Myofacial pain dysfunction syndrome anindya

an overview of muscle pain disorder which regularly create some discomfort for patient to live a normal life as well as to the doctor regarding diagnosis of the problem.

1. MYOFASCIAL PAIN DYSFUNCTION SYNDROME Presented by : Dr. Anindya Chakrabarty

2. Content Introduction History Definition Characteristics Pathophysiology Symptoms Physical examination Goal of treatment Management protocol

3. Introduction It is a muscular pain disorder – most common diagnosis causing chronic pain but one of the most least understood. Complex symptomatology, concomitant disorders and frequent behavioral & psychosocial contributing factors make the disorder difficult to recognize As the name suggest it has three part Myofascial – muscular & connective tissue origin Pain – an unpleasant sensational & emotional experience Dysfunction – deviated from normal function Syndrome – collection of various symptoms

4. History Costen – 1934 – indicate TMJ pain due to occlusal etiology Schwartz – 1956 – coined term TMJ pain dysfunction syndrome – blamed the spasm of masticatory and perimasticatory musculature. Laskin – 1969 – termed as MYOFASCIAL PAIN DYSFUNTION SYNDROME – implicated Psychophysiological theory for such incident.

5. Definition A pain disorder, in which unilateral pain is reffered from the trigger points in myofascial structures, to the muscles of the head and neck. Pain is constant, dull in nature, in contrast to the sudden sharp, shooting, intermittent pain of neuralgias. Pain may range from mild to intolerable

6. Prevalence Common persistent pain in head & neck region 50% of chronic head & neck pain 20-50% of people has this type of pain

7. Types of myofascial pain disorder 6 distinct group Myositis Muscle spasm Myofascial pain dysfunction (Trigger Point Pain) Fibromyalgia Muscle contracture Muscle pain secondary to connective tissue disorder

8. Functional Neuroanatomy and Physiology of the Masticatory System Two major components : (1) neurologic structures (2) muscles.

9. MUSCULAR COMPONENT MOTOR UNIT consists of a number of muscle fibers that are innervated by one motor neuron . Each neuron joins with the muscle fiber at a motor endplate . Depolarization causes the muscle fibers to shorten or contract. fewer the muscle fibers per motor neuron, the more precise the movement. MUSCLE Hundreds to thousands of motor units along with blood vessels and nerves are bundled together by connective tissue and fascia to make up a muscle . Muscles are necessary to overcome this weight and mass imbalance . MUSCLE FUNCTION 3 potential functions isotonic contraction Isometric contraction Controlled relaxation eccentric contraction lengthening of a muscle at the same time that it is contracting

10. Muscles

11. Precise and complex balance of the head and neck muscles must exist to maintain proper head position and function. A, Muscle system. B, Each of the major muscles acts like an elastic band . The tension provided must precisely contribute to the balance that maintains the desired head position. If one elastic band breaks, the balance of the entire system is disrupted and the head position altered.

12. Neurological structure

13. Neuromuscular Function Function of the Sensory Receptors Reflex Action Reciprocal Innervation Regulation of Muscle Activity Influence from the Higher Centers

14. Reflex action Myotic / Stretch Relex Nociceptive reflex

15. MYOTIC REFLEX

16. Nociceptive reflex

17. Pain modulation in trigeminal nerve T he degree of suffering relates more closely to the patient’s perceived threat of the injury and the amount of attention given to the injury Pain modulation means that the impulses arising from a noxious stimulus , which are primarily carried by the afferent neurons from the nociceptors , can be altered before they reach the cortex for recognition. This alteration or modulation of sensory input can occur while the primary neuron synapses with the interneuron when it initially enters the CNS or while the input ascends to the brainstem and cortex. it is important to distinguish the differences among four terms : nociception , pain, suffering , and pain behavior

18. Nociception: Noxious stimulus originating from the sensory receptor Pain: Unpleasant sensation perceived in the cortex, usually as a result of incoming nociceptive input. CNS can alter or modulate nociceptive input before it reaches the cortex for recognition . This ability of the CNS to modulate noxious stimulation is an extremely important function . Suffering: How the human reacts to the perception of pain . Factors such as past experiences, expectations, perceived threat of the injury, and attention drawn to the injury determine to what degree the subject will suffer. Pain Behavior: refers to the individual’s audible and visible actions that communicate suffering to others. Pain behavior is the only communication the clinician receives regarding the pain experience.

19. Mechanism of pain modulation Non painful cutaneous stimulation system It has been postulated that if the larger fibers are stimulated at the same time as the smaller ones, the larger fibers will mask the input to the CNS of the smaller ones The descending inhibitory system assists the brainstem in actively suppressing input to the cortex. In order for an individual to sleep, the brainstem and descending inhibitory system must completely inhibit sensory input (e.g., sound, sight, touch) to the cortex. Without a well-functioning descending inhibitory system, sleep would be impossible. Transcutaneous electrical nerve stimulation (TENS) is an example of the nonpainful cutaneous stimulation system masking a painful sensation. Constant subthreshold impulses in larger nerves near the site of an injury or other lesion block the smaller nerves’ input, preventing painful stimuli from reaching the brain.

20. Intermittent painful stimulation system the stimulation of areas of the body that have high concentrations of nociceptors and low electrical impedance. Stimulation of these areas may reduce pain felt at a distant site . Two basic types of endorphins have been identified : ( 1) the enkephalins and (2) the betaendorphins . This is the basis for acupuncture : A needle placed in a specific area of the body having high concentrations of nociceptors and low electrical impedance is twisted approximately two times a second to create intermittent low levels of pain. The stimulation causes the release of certain enkephalins in the cerebrospinal fluid , and this reduces the pain felt in tissues innervated by that area . Runner’s High – by Beta-endorphin Psychologic modulating system conditions that seem to intensify the pain experience are anxiety, fear , depression, and despair. Certainly the amount of attention drawn to an injury, as well as the consequence of the injury, can greatly influence suffering .

21. CENTRAL EXCITATORY EFFECT F irst explanation suggests that if the afferent input is constant and prolonged, it continuously bombards the interneuron, resulting in an accumulation of neurotransmitter substance at the synapses . If this accumulation becomes great, neurotransmitter substance can spill over to an adjacent interneuron, causing it also to become excited. second explanation of the central excitatory effect is that of convergence. single interneuron may itself be one of many neurons that converge to synapse with the next ascending interneuron. As this convergence nears the brainstem and cortex , it can become increasingly difficult for the cortex to evaluate the precise location of the input .

22. ETIOLOGY OF MPDS TISSUE INJURY Major trauma Exposure to extreme temperature PHYSICAL STRESSES Extreme fatigue Repetitive micro trauma (Clenching & Bruxism) Other disease processes

23. Psychological factors - Pipe smoking - Sleeping on stomach with mandible supported by forearm. - Teeth clenching or grinding - Jaw thrusting, tip sucking, tongue thrusting. - Nail, pen / pencil biting - Constant chewing of tobacco or gum Occlusal factor Developmental occlusal disharmony Acquired occlusal disharmony Iatrogenic occlusal disharmony

24. THEORIES OF MPDS Neurophysiological hypothesis Repetitive strain theory Central hypothesis Central biasing mechanism

25. DIGAMMATIC RERESENTATION OF ETIOLOGY OF MPDS PSYCHOPHYSIOLOGIC THEORY OF MPDS (Modified by LASKIN in 1969)

26. PATHOPHYSIOLOGY OF MUSCLE PAIN Muscular shortening (Calcium excess shortening) Prolonged sustained and muscular contraction Disruption of delicate sarcoplasmic reticulum Release of free calcium ions that are stored within SR Act on sarcomeres containing actin-myosin complex

27. Shortened muscles experience increase in metabolic demands due to more actin and myosin Depletion of ATP (Muscular fatigue) Actin myosin binding intensified (ATP depletion shortening) Mechanical interruption of blood flow through this area of biochemical derangement Vasoconstriction decrease of oxygen in the affected muscular fibres (shift to anaerobic metabolism)

28. Anaerobic metabolism causes propagation of decreased pH & accumulation of Nocigenic and Spasmogenic by-products called the “BIOGENIC AMINES” like serotonin, histamines, kinins & prostaglandins Activation of group III and group IV muscle nociceptive fibres PAIN Pain and further exaggerated central response (reflex response phenomenon) creates increased accumulation of biogenic amines & intensified vasoconstriction Local twitch response & jump signs of myofascial trigger points

29. The constant biochemical cycle results in the production of spasmogenic amines (biogenic amines) Three staged casual theory Calcium pump inactivation, ATP depletion & increase in free Ca++ (creating vicious , deteriorative biochemical cycle) Becomes impossible for muscular fibres to reabsorb the free calcium ions back into the sarcoplasmic reticulum In addition intensified vasoconstriction of central origin coupled with Mechanical vasoconstriction will cause ultimate inactivation of the ATP-dependent calcium pump

30. CLINICAL FEATURES Trigger point are present Presence of zone of reference Generally present at the end of tiresome day Limitation of motion of the jaw Chronic , focal or regional muscle Pain as discomfort (unexplained nature ) Continuous, dull to sharp ache in region of TMJ, preauricular or post auricular areas and at the angle of mandible Joint noises – grating, clicking, snapping etc. Tenderness to palpation of the muscles of mastication.

31. ASSOCIATED SYMPTOMPS Neurologic GIT Musculoskeletal Otologic Tingling Numbness Blurred vision Twiches Trembling Lacrimation Nausea Vomiting Diarrhea Constipation Indigestion Dry mouth Fatigue Tension Stiff joint pain Tiredness Weakness Tinnitus Ear pain Dizziness Vertigo Diminished hearing

32. TRIGGER POINTS Manifestations of abnormal muscles spindles Nodes of degenerated tissues Hyperirritable, localized point of tenderness in muscles **Stimulation of trigger points produces local and referred pain **Pathophysiology unknown although many theories proposed

33. MUSCLES INVOLVED REFERRED PAIN 1. Masseter 2. Temporalis 3. Medial pterygoid 4. Lateral pterygoid 5.Sternocleidomastoid Preauricular, post auricular region and mandibular body Side of the head, masseter origin, orbit maxillary teeth Retromandibular region Ear and TMJ Ear, mastoid and anterior cervical region

34. TEETH source 1. MAXILLARY INCISORS 2. MAXILLARY CANINES 3. MAXILLARY PREMOLARS 4. MAXILLARY MOLARS & MANDIBULAR MOLARS ANTERIOR TEMPORAL MUSCLE ANTERIOR TEMPORAL MUSCLE INTERMEDIATE TEMPORAL MUSCLE,SUPERFICIAL MASSETER MUSCLE, POSTERIOR TEMPORAL MUSCLE, TRAPEZIUS MUSCLE AND STERNO-CLEIDOMASTOID MUSCLE MUSCULAR SOURCES OF REFERRED PAIN TO THE TEETH

35. PAIN REFERENCE POINTS FOR MASSETER MUSCLES (TRIGGER POINTS) SUPERFICIAL LAYER MIDDLE LAYER LOWER DEEP

36. PAIN REFERENCE POINTS FOR TEMPORALIS (TRIGGER POINTS) MIDDLE FIFRES ANTERIOR FIFRES MIDDLE FIFRES POSTERIOR FIFRES

37. PAIN REFERENCE POINTS FOR MEDIAL PTERYGOID (TRIGGER POINTS) BEFORE AND AFTER REMOVAL OF CONDYLE

38. PAIN REFERENCE POINTS FOR LATERAL PTERYGOID (TRIGGER POINTS) BEFORE AND AFTER REMOVAL OF SUPERFICIAL MASSETER

39. STERNAL DIVISION CLAVICULAR DIVISION PAIN REFERENCE POINTS FOR STERNOCLEIDO- MASTOID (TRIGGER POINTS)

40. PAIN REFERENCE POINTS FOR TRAPEZIOUS (TRIGGER POINTS) UPPER RIGHT TRAPEZIUS

41. KEYS IN MAKING A DIFFERENTIAL DIAGNOSIS History Examination Mandibular restriction Mandibular interference Acute malocclusion Loading of the joint Functional manipulation Diagnostic anesthetic blockade Diagnostic imaging & Investigations

42. GENERAL HISTORY: which includes medical, surgical, psychological, occupational and social background SPECIFIC HISTORY: related to present complaint i.e. onset and type of pain, aggrevating and relieving, severity of symptoms, associated symptoms and medicines taken for the problem. HISTORY TAKING

43. CRANIAL NERVE EXAMINATION Olfactory nv Optic nv Occulomotor / Trochlear/ Abducent nv Trigeminal nerve Facial nv Acoustic nv Glossopharyngeal nv Accessory nv Hypoglossal nerve

44. EYE EXAMINATION Testing gross vision Diplopia or blurriness of vision is noted Reddening of the conjunctivae should be recorded Any tearing or swelling of the eyelids EAR EXAMINATION:

45. CERVICAL EXAMINATION EXAMINATION FOR CRANIOCERVICAL DISORDERS . asked to look to the extreme right and the extreme left look upward fully Look downward fully bend the neck to the right and left

46. MUSCLE EXAMINTION Location of muscle pathology Evaluation of muscle tone Location of trigger point Evaluation of temperature change Location of swelling Muscles are palpated bilaterally and simultaneously with firm but gentle pressure for 1-2min. Main pressure is exerted with the middle finger of each hand During palpation subjective pain should be noted. Patient is asked question regarding unilateral / bilateral pain, tenderness is mild / moderate or severe. Reference zone of the pain should be noted

47. Temporalis Examination:

48. Masseter Examination:

49. Sternocleidomastoid Examination:

50. Posterior Neck Muscle examination

51. FUNCTIONAL MANIPULATION Medial Pterygoid Muscle Lateral pterygoid Muscle

52. Interincisal distance Maximal comfortable mouth opening Maximal mouth opening Checking “End Feel”

53. Alteration in Opening pathway

54. Dental / occlusal examination Occlusal discrepancies, prematurities , or interference should be noted. Anterior open bite, collapsed bite, cross bite, reduced vertical dimensions, wear facets, mobility of teeth missing and teeth should be checked. Type of occlusion, skeletal, dentofacial should be checked

55. Examination of Articular joint JOINT SOUND either clicks or crepitation click is a sound of short duration. If it is relatively loud , it is sometimes referred to as a “POP” Crepitation is a multiple gravel-like sound described as grating JOINT RESTRICTION The dynamic movements of the mandible are observed for any irregularities or restrictions.

56. Diagnostic Blocking INDICATIONS: It is essential when differentiating primary from secondary pains useful to identify the pathways that mediate peripheral pain and to localize pain sources when the source of pain is difficult to identify, local anesthetic blocking of related tissues is the key to making the proper diagnosis educate the patient to the source of his or her pain problem GENERAL RULE purpose of an injection is to isolate the particular structure that is to be blocked clinician should have a sound knowledge of the pharmacology of all solutions that will be used clinician should avoid injecting into inflamed or diseased tissues clinician should maintain strict asepsis at all times . TYPES Muscle block Nerve block Intra capsular

57. Technique of Trigger Point Injection

58. AURICULO-TEMPORAL NERVE BLOCKING

59. Radiological investigation Helpful in diagnosis of Intra articular pathologies Osseous pathologies Soft tissue pathologies Conventional Radiograph Panoramic radiograph Transcranial projection Transpharyngeal projection Transmaxillary projection

60. Recent advances CT MRI CBCT Bone scaning

61. Other Investigations Electromyogram Sonography Sonography is the technique of recording and graphically demonstrating joint sounds . Many healthy joints can produce sounds during certain movements Presently sonography does not provide the clinician with any additional diagnostic information over manual palpation or stethoscopic evaluation . Vibration analysis Vibration analysis has been suggested to help in diagnosing intracapsular TMD, and internal derangements in particular Measures the minute vibrations made by the condyle as it translates and has been shown to be reliable . the technique diagnoses up to 25% of normal joints as derangements and misclassifies many deranged joints as normal, especially if the joint sounds are not audible or if the derangement has advanced to a nonreducing stage

62. Thermography Thermography is a technique that records and graphically illustrates surface skin temperatures. Various temperatures are recorded by different colors, producing a map that depicts the surface being studied . Recent studies shows Infrared imaging measurements can provide a useful, non-invasive and nonionizing examination for diagnosis of MTPs in masticatory muscles . Mandibular tracking device If a jaw-tracking device is used, the exact movement of the mandible can be recorded Unfortunately, many intracapsular and extracapsular disorders create deviations and deflections in mandibular movement pathways. A particular deviation may not be specific for a particular disorder, this information should only be used in conjunction with history and examination findings.

63. MANAGEMENT OF MPDS Patients counseling Physiotherapy Pharmacotherapy Occlusal therapy

64. Patient concealing Explaining patient about parafunctional habits such as clenching and bruxism. Soft diet Avoiding tooth to tooth contact. Avoid stressful forces. Resting of the jaw. Relaxation therapy Bio-feedback therapy – yoga, deep breathing, meditation, hypnosis

65. PHYSIOTHERAPY

66. Heat application Superficial: Hot packs, paraffin and radiants (Infra Red) Hot moist application of towels for 15-20 min for 4 times. Hydrocollator : pad filled with clay and heated in water both for 70°-80°, wrapped in a protected towel and placed over the affected area for 15-20 mins Deep Heat application: delivered by diathermy, ultrasound or phonophorosis DIATHERMY ULTRASOUND PHONOPHORESIS

67. DIATHERMY Short Wave Diathermy In chronic conditions, there will be increase in blood flow. Increase in oxygenation on application for 10 mins Mega Pulse Rest period between pulse raise allows dissipation of heat by blood flow. Time of application – 10 mins 60 micro second pulse 100 pulse / sec. Regime: 3 times / week for 4 weeks

68. Ultrasound: Heat is placed on the skin which has to be coated with an acoustic coupling gel and moved in parallel or circular over lapping sweeps 0.7 to 1 volts / cm2 for 10 mins . Regime: 3 times / week for 4 weeks. Uses: Altered cell membrane permeability Intracellular fluid absorption. Decreased collagen viscosity. Vasodilation Relax muscles and analgesia. Phonophorosis : Application of ultrasound instead of acoustic coupling gel. It uses a pad filled with an anesthetic or steroid cream is placed over the treatment kit

69. LASER THERAPY Cold laser therapy cold or soft laser has been investigated for wound healing and pain relief A cold laser is thought to accelerate collagen synthesis, increase vascularity of healing tissues, decrease the number of microorganisms, and decrease pain . increases capillary permeability Time of application: 3min Output: 4 joules / cm 2

70. Cryotherapy / Cold therapy : Ice packs application to the painful area 4 times a day for 20 min. Ice should not be placed over skin not more than 5 to 7 min It lowers thermal gradient in skin, interrupting massive concentration of Histamines, thus lowering pain threshold in the skin. Acupuncture: It is based on a complex relationship between energy through channels or natural elements (wood, earth and water) and positive and negative elements. Energy flow is done merely by placing a needle into a specific site and adding either electric or heat to the needle. It has minimal effect on reducing pain therefore not recommended as primary therapy. Its used as an alternative therapy.

71. Use of vasocoolent sprays : Cold encourages the relaxation of muscles that are in spasm and thus relieves the associated pain . Most commonly used – ethyle chloride and fluromethen Fluromethane or ethylchloride spray is applied to painful area for 5 min. Muscles are then gently stretched after that. Electrogalvanic stimulations: Delivers a wide range of intensity to activate the injured muscles. It stimulate local circulation, achieves excitability and conductivity without painful heating. Pulse at 80 cycles / sec for 10 min followed by excessive for 5 min.

72. TENS (Transcutaneous Electrical Nerve Stimulation) Produced by a continuous stimulation of cutaneous nerve fibers at a sub-painful level When a TENS unit is placed over the tissues of a painful area, the electrical activity decreases pain perception TENS uses a low-voltage, low-amperage , biphasic current of varied frequency and is designed primarily for sensory counter-stimulation in painful disorders . It stimulate local circulation, achieves excitability and conductivity without painful heating. Pulse at 80 cycles / sec for 10 min followed by excessive for 5 min.

73. PENS (Percutaneous Electrical Nerve Stimulation) A new therapy for chronic pain sufferers that uses a low voltage electrical current delivered to the subcutaneous tissue or peripheral nerves to relieve chronic refractory neuropathic pain  I t is a form of neurostimulation or neuromodultation that damping down overactive (sensitized) nerves that are causing pain Does not destroy any nerves. It just makes them less sensitive to pain. A low voltage electrical current is delivered via a specially designed needle to a layer of tissue just below the surface of the skin close to the specific nerve, or to the nerve endings situated in an area that is painful Some patients will have total pain relief, others experience prolonged pain relief for 3 months or more and others get relief for shorter periods of time

74. Manual therapy Soft tissue mobilization Joint mobilization Muscle conditioning Passive muscle stretching Assisted muscle stretching Resistance exercise Postural training

75. PHARMACOTHERAPY Anti inflammatory drugs: NSAIDS : Reduces inflammation and provide pain relief both in the muscles and joints for 14-21 days. Aspirin  2 tab 0.3 to 0.6gm / 4th hourly Piroxican  10-20 mg / 3-4 times /day Ibiprofen  200-600mg / 3-4 times / day Opoids : Pertazacine  50mg / 2-3 times /day. Muscle relaxants: It is used for short duration as they produce addiction. Meprobamate  400mg TDS for 1 days. Vallium  5-10mg 2-3 times /day. It can be used as centrally acting eg Datrium , Succinyl colin , cusara , baclofin , and peripherally acting.

76. ANTI ANXIETY MEDICATION: Propylalcohol derivatives – Meprobamate 1200-1600 mg / day is divided doses. Diphexyl methansis – Antilistamines are used in patients where benzyl diazapines are contra indicated. BENZODIAZEPIENES: Alprazalam – 0.5mg 1-3 times / day Diazepam – 2-5mg 1-4 times / day for 10 days ANTI DEPRESSANT : Amitriptyline  10-25 mg/day for 3 times Fluoxitin 5mg / day LOCAL ANAESTHETICS: Procaine – 0.5% Lidocain – 1%, 2% Ethyl chloride spray or i.m . Local anaesthetic at affected part give relief.

77. PCA (Patient Controlled Analgesia) for MPDS It is an effective method for administrating opiates to patient for pain relief. It gives patients a sense of control over pain

78. USE OF BOTOX Botulinum toxin injections are currently the mainstay of treatment for most focal dystonias . Neurotoxin botulinum toxin A, when injected into a muscle, causes a presynaptic blockade of the release of acetylcholine at the motor end plates. End result is a muscle that can no longer contract (paralysis ). Normally takes 1 to 2 weeks for the effect to be clinically noticeable. Normally , activity of the motor end plate is totally restored in 3 to 4 months Approximately 25 U of botulinum toxin A is normally appropriate for each of these muscles . The greatest number of motor end plates is found in the midbody of the muscle (halfway between the insertion and origin ).

79. OCCLUSAL SPLINT Purpose: To create a balance joint tooth stabilization the mandible. To reduce spasm, contracture and hyperactivity of musculature. To restore vertical dimension Types: Stabilization splint Relaxation splint

80. Stabilization Splint 12-18 hrs / 4-6 months Fabricated over the maxillary teeth covering occlusal and incisal surface made up of acrylic A flat platform perpendicular to mandibular incisors so the splint will disengage the teeth and release the muscles If patient doesn’t have relief at the end of 3 month re-evaluation should be done. Splint reduces the load on the retrodistal area and therapy relieve pain. Pre fabricated rediant splint are also available.

81. Relaxation splint It is used for disengagement of teeth and for only short period ( upto 4 wks ) They are fabricated over the maxillary incisor teeth A platform is added to disengage mandibular anterior

82. Differential diagnosis Type Cause History C/F Treatment Muscle splinting Altered sensory input Constant deep pain Increased stress Recent alteration in local structure Source of deep pain Recent increase in emotional stress Decrease ROM But may achieve normal ROM on request No pain at rest Pain with function Muscle weakness Correction of local causes Removal of source of deep pain Psychological regulation Soft diet Analgesic Local muscle soreness h/o previous muscle splinting Local tissue trauma Emotional stress Pain begun after several hr /day of an event Pain started by- injection, long standing mouth opening Increased emotional stress Decrease ROM & velocity but normal range not achieve on request Minimum pain at rest Pain increase with function Muscle fatigue Elimination of constant deep sensory input Patient motivation and emotional stress management Supportive therapy to control algesia Stabilization appliance Myospasm Continue deep pain Local metabolic factors within muscle tissues Idiopathic myospasm mechanism Sudden onset of restricted jaw movement Marked restriction of jaw movement Acute malocclusion Pain at rest Pain increase with function Affected muscle firm and painful Generalized muscle tightness Passive lightening/ stretching by manual massage 2% lidocaine without vasopressor to stop persistent spasm Muscle rest Reestablishment of electrolyte balance

83. Type Cause History C/F Treatment Myofascial pain Continue deep pain Increased emotional stress Sleep disturbance Local factors – habit, posture, muscle strain, chilling Systemic factors – nutritional imbalance, fatigue, viral infection Idiopathic trigger point c/o heterotropic pain c/o headache or muscle splinting Slight decrease in velocity and range of motion of jaw Presence of trigger point Presence of reference zone Heterotropic pain at rest Pain increase with function On provocation pain at refer zone Eleminate source of deep pain Soft diet Life style modification Analgesic, antianxyti , muscle relaxant Spray and stretch Massage Injection/ theraputic blocking Chronic myositis Mediated by CNS not by masticatory system While CNS exposed to prolonged pain – brain pathway of pain deranged – antidromic effect of afferent nerve Constant, primary, myogenous pain Associated with prolonged history of muscle complain Significant decrease in velocity and range of movement Significant pain at rest Pain increase with rest Generalized muscle tightness Significant pain on muscle palpation May induce muscle atrophy Restricted muscle use Soft diet Slower chewing and smaller bite Avoid exercise or injection – may increase pain – due to neurogenic inflammation Disengage the teeth by relaxation splint Prescribe NSAIDs Fibromyalgia Still not cleared Alteration in musculoskeletal input by CNS Chronic & generalized musculoskeletal pain in ¾ quadrant of body since 3 month or more Presence of sleep disturbances Clinical depression Generalized myogenous pain Decreased ROM Presence of numerous myofascial trigger point Generalized muscle fatigue & weakness Definitive therapy to treat underling causes NSAIDs helpful to some extent If sleep problem – antidepressant can be given

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