|
| Article Access Statistics | | | Viewed | 6570 | | | Printed | 295 | | | Emailed | 15 | | | PDF Downloaded | 0 | | | Comments | [Add] | | | Cited by others | 3 | | |
|
Click on image for details.
|
|
|
|
|
|
| Year : 1999 | Volume
: 47
| Issue : 2 | Page : 94-7 |
Trigeminal evoked potentials in patients with symptomatic trigeminal neuralgia due to intracranial mass lesions.
Sundaram PK, Hegde AS, Chandramouli BA, Das BS
Department of Neurosurgery, National Institute of Mental Health and Neurosciences, Bangalore, India.
Correspondence Address:
Department of Neurosurgery, National Institute of Mental Health and Neurosciences, Bangalore, India.
Trigeminal evoked potentials (TEP) were recorded by electrical stimulation of the lips in 7 patients with symptomatic trigeminal neuralgia due to CT proved mass lesions involving the trigeminal nerve. All the patients showed TEP abnormalities on the affected side. Chronic compression and irritation of the trigeminal nerve may be responsible for these changes. The results obtained were compared with other similar studies and TEP abnormalities observed in idiopathic trigeminal neuralgia. As all the patients had unequivocal compression of the trigeminal nerve and all of them had TEP changes, it can be concluded that TEP abnormality is an accurate predictor of trigeminal nerve compression. TEPs may be a valuable aid in demonstrating a compressive element in patients with trigeminal neuralgia.
How to cite this article:
Sundaram P K, Hegde A S, Chandramouli B A, Das B S. Trigeminal evoked potentials in patients with symptomatic trigeminal neuralgia due to intracranial mass lesions. Neurol India 1999;47:94 |
How to cite this URL:
Sundaram P K, Hegde A S, Chandramouli B A, Das B S. Trigeminal evoked potentials in patients with symptomatic trigeminal neuralgia due to intracranial mass lesions. Neurol India [serial online] 1999 [cited 2023 Jun 3];47:94. Available from: https://www.neurologyindia.com/text.asp?1999/47/2/94/1645 |
Trigeminal evoked potentials (TEPs) have been analysed in patients with tumours involving the trigeminal nerve. Leandri studied TEPs in 23 patients with tumours of the base of the skull arising from the parasellar region or the cerebello-pontine angle region.[1] Only 11 out of these 23 patients had clinical involvement of the trigeminal nerve in the form of facial hypoaesthesia, paraesthesia, weakness of the masticatory muscles or neuralgic pain. In the present study, TEPs were recorded in a specific group of patients who had primarily presented with neuralgic facial pain as a manifestation of posterior fossa or parasellar mass lesions. Other studies of TEPs in compressive mass lesions were reviewed and comparison was made with TEP changes observed in idiopathic trigeminal neuralgia. The reliability of TEPs in demonstrating subclinical trigeminal nerve compression was also assessed.
TEPs were recorded in all patients with the Nihon Kohden Neuropack-8 system by electrical stimulation of the upper and lower lips with surface electrodes. After determining the sensory threshold, a stimulus strength of 3 times was used to average 200 stimuli of 0.2 msec duration at the rate of 2/sec. The active recording electrode was midway between the external auditory meatus and a point 1 cm behind the vertex, the reference at `fpz' as in the 10-20 system and the right ear lobe served as ground. An amplifier band pass of 1 Hz to 3000 Hz and sensitivity of 50 micro volts, sweep time of 100 msec and delay time of 5 msec were used to average the stimuli. The delay time of 5 msec was used to trigger the sweep 5 msec prior to arrival of the stimulus so that the stimulus artifact could be easily delineated from the early waves. The sweep time or analysis time was 100 msec, of which 5 msec preceded the stimuli and 95 msec followed the stimuli. Control data was established by recording TEPs in 10 normal individuals comprising 5 males and 5 females and the procedure was standardized. The mean latency period and normal range ( mean + 2 standard deviation ) of the various waves were calculated. A paired `t' test was used to compare the wave latencies recorded on the right and left sides, in both males and females. In the normal population, there was no significant right left asymmetry or male/female difference in the TEPs recorded. The latency of the waves recorded in the patients with secondary trigeminal neuralgia was considered to be prolonged if they were more than mean + 2 times the standard deviation.
Normal individuals showed the following peaks :
maxillary division N3 P9 N11 P14 N20 P28 N37 P46
mandibular division P4 N9 P14 N20 P28 N38 P48
TEPs were recorded pre-operatively in 7 patients with mass lesions adjacent to the trigeminal nerve. All the patients had neuralgic pain in the distribution of trigeminal nerve, as a primary clinical manifestation. Three out of seven patients had no deficit pertaining to the fifth nerve, three had hypoaesthesia in the trigeminal distribution and one had weakness of the masseters. CT scans with and without contrast were done in all the patients. Histopathology revealed the lesions to be schwannoma in 4, meningioma in 1, epidermoid in 1 and paraganglioma in 1. The TEPs recorded in the patients with symptomatic trigeminal neuralgia were analysed for changes in sensory threshold and changes in the wave configuration between the normal and affected sides.
All the patients in the present study showed changes in the recorded TEPs. A significant increase in sensory threshold on the affected side was noted in 5 out of 7 patients. The difference in sensory threshold was as high as 10 times the difference seen in normal individuals between the two sides. The wave configuration was abnormal in all the 7 patients. The changes affected mainly N20 or later waves in 12 out of 14 TEPs. These were found to be either absent or prolonged. In six patients, there were changes in the earlier waves as well. The changes observed are summarised in [Table I], and [Figure 1] and [Figure 2]. The tumours in these patients were not large enough to cause brainstem distortion. Bilateral changes in TEPs were not noted.
TEP have been studied in patients with tumours adjacent to trigeminal nerve. Singh et al[2] noted that in two patients with acoustic neurinoma, who had unilateral facial anaesthesia to pinprick and loss of corneal reflex, no early or late potentials could be recorded on the affected side, although the TEPs were normal on the asymptomatic side. The sensory threshold was 50 to 75% higher on the symptomatic side. An increased threshold in the maxillary and mandibular divisions with prolonged latencies, was observed in two patients with trigeminal schwannoma.[3] Hafner recorded abnormalities in `very short latency trigeminal evoked potentials' (STEP) in patients with posterior fossa tumours.[4]
In the present study, besides the change in threshold, there were significant changes in the waves and their latencies in the TEPs recorded on the affected side in all the patients. Mechanical compression and chronic irritation of the trigeminal nerve by the tumours may be responsible for these TEP changes. Chronic irritation may result in ectopic action potentials and failure of segmental inhibition, leading to paroxysmal nociceptive discharges in the interneurons of trigeminal nucleus oralis.[5] The large diameter fibres contribute more to the recorded evoked potentials and at the same time are more vulnerable to compression.
It is pertinent to compare TEP changes in idiopathic trigeminal neuralgia where one of the causative factors is extraneous compression. Abnormally prolonged latencies in TEPs were noted in 60% of 66 patients.[6] In another study, comprising 33 patients with maxillary division trigeminal neuralgia, 8 were found to have prolonged TEP latencies.[7] Similarly 41 % of medically treated patients of trigeminal neuralgia had prolonged P19 wave.[8] However, unlike compression by tumours, the role of vascular compression in trigeminal neuralgia remains controversial. Reports show a wide variation in the incidence of vascular compression from 96% of 411 patients[9] to 6 out of 57 patients.[10] It has been suggested that arterial loops and veins in proximity to the nerve, but not in contact, may have been compressing prior to retraction of cerebellum during surgical decompression. A vessel near the nerve in 37% of 52 procedures was considered to be the causative factor.[11] On the contrary, in postmortem studies in patients without pain, 52% had significant arterial compression.[12]
However, in this study there was unequivocal trigeminal nerve compression in all the patients, as all had CT documented tumours adjacent to trigeminal nerve. Further, all the 7 patients had TEP changes indicating that TEP abnormalities were highly predictive of trigeminal nerve compression. While studying early TEPs in 23 patients with tumours of the parasellar region and CP angle, Leandri noted changes in all patients with clinical evidence of fifth nerve involvement (11/23) and in 58% of patients with no such involvement (12/23).[1] Hence, in patients with idiopathic trigeminal neuralgia, TEP abnormalities may indicate the possibility of significant vascular compression. Since recording TEPs is simple, noninvasive and inexpensive, it may routinely be employed in patients with trigeminal neuralgia for planning appropriate investigations and treatment
|
