Hello. Welcome to the revised pain modules presented by the AAPMNR. These have been updated in 2021. We will begin with the pain definitions and classifications. The International Association for the Study of Pain recently revised the definition of pain in 2020, and its definition was an unpleasant sensory and emotional experience associated with or resembling that associated with actual or potential tissue damage. There are some pain terminology definitions that all physiatrists should know, even if you are not going into a pain management field. Some of these are, as you see here, paresthesias. That is an abnormal sensation. Dysesthesia, which is an unpleasant abnormal evoked sensation. Hyperesthesia, which is an increased sensitivity to stimulation. And hyperalgesia, which is an increased response to a stimulus that is normally painful. Other important definitions include hyperpathia, which is a painful syndrome characterized by increased reaction to a stimulus, especially a repetitive stimulus, as well as increased threshold. Also, aloadenia, which is pain due to a stimulus that does not normally provoke pain. This is an example of this would be a light feather touch that should only produce sensation, but that causes pain. This differs from the hyperalgesia, which is seen on the last slide, which is an exaggerated response from a usually painful stimulus. Other common definitions that you'll hear are phantom sensation and phantom pain. The sensation is the non-painful perceptions that occur in the region where the missing body part is after an amputation. Phantom pain is referred to as a surgically removed limb or portion thereof. In regards to classification of pain, when speaking with other physicians or when you are documenting pain in your notes, it is important to talk about the temporality of it. You have acute pain versus subacute pain versus chronic pain. In acute pain, you will have a normal, predictable physiologic response to any adverse physical, chemical, thermal, or mechanical injury. This is usually due to pain resulting from a nociceptor activation due to damage to tissues. Usually once the tissue is repaired, the pain stops. In subacute pain, it is a subset of acute pain with it being present for at least six weeks, but less than three months. And lastly, you have chronic pain. That is pain that lasts longer than usual healing time, typically beyond three months. Nociceptive pathways remain active, often with symptoms greater than the underlying pathology would suggest. You can also classify pain with a physiological classification. There is nociceptive pain, which is pain that is associated with tissue injury. There is neuropathic pain, where there is pain that is associated with injury to the peripheral or central nervous system. And then there is also idiopathic pain, which is pain without identifiable pathology in any tissue substrate. We will cover nociceptive pain and neuropathic pain in their own slide sets after this slide set. Other classifications you can hear about are mechanism-based, regional, ideologic, or multiaxial. Briefly to touch on nociceptive and neuropathic pain, nociceptive pain is pain caused by activation of nociceptive afferent fibers. This type of pain satisfies the criteria for pain transmission, that is, transmission to the spinal cord, thalamus, and then to the cerebral cortex. Within nociceptive pain, you have two different types, somatic and visceral. In somatic pain, the pain is carried along the sensory fibers. This pain is usually discrete and intense and well-localized. Patients can describe it as achy, darp, dull, or sharp, or pressure-like. For example, a bony fracture would be a somatic pain. In visceral pain, pain is carried by the sympathetic fibers. This pain is diffuse and poorly localized. Patients can describe it as deep or gnawing. It can be referred to different sites. An example of this would be cholecystitis. Both are more responsive to treatment overall. With that, you can use NSAIDs or opioids for an acute pain, for example. In regards to neuropathic pain, that is pain initiated or caused by a primary lesion or dysfunction in the peripheral or central nervous system. You can classify these as peripheral pain or central neuropathic pain. In peripheral neuropathic pain, pain is caused by a lesion or dysfunction of the peripheral nervous system. Patients can describe this as burning, tingling, lanceating, or itching. They can have sometimes dysesthesia or allodynia. An example of this would be post-herpetic neuralgia, painful diabetic neuropathy, and complex regional pain syndrome. With central neuropathic pain, there is a lesion in the central nervous system causing pain. Examples of this are pain caused by a spinal cord injury, central nervous system causing pain. Examples of this are thalamic pain syndrome, post-stroke pain, and post-spinal cord injury pain. Both are more resistant to treatment. Both can also be more responsive to anticonvulsants and or antidepressants. Regarding the nociceptive and neuropathic pain, sometimes you can have both at one time. For example, you can have low back pain with a radiculopathy. The low back pain can be axial, very sharp and localized, with the radicular pain shooting down the leg, can be more of a neuropathic burning. Sometimes these can be tricky to treat due to the fact that the pain due to them coming from two different causes of pain. Patients can also present with pain of psychological origin. There are many different types of pain that can stem from a psychological issue, but a few of the main ones that you can see in practice are talked about here. There's hysterical conversion or hypochondriac. A lot of times these patients will attribute the patient's thoughts, process, or personality in the absence of an organic or delusional cause. Sometimes patients can have pain with depression. They will have pain during the course of a depressive illness, not preceding the depression with no other cause. And lastly, there's pain with delusional or hallucinatory issues. Those can be attributed by a patient to a specific delusional cause. There are a few steps that occur when a person feels something painful and the way that their brain perceives it. First, there is transduction, which occurs in the peripheral terminals of the primary affine neurons, where different forms of energy, which can be mechanical, heat, chemical, or cold, are converted to electrical activity, which are action potentials. Next is transmission. Transmission is a process by which electrical activity induced by a stimulus is conducted through the nervous system. There are three major components of the transmission system. The peripheral sensory cells in the dorsal root ganglia transmit impulses from the site of transduction at their peripheral terminal to the spinal cord, where the central terminal synapse with second order neurons. The spinal neurons are the second component in the transmission network. These cells send projections to the thalamus and various brainstem and diencephalon structures. Finally, neurons of the brainstem and diencephalon form the third component of the transmission network as they project to various cortical sites. The third step or stage is modulation. This is a process whereby neural activity may be altered along the pain transmission pathway. A major site of modulation occurs within the dorsal horn of the spinal cord. Modulation at this level of processing involves a magnitude of neurotransmitter systems. Activation of pain modulation systems usually results in less activity in the pain transmission pathway following a noxious stimuli. Examples of activation of this process include stress-induced analgesia. However, in some circumstances, modulation can also result in an enhancement of pain signaling. And finally, there's perception. This is the neural activity in the somatosensory transmission pathway results in a subjective sensation of pain. As described in depth on the last slide, here's a schematic of pain signaling mechanisms involved in transduction, transmission, modulation, and perception of pain. You can see ascending afferent and descending modulation pathways. As discussed in the last few slides regarding the pain signaling mechanisms, that starts in the sensory section you see on the bottom right and interacts with the peripheral nervous system, which then connects and exchanges information with the central nervous system. The peripheral nervous system also has signals into the motor and autonomic, which then is further divided into the sympathetic and parasympathetic nervous systems. There are different sensory fibers in your body that have different functions, especially when they have an obnoxious stimulus. For example, the A-beta sensory fibers are larger and they are myelinated, so they can go faster, with the velocities averaging between 30 and 60 meters per second. The function of the A-beta sensory fibers is the same as the A-beta sensory fibers, 60 meters per second. The function of that is to transmit touch, pressure, and vibration. The A-delta, which is a little bit smaller but also still myelinated, has a velocity of about 10 to 12 meters per second, and the function of that can be to transmit sharp pain and light touch signals. And lastly, there's sensory fibers C. They're very small and also unmyelinated, so they don't transmit signals as quickly as the other. They're less than 1.5 meter per second, and that transmits dull, achy, burning pain as well as temperature. The sensory afferent fibers previously talked on the last slide go to different modalities which project to different parts of the lamina. In the spinal cord, each one of those different fibers project to different areas of the lamina. Some of the supraspinal systems that are involved with pain include the thalamus, hypothalamus, limbic system, and the cerebral cortex. For example, and the cerebral cortex. There's also the periaqueductal gray matter and rostral ventromedial medulla, which have some descending control or influence on pain. There's a phenomena known as facilitation or wind-up, which is a mechanism that is thought to account for the intensification of pain observed with repeated or prolonged application of noxious stimuli. This is referred to as a temporal summation. So, in the second point, you see, again, it's an irritative focus causing constant bombardment of sensory ganglia by some type of stimuli. You have hyperexcitability that spreads from sensory to motor, inducing a hypertonicity, tenderness, or spasm. And once these changes result in dorsal horn neuronal changes, usually at the wide dynamic range neurons, or WDR, it is sensitized afferents are no longer still needed to drive the system. Finally, to wrap up our definitions and classification slide set is the gate control theory. This describes the input along a low threshold A-beta fiber that inhibits responses of nociceptive input along C-fibers. In other words, you have input along fast, unmyelinated fibers that transmit touch, pressure, and vibration, which inhibits responses from slow, unmyelinated fibers that transmit pain. Examples are TENS units, rubbing your knee after a fall. Sometimes parents will go and give their child a kiss, which helps put pressure and vibration on that area that will make the pain sensation less painful.

pain

definitions

classifications

tissue damage

gate control theory