Masticatory muscle pain theory
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MASTICATORY MUSCLE PAIN THEORY. Masticatory OVERLOAD. TMJ SYMPTOMS.

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MASTICATORY MUSCLE PAIN THEORY

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Masticatory muscle pain theory

MASTICATORY MUSCLE PAIN THEORY


Masticatory overload

Masticatory OVERLOAD


Tmj symptoms

TMJ SYMPTOMS

  • Each anatomic portion of the TMJ articulation can tolerate functional change, but if the functional change exceeds a critical level, then alteration within the tissues occur. This level is referred to as structural tolerance. Potential sites of breakdown: muscles, the TMJs, the supportive structures of the teeth, and the teeth.


Muscles of mastication

MUSCLES OF MASTICATION

  • Masseter

  • Temporalis

  • Medial pterygoid

  • Lateral pterygoid

  • Functional d/o of the masticatory muscles are the most common TMD complaint to bring pts into the dental office and of all pain is second only to odontalgia


Muscle pain

MUSCLE PAIN

  • Myalgia: pain felt in muscle tissue

  • This pain can be due to overuse and fatigue but typically TMD is multifactorial i.e. can be centrally mediated, occlusion-related,parafunctional habits, overloading of the joint

  • Severity of the pain is directly related to the functional activity of the muscle involved.


Masticatory muscles

MASTICATORY MUSCLES

  • Activities of the masticatorymusles can be divided into 2 basic types: (1) functional: this describes chewing,speaking and swallowing; and (2)parafunctional: includes clenching or grinding (i.e. bruxism) and various oral habits

  • Parafunctional activity is divided into 2 types: that activity that occurs during the day-diurnal and the activity that occurs at night-nocturnal


Diurnal activity

DIURNAL ACTIVITY

  • Parafunctional habits during the day consists of clenching and grinding, and oral habits like cheek and tongue biting, finger and thumb sucking, unusual postural habits, occupational habits such as biting on pencils, nails or holding objects under the chin like a violin or telephone. Most pts are not even aware of the habit


Nocturnal activity

NOCTURNAL ACTIVITY

  • STAGES OF SLEEP: sleepers pass through 5 stages: 1,2,3,4 and REM sleep. These stages progress cyclically from 1 through REM then begin again with stage 1. A complete cycle will usually last ~90-110 minutes. The first sleep cycles each night have short REM sleeps and long periods of deep sleep but later in the night, REM periods lengthen and deep sleep time decreases.


Sleep stages con t

SLEEP STAGES CON’T

  • Stage 1 is light sleep, easily arousable. Eyes

    move slowly and muscle activity slows

  • Stage 2, eye movement stops and brain waves become slower.

  • Stage 3, extremely slow brain waves(delta) are interspersed with smaller, faster waves(alpha)

  • Stage 4: almost exclusively delta. Stage 3&4 are referred to as deep(delta) sleep. Now Sleep Medicine combines Stage3&4 into 3


Sleep stages con t1

SLEEP STAGES CON’T

  • Stage 3 is when children experience bedwetting, sleepwalking or night terrors.

  • REM period: breathing is rapid,irregular and shallow, pulse and bp increase and dreams most common and can be remembered

  • Adults spend half the sleep cycle in stage 2, abut 20% in REM and the other 30% is divided between the other stages.

  • New class.:REM and NREM1/NREM2/NREM3


Nocturnal bruxism

NOCTURNAL BRUXISM

  • Stages of sleep and bruxist behavior: if a pt is deprived of REM sleep, will see emotional lability-irritability and increased anxiety; if deprived of nonREM sleep, will see musculo-skeletal tenderness,aching and stiffness. The REM pattern is important for psychic rest and nonREM is important for physical rest.


Stages of sleep and bruxism

STAGES OF SLEEP AND BRUXISM

  • If you direct a flashing light toward a sleeping pt’s face, this stimulation will produce tooth grinding, and will occur with sonic and tactical stimulation also.

  • The take home point is bruxism is associated with arousal phases of sleep

  • Bite Force: females 79-99lb

    males 118-143 lb

    greatest bite force recorded 975lb


Dysfunction

DYSFUNCTION

  • Is a commonly used term but the actual definition is a decrease in the range of mandibular movement. If muscle tissue is overused, any contraction or stretching increases pain and the pt will restrict movement. Acute malocclusion-any sudden change in the occlusal condition and occlusal contact changes so the resting length of masticatory muscle is shortened.


Types ofmasticatory muscle disorders 5

TYPES OFMASTICATORY MUSCLE DISORDERS (5)

  • Protective co-contraction (muscle splinting)

  • Local muscle soreness

  • Myofascial (trigger point) pain

  • Myospasm

  • Chronic centrally mediated myalgia

  • Don’t forget about fibromyalgia

    Most of the masticatory muscle d/o occur and recover in a short period of time. Chronic myalgic d/o are centrally mediated myalgia and fibromyalgia


Centrally mediated myalgia chronic myositis

CENTRALLY MEDIATED MYALGIACHRONIC MYOSITIS

  • Causation is at the CNS rather than at the local muscle level. No classic signs of inflammmation. The CNS sends out antidromic neural impulses to muscular and vascular tissues. This process is caused by prolonged myogenous pain and is associated with structural dysfunction, pain at rest local muscle tenderness and muscle contracture.


Protective co contraction

PROTECTIVE CO-CONTRACTION

  • Is a CNS response to injury or threat of injury. Normal sequencing of muscle activity in injury is altered so as to protect the threatened part. Also called protective muscle splinting, and can be caused a source of deep pain or an increase in emotional stress. Clinically described as a feeling of muscle weakness following an event


Local muscle soreness noninflammatory myalgia

LOCAL MUSCLE SORENESSNONINFLAMMATORY MYALGIA

Is a primary, noninflammatory, myogenous pain d/o. It is the first response of muscle tissue to prolonged co-contraction. Local changes seen include release of algogenic substances like bradykinin, substance P and histamine. Causes include protracted co-contraction, local trauma, or excessive muscle use. Is a source of deep muscle pain. Muscle weakness is seen.


Central nervous system effects on muscle pain

CENTRAL NERVOUS SYSTEM EFFECTS ON MUSCLE PAIN

  • After local muscle tissue pain occurs, the CNS may influence progression. This is either due to ongoing deep pain, altered sensory input or upregulation of the autonomic nervous system.

  • Centrally influenced muscle pain divided into ACUTE MYALGIC D/O like myospasm or CHRONIC MYALGIC D/O which is subdivided into myofascial pain or centrally mediated myalgia


Myospasm tonic contraction myalgia

MYOSPASMTONIC CONTRACTION MYALGIA

  • Myospasm is a CNS-induced tonic muscle contraction. Are short-lived, and the muscle is firm to palpation. Like an acute leg cramp. If these contractions are repeated then classified as dystonia


Regional myalgic d o trigger point myalgia

REGIONAL MYALGIC D/OTRIGGER POINT MYALGIA

  • Results from hypersensitive areas within muscles, which feels like bands within the muscle. A trigger point is a localized area of muscle tissue (zone) with a and is few muscle motor units contracting. Are a source of deep pain and can excite a group of afferent interneurons which cause referred pain


Occipital belly of the occipitofrontalis muscle

Occipital belly of the occipitofrontalis muscle

HA pain behind eye


Trapezius muscle with referred pain to ear temple and angle of mand

Trapezius muscle with referred pain to ear,temple and angle of mand.


Scm with referred pain to temple

SCM with referred pain to temple


Semispinalis capitis referred painto anterior temple above eye

Semispinaliscapitis-referred painto anterior temple above eye


Trigger point injections

TRIGGER POINT INJECTIONS

  • Diagnostic nerve blocks may be indicated.

  • The indication may be for diagnosis. If for diagnosis, use a short-acting local anesthesia without vaso. If for long term pain relief, a long-acting local anesthetic may be indicated. Pain referral pathways can be also be demonstrated.

  • All local anesthetics are myotoxic, but the least myotoxic is procaine (1 or 2%). Epi containing solutions cause greater muscle damage.


Trigger con t

TRIGGER CON’T

  • Can be used for diagnostic and therapeutic purposes. Since procaine is not available in carpule form, can use lidocaine or mepivacaine

  • If a trigger point, the muscle will have a band which is palpable, and when injected will shut down the pain referral pattern.


Trigger point injections1

TRIGGER POINT INJECTIONS

  • Use antisepsis to the skin. Needle gauge is usually 27g. Penetrate the band and will elicit exquisite tenderness in the local area and to the referral area. Inject .5 to 2 ccs and fan the injections. After the injections, apply pressure for hemostasis and OK to apply warm moist pack after hemostasis obtained.

  • Stretch and spray with Flouri-Methane. Trying to inactivate myofascial TP’s. Can reperform 2-3 times at each appointment.


Masticatory muscle pain theory

Penetrate band

Fan needle penetration sites


Masseter muscle injection

MASSETER MUSCLE INJECTION

  • Is the most powerful of the muscles of mastication

  • Superfical head arises from inferior border of anterior 2/3 of arch

  • Deep head arises from inferior border of posterior 1/3 of arch


Temporalis muscle injection

TEMPORALIS MUSCLE INJECTION

  • Originates from the entire temporal fossa and faxcia covering the muscle. Insert into coronoid process and anterior border of ramus.

  • Closes mandible and retrudes


Masticatory muscle pain theory

SCM

  • Origin from manubriumsterni and medial third of upper clavicle

  • Inserts after 2 heads join and into mastoid process. Nerve supply via spinal accessory and anterior rami of 2nd and 3rd cervical nerves

  • Action is to extend the head, contraction of one muscle pulls ears down to tip of shoulder

  • Torticollis:congenitalvs spasmodic


Sternocleidomastoid injec

STERNOCLEIDOMASTOID INJEC.


Splenius capitis

SPLENIUS CAPITIS

  • The splenius is a detached part of the deep muscles of the back.

  • Arises from the lower part of the ligamentumnuchae and the 4 upper thoracic spines. Inserts into superior nuchal line of occipital bone and the mastoid process

  • Palpation of mastoid process could produce pain via SCM or Splenius cap.


Splenius capitis1

SPLENIUS CAPITIS


Posterior occipital injec

POSTERIOR OCCIPITAL INJEC.


Trapezius muscle injec

TRAPEZIUS MUSCLE INJEC.


Auriculotemporal block

AURICULOTEMPORAL BLOCK

  • The primary sensory innervation to the joint is via the auriculotemporal nerve, with the massteric br. being secondary.

  • Is a br. of the mandibular br. of V-3

  • Emerges from upper border of parotid gl. behind the jt. It crosses the root of the zygomatic arch behind the superficial temporal artery and in front of the auricle


Art block

ART. BLOCK

  • Needle placement is is just anterior to the junction of tragus and ear lobule. Penetrate skin until posterior neck of condyle is felt.

  • Reposition the needle posteriorly until tip of needle is behind the neck of condyle. Penetrate up to 1 cm and remember the main complication is vascular or neurologic.


Auriculotemporal block1

Auriculotemporal block


Fibromyalgia syndrome fms

FIBROMYALGIA SYNDROME (FMS)

  • Is controversial and of unknown etiology.

  • Characterized by history of bilateral, upper and lower body, “musculoskeletal” pain combined with findings of painful tenderness at 11 or more of 18 anatomically defined soft tissue tender points

  • Other manifestations incl.:lightheadedness, memory loss, insomnia, depression, fatigue, IBS, and urodynia.


Fms con t

FMS CON’T

  • Associated co-morbidities incl.: rheumatic,inflammatory,infectious(Lyme), and endocrine d/o. RA(33%),SLE(40%) and Sjogren’s(50%) prominent

  • Some refer to this entity as “chronic, widespread allodynia”

  • Serotonin, important for regulation of deep sleep and of pain perception, also regulates release of substance P. Substance P [ ] is elevated ~3-fold in the spinal fluid of FMS pts


Masticatory muscle pain theory

FMS

  • Is classified as a soft tissue pain syndrome characterized by widespread pain emanating from periarticular structures outside the joint capsule and periosteum. No synovial joint involvement, so is not arthritic. Effects ligaments, tendons, fascia, bursae, and muscles. These soft tissue structures facilitate function in diarthrodial joints

  • 4-7X more common in females, 50-60 years of age. Interestingly, insulin-like growth factor(produced during delta sleep) decreased


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