CHRONIC PAIN Definition Pain • “An Unpleasant Sensory and Emotional

CHRONIC PAIN Definition Pain “an unpleasant sensory and emotional response to a stimulus associated with actual or potential tissue damage or described in terms of such damage.” IASP Serves an adaptive function, a warning system designed to protect the organism from harm. Pain has never been shown to be a simple function of the amount of physical injury; it is extensively influenced by anxiety, depression, expectation, and other psychological and physiological variables. Acute pain a biologic symptom of an apparent nociceptive stimulus, such as tissue damage that is due to disease or trauma that persists only as long as the tissue pathology itself persists. is generally self-limiting, and as the nociceptive stimulus lessens, the pain decreases. usually lasts a few days to a few weeks (4 to 6 days). If it is not effectively treated, it may progress to a chronic form. nociceptive Chronic Pain disease process in which the pain is a persistent symptom of an autonomous disorder with neurologic,psychological, and physiologic components. pain lasting longer than anticipated (greater than 3 months) within the context of the usual course of an acute disease or injury. The pain may be associated with continued pathology or may persist after recovery from a disease or injury. Principally neuropathic, nociceptive Pain behaviors PAIN Suffering N Psychosocial Tissue factors Nociceptive factors (endogenous Pathways (exogenous/ stress) environmental stress) Term Definition Allodynia Pain caused by a stimulus that does not normally provoke pain Analgesia Absence of pain in response to stimulation that would normally be painful Central pain Pain initiated or caused by a primary lesion or dysfunction in the central nervous system Dysesthesia An unpleasant abnormal sensation, whether spontaneous or evoked Hyperalgesia An increased response to a stimulus that is normally painful Hyperesthesia Increased sensitivity to stimulation, excluding the special senses Neurogenic Pain initiated or caused by a primary lesion, pain dysfunction, or transitory perturbation in the peripheral or central nervous system Neuropathic Pain initiated or caused by a primary lesion or pain dysfunction in the nervous system Noxious A noxious stimulus is one that is damaging to stimulus normal tissues Paresthesia An abnormal sensation, whether spontaneous or evoked, that is not unpleasant Peripheral Pain initiated or caused by a primary lesion, neurogenic dysfunction, or transitory perturbation in the pain peripheral nervous system Peripheral Pain initiated or caused by a primary lesion or Neuropathic dysfunction in the peripheral nervous system pain Psychogenic Pain not caused by an identifiable, somatic pain origin and that may reflect psychologic factors Anatomy of Pain Knowledge of the peripheral anatomy of the human body is essential in evaluating the complex problems found in a patient with pain. It is important to know whether an area is supplied by a single nerve root or a single peripheral nerve or a branch of a peripheral nerve. Somatic Innervation- single cutaneous nerves innervate sharply defined regions with little overlap, but these fibers regroup in the peripheral nerve and are again redistributed in the brachial or lumbosacral plexus. Dermatomes- responsible for mapping out The segmental distribution of each spinal nerve from the skin receptors of the body Myotomes- the distribution of the spinal nerves to the different muscles of the limbs and trunk Sclerotomes- the peripheral nervous system of the skeleton is closely linked to muscle innervation. Most of the bones of the skeleton receive their innervation from nerve twigs of the attached muscles. Autonomic innervation- the peripheral component of the autonomic nervous system is concerned with innervation of visceral glands, blood vessels, and nonstriated muscle. Etiology Pain Pathways The major peripheral receptors for pain are the free nerve endings which are activated when tissue substances are released following a noxious and inflammatory reaction. Two specific types of peripheral nerves transmit pain: Type A delta fibers- larger, myelinated, rapid conducting fibers that are responsible for fast pain or sharp, pricking, well localized type of pain. Type C fibers- smaller, unmyelinated, slow conducting faibers that are responsible for slow type of pain characterized as a burning, poorly localized, slow onset type of pain. The axon fibers that enter the dorsal root ascend and descend on or two cord segments before synapsing at the various lamina in the dorsal horn. These very short longitudinal fibers forms the Posterolateral Fasciculus or Lissauer’s Tract located at the very tip of the dorsal horn. The nerve fibers of Lissauer’s Tract will terminate at either Lamina I (Posteromarginal Nucleus), Lamina II (Substantia Gelatinosa), Lamina III, IV and V for the dorsal horn of the spinal cord. Here it will synapse with the cell body of the second order neuron. The spinothalamic tract already crosses over at the spinal cord level, specifically at the Anterior White Commissure. In the thalamus the spinothalamic tract will synapse ate the Intralaminar and Ventral Posterolateral Nuclei with the cell body of the third order neuron. Anterolateral Systems (both Spinothalamic tract and Spinoreticular tract) is primarily a slowly conducting polysynaptic system. Many of its fibers actually synapse at the brainstem reticular formation. From here the reticular fibers will go to the thalamus. The perception of pain primarily occurs in the higher cortical centers. View of Pain A. Specificity Theory (Von Frey, 1894) o Sensation of pain resulted from a direct communication from specific pain receptors in the periphery to a central pain center in the brain. B. Pattern Theory (Goldschneider, 1894) o All nerve endings are alike, and the perception of pain is produced by intense stimulation of nonspecific receptors. o The combination of direct stimulus added to other sensory inputs informs the CNS that pain is present. C. Gate Control Theory (Melzack and Wall) o Pain is modulated by a “gating” mechanism located in the spinal cord that can increase or decrease the flow of nerve impulse from the brain. o Afferent impulses travel to the dorsal horn along the type A-delta and C fibers that encounter a gate thought to be the substatia gelatinosa cells which may be presynaptic or postsynaptic, can be closed, partially opened, or opened. o When the gate is closed, pain impulses cannot proceed but when the gate is least partially open, T- cells are stimulated in the dorsal horn which ascends the spinal cord to the brain and then pain is perceived. Epidemiology Nearly everyone experiences acute pain. Its incidence approximates the cumulative total of all acute diseases, trauma, and surgical procedures. In studies of the general population, patients have identified the head and lower limbs as the most common sites of acute pain and have identified the back as the most common site of chronic pain Physiology and Pathophysiology The complex interaction between the initial stimulus of tissue injury and the subjective experience of nociception and acute and chronic pain can be described by four general processes known as: Stage Description Transduction The process by which afferent nerve endings (receptor participate in translating noxious stimuli (e.g., a activation) pinprick) into nociceptive impulses Transmission The process by which impulses are sent to the dorsal horn of the spinal cord and then along the sensory tracts to the brain Modulation The process of dampening or amplifying painrelated neural signals, primarily in the dorsal horn of the spinal cord, but also elsewhere, with input from ascending and descending pathways Perception The subjective experience of feeling pain that results from the interaction of transduction, transmission, modulation, and psychological aspects of the individual Clinical Manifestation A. Causative factors: the majority of disorders seen in most clinical settings have two primary causes: 1. Abnormal modeling of tissues during resolution of an acute disorder. a. Malunion of fractures resulting in the change in direction or magnitude of forces acting on the part during use (increased stress) b. Abnormalities in collagen maturation or production (scarring, fibrosis, adhesions) 2. Fatigue response of tissues. a. Tissue breakdown. The rate of attrition exceeds the rate of repair (e.g., stress fractures and cartilage degeneration). The tissue becomes “weaker” and begins to yield under loading conditions. b. Tissue hypertrophy (e.g., fibrosis and sclerosis) occurs with mild to moderately increased stress levels in tissues with good regenerative/repair capacity, acting over a prolonged period. Pain assessment The description of painful symptoms (e.g., burning, throbbing) The location of the pain The temporal nature of the pain o Acute versus chronic o Time of occurrence and duration The severity of the pain o Impact on activities of daily living o Psychological impact o Social impact Exacerbating (e.g., bending) and/or alleviating (e.g., ice) factors Diagnosis A. Physical Examination A detailed history of the pain (origin, radiation, quality, severity, and time intensity attributes, as well as mode of onset, duration, time of occurrence, and factors that aggravate and relieve it) should be obtained. Previous treatments for pain (e.g., past and current medication, physical therapy – types of modalities, exercise and effective regimens) should be noted. Physical examination

Load more