Trigeminal neuralgia in pontine ischaemia.
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Biomedical subjects
Publications and source records attributed to M Leandri.
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This paper reports on the effectiveness of oral lamotrigine in 15 patients suffering from "essential" trigeminal neuralgia and in five patients suffering symptomatic trigeminal neuralgia concomitant with multiple sclerosis. We recorded objective and subjective pain ratings and correlated them to daily dosage (400 mg maximum) and plasma levels of the drug. We detected pain relief proportional to daily dosage and to drug plasma levels. Eleven of the cases affected by the "essential" form of neuralgia showed complete pain relief on reaching their maximum daily dosage. All cases affected by the symptomatic form had complete pain relief. We could detect no changes from these results by the end of the follow-up period (3 to 8 months after the study ended).
This paper presents a complete method for performing trigeminal thermorhizotomy, guided by neurophysiological data, to relieve tic douloureux. The method involves the use of trigeminal evoked potentials (TEPs) produced by stimulation of the supraorbital, infraorbital, and mental nerves and recorded from electrodes at both the scalp and the trigeminal nerve. To perform the thermorhizotomy, a cannula is modified to produce a concentric bipolar electrode that is suitable for both recording and lesion making. The operating procedure is divided into five steps: Step 1, recording of baseline scalp TEPs from the derivation of the cervical vertex to C-7 to ensure that all stimulating electrodes are correctly placed; Step 2, recording of TEPs from the trigeminal electrode after stimulation of the peripheral nerve trunks to ascertain the electrode's position relative to the root bundles; Step 3, fine positioning of the trigeminal electrode by recording the root activity evoked by stimulation of cutaneous trigger points or of the most painful areas; Step 4, assessing the position of the trigeminal electrode relative to the motor root by stimulating the nerve via the electrode and observing the masseter motor responses; and Step 5, recording scalp TEPs immediately before and after each thermolesion. Thermolesions are made until the scalp-recorded wave W2 decreases its amplitude by 20% to 50% of the original value or until it is delayed by 0.30 msec. This procedure has the potential to enable extremely precise monitoring of the position of the trigeminal electrode relative to the activated fibers and provides very effective monitoring of the extent of the lesion. The authors have performed this procedure with very satisfactory results in 30 patients with trigeminal neuralgia in the second branch.
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A cooling system (Mark VII Microclimate System) was used to give six thermosensitive multiple sclerosis patients two 45-minute daily coolings for a period of one month. Before the first cooling, a baseline clinical and electrophysiological examination was performed. The same tests were repeated after the first application and after the thirtieth cooling day, thus providing information relating to acute and chronic efficacy. A clinical improvement was observed after both acute and, more unexpectedly, chronic cooling, whereas a significant improvement in central somatosensory conduction was recorded only under acute conditions. Our data suggest that cooling with this device leads to an improvement in some functional performances (mainly fatigue and strength) of about two hours' duration in thermosensitive patients.
In 20 subjects the supraorbital nerve was stimulated and R1 recorded from electrodes placed over the ipsilateral orbicularis oculi muscle and from locations Fz, F8, F7, Cz, C6, C5, Pz, T4, and T3 on the scalp. The latter were referred either to an extracranial electrode or to Fz. In five subjects an artificial dipole was set at three different positions on the eyebrow and records were taken from the same derivations on the scalp to study the distribution of fields of known intensity originating from known locations. It was found that R1 could be easily detected from all scalp locations. According to its scalp distribution, three patterns were identified, which matched those of the artificial dipole. Conversely from what had been believed by previous authors, the amplitude of R1 could be larger on the contralateral scalp, according to the reference used or to the location of its origin. Therefore, it is remarked that larger amplitude contralateral to the stimulus cannot anymore be considered an exclusive feature of responses arising from the cortex. The evidence we have provided recommends a highly cautious approach in interpreting results describing trigeminal scalp responses in the latency range of R1.
To obtain data about peripheral concentrations of arginine vasopressin in head pain syndromes, the plasma arginine vasopressin secretory pattern in 12 adult male patients with cluster headache was evaluated. Blood samples for plasma arginine vasopressin and osmolality determinations were collected before, and at 15, 30, 45, 60, 90, and 120 minutes during a cluster attack. Blood pressure was also monitored. The same sampling was repeated during an asymptomatic period. During cluster attacks, the mean values of plasma arginine vasopressin before an attack (2.3 (0.1) ng/l) significantly increased, reaching their peak at 45 minutes (4.8 (0.5) ng/l; P < 0.01 v baseline). No significant variations were found in mean arterial pressure and plasma osmolality. These data suggested involvement of neurotransmitter mechanisms regulating arginine vasopressin secretion and a possible role of arginine vasopressin in vasomotor phenomena accompanying cluster attacks.
The R1 component of the blink reflex was evoked by stimulation of the left supraorbital and infraorbital nerves in 10 subjects. In addition, an artificial dipole was placed over the left eyebrow, in order to simulate the occurrence of the R1 component of the blink reflex. These electrical events were recorded at scalp locations Fz, F8, F7, C6, C5, referred either to Cv7 (seventh cervical vertebra) or to Fz. It was found that the blink R1 and the field of the artificial dipole had similar behaviour across the scalp; larger amplitudes were recorded ipsilateral to the stimulus from derivations referred to Cv7, but when referred to Fz larger contralateral amplitudes were measured. In the latter condition, the scalp-recorded R1 shows similar amplitude behaviour to electrical events originating from the cortex and hence its appearance may be deceiving.
A new tool in neurophysiological exploration of the trigeminal nerve has recently been introduced. It has been demonstrated that stimulation of the infraorbital nerve trunk gives rise to very reliable scalp responses reflecting the activity of the afferent pathway between the maximally nerve and the brain stem. The authors demonstrate that alterations of such trigeminal evoked responses fit with documented pathological processes at various locations along the trigeminal pathway (maxillary sinus, parasellar region, and within the brain-stem parenchyma). They report the findings in 68 patients suffering from "idiopathic" trigeminal neuralgia. Alterations of the response were detected in 33 cases, suggesting that some damage of the nerve had taken place either at the root entry zone into the pons (23 cases) or slightly distal to it (10 cases). Such results support the hypothesis that trigeminal neuralgia may be due to a compression of the trigeminal root at the pons entry zone.
A novel calcium entry blocker, nicardipine, has been tested using a dosage of 20 mg twice a day against placebo on 30 patients suffering from migraine without aura, according to a double-blind, cross-over design; overall duration of the study was four months (two with nicardipine and two with placebo). Migraine parameters such as monthly frequency, mean intensity and mean duration of attacks were monitored. Two indexes were also calculated: index A (monthly frequency x mean intensity) and index B (monthly frequency x mean intensity x mean duration). All the parameters considered and the two indexes showed a marked and significant improvement after nicardipine treatment in comparison to both placebo and pre-study scores. Detailed analysis of the cross-over results showed that improvement obtained with nicardipine lasted some time after the drug was discontinued. Nicardipine did not alter the blood and attention tests performed and caused few side effects.
The trigeminal reflexes (corneal reflex, blink reflex, masseter inhibitory periods, jaw-jerk) and far field scalp potentials (nerve, root, brainstem, subcortical) evoked by percutaneous infraorbital stimulation were recorded in 30 patients with "idiopathic" trigeminal neuralgia (ITN) and 20 with "symptomatic" trigeminal pain (STP): seven postherpetic neuralgia, five multiple sclerosis, four tumour, two vascular malformation, one Tolosa-Hunt syndrome, and one traumatic fracture. All the patients with STP and two of those with ITN had trigeminal reflex abnormalities; 80% of patients with STP and 30% of those with ITN had evoked potential abnormalities. The results indicate that 1) trigeminal reflexes and evoked potentials are both useful in the examination of patients with trigeminal pain, and in cases secondary to specific pathologies provide 100% sensitivity; 2) in "symptomatic" and "idiopathic" paroxysmal pain the primary lesion affects the afferent fibres in the proximal portion of the root or the intrinsic portion in the pons; 3) primary sensory neurons of the A-beta fibre group are involved in both paroxysmal and constant pain, but in the latter the damage is far more severe.
In 20 subjects, we stimulated the mental nerve through needle electrodes inserted into the homonymous foramen; recording electrodes were placed on the scalp and along the jaw. Within the 1st 5 msec after the stimulus we recorded 4 constant waves, thought to reflect the afferent activity from the mandibular nerve up to the trigeminal nuclei. These waves have similar characteristics and the same high degree of reliability as those obtained after stimulation of the infraorbital and supraorbital nerves; therefore, they should be a useful complement for a complete exploration of trigeminal nerve function.
The aim of this paper is to evaluate the effectiveness of high-intensity versus low-intensity transcutaneous electrical nerve stimulation (TENS) and versus placebo for treatment of hemiplegic shoulder pain. Three groups of 20 patients each (A, B, C) were studied. In group A high-intensity TENS was delivered at 3 times the sensory threshold with frequency of 100 Hz; in group B low-intensity TENS was delivered at the sensory threshold with frequency of 100 Hz. Group C received placebo stimulation. The treatment protocol consisted of 12 sessions (4 weeks). Before treatment, at the end of it and one month after, passive range of motion (PROM) for flexion, extension, abduction and external rotation were evaluated. Statistically significant improvements of PROMs were recorded for group A, but not for groups B or C.
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Scalp responses following stimulation of the infraorbital nerve have been recorded in awake and anaesthetized subjects from non-cephalic (NCR) and vertex (VR) reference derivations. In awake subjects, after 3 very early potentials (W1, W2 and W3), 4 small components (P4, N5, P6 and N7) with widespread distribution have been constantly recorded from NCR derivations. Sometimes a further component, named N10, could be recorded in VR derivations on the scalp contralateral to the stimulus in the absence of earlier events. Large and inconstant waves were recorded following N7 in NCR and N10 in VR derivations. The muscular origin of these waves was demonstrated by simultaneous records taken from scalp and muscles. Records from NCR derivations in anaesthetized subjects showed that wave N7 was followed by a further event (N10) localized on the scalp contralateral to the stimulus and by a few slow waves. Wave N10 could also be recorded, in the absence of earlier events, from the VR derivation contralateral to the stimulus. All the responses recorded in these patients could be considered of neurogenic origin because curarization abolished any reflex activation of muscles. All the waves following W3 are of postsynaptic nature and, on the basis of their distribution and latency, we suggest that P4, N5, P6, N7 and N10 have their respective origins in the trigeminal nucleus, trigeminal lemniscus, thalamus, thalamic radiation and cortical projection of the stimulated area. It was also demonstrated that stimulation of lips and gums fails to evoke any neural event recordable from the scalp.
The origins of early waves recorded from the scalp of man after stimulation of the infraorbital nerve have been investigated by simultaneous recording from the scalp and from the trigeminal pathway in patients undergoing thermocoagulation rhizotomy. It has been found that the surface-recorded W1, W2 and W3 waves correspond respectively to the activity of the point of entry of the maxillary nerve into the gasserian ganglion, the point of entry of the trigeminal root into the pons and the presynaptic portion of the trigeminal spinal tract. It is remarked that depth recording during surgery may provide useful information about the positioning of the thermocoagulation electrode.
The purpose of this study was to determine whether some types of transcutaneous electrical nerve stimulation cause local vasodilation. The amount of vascular perfusion was monitored using telethermography to gauge the skin temperature of the area to which TENS was applied. We studied the effects of four different modalities of TENS (intensities of 1.5 and 3 times the sensory threshold and frequencies of 3 pulses per second [pps] and 100 pps), delivered through small and large electrodes (1.5 cm and 4 cm in diameter), on 10 healthy subjects. Stimulation at 3 times the sensory threshold produced local hyperthermia, which was maximal when a current of 100 pps was delivered through small electrodes. Because any physical or chemical effects of the current could be eliminated as causes of hyperthermia, the rise in skin temperature was considered to be a result of increased vascular perfusion. The results of the study demonstrate that some types of TENS cause local vasodilation. This effect may represent another mechanism by which such techniques provide pain relief, particularly in the treatment of myofascial syndromes.
Stimulation of the infraorbital nerve evoked a short latency scalp response characterized by a large amplitude triphasic potential (W1), followed by two smaller negative deflections (W2 and W3). All these waves were presynaptic in origin (as shown by double pulse stimulation), but appeared to be generated by separate dipoles. Short distance bipolar recording showed that W1 travelled from the zygoma to the mastoid. This wave was thought to be generated in a nearby neural structure, presumably the proximal part of the maxillary nerve, the gasserian ganglion and possibly even the trigeminal root. W2 and W3 components were probably generated by the trigeminal root fibres running through the brain-stem. Their origin from slowly conducting trigeminal fibres was ruled out by their absence in short distance bipolar records along the line from the zygomatic bone to the mastoid process, and by studies on their thresholds, which were shown to be identical to those of W1. Control experiments with concurrent facial muscle recording excluded any possible contamination of the scalp response to infraorbital nerve stimulation by electromyographic activity, and demonstrated gross muscular artefacts, picked up as far-field activity by scalp electrodes, following electrical stimulation of the upper lip.