Porth's Essentials of Pathophysiology, 4e

869

Somatosensory Function, Pain, and Headache

C h a p t e r 3 5

(i.e., hypoalgesia ). Analgesia , in addition to meaning the relief of pain without loss of consciousness, is a pathol- ogy characterized by the absence of pain on noxious stimulation. The inability to sense pain may result in trauma, infection, and even loss of a body part or parts. It is thought to result from a peripheral nerve defect or a cortical defect, either of which disrupts the perception of pain. Whatever the cause, persons who lack the abil- ity to perceive pain are at constant risk of tissue damage because pain cannot serve its protective function. Allodynia (Greek allo, “other,” and odynia, “painful”) is the puzzling phenomenon of pain that follows a non- noxious stimulus to apparently normal skin. 2 Examples of such non-noxious stimuli are wind, touching sheets, and showering. The condition may arise when otherwise nor- mal tissues are abnormally innervated or are referral sites. It can also result from increased responsiveness within the spinal cord (central sensitization) or a reduction in the threshold for nociceptor activation (peripheral sensitiza- tion). One type of allodynia involves trigger points, which are highly localized points on the skin or mucous mem- brane that can produce immediate intense pain at that site or elsewhere with light tactile stimulation. “Neuropathic pain refers to pain that originates from pathology of the nervous system.” 31 When peripheral nerves are affected by injury or disease, it can lead to unusual and sometimes intractable sensory disturbances. The notable features that point to neuropathic processes as a cause of pain include widespread pain that is not otherwise explainable, evidence of sensory deficit (e.g., numbness, paresthesias), burning pain, pain that occurs with light stroking of the skin, and attacks of pain that occur without seeming provocation. 31 Depending on the cause, few or many axons could be damaged and the condition could be unilateral or bilateral. Causes of neuropathic pain can be categorized according to the extent of peripheral nerve involve- ment. Conditions that can lead to pain by causing dam- age to peripheral nerves in a single area include nerve entrapment, nerve compression from a tumor mass, and various neuralgias (e.g., trigeminal, postherpetic, and post-traumatic). Conditions that can lead to pain by causing damage to peripheral nerves in a wide area include diabetes mellitus, long-term alcohol use, hypo- thyroidism, renal insufficiency, and drug treatment with neurotoxic agents. 32 Diabetes often causes a length- dependent neuropathy (meaning that the longest axons in a peripheral nerve are most vulnerable). Injury to a nerve also can lead to a multisymptom, multisystem syn- drome, called complex regional pain syndrome. Nerve damage associated with amputation is believed to be a cause of phantom limb pain. Neuropathic pain can vary with the extent and loca- tion of disease or injury. There may be allodynia or pain that is stabbing, jabbing, burning, or shooting. Special Types of Pain Neuropathic Pain

Alterations in Pain Sensitivity and Special Types of Pain Pain sensitivity and types of pain vary according to the body structures, the initiating event, and the duration of the pain. It also varies among persons and in the same person under different conditions. Alterations in Pain Sensitivity Sensitivity to and perception of pain varies among persons and in the same person under different condi- tions and in different parts of the body. Irritation, mild hypoxia, and mild compression of a peripheral nerve often result in hyperexcitability of the sensory nerve fibers or cell bodies. This is experienced as unpleas- ant hypersensitivity (i.e., hyperesthesia ) or increased painfulness (i.e., hyperalgesia ). Primary hyperalgesia describes pain sensitivity that occurs directly in damaged tissues. Secondary hyperalgesia occurs in the surround- ing uninjured tissue. An example of primary hyperalge- sia is the extreme sensitivity of sunburned skin, which results from sensitization of the skin pain endings by local products from the burn. More severe pathologic processes can result in reduced or lost tactile (e.g., hypoesthesia, anesthesia ), tempera- ture (e.g., hypothermia, athermia ), and pain sensation ■■ Modulation of the pain experience occurs by way of the endogenous analgesic center in the midbrain, the pontine noradrenergic neurons, and the nucleus raphe magnus in the medulla, which sends inhibitory signals to dorsal horn neurons in the spinal cord or trigeminal nerve. ■■ Pain can be classified according to location, referral, and duration as well as associated medical diagnoses. Pain can arise from stimulation of cutaneous, deep somatic, or visceral pain receptors. Referred pain is pain perceived at a site different from its origin. Acute pain is self-limiting pain that ends when the injured tissue heals. Chronic pain is pain that lasts much longer than the anticipated healing time for the underlying cause of the pain. ■■ Treatment modalities for pain include the use of nonpharmacologic and pharmacologic agents either singly or in combination. Management of acute pain includes therapy directed at providing pain relief by interrupting the nociceptive stimulus. Chronic pain management is much more complex and is based on multiple considerations, including life expectancy.