Neurophysiological mechanisms of TMDS.C.Ahn

1.The charcteristics of peripheral nociceptors.->the reason why inflamed tissues become sensitive to palpation and movement.2.Central nociceptive neurons.->the nature of the pain.3.Functional changes in central reflex. ->the effect of pain on movement.Introduction

Properties of pain receptors in muscles and joints Nociceptors ->unencapsulated nerve endings fromsmall myelinated(A-delta fiber)unmyelinated(C-fiber)some of these receptors begin to fire when noxious stimuli or algesic chemicalanother group of these receptors become sensitized to mechanical stimuli,and respond to previously innocuous pressure

Properties of pain receptors in muscles and joints

Properties of pain receptors in muscles and joints Peripheral changes Sensitization of nociceptive ending : defence mechanism that protects injured tissues from repeated injury by providing a sharp reminder to cease movement or contactCentral changesDeep pain(poor localization & referral)Hyperalgesia --> these have more to do with central changes

Properties of pain receptors in muscles and jointsNoxious stimuliTissuemast cellsbasophilsmacrophagesplateletsendothelial cellsEndogenous substances

Properties of pain receptors in muscles and jointssome of these endogenous substances produce pain when they are applied locally (histamine, bradykinin, serotonin, potassium)other substances facilitate the pain evoked by stimuli, but themselves are relatively ineffective in evoking pain (prostaglandins)

Roles of sensory & sympathetic neurons in inflammationAntidromic stimulation of sensory nerves causes vasodilation & inflammation in the areas that they innervate ---->Neurogenic inflammationThe branches of primary afferents that ramify in tissues outside the site of injury --->a essential role in the spread of inflammation

Roles of sensory & sympathetic neurons in inflammation

Roles of sensory & sympathetic neurons in inflammationThis process is associated with peripheral spread of the zone of hyperalgesia or tenderness of injuryHyperalgesia1)primary hyperalgesia : in the primary zone of injury2)secondary hyperalgesia : in the secondary zone that surrounds the primary site

Roles of sensory & sympathetic neurons in inflammation The release of neuropeptides from the terminals of thin afferent fibers is the critical event in neurogenic inflammation (sustance P, neurokinin A, somatostatin, Calcitonin Gene-Related Peptide, Vasoactive Intestinal Peptide)

Roles of sensory & sympathetic neurons in inflammationIt is an important transmitter in the nociceptive pathways because it excites spinal cord and trigeminal nociceptive neurons.Sunstance P has many actions : vasodilation, increases vascular permeability, activate lymphocyte, initiate pavementation of lymphocyte, release of histamin and 5-hydroxytryptamine(5-HT) from mast cell

Roles of sensory & sympathetic neurons in inflammationThese promote both vasodilation and vascular permeability and increase the rate of release of substance P. Neural mechanism for suppressing neurogenic inflammation : second population of primary afferents containing somatostatin which inhibits the liberation

Roles of sensory & sympathetic neurons in inflammationNeurogenic effect in inflammationinflammation is greatest in the joints that have the highest levels of substance PWhen rats were treated systemically with capsaicin, which destroys unmyelinated afferent fibers and depletes substance P, they were protected against the experimental arthritis.

Roles of sensory & sympathetic neurons in inflammationNeurogenic effect in inflammation in humans gold has been used for many years to treat rheumatoid arthritis,is now known to be a selective neurotoxin that attcks unmyelinated nerve fibersLocal microvasculature and the sympathetic efferent fiber are important in inflammation. Substance P released from afferent terminals at the site of injury and in the secondary zone acts on the blood vessels

Roles of sensory & sympathetic neurons in inflammationThe substance P causes sympathetic neurohumoral agents to bo secreted by sympathetec terminals inderectly via histamine : norepinephrine->vasoconstrictionprostanoid PGE2->vascular permeability

Roles of sensory & sympathetic neurons in inflammationNociceptive afferents increase the release of substances from sympathetic terminalssubstance P-containg terminals of sensory neurons innervate sympathetic gangliathere are reflex connectons between primary afferents and sympathetic preganglionic neurons that aldo lead to increased sympathetic tone.Stress, which increases sympathetic activity, exacerbates the symptoms of TMDs

Central mechanismsThe spinal cord dorsal horn and trigeminal subnucleus caudalis are key structrues for pain perception. They contain neurons with several different types of somatosensory receptive fields. Low-Threshold mechanoreceptive(LTM) neurons. :Nociceptive specific(NS) neurons :Wide dynamic range(WDR) neurons :

Central mechanismsWDR & NS neurons code the intensity and spatial localization of noxious stimuli. Many neurons of all three types project to higher centers and contribute to sensory perception. A characteristic of many spinal & trigeminal WDR and NS somatosensory neurons transmitting deep nociceptive information is that they receive additional inputs from afferents supplying other tissues

Central mechanismsExtensive convergence and large mechanoreceptive fields are typical of myofascial or TMJ-activated WDR and NS neurons in subnucleus caudalis. These features contribute to the poor localization, spread and referral of pain that are characteristic of pain conditions involving the TMJ and associated musculature.

Central mechanismsExtensive convergencePoor localization Referral of painSpread of pain

Central mechanismsCentral sensitization of spinal dorsal horn nociceptive neurons can occurInjection of algesic chemical into muscle or localized inflammation can result in change in neurons of the spinal dorsal horn and primary somatosensory cortex.Their responsiveness to afferent inputs is enhanced, not only from the site of inflammation, but also from other tissues.

Central mechanismsHyperalgesiaPeripherial sensitizatonCentral sensitizationHyperalgesia

Central mechanismsCentral sensitizationLocalized inflammationSpinal dorsal hornThalamusPrimary somatosensory cortexResponsiveness is enhancedHyperalgesia

Central mechanismsThese process may influence the cutaneous as well as the deep receptive field properties of central spmatosensory neuronsNot only more responsive to gentle movement of the inflamed site, but some also show prolonged changes in receptive field size.C-fibers appear to be especially important for inducing these effects.

Central mechanismsThe remarkable properties of trigeminal nociceptive neurons, and in particular the enhanced excitability that follows the stimulation of small-diameter afferent fibers from muscle, joints and other deep tissues, appear to contribute to the tenderness and hyperalgesia, as well as to the spread and referral of pain , that characterize conditions such as TMD.

Central mechanismsThe cause of the pain that is the primary sign of the TMD is still not known.It is likely that many of the neural mechanisms are important in TMJ arthritis and that they will later be linked to myofascial pain.1)neurogenic inflammation2)peripheral sensitization3)central sensitization

Central mechanisms

The relationship between pain and muscle dysfunctionSustained muscle hyperactivity in the development and persistence of TMD pain is not a factor in the large majority of cases.

TMD is separated into distinct1)Myogenous2)Internal derangement3)Arthritis

The relationship between pain and muscle dysfunctionThe ability of patients with these conditions to move the jaws is abnormal. This can be caused by mechanical impediments to movement and be related to the presence of painAt past, it is thought that the soreness and tenderness lead to overwork and fatigue, and muscle hyperactivity causes pain, and that pain in its turn promotes hyperactivity -->a chronic vicious cycle

The relationship between pain and muscle dysfunctionFunctioning abnormallyMuscle hyperactivityPainChronic vicious cycle

The relationship between pain and muscle dysfunctionIt is certainly true that heavy exercise can lead to microtrauma in muscles and connective tissue. This is followed by pain that peaks in about 24hours. --->Post-Exercise Muscle Soreness(PEMS)

However, pain interacts with the neurons that program movements.

Postural activity in TMDIt was accepted for a long time that people suffering from TMD had an abnormally high level of postural activity in their jaw closing muscles, and that this was the cause of fatigue, ischemia and pain.In EMG activity of the masseter and temporalis muscles of TMD patients and people without pain, the average activity in the patients was a few millivolts higher than normal.

Postural activity in TMDIt seems a little extravagant to label such small increases hyperactivity, because they represented only 1~2% of the maximum output of the muscle. These small differences between the patients and the other proups were due to other factors that were not controlled in the experiments, such as sex, age and prevalence of bruxism

Postural activity in TMDChronic bruxers have higher resting activity than non-bruxers, presumably because their jaw muscles are relatively hypertrophied, there is no difference between the resting activity of bruxers who report pain and those who do not. The evidence does not support the idea that there is a systematic increase in the postural activity of muscles in TMD.

Biting forceChronic pain patients cannot exert maximal force. The maximal biting force of TMD patients is significantly less than controls. Biting force increased over time as pain fell.The pain does not even have to be associated with muscles or joints to cause a fall in bite force. For example, the bite force after extraction was lower and that there was a weak inverse correlation with pain intensity

Voluntary jaw movements and masticationPain often changes movement.TMD patients cannot open their mouths widely without painThe restriction on movement must rarely be structural, because the TMD subjects could open an average of more than 7mm more if they were encouraged or assisted.

Voluntary jaw movements and masticationHyperalgesia and tenderness cause most TMD patients to reduce the amplitude of voluntary movements so as to avoid pain, it also seems that unconscious reflexes, heightened by the peripheral and central sensitization, participate. Jaw-closing muscles were more active in TMD patients than in controls during the jaw-opening phase of mastication.

Voluntary jaw movements and mastication

The mean activity of the masseter and temporalis muscles of individual TMD patients is significantly greater during the jaw-opening phase of painfl masticatory cycles than during pain-free cycles.

Voluntary jaw movements and masticationPain in the masseter muscle : 1)A decrease in the velocity and amplitude of jaw movement2)The activity of masseter muscles are less active3)EMG of the masseter become more active during jaw-opening

The pain-adaptation modelPain has a similar effect on muscle activity throughout the body.Vicious cycle theory has been rejected Pain-adaptation model proposed to explain the effects of pain on motor activity.It incorporates how sensory-motor interactions take place, and it can account for the changes in motor patterns that accompany chronic pain.

The pain-adaptation model

Pain in a body part causes agonist muscles to become less active and antagonist muscles to become more active than normal

A decrease in the amplitude and speed of movements, which probably reduces the chance of aggravating the injury and therefore aids healing.

The pain-adaptation modelAt least, part of the effect of pain is involuntary.Pain can change movements by acting at the level of the brainstem or spinal cord.

Summary

Inflammatory processes, the peripheral sensitization of muscle and joint nociceptors, and the central sensitization of the nociceptive neurons in the spinal cord and brainstem is important for pain on TMJ.

Summary

The properties of the peripheral and central neural elements can explain many of the signs and symptoms of TMD, including the tenderness the poor localization, spread and referral of pain, as well as the limitation of jaw-opening and slowing of movement

ReferenceGeorge A.Zarb. Gunnar E.Carlsson. Temporomandibular joint and masticatory muscle disorders. 158-207Epker J.et al. A model for predicting chronic TMD : practical application in clinical settings. J Am Dent Assc. 1999 Oct: 130(10):1470-5

Wight EF. Referred craniofacial pain patterns in patients with temporomandibular disorder. J Am Dent Assoc.2000 Sep:131(9):1307-15Maixner W.et al. Sensitivity of a patients with painful temporomandibular disorders to experimentally evoked pain: evidence for altered temporal summation of pain. Pain..1998 May:76(1-2):71-81

Colpaert FC, Donnerer J, Lembeck F. Effects of capsaicin on inflammation and on the substance P content of nervous tissues in rat with adjuvant arthritis. Life Sci 1983;32:1827-34