Electrotherapy Pain Mechanisms Lecture Notes PDF

 ELECTROTHERAPY MECHANISMS OF PAIN By: Dr. Mohamed Gamal AbouElYazeed Ali Lecturer of Physical Therapy South Valley University  MECHANISMS OF PAIN *Pain is the most common complaint and the most prevalent symptom that requires intervention among patients in r...

 ELECTROTHERAPY MECHANISMS OF PAIN By: Dr. Mohamed Gamal AbouElYazeed Ali Lecturer of Physical Therapy South Valley University  MECHANISMS OF PAIN *Pain is the most common complaint and the most prevalent symptom that requires intervention among patients in rehabilitation programs. *Pain perception is influenced by various factors such as cultural differences, motivation, emotional states, and past experiences with pain (Sluka., 2009). *Pain is undoubtedly the main reason people seek treatment from health professionals (Turk et al., 2011). *The International Association for the Study of Pain (IASP) defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage” that has physiologic and psychological aspects.  TYPES OF PAIN 1) Acute Pain: -Acute pain is a symptom that results from injury and/ or disease that causes or can cause tissue damage through infection, trauma, or the progression of a metabolic disorder. -Acute pain is described as pain lasting less than 12 weeks (i.e., 3 months). -Acute pain is typically well-located and defined, depending on the type of tissue involved. Superficial (e.g., skin) pain is typically sharp and easy to locate. On the other hand, acute deep- tissue pain from muscles, joints, or viscera can be diffuse and difficult to locate. -The clinical treatment of acute pain can be pharmacological or nonpharmacological, involving rehabilitation or surgery. -Acute pain is often associated with changes in heart rate, blood pressure, and even respiratory rate, measurement of vital signs is warranted. 2) Chronic Pain: -Chronic pain is commonly defined as persistent or recurrent pain existing for 3 to 6 months or pain that persists beyond the normal time expected for the healing of injured tissue. -Chronic pain follows acute pain and is also associated with structural and functional changes in the central nervous system that require multiple therapeutic approaches. ‫ﻻزم ﯾﻌﻧﻰ اﻟﺟﮭﺎز اﻟﻌﺻﺑﻰ اﻟﻣرﻛزى ھو اﻟﻠﻰ ﯾﺗﺻﺎب؟‬ -Central sensitization, or the amplification of neural signaling within the central nervous system that underlies pain hypersensitivity, is a characteristic of chronic pain. -The persistence of chronic pain associated with injury or disease, such as diabetes or arthritis. -Chronic pain is no longer considered a symptom and may even be considered a disease itself. -Generally, chronic pain is associated with physical, emotional, social, and financial disability. -As chronic pain is difficult to manage, Clinicians must rely on a multidisciplinary approach and should involve more than one therapeutic modality. physician , pt , psychologist , socialist 3) Referred Pain: -Referred pain is defined as pain that occurs at a site remote from the source of the disease or injury, usually a visceral or muscle source. -It is generally believed that referred pain occurs due to the convergence of cutaneous, visceral, and skeletal muscle nociceptors on the common nerve root of the spinal cord. -The brain interprets the afferent input as arising from cutaneous structures because of the higher proportion of cutaneous afferents converging on second-order transmission neurons. -A common example is referred pain that radiates to the left shoulder, arm, jaw, or chest during angina or myocardial infarction. -###Treating pain of unknown or unidentifiable origin is considered a contraindication tosome common pain modalities like TENS. Masking undiagnosed pain with TENS can postpone proper treatment and lead to a worsening of the underlying condition ###. ‫‪12 weeks‬‬ ‫ﻣﺎ ﻣﻌﻧﺎھﺎ‬  DIMENSIONS OF PAIN A. Intensity: *Pain intensity may be defined as how much a person hurts (Jensen et al., 2011). Intensity is the dimension of pain most frequently assessed by clinicians. *In most cases, the more intense the pain, the more aggressive the treatment delivery and the less rapid the discharge. Inversely, the lesser the pain is, the less aggressive the treatment and the more rapid the patient’s discharge. B. Quality: *It refers to the specific physiologic sensations associated with pain. It reveals how the person feels or senses the pain (e.g., burning, itching).(colicky , dull aching ,sharp) *This dimension is very informative in determining the cause or nature of pain. C. C. Affect: *The affective dimension of pain is very complex because it relates to the degree of emotional arousal—that is, the changes in action readiness caused by the sensory experience of pain (Jensen et al., 2011). - ‫ﻣﯾول رد اﻟﻔﻌل‬ - ‫ﻋﺎطﻔﺔ رد اﻟﻔﻌل‬ ‫ﺗﺧﻣﯾن‬ *Pain affect is a mental state triggered by an implicit or explicit appraisal of a threat. In chronic pain, the emotional aspects can come to dominate the clinical picture. *This pain dimension is very important to clinicians and helps them determine the extent to which the patient is emotionally affected by his or her pain condition. This information can help to make a better choice of pain therapy—a psychological versus somatic approach, for example. D. Location: *Pain location is defined as the perceived location(s) of pain sensation that patients experience on or in their bodies. *Assessing pain location is important because the number of locations and sites indicated by the patients may be related to physical and psychological functioning (Jensen et al., 2011). The process of pain experience is made of five distinct and successive physiologic phases: 1) Transduction ‫ﺗﺣوﯾل اﻟطﺎﻗﺔ ﻣن ﺻورة‬ ‫إﻟﻰ ﺻورة أﺧرى‬ 2) Peripheral transmission 3) Modulation 4) Central transmission 5) Perception *Nociceptors: Most nociceptors have a high stimulation or activation threshold and, as a ‫ ﻣﺑﺗذل‬stimuli (Mense, 2003). This means, for example, that the result, do not respond to everyday nociceptors in our skin are not activated when we are sitting (compression of the gluteal skin area) or when muscle nociceptors are not activated when we are walking (muscle fiber contraction and elongation). *Only when their activation thresholds are exceeded is a noxious stimulus message generated. Nociceptors respond to intense mechanical, thermal, and chemical stimuli capable of damaging the tissues surrounding them. Stimuli that activate nociceptors are called noxious stimuli. Cutaneous mechanoreceptors, such as Meissner and Pacinian corpuscles and Merkel tactile disks, provide us with the senses of touch, pressure, and vibration. Cutaneous thermoreceptors provide our thermal sense for detecting heat (Ruffini corpuscles) and cold (Krause end bulbs). *It is important to always keep in mind that the pain threshold is the level of noxious stimulus required to alert the individual to a potential threat to tissue. Pain tolerance, on the other hand, is a measure of how much pain a person can or will withstand (Sikes, 2004). Both pain threshold and pain tolerance can vary greatly between individuals. Cutaneous Sensory Receptors 1. Transduction Phase: *Transduction is the phase of converting energy (i.e., of mechanical, thermal, and chemical forms) affecting nociceptors at the site and around the wound into electrical energy, which generates action potentials that lead to the production of nerve impulses. As stated previously, pain initially develops in nociceptors, the specialized nerve endings that are activated by strong mechanical and thermal stimuli, and by chemical substances produced and released (inflammatory response) in the tissue at the wound site. *This transduction, or conversion, of energy results from a change in the nociceptor’s structural confirmation with the formation of pores (ionic channels) within its cell membrane. Ion exchanges in and out of the nociceptor’s cell membrane generate action potentials leading to the production of nerve impulses, which will subsequently be transmitted along specialized sensory afferent fibers toward the spinal cord. *For transduction to occur, the quantum of physical energy available at the tissue injury site must be large enough, or intense enough, to exceed the nociceptor’s membrane threshold of activation. 2. Peripheral Transmission Phase: *The peripheral transmission phase includes the propagation or transmission of nerve impulses generated as a result of transduction from the nociceptors to the spinal cord. *The terminal ends of the nociceptors—that is, the free nerve endings—connect with the spinal cord through two distinct afferent sensory nerve fibers: A-delta fibers and C fibers (Wright, 2002; Weisberg et al., 2006). *The noxious message, now coded in nerve impulses, is transmitted to the dorsal horn of the spinal cord along these two afferent sensory fibers, whose cell body (neuron) resides in the dorsal root ganglia. *Impulse transmission in the A-delta fibers occurs more rapidly than in the C fibers (approximately 15 m/s vs. 1 m/s) because the axons of the former are lightly myelinated (larger in diameter), whereas those of the latter are unmyelinated (smaller in diameter). *A-delta fibers conduct mechanical as well as thermal noxious stimuli. C fibers, on the other hand, conduct mechanical, thermal, and chemical noxious stimuli.  A delta C fiber 3. Modulation Phase: - mechanical -mechanical *Modulation is the third phase leading to the - thermal noxious - mechanical noxious experience of pain. This phase is characterized - thermal by a diminution, suppression, or amplification of pain (hence the word modulation). *Research has shown that pain modulation occurs because of the action of nociceptive nerve impulses on the spinal gating system located in the dorsal horn of the spinal cord (McMahon et al., 2006). *Because pain modulation reflects the action of our own thoughts and emotions, it is logical that the two remaining phases, central transmission (fourth phase) and perception (fifth phase), are addressed before the modulation phase. 4. Central Transmission Phase: *Central transmission is the phase that encompasses the ascending transmission, or projection, of nociceptive nerve impulses, generated by the spinal pain-transmitting neurons, also referred to as T neurons. VPLNT *The lateral spinothalamic tract has two types of T neurons: fast-conducting, lightly myelinated A- delta fibers and slow-conducting, unmyelinated C fibers, representing the pathway of the second-order neurons from the dorsal horn of the spinal cord to the thalamus. *The third-order neurons, a new set of nerve impulses carrying the nociceptive message from the thalamus to the cortical neurons for pain perception to finally occur. 5. Perception Phase: *Perception relates first to the detection of pain and subsequently to the determination of its meaning (Bushnell et al., 2006). During this crucial phase, nociception (the organic aspect) finally becomes a pain (the cognitive aspect). It is also during this phase that pain is processed. *There is evidence from brain imaging and electrophysiologic studies that different cortical regions may be preferentially involved in different aspects of the complex experience of pain (Melzack et al., 2008). Most evidence suggests that the somatosensory cortex is more important for the perception.‫ﻰ‬ ٌ ‫زﻣﻧ‬ of spatial and temporal features, such as the location and duration of pain, whereas the limbic system is more important for the emotional and motivational aspects of pain (Bushnell et al., 2006). *As soon as we perceive pain, we try to modulate it downward.  SOMATIC PAIN MODULATION A. The Spinal Gating System: *According to the gate control theory, pain is perceived only if the spinal gate is open. It thus follows that to suppress the perception of pain, we need therapeutic interventions designed to close this gate. *The gating system is located in the dorsal horn of the spinal cord, more precisely within the anatomic laminae II and V. *The gating effect (open or closed) occurs after physiologic interaction between the inhibitory neurons located in the substantia gelatinosa (SG) and the pain-transmitting neurons (T) located deeper in the dorsal horns. *The fast-conducting, lightly myelinated A-delta fibers and slow-conducting, unmyelinated C fibers, have an inhibitory effect on the neurons of SG and an excitatory effect on the T neurons. Whereas the large-diameter, heavily myelinated A-beta (mechanoreceptors) fibers have an excitatory effect on the neurons of the SG and an inhibitory effect on the T neurons. *Different mechanical stimulation techniques like massaging the skin area over and around the site of pain, joint mobilization, tissue heating, and electrical stimulation, can potentially activate the mechanoreceptors attached to the very fast-conducting, large-diameter A-beta fibers. *The large-diameter A-beta fibers induce the secretion of Gamma- aminobutyric acid (GABA), the common inhibitory neurotransmitter in the central nervous system. Also, stimulation of A-beta fibers inhibits the production of both: 1) Glutamate, the chemical substance that triggers the firing of the second-order neuron of acute pain perception. 2) Substance P, the chemical substance that triggers the firing of the chronic second-order neuron of acute pain perception. *As a result of GABA release and inhibition of glutamate production, there is an excitatory effect on neurons of the SG and an inhibitory effect on the T neurons that block the ascending signals and prevent the firing of the second-order neuron and so on, pain perception at the higher centers. B. Descending Endogenous Opiate System (DEOS): *The DEOS originates primarily from neurons located in the periaqueductal gray matter (PAG) and the nucleus raphe magnus (NRM) areas, both located in the midbrain. *The DEOS exerts a descending (from central to spinal level) inhibitory effect (closing the gate) on the T neurons by releasing endogenous opiate, morphinelike substances known as enkephalins, endorphins, and Serotonin into the bloodstream and cerebrospinal fluid. *Research also suggests that the patient’s cognitive (thoughts) and emotional responses to painful events can also inhibit the spinal gating system simply with positive modification of the patient’s thoughts and emotional response to pain which leads to activation of the DEOS.