question: what makes pain differentiate into various sensations such as shooting, stabbing, throbbing, aching, sharp, dull, etc?
comment: How big the area causing the pain is, plus the method of damage of the tissue e.g. are the cells too hot, or physically cut, and therefore which types of nerve cells are stimulated (e.g. A-d fibres can be stimulated by mechanical or thermal stimuli, or C fibres which can be mechanical, thermal or chemical). Some nerve fibres have special coatings (myelination) which allows the signal to travel faster e.g. A-d pain fibres
passages: Section::::Theory.:Three dimensions of pain.
  
  In 1968 Ronald Melzack and Kenneth Casey described chronic pain in terms of its three dimensions:
  
  BULLET::::- "sensory-discriminative" (sense of the intensity, location, quality and duration of the pain),
  
  BULLET::::- "affective-motivational" (unpleasantness and urge to escape the unpleasantness), and
  
  BULLET::::- "cognitive-evaluative" (cognitions such as appraisal, cultural values, distraction and hypnotic suggestion).
   There are two main types of pain that we experience in our bodies: pain caused by damage of body tissue and pain caused by nerve damage. Nociceptive pain serves as a warning or signal for tissue damage and works to preserve the body’s equilibrium and functionality. This pain is signaled by the interworkings of both the peripheral and central nervous systems. Another type of pain, known as neuropathic pain, is caused by a direct problem or disease that affects the nerves in the central nervous system.
   Section::::Interoceptive physiology.:Nociceptive system.
  
  Nociception refers to the receiving and processing of pain inducing stimuli by the central nervous system. Functional brain imaging studies during painful stimulation of the skin with heated probes, during mechanical compression, and electric shock have suggested that the insular cortex is prominently activated during pain processing. Thus while pain was once thought of as an exteroceptive sensation, based on functional imaging and anatomical evidence it is now understood that it has an interoceptive component.
  
  Section::::Interoceptive physiology.:Thermoregulatory system.
   Hyperexcitability hypothesizes that referred pain has no central mechanism. However, it does say that there is one central characteristic that predominates. Experiments involving noxious stimuli and recordings from the dorsal horn of animals revealed that referred pain sensations began minutes after muscle stimulation. Pain was felt in a receptive field that was some distance away from the original receptive field. According to hyperexcitability, new receptive fields are created as a result of the opening of latent convergent afferent fibers in the dorsal horn. This signal could then be perceived as referred pain.
   Nociceptive pain may also be classed according to the site of origin and divided into "visceral", "deep somatic" and "superficial somatic" pain. Visceral structures (e.g., the heart, liver and intestines) are highly sensitive to stretch, ischemia and inflammation, but relatively insensitive to other stimuli that normally evoke pain in other structures, such as burning and cutting. Visceral pain is diffuse, difficult to locate and often referred to a distant, usually superficial, structure. It may be accompanied by nausea and vomiting and may be described as sickening, deep, squeezing, and dull. "Deep somatic" pain is initiated by stimulation of nociceptors in ligaments, tendons, bones, blood vessels, fasciae and muscles, and is dull, aching, poorly-localized pain. Examples include sprains and broken bones. "Superficial" pain is initiated by activation of nociceptors in the skin or other superficial tissue, and is sharp, well-defined and clearly located. Examples of injuries that produce superficial somatic pain include minor wounds and minor (first degree) burns.
   "Nociceptive" pain is a physiological response described as stabbing, throbbing, aching, or sharp. Nociceptive pain is considered to be an appropriate to painful stimuli that occurs as a result from underlying tissue damage and may be acute or chronic. Nociceptive pain that is persistent may due to conditions causing ongoing tissue damage such as ischemia, or edema.
  
  "Neuropathic" pain is associated with chronic pain and results from a nervous system dysfunction, which causes an inappropriate response to pain. Neuropathic pain is described as burning or tingling persistent pain.
   Section::::Mechanism.:Thalamic-convergence.
  
  Thalamic convergence suggests that referred pain is perceived as such due to the summation of neural inputs in the brain, as opposed to the spinal cord, from the injured area and the referred area. Experimental evidence on thalamic convergence is lacking. However, pain studies performed on monkeys revealed convergence of several pathways upon separate cortical and subcortical neurons.
  
  Section::::Laboratory testing methods.
   Nerves are categorized into three groups based on the direction that signals are conducted:
  
  BULLET::::- "Afferent nerves" conduct signals from sensory neurons to the central nervous system, for example from the mechanoreceptors in skin.
  
  BULLET::::- "Efferent nerves" conduct signals from the central nervous system along motor neurons to their target muscles and glands.
  
  BULLET::::- "Mixed nerves" contain both afferent and efferent axons, and thus conduct both incoming sensory information and outgoing muscle commands in the same bundle.
  
  Nerves can be categorized into two groups based on where they connect to the central nervous system:
   Spontaneous pain or allodynia (pain resulting from a stimulus which would not normally provoke pain, such as a light touch of the skin) is not limited to the territory of a single peripheral nerve and is disproportionate to the inciting event.
  
  BULLET::::1. There is a history of edema, skin blood flow abnormality, or abnormal sweating in the region of the pain since the inciting event.
  
  BULLET::::2. No other conditions can account for the degree of pain and dysfunction.
   Although thresholds for touch-position perception are relatively easy to measure, those for pain-temperature perception are difficult to define and measure. "Touch" is an objective sensation, but "pain" is an individualized sensation which varies among different people and is conditioned by memory and emotion. Anatomical differences between the pathways for touch-position perception and pain-temperature sensation help explain why pain, especially chronic pain, is difficult to manage.
  
  Section::::Trigeminal nucleus.
   From a stimulus-response perspective, the perception of physical pain starts with the nociceptors, a type of physiological receptor that transmits neural signals to the brain when activated. These receptors are commonly found in the skin, membranes, deep fascias, mucosa, connective tissues of visceral organs, ligaments and articular capsules, muscles, tendons, periosteum, and arterial vessels. Once stimuli are received, the various afferent action potentials are triggered and pass along various fibers and axons of these nociceptive nerve cells into the dorsal horn of the spinal cord through the dorsal roots. A neuroanatomical review of the pain pathway, "Afferent pain pathways" by Almeida, describes various specific nociceptive pathways of the spinal cord: spinothalamic tract, spinoreticular tract, spinomesencephalic tract, spinoparabrachial tract, spinohypothalamic tract, spinocervical tract, postsynaptic pathway of the spinal column.
   Nociception (physiological pain) signals nerve-damage or damage to tissue. The three types of pain receptors are cutaneous (skin), somatic (joints and bones), and visceral (body organs). It was previously believed that pain was simply the overloading of pressure receptors, but research in the first half of the 20th century indicated that pain is a distinct phenomenon that intertwines with all of the other senses, including touch. Pain was once considered an entirely subjective experience, but recent studies show that pain is registered in the anterior cingulate gyrus of the brain. The main function of pain is to attract our attention to dangers and motivate us to avoid them. For example, humans avoid touching a sharp needle, or hot object, or extending an arm beyond a safe limit because it is dangerous, and thus hurts. Without pain, people could do many dangerous things without being aware of the dangers.
   Section::::Classification.:Nociceptive.
  
  Nociceptive pain is caused by stimulation of sensory nerve fibers that respond to stimuli approaching or exceeding harmful intensity (nociceptors), and may be classified according to the mode of noxious stimulation. The most common categories are "thermal" (e.g. heat or cold), "mechanical" (e.g. crushing, tearing, shearing, etc.) and "chemical" (e.g. iodine in a cut or chemicals released during inflammation). Some nociceptors respond to more than one of these modalities and are consequently designated polymodal.
   Section::::Mechanism of action.
  
  Nociceptive pain is immediate pain felt as a result of injury inflicted upon tissue. Neuropathic pain, in contrast, is long-lasting pain that develops when the peripheral and the central nervous system are sensitized following injury to these systems. Neuropathic pain may be continuous pain, spontaneous, or pain caused by hypersensitivity to non-nociceptive levels of stimulus.
   Section::::Role in neuropathic pain.
  
  Activation of nociceptors is not necessary to cause the sensation of pain. Damage or injury to nerve fibers that normally respond to innocuous stimuli like light touch may lower their activation threshold needed to respond; this change causes the organism to feel intense pain from the lightest of touch. Neuropathic pain syndromes are caused by lesions or diseases of the parts of the nervous system that normally signal pain. There are four main classes: 
  
  BULLET::::- peripheral focal and multifocal nerve lesions
  
  BULLET::::- traumatic, ischemic or inflammatory
  
  BULLET::::- peripheral generalized polyneuropathies
   Nociceptive pain may be divided into "superficial" and "deep", and deep pain into "deep somatic" and "visceral". "Superficial" pain is initiated by activation of nociceptors in the skin or superficial tissues. "Deep somatic" pain is initiated by stimulation of nociceptors in ligaments, tendons, bones, blood vessels, fasciae and muscles, and is dull, aching, poorly-localized pain. "Visceral" pain originates in the viscera (organs). Visceral pain may be well-localized, but often it is extremely difficult to locate, and several visceral regions produce "referred" pain when damaged or inflamed, where the sensation is located in an area distant from the site of pathology or injury.
   Depending on the sensation associated with neuropathic pain, it may be considered as acute or chronic. Acute neuropathic pain is associated with burning, squeezing, throbbing, shooting, or electric shock sensations that resolve. Neuropathic sensations such as numbness, tingling, and prickling are considered as chronic neuropathic pain. Chronic neuropathic pain may be intermittent or continuous, and may remain unresolved post tissue healing.
  
  Section::::Classifications.
   Sensory feelings, especially pain, are stimuli that can elicit a large response and cause neurological changes in the body. Pain also causes a behavioral change in the body, which is proportional to the intensity of the pain. The feeling is recorded by sensory receptors on the skin and travels to the central nervous system, where it is integrated and a decision on how to respond is made; if it is decided that a response must be made, a signal is sent back down to a muscle, which acts appropriately according to the stimulus. The postcentral gyrus is the location of the primary somatosensory area, the main sensory receptive area for the sense of touch.
   The pain signal travels from the periphery to the spinal cord along an A-delta or C fiber. Because the A-delta fiber is thicker than the C fiber, and is thinly sheathed in an electrically insulating material (myelin), it carries its signal faster (5–30 m/s) than the unmyelinated C fiber (0.5–2 m/s). Pain evoked by the A-delta fibers is described as sharp and is felt first. This is followed by a duller pain, often described as burning, carried by the C fibers. These "first order" neurons enter the spinal cord via Lissauer's tract.
   Neuropathic pain is divided into "peripheral" (originating in the peripheral nervous system) and "central" (originating in the brain or spinal cord). Peripheral neuropathic pain is often described as "burning", "tingling", "electrical", "stabbing", or "pins and needles".
  
  Section::::Causes.
  
  Section::::Causes.:Pathophysiology.
   Section::::Pressure modality.:Somatosensory information.:Mechanoreceptors.
  
  There are four types of mechanoreceptors: Meissner corpuscles and merkel cell neurite complexes, located between the epidermis and dermis, and Pacinian corpuscles and Ruffini endings, located deep within the dermis and subcutaneous tissue. Mechanoreceptors are classified in terms of their adaptation rate and the size of their receptive field. Specific mechanoreceptors and their functions include:
  
  BULLET::::- Thermoreceptors that detect changes in skin temperature.
  
  BULLET::::- Kinesthetic receptors detect our movements and the position of our limbs.
  
  BULLET::::- Nociceptors that have bare nerve endings that detect tissue damage and give the sensation of pain.
  
  Section::::Pressure modality.:Tests.
   Nociceptors respond to potentially damaging stimuli by sending signals to the spinal cord and brain. This process, called nociception, usually causes the perception of pain. They are found in internal organs, as well as on the surface of the body. Nociceptors detect different kinds of damaging stimuli or actual damage. Those that only respond when tissues are damaged are known as "sleeping" or "silent" nociceptors.
  
  BULLET::::- Thermal nociceptors are activated by noxious heat or cold at various temperatures.
  
  BULLET::::- Mechanical nociceptors respond to excess pressure or mechanical deformation.
   Pain receptors are known as nociceptors. Two main types of nociceptors exist, A-fiber nociceptors and C-fiber nociceptors. A-fiber receptors are myelinated and conduct currents rapidly. They are mainly used to conduct fast and sharp types of pain. Conversely, C-fiber receptors are unmyelinated and slowly transmit. These receptors conduct slow, burning, diffuse pain.
   BULLET::::- Referred pain is often experienced on the same side of the body as the source, but not always.
  
  Section::::Mechanism.
  
  There are several proposed mechanisms for referred pain. Currently there is no definitive consensus regarding which is correct. The cardiac general visceral sensory pain fibers follow the sympathetics back to the spinal cord and have their cell bodies located in thoracic dorsal root ganglia 1-4(5).
  
  As a general rule, in the thorax and abdomen, general visceral afferent (GVA) pain fibers follow sympathetic fibers back to the same spinal cord segments that gave rise to the preganglionic sympathetic fibers.
   Section::::Mechanism.:Convergent-projection.
  
  This represents one of the earliest theories on the subject of referred pain. It is based on the work of W.A. Sturge and J. Ross from 1888 and later TC Ruch in 1961. Convergent projection proposes that afferent nerve fibers from tissues converge onto the same spinal neuron, and explains why referred pain is believed to be segmented in much the same way as the spinal cord. Additionally, experimental evidence shows that when local pain (pain at the site of stimulation) is intensified the referred pain is intensified as well.
  