Electrical stimulation of the trigeminal nerve root for the treatment of chronic facial pain

1995 ◽  
Vol 83 (1) ◽  
pp. 72-78 ◽  
Author(s):  
Ronald F. Young
Keyword(s):  
Electrical Stimulation ◽  
Pain Intensity ◽  
Trigeminal Nerve ◽  
Nerve Root ◽  
Facial Pain ◽  
Content Type ◽  
Number Of Patients ◽  
Trigeminal Nerve Root ◽  
Fine Print ◽  
Stimulation Of

✓ Between March 1990 and December 1992, 23 patients with chronic intractable facial pain due to various forms of injury to the trigeminal nerve or nerve root underwent implantation of an electrical stimulating system to treat their pain. All patients had failed previous extensive pain treatment efforts. A monopolar platinum-iridium electrode was implanted on the trigeminal nerve root via percutaneous puncture of the foramen ovale. All patients experienced at least 50% reduction in pain intensity during a period of trial stimulation and underwent internalization of the electrode and connection to a completely implanted pulse generator. Independent assessment of the effect of stimulation was obtained by a specially trained nurse practitioner. Over a mean follow-up period of 24 months, six patients reported nearly complete relief of pain and six others reported at least a 50% reduction in pain intensity using a visual analog scale. Thus, 12 (52%) of the 23 patients achieved 50% or greater reduction in pain intensity. Although changes in the patterns of analgesic medication usage were few, six patients (26%) now experience a normal life style. Only one complication was seen, namely a dislocated electrode, which was easily replaced. Chronic electrical stimulation of the trigeminal nerve root appears to be an easy and safe technique for providing relief of chronic facial pain related to injury to the trigeminal nerve in a significant number of patients.

Microvascular relations of the trigeminal nerve

1980 ◽  
Vol 52 (3) ◽  
pp. 381-386 ◽  
Author(s):  
Stephen J. Haines ◽  
Peter J. Jannetta ◽  
David S. Zorub
Keyword(s):  
Trigeminal Neuralgia ◽  
Trigeminal Nerve ◽  
Facial Pain ◽  
Entry Zone ◽  
Content Type ◽  
Root Entry Zone ◽  
Venous Compression ◽  
Trigeminal Nerve Root ◽  
Trigeminal Nerves ◽  
Fine Print

✓ The vascular relationships of the trigeminal nerve root entry zone were examined bilaterally in 20 cadavers of individuals known to be free of facial pain. Fourteen of 40 nerves made contact with an artery, but only four of these showed evidence of compression or distortion of the nerve. In addition, the vascular relationships of 40 trigeminal nerves exposed surgically for treatment of trigeminal neuralgia were studied, and 31 nerves showed compression by adjacent arteries. Venous compression was seen in four of the cadaver nerves and in eight nerves from patients with trigeminal neuralgia. These data support the hypothesis that arterial compression of the trigeminal nerve is associated with trigeminal neuralgia.

Chronic electrical stimulation of the gasserian ganglion for the relief of pain in a series of 34 patients

1997 ◽  
Vol 86 (2) ◽  
pp. 197-202 ◽  
Author(s):  
Ethan Taub ◽  
Michael Munz ◽  
Ronald R. Tasker
Keyword(s):  
Electrical Stimulation ◽  
Facial Pain ◽  
Prophylactic Antibiotic ◽  
Stage Ii ◽  
Gasserian Ganglion ◽  
Content Type ◽  
Antibiotic Drugs ◽  
Chronic Electrical Stimulation ◽  
Fine Print ◽  
Stimulation Of

✓ The use of an implanted system for chronic electrical stimulation of the gasserian ganglion for relief of facial pain was described in 1980 by Meyerson and Håkansson. Between 1982 and 1995, the senior author (R.R.T.) performed gasserian ganglion stimulation in 34 patients for the relief of chronic medically intractable facial pain. The etiology of pain was peripheral damage to the trigeminal nerve in 22 patients (65%), central (stroke) damage in seven (21%), postherpetic neuralgia in four (12%), and unclassifiable cause in one (3%). All patients received a trial of transcutaneous stimulation (Stage I). Successful trials in 19 patients (56%) were followed by implantation of a permanent system (Stage II). Trial and postimplantation stimulation were deemed successful when there was a reduction of pain by at least 50% whenever the stimulator was on. Success rates varied from five (71%) of seven patients for central pain to five (23%) of 22 for peripheral pain and none (0%) of four for postherpetic neuralgia. The median follow-up duration in successful cases was 22.5 months. Infections occurred in seven patients, all of whom had undergone Stage II treatment. Infections were more frequent when the stimulating electrode from Stage I was left in place for Stage II (six [43%] of 14) than when completely new hardware was used and prophylactic antibiotic drugs were administered (one [20%] of five). Other complications included iatrogenic injury to the trigeminal nerve or ganglion in three cases (9%), transient diplopia in two (6%), increased pain in two (6%), and various technical problems in 10 (29%). It is concluded that pain of central origin (stroke) is the type most likely to be relieved by this procedure. This finding is new, as the few other clinical series reported to date contain no patients with this type of pain. The risk of infection seems to be lower when completely new hardware is used for Stage II and prophylactic antibiotic drugs are administered.

Trigeminal neuralgia associated with seizure and syncope

1984 ◽  
Vol 61 (3) ◽  
pp. 594-595 ◽  
Author(s):  
Wishwa N. Kapoor ◽  
Peter J. Jannetta
Keyword(s):  
Trigeminal Neuralgia ◽  
Trigeminal Nerve ◽  
Mechanical Stimulation ◽  
Microvascular Decompression ◽  
Facial Pain ◽  
Loss Of Consciousness ◽  
Content Type ◽  
Vascular Decompression ◽  
Fine Print ◽  
Stimulation Of

✓ A patient with trigeminal neuralgia experienced a generalized seizure and a prolonged syncopal episode. He was found to be asystolic during the syncopal episode. There was no recurrence of loss of consciousness after implantation of a pacemaker. Mechanical stimulation of the trigeminal nerve during craniotomy for microvascular decompression of the trigeminal nerve resulted in bradycardia. Since vascular decompression of the trigeminal nerve, there has been no recurrent facial pain, and no further syncope, seizures, or bradycardia. Syncope and seizures have not been previously reported in association with trigeminal neuralgia, although they are well described with glossopharyngeal neuralgia.

Trigeminal neuralgia caused by microarteriovenous malformations of the trigeminal nerve root entry zone: symptomatic relief following complete excision of the lesion with nerve root preservation

2002 ◽  
Vol 97 (4) ◽  
pp. 874-880 ◽  
Author(s):  
Richard J. Edwards ◽  
Yvonne Clarke ◽  
Shelley A. Renowden ◽  
Hugh B. Coakham
Keyword(s):  
Trigeminal Neuralgia ◽  
Trigeminal Nerve ◽  
Nerve Root ◽  
Preoperative Imaging ◽  
Posterior Fossa Surgery ◽  
Entry Zone ◽  
Content Type ◽  
Root Entry Zone ◽  
Trigeminal Nerve Root ◽  
Fine Print

Object. Within a series of 341 consecutive patients who underwent posterior fossa surgery for trigeminal neuralgia (TN), in five the cause was found to be a microarteriovenous malformation (micro-AVM) located in the region of the trigeminal nerve root entry zone (REZ). The surgical management and clinical outcomes of these cases are presented. Methods. Patients were identified from a prospectively collected database of all cases of TN treated at one institution between 1980 and 2000. Presentation was clinically indistinguishable from TN caused by vascular compression. Preoperative imaging, including computerized tomography scanning (two cases) and magnetic resonance (MR) imaging and MR angiography (three cases), failed to demonstrate an AVM except for one case in which multiple abnormal vessels were identified in the trigeminal REZ on an MR image obtained using a 1.5-tesla magnet. All patients underwent a standard retromastoid craniotomy. In all cases a small AVM embedded in the trigeminal REZ was identified and completely excised, with preservation of the trigeminal nerve. All patients experienced immediate relief of pain following surgery. Postoperatively, in one patient a small pontine hematoma developed, resulting in permanent trigeminal nerve anesthesia in the V2 and V3 divisions. All patients were free from pain at a mean follow-up period of 30 months. Conclusions. These rare lesions are usually angiographically occult, but may sometimes be identifiable on high-resolution MR images. Total microsurgical resection with nerve preservation is possible, although operative complications are relatively common, reflecting the intimate association between these lesions and the pons. Complete resection is advised not only for symptom relief, but also to eliminate the theoretical risk of pontine hemorrhage.

The mechanism and effect of chronic electrical stimulation of the globus pallidus for treatment of Parkinson disease

2004 ◽  
Vol 100 (6) ◽  
pp. 997-1001 ◽  
Author(s):  
Mitsuhiro Ogura ◽  
Naoyuki Nakao ◽  
Ekini Nakai ◽  
Yuji Uematsu ◽  
Toru Itakura
Keyword(s):  
Electrical Stimulation ◽  
Parkinson Disease ◽  
Globus Pallidus ◽  
Rating Scale ◽  
Underlying Mechanism ◽  
Clinical Effects ◽  
Content Type ◽  
Chronic Electrical Stimulation ◽  
Fine Print ◽  
Stimulation Of

Object. Although chronic electrical stimulation of the globus pallidus (GP) has been shown to ameliorate motor disabilities in Parkinson disease (PD), the underlying mechanism remains to be clarified. In this study the authors explored the mechanism for the effects of deep brain stimulation of the GP by investigating the changes in neurotransmitter levels in the cerebrospinal fluid (CSF) during the stimulation. Methods. Thirty patients received chronic electrical stimulation of the GP internus (GPi). Clinical effects were assessed using the Unified PD Rating Scale (UPDRS) and the Hoehn and Yahr Staging Scale at 1 week before surgery and at 6 and 12 months after surgery. One day after surgery, CSF samples were collected through a ventricular tube before and 1 hour after GPi stimulation. The concentration of neurotransmitters such as γ-aminobutyric acid (GABA), noradrenaline, dopamine, and homovanillic acid (HVA) in the CSF was measured using high-performance liquid chromatography. The treatment was effective for tremors, rigidity, and drug-induced dyskinesia. The concentration of GABA in the CSF increased significantly during stimulation, although there were no significant changes in the level of noradrenaline, dopamine, and HVA. A comparison between an increased rate of GABA concentration and a lower UPDRS score 6 months postimplantation revealed that the increase in the GABA level correlated with the stimulation-induced clinical effects. Conclusions. Stimulation of the GPi substantially benefits patients with PD. The underlying mechanism of the treatment may involve activation of GABAergic afferents in the GP.

Transcorneal stimulation of trigeminal nerve afferents to increase cerebral blood flow in rats with cerebral vasospasm: a noninvasive method to activate the trigeminovascular reflex

2002 ◽  
Vol 97 (5) ◽  
pp. 1179-1183 ◽  
Author(s):  
Basar Atalay ◽  
Hayrunnisa Bolay ◽  
Turgay Dalkara ◽  
Figen Soylemezoglu ◽  
Kamil Oge ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Vasospasm ◽  
Trigeminal Nerve ◽  
Nerve Endings ◽  
Noninvasive Method ◽  
Direct Stimulation ◽  
Content Type ◽  
Fine Print ◽  
Stimulation Of

Object. The goal of this study was to investigate whether stimulation of trigeminal afferents in the cornea could enhance cerebral blood flow (CBF) in rats after they have been subjected to experimental subarachnoid hemorrhage (SAH). Cerebral vasospasm following SAH may compromise CBF and increase the risks of morbidity and mortality. Currently, there is no effective treatment for SAH-induced vasospasm. Direct stimulation of the trigeminal nerve has been shown to dilate constricted cerebral arteries after SAH; however, a noninvasive method to activate this nerve would be preferable for human applications. The authors hypothesized that stimulation of free nerve endings of trigeminal sensory fibers in the face might be as effective as direct stimulation of the trigeminal nerve. Methods. Autologous blood obtained from the tail artery was injected into the cisterna magna of 10 rats. Forty-eight and 96 hours later (five rats each) trigeminal afferents were stimulated selectively by applying transcorneal biphasic pulses (1 msec, 3 mA, and 30 Hz), and CBF enhancements were detected using laser Doppler flowmetry in the territory of the middle cerebral artery. Stimulation-induced changes in cerebrovascular parameters were compared with similar parameters in sham-operated controls (six rats). Development of vasospasm was histologically verified in every rat with SAH. Corneal stimulation caused an increase in CBF and blood pressure and a net decrease in cerebrovascular resistance. There were no significant differences between groups for these changes. Conclusions. Data from the present study demonstrate that transcorneal stimulation of trigeminal nerve endings induces vasodilation and a robust increase in CBF. The vasodilatory response of cerebral vessels to trigeminal activation is retained after SAH-induced vasospasm.

Pain relief by electrical stimulation of the periaqueductal and periventricular gray matter

1987 ◽  
Vol 66 (3) ◽  
pp. 364-371 ◽  
Author(s):  
Ronald F. Young ◽  
V. Israel Chambi
Keyword(s):  
Pain Relief ◽  
Pain Intensity ◽  
Gray Matter ◽  
Cross Tolerance ◽  
Endogenous Opioid ◽  
Double Blind ◽  
Content Type ◽  
Fine Print ◽  
Development Of Tolerance ◽  
Stimulation Of

✓ Pain relief following stimulation of the periaqueductal gray matter (PAG) or periventricular gray matter (PVG) in man has been ascribed to stimulation-induced release of endogenous opioid substances. Forty-five patients were studied and followed for at least 1 year after placement of chronic stimulating electrodes in the PAG or PVG to determine if pain relief due to stimulation could be ascribed to an endogenous opioid mechanism. Three criteria were assessed: 1) the development of tolerance to stimulation; 2) the possibility of cross-tolerance to morphine; and 3) reversibility of stimulation-induced pain relief by the opiate antagonist naloxone. Sixteen patients (35.6%) developed tolerance to stimulation, that is, they obtained progressively less effective pain relief. Twelve (44.4%) of 27 patients undergoing stimulation of the thalamic sensory relay nuclei for treatment of chronic pain (a presumably non-opioid mechanism) also developed tolerance. Morphine sulfate was administered in a blind, placebo-controlled protocol to 10 patients who had become tolerant to PAG-PVG stimulation and none showed evidence of cross-tolerance. Fifteen of 19 patients, already tolerant to morphine at the time of PAG-PVG electrode implantation, experienced excellent pain relief by stimulation, also indicating a lack of cross-tolerance. Twenty-two patients who experienced excellent pain relief from chronic PAG-PVG stimulation received intravenous naloxone in a double-blind, placebo-controlled protocol. Pain intensity as assessed by the visual analog scale was increased to the same degree by both placebo and naloxone. Eight patients showed no increase in pain intensity with either placebo or naloxone. Although tolerance to PAG-PVG stimulation developed in these patients, the frequency of tolerance was similar to that seen in patients undergoing thalamic sensory nuclear stimulation. Since the latter technique presumably relieves pain by a non-opioid mechanism, the development of tolerance to PAG-PVG stimulation does not, in itself, confirm an opioid mechanism. Cross-tolerance between PAG-PVG stimulation and morphine was not seen and cross-tolerance to PAG-PVG stimulation in patients already tolerant to morphine was rare. The pain-relieving effect of PAG-PVG stimulation was reversed to an approximately equal degree by naloxone and placebo. The authors do not believe that, in most patients, pain relief elicited by PAG-PVG stimulation depends on an endogenous opioid mechanism. It appears that other, non-opioid mechanisms are primarily responsible for such pain relief.

Functional magnetic resonance imaging of somatosensory cortex activity produced by electrical stimulation of the median nerve or tactile stimulation of the index finger

2000 ◽  
Vol 93 (5) ◽  
pp. 774-783 ◽  
Author(s):  
Maxwell Boakye ◽  
Sean C. Huckins ◽  
Nikolaus M. Szeverenyi ◽  
Bobby I. Taskey ◽  
Charles J. Hodge
Keyword(s):  
Electrical Stimulation ◽  
Median Nerve ◽  
Somatosensory Cortex ◽  
Tactile Stimulation ◽  
Index Finger ◽  
Functional Magnetic Resonance ◽  
Content Type ◽  
The Right ◽  
Fine Print ◽  
Stimulation Of

Object. Functional magnetic resonance (fMR) imaging was used to determine patterns of cerebral blood flow changes in the somatosensory cortex that result from median nerve stimulation (MNS).Methods. Ten healthy volunteers underwent stimulation of the right median nerve at frequencies of 5.1 Hz (five volunteers) and 50 Hz (five volunteers). The left median nerve was stimulated at frequencies of 5.1 Hz (two volunteers) and 50 Hz (five volunteers). Tactile stimulation (with a soft brush) of the right index finger was also applied (three volunteers). Functional MR imaging data were transformed into Talairach space coordinates and averaged by group. Results showed significant activation (p < 0.001) in the following regions: primary sensorimotor cortex (SMI), secondary somatosensory cortex (SII), parietal operculum, insula, frontal cortex, supplementary motor area, and posterior parietal cortices (Brodmann's Areas 7 and 40). Further analysis revealed no statistically significant difference (p > 0.05) between volumes of cortical activation in the SMI or SII resulting from electrical stimuli at 5.1 Hz and 50 Hz. There existed no significant differences (p > 0.05) in cortical activity in either the SMI or SII resulting from either left- or right-sided MNS. With the exception of the frontal cortex, areas of cortical activity in response to tactile stimulation were anatomically identical to those regions activated by electrical stimulation. In the SMI and SII, activation resulting from tactile stimulation was not significantly different (p > 0.05) from that resulting from electrical stimulation.Conclusions. Electrical stimulation of the median nerve is a reproducible and effective means of activating multiple somatosensory cortical areas, and fMR imaging can be used to investigate the complex network that exists between these areas.

Magnetic and electrical stimulation of the auditory cortex for intractable tinnitus

2004 ◽  
Vol 100 (3) ◽  
pp. 560-564 ◽  
Author(s):  
Dirk De Ridder ◽  
Gert De Mulder ◽  
Vincent Walsh ◽  
Neil Muggleton ◽  
Stefan Sunaert ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Transcranial Magnetic Stimulation ◽  
Auditory Cortex ◽  
Magnetic Stimulation ◽  
Cortical Plasticity ◽  
Cortical Reorganization ◽  
Complete Suppression ◽  
Content Type ◽  
Fine Print ◽  
Stimulation Of

✓ Tinnitus is a distressing symptom that affects up to 15% of the population for whom no satisfactory treatment exists. The authors present a novel surgical approach for the treatment of intractable tinnitus, based on cortical stimulation of the auditory cortex. Tinnitus can be considered an auditory phantom phenomenon similar to deafferentation pain, which is observed in the somatosensory system. Tinnitus is accompanied by a change in the tonotopic map of the auditory cortex. Furthermore, there is a highly positive association between the subjective intensity of the tinnitus and the amount of shift in tinnitus frequency in the auditory cortex, that is, the amount of cortical reorganization. This cortical reorganization can be demonstrated by functional magnetic resonance (fMR) imaging. Transcranial magnetic stimulation (TMS) is a noninvasive method of activating or deactivating focal areas of the human brain. Linked to a navigation system that is guided by fMR images of the auditory system, TMS can suppress areas of cortical plasticity. If it is successful in suppressing a patient's tinnitus, this focal and temporary effect can be perpetualized by implanting a cortical electrode. A neuronavigation-based auditory fMR imaging-guided TMS session was performed in a patient who suffered from tinnitus due to a cochlear nerve lesion. Complete suppression of the tinnitus was obtained. At a later time an extradural electrode was implanted with the guidance of auditory fMR imaging navigation. Postoperatively, the patient's tinnitus disappeared and remains absent 10 months later. Focal extradural electrical stimulation of the primary auditory cortex at the area of cortical plasticity is capable of suppressing contralateral tinnitus completely. Transcranial magnetic stimulation may be an ideal method for noninvasive studies of surgical candidates in whom stimulating electrodes might be implanted for tinnitus suppression.

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