methylprednisone (intrathecal)• Adenosine• Glycine antagonist• Desipramine• VenlafaxineStatic mechanical allodynia - sodium channel blockers, opioids• Lidocaine (IV)• Alfentanil (IV)• Adenosine (IV)• Ketamine (IV)• Glycine antagonist• VenlafaxineCold allodynia• Lamotrigine• Lidocaine (IV)The list of compounds that can be used to treat allodynia is even longer than this. For example, many non-steroidal anti-inflammatory drugs, such as naproxen, can inhibit COX-1 and/or COX-2, thus preventing the sensitization of the central nervous system. Another effect of naproxen is the reduction of the responsiveness of mechano- and thermoreceptors to stimuli.Other compounds act on molecules important for the transmission of an action potential from one neuron to another. Examples of these include interfering with receptors for neurotransmitters or the enzymes that remove neurotransmitters not bound to receptors.YM-230888 is a compound that can bind to one of the metabotropic receptors, preventing glutamate from binding and the transmission of the signal. This compound can also overcome the blood-brain barrier, allowing it to be useful in the thalamus.Endocannabinoids are molecules that can relieve pain by modulating nociceptive neurons. When anandamide, an endocannabinoid, is released, pain sensation is reduced. Anandamide is later transported back to the neurons releasing it using transporter enzymes on the plasma membrane, eventually disinhibiting pain perception. However, this re-uptake can be blocked by AM404, elongating the duration of pain inhibition.
    Anonymous 42789 Replies
    • January 9, 2011
    • 04:35 PM
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