Abstract: We assessed the trigeminal nociceptive pathways in patients with painful temporomandibular disorders (TMD) and control subjects using a CO(2)-laser stimulator which provides a predominant activation of the nociceptive system. Fifteen patients with unilateral pain were examined in accordance with the Research Diagnostic Criteria for TMD and 30 gender- and age-matched individuals were included as a control group. Laser-evoked potentials (LEPs) and laser silent periods (LSPs) after stimulation of the perioral region (V2/V3) on the painful and non-painful sides were recorded in all subjects. LEPs were evoked by low-intensity pulses (1.5 x perception threshold (PTh)) and recorded from scalp electrodes at the vertex. LSPs were evoked by high-intensity pulses (4 x PTh) and recorded bilaterally from masseter muscles with surface electromyogram (EMG) electrodes. Subjects also assessed the stimulus intensity on a 0-10 rating scale. LEPs had normal latency but smaller amplitude in TMD patients compared to the control group (P<0.001). Side-to-side comparison within patients showed that LEP amplitude was even more reduced after stimulation on the painful than the non-painful side (P<0.001). TMD patients showed a significant side-asymmetry of the pre-stimulus EMG activity, with a smaller value in the muscle on the painful side (P<0.001). LSPs were completely absent bilaterally in 12 TMD patients and unilaterally in two patients; only one patient had normal and bilateral LSPs. TMD patients perceived the laser stimulus less intense on the painful than the non-painful side (P<0.05). We found suppression of cortical responses and brainstem reflexes elicited by a predominantly nociceptive input in TMD patients. These findings are consistent with recent experimental pain studies and suggest that chronic craniofacial pain in TMD patients may be associated with a dysfunction of the trigeminal nociceptive system.

Abstract: Much is unclear about the pathophysiological mechanisms underlying painful temporomandibular disorders. In addition to various other theories, masticatory muscle dysfunction and pain have also been attributed to primary central nervous system hyperactivity. We assessed this possibility in a study using recent neurophysiological techniques. From among outpatients whose diagnosis of temporomandibular disorders had been obtained in stomatognathic facilities, we studied 10 patients with bilateral pain and 15 patients with unilateral pain, in whom electromyographic examination of the trigeminal reflexes disclosed normal findings except for absence or amplitude asymmetry of the jaw jerk. Transcranial magnetic stimulation yielded masseter motor evoked potentials of normal latency and amplitude, but five patients had to exert a near-maximum contraction to obtain their responses. The masseter silent periods elicited by the double-shock technique recovered normally. Because these tests measure the excitability of the masticatory system (including motor cortex, corticobulbar and corticoreticular connections, reticular interneurones and lower motoneurones), the lack of facilitation in these patients' responses excluded central hyperactivity as the primary cause of their masticatory dysfunction and pain.

Abstract: This investigation is focused on the analysis of the masseter responses evoked by means of magnetic and electric stimulation of the cortex and root of the trigeminal system of 20 healthy subjects. Moreover, in order to determine jaw elevation in centric occlusion, the analysis also focused on the motor response of the trigeminal bilateral roots evoked simultaneously using two stimulators. The masseter responses show a high level of symmetry in both latency and amplitude. The difference between the hinge axis in natural centric occlusion (CO) and in centric relation (CR) as determined by electric and magnetic transcranial stimulation is lesser than 2.5 mm. This is due to two main factors: (i) the response is evoked from the trigeminal motor neural pool involving all the masticatory muscles and hence simulating the natural 'muscular coactivation'; (ii) there is no manual manipulation to guide the jaw into the centric relation (CR). This method could be of some help for diagnosis in patients suffering from TMJ dysfunction who have lost stereognostic control over the jaw and display obvious signs of deviation during closure of the mandible.

Abstract: The main purpose of this study is to examine whether the stimulation of an exclusively pain-sensing receptive field (dental pulp) could determine cardiorespiratory effects in animals in which the cortical integration of the peripheral information is abolished by deep anesthesia. In 15 anesthetized (alpha-chloralose and urethan) rabbits, low (3-Hz)- and high-frequency (100-Hz) electrical dental pulp stimulation was performed. Because this stimulation caused dynamic and static reflex contractions of the digastric muscles leading to jaw opening jaw-opening reflex (JOR); an indirect sign of algoceptive fiber activation], experimentally induced direct dynamic and static contractions of the digastric muscle were also performed. The low- and high-frequency stimulation of the dental pulp determined cardiovascular [systolic arterial pressure (SAP): -21.7 +/- 4.6 and 10.8 +/- 4.7 mmHg, respectively] and respiratory [pulmonary ventilation (VE): 145.1 +/- 44.9 and 109.3 +/- 28.4 ml/min, respectively] reflex responses similar to those observed during experimentally induced dynamic (SAP: -17.5 +/- 4.2 mmHg; VE: 228.0 +/- 58.5 ml/min) and static (SAP: 5.8 +/- 1.5 mmHg; VE: 148.0 +/- 75.3 ml/min) muscular contractions. The elimination of digastric muscular contraction (JOR) obtained by muscular paralysis did away with the cardiovascular changes induced by dental pulp stimulation, the effectiveness of which in stimulating dental pulp receptors has been shown by recording trigeminal-evoked potentials in six additional rabbits. The main conclusion was that, in deeply anesthetized animals, an algesic stimulus is unable to determine cardiorespiratory effects, which appear to be exclusively linked to the stimulation of ergoreceptors induced by muscular contraction.

Abstract: Two patients aged 21 and 50 years presented with facial hemiatrophy and unilateral spasms of the masticatory muscles. Masticatory muscle biopsy showed normal findings in both patients and facial skin biopsy specimens only showed atrophy, although morphoea (localised facial scleroderma) had been diagnosed nine years previously in the second patient. The involuntary movements consisted of brief twitches and prolonged contractions clinically and electromyographically similar to those of hemifacial spasm and cramps. The jaw jerk and the silent periods were absent in the affected muscles. Direct stimulation of the muscle nerve and transcranial stimulation of the trigeminal root demonstrated slowing of conduction and after-activity due to autoexcitation. Observations in other reported cases and these two patients suggest that hemimasticatory spasm is produced by ectopic activity secondary to focal demyelination of the trigeminal motor nerve fibres. The proposed cause of the neuropathy is focal damage to the masticatory nerves caused by compression, possibly resulting from the deep tissue changes that occur in facial hemiatrophy.

Abstract: An alternative method for fabricating occlusal splints by means of electric transcortical stimulation is presented. Ensuing results in one patient suggest neuromuscular benefits. However, the centric occlusal position determined by this method is a painful procedure because of electric stimulation on the scalp. Further and extensive investigations must be carried out to assess the clinical benefits and limits of this method.

Abstract: The jaw jerk elicited by tapping the chin with a reflex hammer was electromyographically recorded in 14 patients with craniomandibular dysfunction, who were selected because of their strictly unilateral symptoms. Mandibular deviation, as measured by means of a kinesiograph, was on the same side as the pain. Neurological and neurophysiological investigations, including the recording of masseter motor potentials evoked by transcranial stimulation, showed normal function of the sensory and motor trigeminal nerve fibres. Latency and amplitude of the jaw jerk recorded in postural position and intercuspal occlusion were, respectively, longer and smaller on the affected side. In some cases the latency difference exceeded 1 ms, the limit usually considered significant for trigeminal neuropathy or brainstem lesions. Jaw-jerk asymmetry is probably due to facilitation on the side contralateral to mandibular deviation. In intercuspal occlusion, contralateral facilitation might be produced by a stronger input from muscle spindles and periodontal mechanoreceptors. In postural position, other factors probably intervene.