Electrotherapy I Lecture 2 PDF

Electrotherapy I Lecture 2 By Prof.Dr:Fathy Elshazly Professor Of Physical Therapy, Cairo University Dean Of Faculty Of Physical Therapy, Badr University In Assuit (BUA) Dr.Taher Mohamed AbdElhamed Lecturer of Integumentary physical thera...

Electrotherapy I Lecture 2 By Prof.Dr:Fathy Elshazly Professor Of Physical Therapy, Cairo University Dean Of Faculty Of Physical Therapy, Badr University In Assuit (BUA) Dr.Taher Mohamed AbdElhamed Lecturer of Integumentary physical therapy Badr University In Assuit (BUA)  Lecture 2 MECHANISMS OF PAIN & TISSUE REPAIR Objectives 1. The sensory system 2. Definition of pain 3.Physiology of pain 4. Pain modulation 5- Principles of tissue repair The central nervous system include: Sensory-Motor –autonomic  Sensory system provides Information about ( internal & external) environment autonomic afferent Visceral e.g. : BP , ECF volume Sensation Somatic Somatic afferent  Receptors Sensory receptors are detectors and transducers that convert various form of energy (light, sound, chemical ,mechanical ) in to action potentials in neuron. Anatomically : receptor are specialized structures present at peripheral termination of afferent nerve fiber. Classification of receptors Traditional classification :  According to the Site of Event Distance events Teleceptors Visual receptors exteroceptors Immediate external environment Touch receptors Interoceptors internal environment e.g. chemoreceptors Change in body position Proprioceptors Joints , tendons , ligaments According to the degree of adaptation Slowly Rapidly adapting adapting Moderately non adapting adapting According to the type (Energy) of stimulus Mechanoreceptors Pressure, stretch, sound. information about the total solute concentration of a Chemoreceptors solution. Thermo receptors hot, cold. Nociceptors pain receptor stimulated by any energy form that cause tissues damage. Baroreceptors elevation of BP photoreceptor  Nociceptors Most nociceptors have a high stimulation or activation threshold and, as a result, do not respond to everyday stimuli. This means, for example, that the 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 and cold. 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.  Cutaneous Sensory Receptors (Nociceptors) PAIN  Definition of Pain 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. Pain is the most common complaint and the most prevalent symptom that requires intervention among patients in rehabilitation programs.  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 non-pharmacological, 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. -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.  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. -A common example is referred pain that radiates to the left shoulder, arm, jaw, or chest during angina or myocardial infarction. The process of pain 1) Transduction experience is made of five distinct and 2) Peripheral successive physiologic transmission phases: 3) Modulation 4) Central transmission 5) Perception  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. 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 The noxious Transmission Phase: message, now The peripheral transmission phase coded in nerve includes the propagation or impulses, is transmission of nerve impulses transmitted to the generated as a result of transduction dorsal horn of the from the nociceptors to the spinal spinal cord along cord. these two afferent The terminal ends of the nociceptors sensory fibers, that is, the free nerve endings— whose cell body connect with the spinal cord through (neuron) resides in two distinct afferent sensory nerve the fibers: A-delta fibers and C fibers. dorsal root ganglia.  Note……! A-delta fibers conduct mechanical as well as thermal noxious stimuli. C fibers, on the other hand, conduct mechanical, thermal, and chemical noxious stimuli.  3. Modulation Phase Modulation is the third phase leading to the experience of pain. This phase is characterized by a diminution, suppression, or amplification of pain (hence the word modulation). 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.  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. 5. Perception Phase: Perception relates first to the detection of pain and subsequently to the determination of its meaning.  NOTE: 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. somatosensory cortex: Is more important for the perception 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  Pain Modulation A. The Spinal Gating System B. Descending Endogenous Opiate System (DEOS  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 large-diameter A-beta fibers induce the secretion of Gammaaminobutyric 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 second-order neuron of acute pain perception. Note: 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)(A) and the nucleus raphe magnus (NRM) areas(B), 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.  Part 2 Principals of soft tissue repair Soft-Tissue Healing Process The Healing Phases: A. Hemostasis Phase B. Inflammatory Phase C. Proliferative Phase D. Remodeling/Maturation Phase  A. Hemostasis Phase: The first phase of healing, called hemostasis, is characterized by the arrest of bleeding at the wound site. *This phase usually lasts a few seconds or, in case of moderate to severe pathologies that involve multiple well-vascularized tissues, up to several minutes. The hemostatic response to injury is a complex series of regulatory events that require the interaction of both cellular elements and blood plasma proteins.  B. Inflammatory Phase: The inflammatory phase relates to the process of inflammation, of which the aim is to clean the wound of its cellular debris, preparing it for the deposition of new, repaired, or regenerated tissues. There are six clinical cardinal signs and symptoms associated with this phase: Erythema , Hyperthermia, Edema, Pain and temporary partial to total dysfunction. This phase is a time-dependent process, characterized by vascular, chemical, and cellular events that lead to the proliferative phase of healing. *The inflammatory phase may last hours, days, or weeks depending on the severity of the pathology. It is the crucial phase of healing—without it, no tissue healing is possible.  C. Proliferative Phase The inflammatory phase is followed by the proliferative phase, which deals with the formation and proliferation of new and immature repair tissues to replace the damaged tissues. *Fibroplasia and angiogenesis are key processes during this phase. Fibroplasia is the formation of fibrous tissue. Angiogenesis is the process of growing new blood vessels. These processes are concomitant with all the other cellular responses during this phase of healing. *The proliferative phase may last for weeks and sometimes months depending on the severity of the pathology and the type of soft-tissue affected.  D. Remodeling/Maturation Phase: The fourth and final phase of healing is the remodeling (fiber alignment) and maturation (increase of mechanical strength) of immature tissue to form the most structurally functional tissue possible at the wound site. *This phase usually lasts for months, sometimes more than a year, depending, again, on the severity of the pathology and the type of tissue affected.  Tissue Regeneration and Repair *Tissue healing is defined as the natural response to pathology through which damaged and dead tissue is replaced by living tissue. *The purpose of this healing process is to restore the structural and functional continuity of body tissues that has been disrupted by the pathologic processes. *Research has shown that injured soft tissues heal through one of two Primary mechanisms: regeneration and repair  Regeneration refers to the restoration of tissue that is identical in structure and function to the tissue that has been damaged or destroyed.  Repair Repair on the other hand, involves fibrous scar formation, which alters the normal structure and functional properties of the affected tissues.  *Soft-tissue healing Soft-tissue healing occurs, in most cases, through a combination of regeneration and repair mechanisms.  Healing Quality Qualities of soft-tissue healing may be defined as ideal, acceptable, minimal, and failed. 1-Ideal healing is obtained when the wound is totally replaced by normal tissue structure, function, and appearance. This implies regeneration, meaning that the repaired tissue is identical to the original one. 2-Acceptable healing is observed when the healed wound shows almost normal structure and appearance, and less than optimal function. 3-Minimal healing is obtained when the healed wound shows minimal normal structure and appearance, and partial function. 4-Failed healing is present when the repair tissue shows abnormal structure, appearance, and function.