CHRONIC PAIN Definition Pain an unpleasant sensory and emotional response to a stimulus associated with actual or potential tissue

e 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 N

Suffering

Tissue factors (endogenous stress)

Nociceptive Pathways

Psychosocial factors (exogenous/ environmental stress)

Term Allodynia

Definition Pain caused by a stimulus that does not normally provoke pain Absence of pain in response to stimulation that would normally be painful Pain initiated or caused by a primary lesion or dysfunction in the central nervous system An unpleasant abnormal sensation, whether spontaneous or evoked An increased response to a stimulus that is normally painful Increased sensitivity to stimulation, excluding the special senses Pain initiated or caused by a primary lesion, dysfunction, or transitory perturbation in the peripheral or central nervous system Pain initiated or caused by a primary lesion or dysfunction in the nervous system A noxious stimulus is one that is damaging to normal tissues An abnormal sensation, whether spontaneous or evoked, that is not unpleasant Pain initiated or caused by a primary lesion, dysfunction, or transitory perturbation in the peripheral nervous system Pain initiated or caused by a primary lesion or dysfunction in the peripheral nervous system

Analgesia

Central pain

Dysesthesia

Hyperalgesia

Hyperesthesia

Neurogenic pain

Neuropathic pain Noxious stimulus Paresthesia

Peripheral neurogenic pain Peripheral Neuropathic pain Psychogenic pain

Pain not caused by an identifiable, somatic 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 Lissauers Tract located at the very tip of the dorsal horn. The nerve fibers of Lissauers 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)

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, Tcells 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 Transduction (receptor activation) Transmission Description The process by which afferent nerve endings participate in translating noxious stimuli (e.g., a pinprick) into nociceptive impulses The process by which impulses are sent to the dorsal horn of the spinal cord and then along the sensory tracts to the brain The process of dampening or amplifying painrelated neural signals, primarily in the dorsal

Modulation

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 begins when the patient is first seen and continues through every contact made with the patient. Painful regions need to be compared with normal areas on the contralateral side of the patient for sensation, temperature, and sensitivity to palpation. B. Diagnostic Procedures a. Laboratory tests Drug screening tests of the blood and urine provide information as to the variety and type of pain medications being ingested Serum drug level testing provides data to determine the bioavailability of medications being taken by the patient. b. Radiology Radiography, Computed tomography (CT), Magnetic resonance imaging (MRI) demonstrate anatomic or structural disorders, which account for a low percentage of functional abnormalities. c. Psychological evaluation Psychological evaluation often involves the use of questionnaires, inventories, and the clinical interview. o McGill Pain Questionnaire is an often-used instrument designed to measure three dimensions of the pain experience: sensory, affective, and evaluative. o Minnesota Multiphasic Personality Inventory (MMPI or MMPI) has been used in the United States perhaps more than any other psychological instrument in the assessment of personality factors contributing to the experience of chronic pain

d. Electrodiagnosis It is an objective neurophysiologic extension of the physical examination. It typically includes the determination of nerve conduction velocities and needle electromyographic (EMG) studies of individual muscles. Measuring Pain Intensity A. Unidimensional Scales Visual Analogue Scale o a 10-cm line with anchors at both ends. Common anchors are no pain and worst pain. o Patients are asked to draw a vertical line through the horizontal line to indicate their pain intensity. The line is measured in millimeters, yielding a number between 0 and 100. Numerical Rating Scale o The numerical rating scale (NRS), sometimes referred to as a verbal rating scale (VRS), is an 11point scale on which patients rate the intensity of their pain by choosing a number from 0, (no pain), to 10 (pain as bad as it could be). o This rating scale is commonly used and easy to understand. B. Categorical Scale -verbal categorical pain scales that provide a simple means for patients to rate their pain intensity using verbal or visual descriptions of their pain. Simple Descriptive Pain Intensity Scale Face Pain Scale

Complications/ Prognosis

 Physical o Secondary pain loci as a result of inactivity. o Decreased range of motion, myofascial pain, and weakness because of disuse. Psychological o Depression Environmental Pharmacological Management Nonsteroidal Antiinflammatory Drugs and Cyclooxygenase-2 Inhibitors Opioid Analgesics o Methadone Anticonvulsant Medications as a Treatment for Neuropathic Pain Conditions Antidepressants o Tricyclic Antidepressants and Selective Serotonin Reuptake Inhibitors. o SerotoninNorepinephrine Reuptake Inhibitors. Medication for Insomia Topical Agents Universal Precautions in Pain Medicine 1. Diagnosis with appropriate differential 2. Psychologic assessment, including risk of addictive disorder 3. Informed consent 4. Treatment agreement 5. Preintervention and postintervention assessment of pain level and function 6. Appropriate trial of opioid therapy with/without adjunctive medications 7. Reassessment of pain score and level of function 8. Regularly assess the 4 As of pain medicine (analgesia, activities of daily living, adverse effects, aberrant behavior) 9. Periodically review pain diagnosis and comorbid conditions, including addictive disorders 10. Documentation PT Management A. Objective of Care Increase soft tissue, muscle and/or joint mobility. Improve neuromuscular control, strength, muscle endurance.

 Improve cardiovascular endurance. Progress functional activities. B. Appropriate Interventions Physical Modalities o Heat Therapy Examples: (Superficial) Hydrocollator packs, Paraffin baths, Whirlpool baths (Deep) Ultrasound, Shortwave diathermy Indication: Pain, contracture, hematoma, muscle spasm, arthritis, before stretching program to increase collagen extensibility Precautions and Contraindications: Acute trauma, hemorrhage, bleeding diathesis, impaired sensation, altered thermal regulation, malignancy, ischemia, cognitive deficits, or inability to report pain o Cryotherapy Examples: Ice, Cold packs, Whirlpool baths, Vapocoolant spray Indications: Pain, acute trauma, acute inflammation, joint effusion, hemorrhage, muscle spasm, spasticity Precautions and Contraindications: Cold hypersensitivity, ischemia, impaired sensation, cognitive deficits, areas over superficial peripheral nerves, Raynaud phenomenon or disease, cryoglobulinema, arterial vascular disease PRICE (protection, rest, ice, compression, and elevation) method is commonly prescribed for acute sports-related injuries o Electrical Stimulation Therapy Example: Transcutaneous electrical nervestimulation Indications: Rheumatoid arthritis, osteoarthritis, deafferentation pain syndromes, visceral pain, sympathetically mediated pain, tension headache, acute postoperative pain, Raynaud disease, ischemic pain, urogenital dysfunction Precautions and Contraindications:

 Demand-type cardiac pacemaker; carotid sinus, laryngeal or pharyngeal muscles, eyes, and mucosal membranes; cognitive deficits; abdominal, lumbrosacral, or pelvic areas of pregnant women; edema; open wounds or skin irritation Therapeutic Exercises o Stretching techniques specific to tight tissue: Joint and selected ligaments (joint mobilization). Ligaments, tendons and soft tissue adhesions (cross-fiber massage). Muscles (neuromuscular inhibition, passive stretch, massage, and flexibility exercises). o Progress exercises: Submaximal to maximal resistance. Specificity of exercise using resisted concentric and eccentric, weight bearing and non-weightbearing. Single plane to multiplane motions. Simple to complex motions, emphasizing movements that simulate functional activities. Controlled proximal stability, superimpose distal motion. Safe biomechanics. Increase time at slow speed; progress complexity and time; progress speed and time. o Progress aerobic exercises using safe activities. o Continue using supportive and/or assistive devices until the ROM is functional with joint play, and strength in supporting muscles is adequate. o Progress functional training with simulated activities from protected and controlled to unprotected and variable. o Continue progressive strengthening exercises and advanced training activities until the muscles are strong enough and able to respond to the required functional demands. Precautions: There should be no signs of inflammation. Some discomfort will occur as the activity level is progressed, but it should not last longer than a couple of hours. Signs that activities are progressing too quickly or with too great a dosage are joint swelling, pain that lasts longer than 4 hours or that requires medication for relief, a decrease in strength, or fatiguing more easily.

C. Rationale of each action To maximize and maintain physical activity and function To reduce the misuse or abuse of dependency producing medications, invasive procedures, and passive modalities, fostered by a change toward active patient self-management To return to previous levels of activity at home, in the workplace, and in leisure pursuits To reduce subjective reported pain intensity and maladaptive pain behaviors To assist patients in obtaining resolution and/or closure of contentious work-related or litigation aspects of the pain condition D. Relevant health teaching to patient and family Patient education by instructing patient in safe progressions of exercises and stretching. o Monitor understanding and compliance. o Teach ways to avoid reinjuring the part. o Teach safe body mechanics. o Provide ergonomic counseling. Family education by exhibiting that encourage and help the coping mechanism of the patient

Myofascial Pain Syndrome Definition a chronic, regional pain syndrome. hallmark classification of MPS :myofascial trigger points (MTrPs) can be secondary to pathologic conditions such as chronic repetitive minor muscle strain, poor posture, systemic diseases, and neuromusculoskeletal lesions (such as strain, sprain, enthesopathy, bursitis, arthritis, spinal disk lesion, etc.). Myofascial trigger points (MTrPs) most tender (hyperirritable) circumscribed spot in a palpable taut band of skeletal muscle fibers. pressure stimulation of a typical MTrP can elicit pain, referred pain, and LTR (Local Twitch Response)

 Latent MTrP- are tender but not spontaneaously painful. - asymptomatic unless palpated. Active MTrP- painful spontaneously or in response to movement of the involved muscle and are often so painful on palpation that the patient jumps. (the jump sign).

Note: - A latent MTrP can be observed clinically to evolve into an active MTrP. When an active MTrP is suppressed with treatment, it is still tender but not spontaneously painful because it has become a latent MTrP. - The syndrome begins with one active MTrP in the affected muscle as a result of a soft tissue lesion. The underlying lesion should be treated properly to avoid developing additional active MTrPs to other regions. Etiology Although the etiology of trigger points is not completely understood, some potential causes are: Chronic overload of the muscle that occurs with repetitive activities or that maintain the muscle in a shortened position. Acute overload of muscle, such as slipping and catching oneself, picking up an object that has an unexpected weight, or following trauma such as in a motor vehicle accident. Poorly conditioned muscles compared to muscles that are exercised on a regular basis. Postural stresses such as sitting for prolonged periods of time, especially if the workstation is not ergonomically correct, and leg length differences. Poor body mechanics with lifting and other activities.

Precipitating and Perpetuating Factors Trauma o Macrotrauma Contusions, sprains and strains may give rise to MFP acutely. o Microtrauma The onset is more subtle. Chronic repetitive overloading or overuse of muscles may lead to fatigue and gradual onset of MFP. Mechanical o Internal factors Poor posture, scoliosis o External factors Poor ergonomics, when the working environment of an individual is poorly molded to his or her physique. Degeneration Ageing, structural degeneration of bones and joints, with gradual loss of myofascial flexibility, may lead to MFP Nerve Root Compression Irritation of the nerve root may lead to sensitisation of the spinal segment and MFP in the innervated muscles. Emotional Psychological Stress Anxiety, increased sympathetic output and sleep deprivation may lead to increased muscle tension, fatigue and decreased MFP threshold. Endocrine and Metabolic Deficiencies Thyroid and oestrogen insufficiencies are known to cause MFP. Nutritional Deficiencies Vitamins and minerals insufficiencies may perpetuate MFP. Chronic Infection Chronic virus or parasite infections may perpetuate MFP Epidemiology has a high prevalence among individuals with regional pain complaints. the prevalence varies from 21% of patients seen in a general orthopedic clinic to 30% of general medical clinic patients with regional pain to as high as 85% to 90% of patients presenting to specialty pain management centers. Women and men are affected evenly. Pathophysiology Precipitating factors of MFP may cause the facilitated release of acetylcholine at motor end plates, sustained muscle

fiber contractions and local ischemia with release of vascular and neuroactive substances, and muscle pain. More acetylcholine may then be released, thus perpetuating the muscle pain and spasm. Clinical Manifestation Characteristics of Myofascial Trigger Points Painful or Tender spot - a circumscribed spot in the muscle with pain and tenderness which is approximately located in the same region in different persons. Taut Band - are groups of muscle fibres that are hard and painful on palpation. - is an objective and consistent palpatory finding in muscles with myofascial pain. Within TB, the most painful and sensitive areas are the trigger point and tender spot. Referred Tenderness and Referred Pain - referred tenderness occurs when a distant muscle has pain in response to compression of an MTrP while referred pain occurs when spontaneous pain is referred to remote sites from an MTrP. Local Twitch Response (LTR) - is a brisk contraction of a group of muscle fibers in response to snapping palpation. Motor Dysfunction - a pain-induced weakness and usually occurs only in severe cases of myofascial pain. - other motor dysfunctions related to MTrP: increased responsiveness (muscle hyperactivity, referred muscle hyperactivity, referred inhibition), delayed relaxation, and increased fatigability. Autonomic Phenomena - abnormal sweating, tearing, salivation, and increased vasomotor response and pilomotor response). Diagnosis Basic diagnostic criteria Exquisite spot tenderness Pain recognition Taut band Confirmatory signs Referred pain Local twitch response

 History and Physical examination Pain distribution pattern Pointed out by the patient Palpation: tender spot, taut band, referred pain, local twitch response Laboratory findings Biochemicals associated with pain and inflammation Thermography Sonography MRI Differential Diagnosis Fibromyalgia vitamin D deficiency rheumatoid arthritis Localized and generalized osteoarthritis degenerative shoulder or hip joint Pain Visceral disorders such as heart disease, kidney stones, irritable bladder, irritable bowel syndrome, and endometriosis Mechanical Dysfunction - hypermobility and structural bodily asymmetries such as leg-length inequality. Complications/ Prognosis physical inactivity that may lead to cardiovascular disease. reduced sleep quality. Pharmacological Management Muscle Relaxants Nonsteroidal Antiinflammatory Drugs Antidepressants PT Management A. Objective of care: Treatment consists of three main components: Eliminating the trigger point o Contractrelaxpassive stretch done repeatedly until the muscle lengthens o Contractrelaxactive stretch also done in repetition o Trigger point release o Spray and stretch o Dry needling or injection

Correcting the contributing factors - if the cause of the trigger point is a chronic overload of the muscle, the contributing factor should be eliminated prior to addressing the trigger point. and Strengthening the muscle. - when ROM is restored and the trigger point has been addressed, muscle strengthening is initiated.

B. Appropriate intervention Manual Therapy Stretching: intermittent cold and stretch Deep pressure soft tissue massage Trigger point pressure release Ischemic compression, acupressure, myotherapy, shiatsu Spinal and joint manipulation and mobilization Voluntary contraction and release method o Muscle energy technique o Reciprocal inhibition o Postisometric relaxation Modality application Thermotheraphy: Hydrocollator hot pack, ultrasound Electrotheraphy: interferential current, TENS Laser therapy: Cold laser Needling Traditional acupuncture Dry needling Myofascial trigger point injection and preinjection block

*Basic Principles of Myofascial Trigger Point Injection Before considering MTrP injection Treat etiologic lesions

Treat with conservative techniques for MTrP inactivation Pain recognition Identification of key trigger points

During MTrP injection Accurately localize the area of sharp tenderness and taut band Accurate placement of needle tip Quick movement of needle (fast-in and fast-out technique) Multiple needle insertions to elicit as many local twitch response as possible After MTrP injection Hemostasis: Firm compression on the area of injection Home program Physical therapy as indicated *Procedure of Myofscial Trigger Point Injection

Identification of MTrP Skin preparation: sterilization (and analgesia) Skin penetration: to subcutaneous tissue layer Palpation of MTrP: firm compression of MTrP with index or middle finger of the nondominant hand to direct the needle placement Insertion of the needle into the minute tender site with a fast-in and fast-out technique for searching sensitive loci (eliciting LTRs) Pulling the needle back to the subcutaneous layer after each insertion Injection of MTrP with a drop of 0.5% lidocaine if an LTR elicited Eliciting as many LTRs as possible by repeated needle insertions

Note : After needling the TRP/TS, it is essential to correct the muscle imbalance to achieve a good therapeutic result. It is important to try to restore normal length and flexibility to the muscles. However, one should be careful of achieving this by direct stretching exercises when a muscle is still in pain and spasm. Direct stretching may cause more pain and more spasm in the painful muscle. Instead, flexibility may be restored to the

painful muscle through limbering exercises. The following neuromuscular relaxation techniques may be applied: o o o o Muscle relaxation by exhalation. Muscle relaxation by eye movement, inferiorly and in the direction in which relaxation is desired. Muscle relaxation following isometric contraction, by autogenic inhibition. Muscle relaxation following minimal activation of the antagonist muscle, by reciprocal inhibition.

C. Rationale of treatment It is also important that strengthening exercises should not be started too early. Before pain has fully subsided, the muscles are still tight and in spasm. Strengthening exercises, if started too early, may cause more pain, spasm and tightness. Strengthening exercises should only commence after the pain has been fully treated and resolved. It should then begin gradually with isometric exercises and progress to repetitive low resistance exercises to develop endurance, before high resistance exercises to develop strength, as well as stabilisation exercises. D. Patient education and Home program Patient education is critical in the treatment of myofascial pain. The patient should be schooled in the causes of MTrPs, principles of treatment, and prevention strategies (e.g., body mechanics). Demonstrations about self-stretch techniques, focal massage, local heat application, therapeutic home exercise program, etc. are also required to help the patient eliminate or control pain.

Fibromyalgia Definition a generalized chronic pain syndrome characterized by widespread pain and tenderness to palpation at multiple anatomically defined soft tissue body sites that has lasted for more than 3months. Primary FMS

defined as pure FMS having no association with any other medical condition.

Secondary FMS - FMS associated with another medical condition * The 1990 American College of Rheumatology Criteria for the Classification of Fibromyalgia Syndrome From history: Widespread musculoskeletal pain Definition: For the past 3 months, pain has been experiencedin four quadrants; the locations are counted as follows: bothsides of the body, above and below the waist, in the trunk(e.g., cervical spine, anterior chest, thoracic spine, low backareas). Shoulder and buttock involvement count for bothsides of the body. Low back counts as lower segment. From examination: Pain induced by palpation of tender points Definition: Pain must be inducible at 11 or more of the following 18 (9 bilateral) tender point sites: 1, 2. Occipitus: At the suboccipital muscle insertion 3, 4. Low cervical: At the anterior aspects of the intertransverse spaces at C5C7 5, 6. Trapezius: At the midpoint of the upper muscle border 7, 8. Supraspinatus: Near the origins, above the spine of the scapula 9, 10. Second rib: Upper surface just lateral to the second costochondral junction 11, 12. Lateral epicondyle: Extensor muscle, 2 cm distal to the epicondyle 13, 14. Gluteal: In upper outer quadrants of buttocks in anterior fold of muscle 15, 16. Greater trochanter: Posterior to the trochanteric prominence 17, 18. Knees: At the medial fat pad proximal to the joint line and condyle

Characteristics of FM The first symptoms of FM can occur at any age but usually appear during early to middle adulthood. For more than 30% of those diagnosed, the symptoms develop after physical trauma such as a motor vehicle accident or a viral infection. Although the symptoms vary from individual to individual, there are several hallmark complaints. Pain is usually described as muscular in origin and is predominantly reported to be in the scapula, head, neck, chest, and low back. A significant fluctuation in symptoms. Some days an individual may be pain-free, whereas other days the pain is markedly increased. Most individuals report that when they are in a cycle where the symptoms are diminished they try to do as much as possible. This is usually followed by several days of worsening symptoms and an inability to carry out their normal daily activities. This is often the response to exercise. Individuals with FM have a higher incidence of tendonitis, headaches, irritable bowel, temporal mandibular joint dysfunction, restless leg syndrome, mitral valve prolapse, anxiety, depression, and memory problems. Etiology Although FM is a noninflammatory, nondegenerative, nonprogressive disorder, several factors may affect the severity of symptoms. These factors include environmental stresses, physical stresses, and emotional stresses. Environmental stresses -include weather changes, especially significant changes in barometric pressure, cold, dampness, fog, and rain. An additional environmental stress is fluorescent lights. Physical stresses - include repetitive activities, such as typing, playing piano, vacuuming; prolonged periods of sitting and/or standing; and working rotating shifts. Emotional stresses- are any normal life stresses.

Epidemiology

The prevalence of fibromyalgia is reported to be 3% to 5% with a significant female predominance. Recent evidence suggests that fibromyalgia and related syndromes may share heritable pathophysiologic features. A much higher prevalence of FMS among females than among males can be explained by the fact that females have lower antinociceptive activity than males. Pathophysiology Although the etiology remains unclear, characteristic alterations in the pattern of sleep and changes in neuroendocrine transmitters such as serotonin, substance P, growth hormone and cortisol suggest that regulation of the autonomic and neuroendocrine system appears to be the basis of the syndrome. Fibromyalgia is not a life-threatening, deforming, or progressive disease. Anxiety and depression are the most common association. Clinical Manifestation The symptoms of fibromyalgia vary from person to person. The most common symptoms and conditions associated with FM include: marked fatigue stiffness sleep disorders cognitive disturbances psychological distress temporomandibular joint syndrome paresthesias, headache genitourinary manifestations irritable bowel syndrome and orthostatic intolerance

Diagnostic Criteria The tender point test is being replaced with a widespread pain index and a symptom severity (SS) score. A tender point evaluation is no longer required although a full physical exam is still recommended along with other diagnostic tests to identify causes for the patients' symptoms besides fibromyalgia. In place of the tender point count, patients (or their physician) may endorse 19 body regions in which pain has been experienced during the past week. One point is given

for each area, so the score is between 0-19. This number is referred to as the Widespread Pain Index (WPI) and it is one of the two required scores needed for a doctor to make a diagnosis of fibromyalgia. The second part of the score required to assess the diagnosis of fibromyalgia involves the evaluation of a person's symptoms. The patient ranks specific symptoms on a scale of 0-3. These symptoms include: Fatigue, Waking unrefreshed, Cognitive symptoms, Somatic (physical) symptoms in general (such as headache, weakness, bowel problems, nausea, dizziness, numbness/tingling, hair loss). The numbers assigned to each are added up, for a total of 0-12. The diagnosis is based on both the WPI score and the SS score either: WPI of at least 7 and SS scale score of at least 5, or WPI of 3-6 and SS scale score of at least 9.

New ARC Diagnostic Criteria Fatigue 0= No problem 1= Slight or mild problems; Generally mild or intermittent 2= Moderate; considerable Problems; often present and/or at a moderate level 3= Severe: pervasive, continuous, Life disturbing problems Walking unrefreshed 0= No problem 1= Slight or mild problems; Generally mild or intermittent 2= Moderate; considerable Problems; often present and/or at a moderate level 3= Severe: pervasive, continuous, Life disturbing problems Cognitive symptoms 0= No problem 1= Slight or mild problems; Generally mild or intermittent 2= Moderate; considerable Problems; often present and/or at a moderate level 3= Severe: pervasive, continuous, Life disturbing problems

Differential diagnosis Joint disorders: zygoapophyseal joint disorder, osteoarthritis, loss of normal joint motion Inflammatory disorders: polymyositis, polymyalgia rheumatica, rheumatoid arthritis

 Neurologic disorders: radiculopathy, entrapment neuropathy, metabolic myopathy Regional soft tissue disorders: bursitis, epicondylitis, tendonitis, cumulative trauma Diskogenic disorders: degenerative disk disease, annular tears, protrusion, herniation Visceral referred pain: gastrointestinal, cardiac, pulmonary, renal Mechanical stresses: postural dysfunction, scoliosis, leg length discrepancy Nutritional, metabolic, and endocrine conditions: deficiency in vitamins B1, B12, or folic acid; alcoholic and toxic myopathy; iron, calcium, magnesium deficiency; hypothyroidism Psychologic disorders: depression, anxiety, disordered sleep Infectious diseases: viral illness, chronic hepatitis, bacterial or viral myositis Widespread chronic pain Complications/ Prognosis Rheumatoid arthritis Systemic Lupus Erythematosus Hypothyroidism Pharmacological management low-dose tricyclic sedative hypnotic medication analgesic-level dosage of a nonsteroidal antiinflammatory drug (NSAID) PT Management A. Objective of care A major therapeutic goal is to empower patients to trust their own experiences and enhance their ability to recognize the consistency of some symptoms and the fluctuation and interaction of others, so they can achieve a lifeworld environment in which they can be as active as possible without aggravating their symptoms, and then gradually expand their activity boundaries. B. Appropriate Intervention & Patient and family education

Accepting the existence of fibromyalgia syndrome by both physician and patient Instruction in pacing activities, in an attempt to avoid fluctuations in symptoms Avoidance of stress factors Decreasing alcohol and caffeine consumption Diet modification. Making accurate diagnosis via comprehensive evaluation Educating the patient, family, and society Encouraging patient to take an active role in self-care Supporting patient with psychologic or psychiatric management Treating patient with rehabilitation programs (including physical therapy, occupational therapy) Treating patient with medication Monitoring progress via regular follow-up evaluation

*Research supports the use of exercise, particularly aerobic exercise, to reduce the most common symptoms associated with FM.

Similarities and Differences between Fibromyalgia and Myofascial Pain Syndrome Fibromyalgia Similarities Pain in muscles Decreased range of motion Postural stresses Differences Tender points Poor sleep No referred patterns of pain Fatigue Trigger points in muscle Referred patterns of pain Tight band of muscle Myofascial Pain Syndrome

Chronic Regional Pain Syndrome (CRPS) Definition This is a grouping of complex regional painful disorders that develop as a consequence of trauma affecting the extremities with or without an obvious nerve lesion. This group of conditions that are described under the heading complex regional pain syndrome were previously known as reflex sympathetic dystrophy and causalgia. Two distinct types of CRPS: Type 1 (reflex sympathetic dystrophy) does not involve a nerve lesion. Type 2 (causalgia) a describable nerve injury jas occurred. Related Diagnosis for RSD: shoulder-hand syndrome Sudecks atrophy reflex neurovascular dystrophy traumatic angiospasm or vasospasm, sympathetically maintained pain (SMP). Classification and Clinical Features of CRPS CRPS type I (reflex sympathetic dystrophy) Develops after an initiating noxious event Spontaneous pain or allodynia/hyperalgesia Edema, vascular abnormalities Abnormal sudomotor activity Non-nerve origin CRPS type II (causalgia) Develops after nerve injury Not limited to territory of injured nerve Edema; skin blood flow abnormality Abnormal sudomotor activity Clinical Features of CRPS Symptoms more marked distally in an extremity Symptoms progress in intensity and spread proximally Symptoms vary with time Disproportion of symptoms in relation to the causing event

A specific diagnosis, such as diabetes or fibromyalgia, has been excluded

Etiology The underlying mechanism that stimulates the onset of these syndromes is unclear. They usually develop in association with a persistent, painful lesion, such as a painful shoulder; after a cardiovascular accident or myocardial infarction; with cervical osteoarthritis; after trauma such as a fracture or sympathetic nervous system is usually involved in CPRS sprain; with burns or immobilization; or after surgery or cardiac catheterization. There may or may not be an obvious nerve lesion. CPRS may be the result of various organic or psychiatric disorders that involve the nervous system. Epidemiology Women are affected with RSD three times as often as men. Because there seems to be an increased risk of the condition in family members of RSD patients, a possible genetic predisposition has been suggested, especially in patients who are resistant to therapy. Pathophysiology Normally, sympathetic stimulation secondary to injury results in vasoconstriction, which decreases blood loss and swelling. Sympathetic tone then decreases after injury, allowing increased blood flow. In the abnormal situation (RSD), inappropriate continuation of sympathetic activity results in edema, with capillary collapse, and ischemia, causing continued pain (positive feedback loop). Characteristics of CRPS A. Common sensory signs and symptoms associated with CRPS: 1. Continuous burning pain in the distal part of the affected extremity. 2. Pain is disproportionate in intensity to the inciting event and usually increases when the extremity is in a dependent position. 3. Stimulus-evoked pains include mechanical and thermal and deep somatic allodynia (pain due

to touching the joints and movement of joints) or hyperalgesia 4. Sensory abnormalities are most pronounced distally, and have no consistent spatial relationship to individual nerve territories or to the site of the inciting lesion. B. Common autonomic abnormalities associated with CRPS: 1. Swelling of the distal extremity especially in the acute phase 2. Hyper- or hypohidrosis 3. Vasodilatation or vasoconstriction 4. Changes in skin temperature C. Common trophic changes associated with CRPS: 1. Abnormal nail growth 2. Increased or decreased hair growth 3. Fibrosis 4. Thin, glossy skin 5. Osteoporosis D. Common motor abnormalities associated with CRPS: 1. Weakness 2. Coordination deficits 3. Tremor 4. Dystonia 5. Neglect-like symptoms or symptoms of disturbed body perception of the affected extremity Clinical Manifestations It is important to recognize the early symptoms to prevent progression of the disease. Three clinical stages of RSD: Stage 1: Acute/ Reversible Stage Lasts 3 weeks to 6 months This is a stage of vaspdilation Pain is usually out of proportion to the severity of injury Hyperhydrosis, warmth, erythema, rapid nail growth, and edema in the distal extremity Stage 2: Dystrophic or Vasoconstriction (Ischemic Stage)

 Lasts 3 to 6 months Characterized by sympathetic hyperactivity, burning pain, and hyperesthesia aggravated by cold weather Mottling, coldness, brittle nails and osteoporosis Stage 3: Atrophic Stage Most severe stage Condition can last for months to years, but spontaneous recovery often occur within a span of 18 to 24 months Characterized by pain (either decreasing or becoming worse) and by severe osteoporosis. Muscle wasting and contractures occur Diagnosis Diagnosis of CRPS is difficult. The patients pain is usually diffuse and does not correspond to dermatomal or peripheral nerve patterns. Thus, these patients are often diagnosed as having psychogenic pain. Anatomic or pharmacologic nerve blocks may establish the diagnosis. Psychogalvanic reflex tests and thermography may be useful in documenting sympathetic nervous system hyperactivity. Differential Diagnosis Cellulitis Lymphedema Occult or stress fracture Acute synovitis Septic arthritis Septic tenosynovitis Upper or lower limb venous thrombosis Scleroderma Plexitis, peripheral neuropathy Pharmacological Management NSAIDs (tramadol), sodium channel blockers (intravenous [IV] lidocaine), N-methyl-D-aspartate [NMDA] receptor blockers (ketamine, dextromethorphan, memantine) calcium-regulating drugs (calcitonin, clodranate, alendronate) and oral phenoxybenzamine

PT Management A. Objective of care: The best intervention is prevention when it is recognized that development of CRPS type I (RSD) is a possibility, such as when there has been trauma to the extremity or when the extremity is immobilized. It requires that the therapist motivate the patient to: - move the entire extremity safely - minimize edema and vascular stasis with elevation - activity of the distal segments (squeeze and open hand with upper extremity lesions, or ankle pumping and toe curls with lower extremity lesions) - be alert to the development of adverse symptomatology. B. Appropriate interventions for CRPS Pain and edema control. Modalities( such as ultrasound, vibration, transcutaneous electrical nerve stimulation (TENS), or ice. Retrograde massage. Elevate and use elastic compression when not undergoing pneumatic compression treatment. Mobility. In the early stages, use gentle, active exercises to manage the increasing stiffness. With patient actively contracting the musculature while the part is held near the end of the pain-free range. Avoid increasing painful reactions. Support and have the patient actively move each joint for a short period of time. Patient should perform brief motions frequently throughout the day. Tendon glide exercises in the hands Mobilization of the nervous system Muscle performance. Facilitate active muscle contractions of the joints proximal to the symptoms (shoulder/ hip) Provide tissue stress with minimal joint motion by using both dynamic and isometric exercise and alternating controlled stress loading (compressive loading) with distraction activities for neuromuscular control as well as afferent fiber stimulation. Suggested exercises:

Stress load the upper extremity by scrubbing with a brush in the quadruped position, beginning at 3 minutes and incrementally increasing to 10 minutes 3x a day. for the lower extremity, utilize progressive weight-bearing activities. Distraction carry 1 to 5 pounds up to 10 minutes at a time frequently throughout the day Total body circulation and cardiac output. low-impact aerobic exercises. Desensitization. desensitization techniques for brief periods 5x/day, such as having the patient work with various textures and tap or vibrate over the sensitive area. The patient is instructed to wear a protective glove during activities of daily living.

C. Rationale of interventions for CRPS Stage II and III Pain management. Modalities are often used as palliative interventions prior to or in conjunction with exercise to minimize pain. Desensitization. Progress the desensitization techniques to increase the patients tolerance to various textures. Mobility. Use joint mobilization, neuromobilization, and stretching techniques to address tissues limiting mobility. Because of the pain and significant limitations, little progress is sometimes seen with the stretching maneuvers, so surgical intervention may be required to gain motion. Muscle performance. Develop an exercise program to improve strength, endurance, and overall functional performance that meets the specific needs of the patient. D. Patient Education RSD affects all aspects of a patients life and for this reason; a referral to an interdisciplinary pain clinic may be most useful, it is important that CRPS patients receive the support of family, friends, and all members of the health care team in their efferts to become better from this devastating syndrome. Emphasize the importance of following the program of increased activity.

Teach the patient interventions that deal with the variable vasomotor responses with the use of gentle heat when at home, gentle exercises for short periods throughout the day, and use of associated parts of the extremity.

Delayed-Onset Muscle Soreness (DOMS) Definition The pain or discomfort in the muscles that have undergone unaccustomed exercise, particularly exercise involving eccentric muscle actions. Exercise-induced muscle soreness or Post Exercise Muscle Soreness begins to develop approximately 12 to 24 hours after the cessation of exercise. High-intensity eccentric muscle contractions consistently cause the most severe DOMS symptoms. DOMS sensation usually intensifies and peaks 24 to 48 hours after exercise. Although the time course varies, the signs and symptoms, which can last up to 10 to 14 days, gradually dissipate. Acute muscle soreness develops during or directly after strenuous exercise performed to the point of muscle exhaustion.This response occurs as a muscle becomes fatigued during acute exercise because of the lack of adequate blood flow and oxygen (ischemia) and a temporary buildup of metabolites, such as lactic acid and potassium, in the exercised muscle Anatomy Although much research has been developed, the cause of soreness is less well understood. Since the location of soreness can be quatified using pressure algometers, manual palpation techniques have been useful to document the distribution of pain following exercise-induced muscle injury. Researchers believe that the myotendinous junction is more susceptible to damage. Morphologic studies also revealed that there is myofiber damage along the entire length of the muscle. Etiology The underlying mechanism of tissue damage associated with DOMS is still unclear. Several theories have been proposed, and some have subsequently been refuted. DOMS is linked to some form of contraction-induced, mechanical disruption (microtrauma) of muscle fibers and/or

connective tissue in and around muscle that results in degeneration of the tissue. Evidence of tissue damage such as elevated blood serum levels of creatine kinase, is present for several days after exercise and is accompanied by inflammation and edema. Epidemiology Almost every individual unaccustomed to exercise who begins a resistance training program, particularly one that includes eccentric exercise, experiences muscle soreness. Pathophysiology The temporary loss of strength and the perception of soreness or aching associated with DOMS appear to occur independently and follow different time courses. Strength deficits develop prior to the onset of soreness and persist after soreness has remitted. Thus, force production deficits appear to be the result of muscle damage, possibly myofibrillar damage at the Z bands,which directly affects the structural integrity of the contractile units of muscle, not neuromuscular inhibition as the result of pain. Clinical Manifestation Muscle soreness and aching beginning 12 to 24 hours after exercise and peaking at 48 to 72 hours Tenderness with palpation throughout the involved muscle belly or at the myotendinous junction Increased soreness with passive lengthening or active contraction of the involved muscle Local edema and warmth Muscle stiffness reflected by spontaneous muscle shortening before the onset of pain Decreased ROM during the time course of muscle soreness Decreased muscle strength prior to onset of muscle soreness that persists for up to 1 to 2 weeks after soreness has remitted Muscle Strain Continuum Failure Disruption Sarcomere, Disruption in sarcolemma, structures smaller cytoskeleton, than the myofiber extracellular matrix

Damage Subcellar

Cellular

Myofiber

Ruptured and retraction of one or more muscle cells Rupture of a fascicle or entire muscle, involving myofiber fascia, and blood vessels (e.g., hamstring tears)

Organ

Muscle

The common burning experienced during and immediately after a maximal exercise bout is similar in experience to the pain resulting from defective energy supply. The pain results from metabolic processes that produce noxious substances (e.g., low pH, potassium ion). Local ionic disturbances following alterations in pH and ion homeostasis can stimulate free nerve endings. Another type of pain, closely related to burning, results from muscle cramps. The reason for the similarity in experience stems from the physiologic outcome of muscle cramp which is the result of an uncontrolled muscle activation caused by high stimulation frequencies and muscle working in shortened positions. Stretching the muscle relieves a cramp but exacerbates DOMS.

Pharmacological Management Topical salicylate creams- which provide an analgesic effect. Anti-inflammatory or analgesic drugs- if inflammation were the cause of pain Calcium blockers- given to patients with execptional pain syndromes. Protease inhibitors- given to patients with intermittent claudication. PT Management Prevention: progressing the intensity and volume of exercise gradually, by performing low-intensity warm-up and cool-down

activities,or by gently stretching the exercised muscles before and after strenuous exercise. repetitive concentric exercise prior to DOMS-inducing eccentric exercise a regular routine of exercise, particularly eccentric exercise, after an initial episode of DOMS has developed and remitted

Treatment Light, high-speed (isokinetic), concentric exercise has been reported to reduce muscle soreness and hasten the remediation of strength deficits associated with DOMS Electrical Stimulation Cryotherapy (cold water immersion) after vigorous eccentric exercise reduces signs of muscle damage (creatine kinase activity)

References:

Chronic Pain: Braddom, R.L., Physical Medicine & Rehabilitation. 4th ed.,pp.936-963 DeLisa, J.A., Rehabilitation Medicine: Principles & Practice, 4th ed., pp. 494-498, 506-509 Hertling, D., & Kessler, R. M., Management of Common Musculoskeletal Disorders: Physical Therapy Principles and Methods, 4th ed., pp. 54-55, 104 Kisner, C. & Colby, L.A., Therapeutic Exercise: Foundations and Techniques, 5th ed., p. 304

Santos, Ramona Luisa Pablo, Clinical Integration of Neuroanatomy & Neurophysiology, pp.147, 239-242

Zacharoff, K.L, Pujol, L. M. & Corsini, E., Pain EDU.org Manual: A Pocket Guide to Pain Management, 4th ed., pp. 28,34-36

Myofascial Pain Syndrome:

Borg-Stein, J. (2006)., Treatment of Fibromyalgia, Myofascial Pain, and Related Disorders, Rehabilitation Center, Spaulding Newton-Wellesley Rehabilitation Hospital, 65 Walnut Street, Wellesley, MA 02481, USA., p. 492 Braddom, R.L., Physical Medicine & Rehabilitation. 4th ed.,pp. 974-994 Frontera, W.R., Silver, J.L. & Rizzo Jr., T. D., Essentials of Physical Medicine and Rehabilitation: Musculoskeletal Disorders, Pain, and Rehabilitation, 2nd ed., p.534 Kisner, C. & Colby, L.A., Therapeutic Exercise: Foundations and Techniques, 5th ed., p. 318 Mense, S., Gerwin, R., Muscle Pain: Diagnosis and Treatment, p.53 Rakel, D., Integrative Medicine, 3rd ed., pp 580,584 Yap, E. (2007)., Myofascial Pain An Overview., Tan Tock Seng Hospital Rehabilitation Centre, 17 Ang Mo Kio Ave 9, Singapore 569766., pp. 44-47

Fibromyalgia:

Borg-Stein, J. (2006)., Treatment of Fibromyalgia, Myofascial Pain, and Related Disorders, Rehabilitation Center, Spaulding Newton-Wellesley Rehabilitation Hospital, 65 Walnut Street, Wellesley, MA 02481, USA., p.494-495 Braddom, R.L., Physical Medicine & Rehabilitation. 4th ed.,pp. 995-997 Carruthers, B. M., & van de Sande, M.I., Fibromyalgia Syndrome: A Clinical Case Definition and Guidelines for Medical Practitioners. An Overview of the Canadian Consensus Document., p. 22 DeLisa, J.A., Rehabilitation Medicine: Principles & Practice, 4th ed., p. 1309

Franciscus, A. (2012). Fibromyalgia. PO Box 427037 San Francisco, CA 94142-7037. Page 2 Frontera, W.R., Silver, J.L. & Rizzo Jr., T. D., Essentials of Physical Medicine and Rehabilitation: Musculoskeletal Disorders, Pain, and Rehabilitation, 2nd ed., p. 525 Jahan F, Nanji K, Qidwai W, Qasim R., Fibromyalgia Syndrome: An Overview of Pathophysiology, Diagnosis and Management,Oman Med J 2012 May; 27(3):192-195 Kisner, C. & Colby, L.A., Therapeutic Exercise: Foundations and Techniques, 5th ed., pp. 316-317

Chronic Regional Pain Syndrome Brotzman, S.B., Wilk, K.E., Clinical Orthopeadic Rehabilitation, 2nd ed., p. 544

Charlton, J. E., Core Curriculum for Professional Education in Pain, p. 1-2 DeLisa, J.A., Rehabilitation Medicine: Principles & Practice, 4th ed., p. 1303 Frontera, W.R., Silver, J.L. & Rizzo Jr., T. D., Essentials of Physical Medicine and Rehabilitation: Musculoskeletal Disorders, Pain, and Rehabilitation, 2nd ed., p. 513 Kisner, C. & Colby, L.A., Therapeutic Exercise: Foundations and Techniques, 5th ed., pp 378-380 Strong, J., Unruh, A. M., Wright, A., Pain: A Textbook for Therapists, p. 368 Wittink, H., Michel, T. H., Chronic Pain Management for Physical Therapists, 2nd ed., p. 259

Delayed-Onset Muscle Soreness Kisner, C. & Colby, L.A., Therapeutic Exercise: Foundations and Techniques, 5th ed., pp 184-185

Zachazewski, J. E., Magee, D. J., Quillen, W. S., Athletic Injuries and Rehabilitation, pp 92, 95-96