Difference between revisions of "Trigeminal Nociceptive Evaluation in TMD Patients by studying CO2-Laser Evoked Potentials and Masseter Laser Silent Periods"

Trigeminal Nociceptive Evaluation in TMD Patients by studying CO2-Laser Evoked Potentials and Masseter Laser Silent Periods (view source)

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-=Chapter 6=
-'''Evaluation of the trigeminal nociceptive system in patients with temporomandibular dysfunction through CO2 laser-evoked potentials and masseter laser silent periods study'''
 '''Antonietta Romaniello'''
-Department of Neurological Sciences, University of Rome “La Sapienza”
 ===Introduction===
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 ===Discussion===
 ===Modulation of Laser-Evoked Potentials (LEPs)===
-Several studies have described modulation of brain responses evoked by phasic nociceptive experimental stimuli in patients with various types of chronic pain. In patients with the so-called "benign intractable chronic pain syndrome," a reduction in LEP amplitude compared to controls was observed<ref name="Coger1980" />. LEP amplitude is also reduced in patients with cervico-brachial pain<ref name="Gibson1991" /> and central pain<ref name="Casey1996" />. A study conducted on patients with "chronic burning mouth syndrome" showed reduced sensitivity to laser stimuli both in the painful area and in non-painful areas<ref name="Svensson1993" />. The collective data suggest inhibition of phasic nociceptive inputs in patients with chronic pain. The results of this study on patients with chronic craniofacial pain provide further support for this interpretation.
+Several studies have described modulation of brain responses evoked by phasic nociceptive experimental stimuli in patients with various types of chronic pain. In patients with the so-called "benign intractable chronic pain syndrome," a reduction in LEP amplitude compared to controls was observed<ref>Coger RW, Kenton B, Pinsky JJ, Crue BL, Carmon A, Friedman Y. Somatosensory evoked potentials and noxious stimulation in patients with intractable, noncancer pain syndromes. Psychiatry Res 1980; 2: 279-294.</ref>. LEP amplitude is also reduced in patients with cervico-brachial pain<ref>Gibson SJ, LeVasseur SA, Helme RD. Cerebral event-related responses induced by CO2 laser stimulation in subjects suffering from cervico-brachial syndrome. Pain 1991; 47: 173-182.</ref> and central pain<ref>Casey KL, Beydoun A, Boivie J, Sjolund B, Holmgren H, Leijon G, Morrow TJ, Rosen I. Laser-evoked cerebral potentials and sensory function in patients with central pain. Pain 1996; 64: 485-491.</ref>. A study conducted on patients with "chronic burning mouth syndrome" showed reduced sensitivity to laser stimuli both in the painful area and in non-painful areas<ref>Svensson P, Bjerring P, Arendt-Nielsen L, Kaaber S. Sensory and pain thresholds to orofacial argon laser stimulation in patients with chronic burning mouth syndrome. Clin J Pain 1993; 9:207-215.</ref>. The collective data suggest inhibition of phasic nociceptive inputs in patients with chronic pain. The results of this study on patients with chronic craniofacial pain provide further support for this interpretation.
 TMD patients exhibited reduced sensitivity to phasic experimental pain, as the suprathreshold laser stimulus was perceived as less intense on the painful side compared to the non-painful side, and at the same time, LEP amplitude was significantly reduced. These observations suggest hypoactivity of the trigeminal nociceptive system projecting to the cortex in TMD patients. It is not possible to determine at which level of the central pathways this modulation occurs. However, peripheral involvement is unlikely since the perceptual threshold in TMD patients did not differ from that of controls. It is probable that the inhibition of LEP amplitude represents an alteration in the cognitive evaluation of nociceptive information, which could derive either from a psychological adaptation process, where discomfort caused by phasic experimental pain is reduced due to comparison with the considerably greater discomfort caused by clinical pain, or from a physiological phenomenon of compensatory inhibition of nociceptive information<ref name="Gracely1984">Gracely RH. Subjective quantification of pain perception. In: Bromm B (ed.), Pain Measurement in Man: Neurophysiological Correlates of Pain, Elsevier, Amsterdam, 1984: 111-137.</ref>.
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 ===Modulation of Laser Silent Period (LSP)===
-Studies on the EMG activity of muscles affected by pain have yielded conflicting results, and the literature on EMG changes in TMD provides inconclusive data<ref name="Stohler1995">Stohler CS. Craniofacial Pain and Motor Function, Exp Brain Res 1995; 99: 46-53.</ref><ref name="Svensson2000" />. However, there is evidence that pain alters motor performance by facilitating the motoneuron when the muscle acts as an agonist and inhibiting it when the muscle acts as an antagonist<ref name="Lund1991" />. Motor performance modulation has been observed in various types of chronic pain and likely reflects an adaptive process<ref name="Lund1991" />. At the trigeminal level, nociceptive inputs from the masticatory muscles reduce both the amplitude and speed of voluntary jaw movements<ref name="Lund1991" /> and chewing movements<ref name="Svensson1996a" /><ref name="Svensson1996b" />. The reduction in pre-stimulus EMG activity observed in our study is consistent with the above theory. Unilateral reduction in pre-stimulus EMG activity was associated with significant bilateral inhibition of the brainstem reflex pathways mediating nociceptive reflex responses (LSPs were absent bilaterally in most TMD patients). It is unlikely that the absence of LSPs was caused by reduced pre-stimulus EMG activity. Miles and Turker<ref name="Miles1986" /> demonstrated that motoneuron susceptibility to inhibition is proportional to their firing rate. Therefore, at equal stimulus intensity, it should be easier to inhibit motoneurons with lower pre-stimulus firing levels<ref name="Miles1986" />. Hence, the absence of LSP in TMD patients was most likely caused by chronic pain and not reduced pre-stimulus EMG activity.
+Studies on the EMG activity of muscles affected by pain have yielded conflicting results, and the literature on EMG changes in TMD provides inconclusive data<ref name="Stohler1995">Stohler CS. Craniofacial Pain and Motor Function, Exp Brain Res 1995; 99: 46-53.</ref><ref name="Svensson2000" />. However, there is evidence that pain alters motor performance by facilitating the motoneuron when the muscle acts as an agonist and inhibiting it when the muscle acts as an antagonist<ref name="Lund1991" />. Motor performance modulation has been observed in various types of chronic pain and likely reflects an adaptive process<ref name="Lund1991" />. At the trigeminal level, nociceptive inputs from the masticatory muscles reduce both the amplitude and speed of voluntary jaw movements<ref name="Lund1991" /> and chewing movements<ref>Svensson P, Arendt-Nielsen L, Bjerring P, Bak P, Hjorth T, Troest T. Human mastication modulated by experimental trigeminal and extra-trigeminal painful stimuli. J Oral Rehabil 1996a; 23: 838-848.</ref><ref>Svensson P, Arendt-Nielsen L, Houe L. Sensory-motor interactions of human experimental unilateral jaw muscle pain: a quantitative analysis. Pain 1996b; 64: 241-249.</ref>. The reduction in pre-stimulus EMG activity observed in our study is consistent with the above theory. Unilateral reduction in pre-stimulus EMG activity was associated with significant bilateral inhibition of the brainstem reflex pathways mediating nociceptive reflex responses (LSPs were absent bilaterally in most TMD patients). It is unlikely that the absence of LSPs was caused by reduced pre-stimulus EMG activity. Miles and Turker<ref name=":0">Miles TS, Turker KS. Does reflex inhibition of motor units follow the "size principle"? Exp Brain Res 1986; 62: 443-445. </ref> demonstrated that motoneuron susceptibility to inhibition is proportional to their firing rate. Therefore, at equal stimulus intensity, it should be easier to inhibit motoneurons with lower pre-stimulus firing levels<ref name=":0" />. Hence, the absence of LSP in TMD patients was most likely caused by chronic pain and not reduced pre-stimulus EMG activity.
 LSP is a purely nociceptive reflex<ref name="Ellrich1997">Ellrich J, Hopf HC, Treede RD. Nociceptive masseter inhibitory reflexes evoked by laser radiant heat and electrical stimuli. Brain Res 1997; 764: 214-220.</ref><ref name="CruccuRomaniello1998">Cruccu G, Romaniello A. Jaw-opening reflex after CO2 laser stimulation of the perioral region in man. Exp Brain Res 1998; 118: 564-568.</ref>, whose circuit remains partially unknown. A common center has been suggested, represented by wide-dynamic-range (WDR) neurons of the reticular nucleus, corresponding to lamina V of the subcaudal nucleus<ref name="Sessle1999">Sessle BJ. Neural mechanisms and pathways in craniofacial pain. Can J Neurol Sci 1999; 26: 7-11.</ref><ref name="CruccuRomaniello1998" />, capable of mediating the second silent period of the masseter evoked electrically (SP2), the single silent period evoked by supraorbital nerve stimulation, and LSP. Experimental studies have shown that SP2 is modulated by experimental painful stimuli applied both in the trigeminal area<ref name="Wang1999">Wang K, Svensson P, Arendt-Nielsen L. Modulation of exteroceptive suppression periods in human jaw-closing muscles by local and remote experimental muscle pain. Pain 1999; 82: 253-262.</ref> and in extra-trigeminal areas<ref name="Bendtsen1993">Bendtsen L, Jensen R, Brennum J, Arendt-Nielsen L, Olesen J. Exteroceptive suppression periods in jaw-closing muscles. Variability and relation to experimental pain and sustained muscle contraction. Cephalalgia 1993; 13: 184-191.</ref><ref name="Bendtsen1996">Bendtsen L, Jensen R, Brennum J, Arendt-Nielsen L, Olesen J. Exteroceptive suppression of temporal muscle activity is normal in chronic tension-type headache and not related to actual headache state. Cephalalgia 1996; 16: 251-256.</ref><ref name="Cadden1994">Cadden SW, Newton JP. The effects of inhibitory controls triggered by heterotopic noxious stimuli on a jaw reflex evoked by perioral stimuli in man. Arch Oral Biol 1994; 39: 473-480.</ref><ref name="Schoenen1994">Schoenen J, Wang W, Gerard P. Modulation of temporalis muscle exteroceptive suppression by limb stimuli in normal man. Brain Res 1994; 657: 214-220.</ref>. Conversely, data in TMD patients<ref name="DeLaat1998">De Laat A, Svensson P, Macaluso GM. Are jaw and facial reflexes modulated during clinical or experimental orofacial pain? J Orofac Pain 1998; 12: 260-271.</ref>, as well as in other patients with chronic craniofacial pain<ref name="Schoenen1993">Schoenen J. Exteroceptive suppression of temporalis muscle activity: Methodological aspects and pathophysiological implications. Cephalalgia 1993; 13: 82-91.</ref>, remain controversial.