Classification Of Pain PDF

Classification of Pain ○ For scientific and clinical purposes, pain is defined by International Association for the study of Pain (IASP) as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.” ○ This is to be disting...

Classification of Pain ○ For scientific and clinical purposes, pain is defined by International Association for the study of Pain (IASP) as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.” ○ This is to be distinguished from the term nociception that the IASP defines as the unconscious activity induced by a harmful stimulus applied to sense receptors. ○ Pain is frequently classified as physiologic or acute pain and pathologic or chronic pain ○ Acute pain typically has a sudden onset and recedes during the healing process; it can be regarded as “good pain” as it serves an important protective mechanism This withdrawal reflex is an expression of this protective role of pain ○ Chronic pain can be considered “bad pain” because it persists long after recovery from an injury and is often refractory to common analgesic agents, including nonsteroidal anti-inflammatory drugs (NSAIDs) and opioids. Chronic pain can result from inflammation (inflammatory pain) or nerve injury (neuropathic pain) including diabetic neuropathy, toxin induced nerve damage, and ischemia ! Hyperalgesia and Allodynia ○ Pain is often accompanied by hyperalgesia and allodynia ○ Hyperalgesia is an exaggerated response to noxious stimulus ○ Allodynia is a sensation of pain in response to a normally innocuous stimulus An ex: painful stimulus from a warm shower when the skin is damaged by sunburn ○ Hyperalgesia and allodynia signify increased sensitivity of nociceptive afferent fibers ○ Chemicals released at the site of injury can further directly activate receptors on sensory nerve endings leading to inflammatory pain ○ Injured tissues also release chemicals such as K+ that directly depolarize nerve terminals, making nociceptors more responsive (Sensitization). ○ Injured tissues also release bradykinin and substance P to further sensitize nociceptive terminals. ○ Histamine is released from mast cells, serotonin (5HT) from platelets, and prostaglandins from cell membranes, all contributing to the inflammatory process and they activate or sensitize the nociceptors ○ Some released substances act by releasing another one (ex: bradykinin activates both As and C nerve endings and increases synthesis and release of prostaglandins). ○ Prostaglandin E2 (a cyclooxygenase metabolite of arachidonic acid) is released from damaged cells and produces hyperalgesia. ○ This explains why aspirin and other NSAIDs (nonselective inhibitors of cyclooxygenase) alleviate pain Deep and visceral pain ○ The main difference between superficial (cutaneous) and deep or visceral pain is the nature of the pain evoked by noxious stimuli. ○ This may be due to a relative deficiency of As nerve fibers in deep structures, so there is little rapid, sharp pain. ○ Also deep pain and visceral pain are poorly localized, nauseating and frequently accompanied by sweating and changes in blood pressure ○ Muscle spasms can result from injuries to bones, tendons, and joints ○ The steadily contracting muscles become ischemic, and ischemia stimulates the pain receptors in the muscle ○ The pain in turn initiatives more spasms, setting up a vicious cycle ○ Nociceptors are present in visceral organs, but they are more sparsely distributed than in somatic structures. ○ Afferent fibers from visceral structure reach the CNS via sympathetic and parasympathetic nerves. ○ Their cell bodies are in the dorsal root ganglia and cranial nerve ganglia ○ Specifically, there are visceral afferents in the facial, glossopharyngeal, and vagus nerves in the thoracic, upper lumbar and sacral dorsal roots ○ Visceral pain can be severe, the receptors in the walls of the viscera are especially sensitive to distention of these organs. ○ Intestinal colic is a pain that waxes and wanes to due muscle spasms that occur after an intestinal obstruction ○ When a visceral organ is inflamed, or hyperemic, relatively minor stimuli cause severe pain, a form of hyperalgesia. Somatosensory pathways ○ The sensation evoked by impulses generated in a sensory receptor depends in part on the specific part of the brain they ultimately activate ○ Ascending sensory pathway that mediates touch, vibratory sense and proprioception (dorsal column or medial lemniscal pathway) and that which mediates pain and temp (ventrolateral spinothalamic pathway) Dorsal column pathway ○ Fibers mediating these sensations ascend ipsilaterally in the dorsal columns of the spinal cord to the medulla, where they synapse in the gracilis and cuneate nuclei. ○ The second order neurons from the nuclei cross the midline and ascend in the medial lemniscus to end in the contralateral ventral posterior lateral (VPL) nucleus. ○ The ascending system is called the dorsal column or medial lemniscal system. ○ The fibers within the dorsal column pathway are joined in the brainstem by fibers mediating sensation from the head. ○ Touch and proprioception from the head are relayed mostly via the main sensory and mesencephalic nuclei of the trigeminal nerve Brown-Sequard syndrome ○ A functional hemisection of the spinal cord causes a characteristic and easily recognized clinical picture that reflects damage to ascending sensory (dorsal column pathway, ventrolateral spinothalamic tract) and descending motor (corticospinal tract) Pathways, which is called the Brown-Sequard syndrome. ○ The lesion to fasciculus gracilis or facilis cuneatus leads to ipsilateral loss of discriminative touch, vibration, and proprioception below the level of the lesion. ○ The loss of the spinothalamic tract leads to contralateral loss of pain and temperature sensation beginning one or 2 segments below the lesion. ○ Damage to the corticospinal tract produces weakness and spasticity in certain muscle groups on the same side of the body ○ Although a precise spinal hemisection is rare, the syndrome is common because it can be caused by a spinal cord tumor, spinal cord trauma, degenerative disk disease and ischemia Therapeutic highlights ○ Spinal or vertebral stabilization is needed when spinal trauma is indicated. Drug treatments for brown-sequard syndrome are based on the etiology and time since onset ○ High doses of corticosteroids have been shown to be of value particularly of administered soon after the onset of such a spinal cord injury ○ Corticosteroids decrease the inflammation by suppressing polymorphonuclear leukocytes and reverse the increase in capillary permeability ○ Drugs may be needed to treat spasticity, pain or other possible complications of the spinal cord injury ○ Physical therapy is important to maintain strength and joint mobility and improving respiratory function Stress induced analgesia ○ It is well known that soldiers wounded in the heat of battle usually feel no pain until after the battle is over. This is an example of stress induced analgesia that can be exemplified by reduced pain sensitivity when being attacked by a predator or other stressful events ○ Release of norepinephrine, perhaps from brainstem catecholaminergic neurons, in the amygdala may contribute to this phenomenon. ○ The amygdala is a part of the limbic system that is involved in mediating the motivational affective responses to pain ○ The release of the endogenous cannabinoids such as 2-arachidonoylglycerol (2AG) and anandamide may contribute to stress induced analgesia. ○ These chemicals can act on 2 types of G protein coupled receptors (CB1 and CB2) ○ CB1 receptors are found in many brain regions, and activation of these receptors accounts for the euphoric actions of cannabinoids. ○ CB2 receptors are expressed in activated microglia under pathologies that are associated with chronic neuropathic pain ○ Binding of an agonist to CB2 receptors on microglia reduces the inflammatory response and has an analgesic effect ○ Work is underway to develop selective CB2 agonists for therapeutic treatment of neuropathic pain