Neurophysiology of pain

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Physiology of Pain

Neurophysiology of PainDr. karishma R. PandeyAssistant professorDepartment of basic and clinical physiology

Topics What is pain?TypesReceptorsStimulated byPathways Visceral painReferred painProjected pain/ phantom painModulation

What is pain?Pain is an unpleasant experience associated with acute tissue damage.

Experienced: following injury,organic diseases such as advanced cancer, its origin within the CNS itself (not associated with tissue damage)Accompanied byemotional reaction (fear or anxiety)autonomic responses such as sweating and an increase BP and HR.

Sherrington Pain is the physical adjunct of an imperative protective reflex." Painful stimuli generally initiate potent withdrawal and avoidance responses.

Pain differs from other sensations in that it sounds a warning that something is wrong, it preempts other signals, and it is associated with an unpleasant affect. It turns out to be immensely complex because when pain is prolonged and tissue is damaged, central nociceptor pathways are facilitated and reorganized. Much still needs to be learned, but in a general way it is convenient to talk about physiologic or acute pain and two pathologic states: inflammatory pain and neuropathic pain. The weight of evidence now suggests that pain is conveyed by specific sets of afferent nerve fibers and is not simply the result of a massive stimulation of afferent fibers. Nevertheless, pain may arise spontaneously without an obvious organic cause or in response to an earlier injury, long since healed. This kind of pain often has its origin within the CNS itself. Although it is not obviously associated with tissue damage, pain of central origin is no less real to the sufferer.Furthermore, pain is unique among the sensations in that it has a "built-in" unpleasant affect.

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Functions of PainProtects body against further injuryGuides functional recoveryMay enhance disability

Classification

Fast PainSlow Pain2-5 micro met dia0.4-1.2 miro met dia12-30 m/s0.5-2 m/sA fibreC fibreMonomodalPolymodalActivated by either high intensity mechanical stimuli or thermal stimuli(43

VRL-1: temp > 50

There may be many types of receptors on single peripheral C fiber endings, so single fibers can respond to many different noxious stimuli. However, the different properties of the VR1 and the VRL-1 receptors make it likely that there are many different nociceptor C fibers systems as well.

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Stimulation of Pain FibersAs almost everyone knows from personal experience, visceral pain can be very severe. The receptors in the walls of the hollow viscera are especially sensitive to distention of these organs. Such distention can be produced experimentally in the gastrointestinal tract by inflation of a swallowed balloon attached to a tube. This produces pain that waxes and wanes (intestinal colic) as the intestine contracts and relaxes on the balloon. Similar colic is produced in intestinal obstruction by the contractions of the dilated intestine above the obstruction. When a viscus is inflamed or hyperemic, relatively minor stimuli cause severe pain. This is probably a form of primary hyperalgesia (see below).

Nociceptors are activated by specific substances released from damaged tissueAs for the sense of touch and temperature, the distribution of the pain receptors in the skin is punctate. Histological examination of a pain spot reveals a dense innervation with bare nerve endings, which are believed to be the nociceptors. The adequate stimulus for the nociceptors is not known with certainty, but the application of pain-provoking stimuli such as radiant heat elicits reddening of the skin and other inflammatory changes. It is probable that a number of chemical agents called pain-producing substances (algogens) are released following injury to the skin and cause the pain endings to discharge. These agents include ATP, bradykinin, histamine, serotonin (5-HT), hydrogen ions, and a number of inflammatory mediators such as prostaglandins.

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Organization of Spinal Cord

Anterolateral Pathway: Spinothalamic Pathway

Sensations of pain, thermal and crude touch

Some of the axons of the dorsal horn neurons end in the spinal cord and brainstem. Others enter the ventrolateral system, including the lateral spinothalamic tract. A few ascend in the dorsal portion of the cord. Some of the ascending fibers project to the ventral posterior nuclei, which are the specific sensory relay nuclei of the thalamus, and from there to the cerebral cortex. PET and fMRI studies in normal humans indicate that pain activates cortical areas SI, SII, and the cingulate gyrus on the side opposite the stimulus. In addition, the mediofrontal cortex, the insular cortex, and the cerebellum are activated. In experimental animals and humans, lesions of the insular cortex cause analgesia, as do local increases in GABA in this cortical area in animals.

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Neospinothalamic Pathway: Fast Pain (More Localized)

Paleospinothalamic Pathway: Slow Pain (Less Localized)Diffuse projection to cerebral cortex and limbic system

Visceral pain Deep pain Pain in deeper region of the body especially due to injuries to bones, tendons, and jointsdull aching and poor localization (probably d/t relative deficiency of A nerve fibers)Usu accompanied by prolonged contraction of skeletal muscles--- induce ischaemia and aggravate painPain in visceral organs. chronic-aching-suffering type of pain, st burning and intense sharp painDiffuse and poor localizationCauses of pain are distention of organ, chemical irritation or ischemiaMuscle spasm and rigidity (guarding)Pain impulses are carried by C fibers.pain often radiates or is referred to other areas

Deep pain arises when deep structures such as muscles or visceral organs are diseased or injured. Deep pain has an aching quality, sometimes with the additional feeling of burning. It is usually difficult to localize and, when it arises from visceral organs, it may be felt at a site other than that at which it originates. This is known as referred pain (see below).Both deep pain and visceral pain are poorly localized, nauseating, and frequently associated with sweating and changes in blood pressureMuscle Spasm & RigidityVisceral pain, like deep somatic pain, initiates reflex contraction of nearby skeletal muscle. This reflex spasm is usually in the abdominal wall and makes the abdominal wall rigid. It is most marked when visceral inflammatory processes involve the peritoneum. However, it can occur without such involvement. The spasm protects the underlying inflamed structures from inadvertent trauma. Indeed, this reflex spasm is sometimes called "guarding."

Deep Pain

This is probably due to a relative deficiency of A nerve fibers in deep structures, so there is little rapid, bright pain. In addition, deep pain and visceral pain are poorly localized, nauseating, and frequently associated with sweating and changes in blood pressure. Pain can be elicited experimentally from the periosteum and ligaments by injecting hypertonic saline into them. The pain produced in this fashion initiates reflex contraction of nearby skeletal muscles. This reflex contraction is similar to the muscle spasm associated with injuries to bones, tendons, and joints. The steadily contracting muscles become ischemic, and ischemia stimulates the pain receptors in the muscles (see below). The pain in turn initiates more spasm, setting up a vicious cycle.

Visceral Painpoorly localized, unpleasant, and associated with nausea and autonomic symptoms, visceral pain often radiates or is referred to other areas.The receptors for pain and the other sensory modalities present in the viscera are similar to those in skin, but there are marked differences in their distribution. There are no proprioceptors in the viscera, and few temperature and touch receptors. Pain receptors are present, although they are more sparsely distributed than in somatic structures.Afferent fibers from visceral structures reach the CNS via sympathetic and parasympathetic pathways. Their cell bodies are located in the dorsal roots and the homologous cranial nerve ganglia. Specifically, there are visceral afferents in the facial, glossopharyngeal, and vagus nerves; in the thoracic and upper lumbar dorsal roots; and in the sacral roots (Figure 76). There may also be visceral afferent fibers from the eye in the trigeminal nerve. At least some substance P-containing afferents make connections via collaterals to postganglionic sympathetic neurons in collateral sympathetic ganglia such as the inferior mesenteric ganglion. These connections may play a part in reflex control of the viscera independent of the CNS.In the CNS, visceral sensation travels along the same pathways as somatic sensation in the spinothalamic tracts and thalamic radiations, and the cortical receiving areas for visceral sensation are intermixed with the somatic receiving areas.

Muscle PainIf a muscle contracts rhythmically in the presence of an adequate blood supply, pain does not usually result. However, if the blood supply to a muscle is occluded, contraction soon causes pain. The pain persists after the contraction until blood flow is reestablished.These observations are difficult to interpret except in terms of the release during contraction of a chemical agent (Lewis's "P factor") that causes pain when its local concentration is high enough. When the blood supply is restored, the material is washed out or metabolized. The identity of the P factor is not settled, but it could be K+.Clinically, the substernal pain that develops when the myocardium becomes ischemic during exertion (angina pectoris) is a classic example of the accumulation of P factor in a muscle. Angina is relieved by rest because this de