Tinnitus and pain.

Tinnitus has many similarities with the symptoms of neurological disorders such as paresthesia and central neuropathic pain. There is considerable evidence that the symptoms and signs of some forms of tinnitus and central neuropathic pain are caused by functional changes in specific parts of the central nervous system and that these changes are caused by expression of neural plasticity. The changes in the auditory nervous system that cause tinnitus and the changes in the somatosensory systems that cause central neuropathic pain may have been initiated from the periphery, i.e. the ear or the auditory nerve for tinnitus and receptors and peripheral nerves in the body for pain. In the chronic condition of tinnitus and pain, abnormalities in the periphery may no longer play a role in the pathology, but the tinnitus is still referred to the ear and central neuropathic pain is still referred to the location on the body of the original pathology. In this chapter we will discuss specific similarities between tinnitus and pain, and compare tinnitus with other phantom disorders. Since much more is known about pain than about tinnitus, it is valuable to take advantage of the knowledge about pain in efforts to understand the pathophysiology of tinnitus and find treatments for tinnitus.

Hemifacial spasm: results of electrophysiologic recording during microvascular decompression operations.

Electrophysiologic recordings were made from patients with hemifacial spasm (HFS) during microvascular decompression (MVD) operations to see if spasm and synkinesis are caused by ephaptic transmission at the site of lesion (root entry zone [REZ] of the facial nerve). The response from the orbicularis oculi muscle to electrical stimulation of the marginal mandibular nerve had a 2.2-msec longer latency (average of 16 patients) than the sum of the conduction times of the parts of the facial nerve that would be involved if the response was the result of ephaptic transmission at the REZ of the seventh cranial nerve. Similar results were obtained when the zygomatic branch of the facial nerve was stimulated. These results indicate that the facial motonucleus is involved in HFS.

Laboratory methods of assessing hearing loss.

Methods for assessing hearing loss in human loss in human and in animal are reviewed with special reference to the use of brainstem auditory evoked potentials (BSEP). The technique of recording and digital filtering of BSEP is described and compared with the results obtained by use of traditional analog filtering. The use of electrophysiological methods in assessing threshold shifts in studies of the effect of noise exposure on hearing in experimental animals is described for examples of results obtained in rats.

Neuromonitoring in operations in the skull base.

Methods to monitor the integrity of cranial motor nerves during operations on skull base tumors have been developed over the past decade. These methods can help the surgeon to identify cranial motor nerves that are located in the surgical field but which may not be visible directly. Methods have also been developed that allow monitoring of the function of sensory systems such as the auditory system and it has been shown that brainstem auditory evoked potentials can provide important information about the integrity of the auditory nervous system. It has been shown in several studies that such neuromonitoring, when performed during operations in the skull base, can help reduce the incidence of permanent neurological deficits that may occur with the removal of large tumors. We have also shown that such monitoring can be performed routinely without interfering noticeably with the actual surgical procedures.

Latency in the ascending auditory pathway determined using continuous sounds: comparison between transient and envelope latency.

The gross responses from the cochlea (round window) and two nuclei of the ascending auditory pathway of the rat in response to tone and noise bursts (compound action potentials) were compared with those recorded in response to continuous tones and noise that was amplitude modulated with pseudorandom noise. The cross-correlation function between: (1) the averaged response to the sounds that were amplitude modulated with the pseudorandom noise, and (2) one period of the pseudorandom noise, were obtained. The compound action potentials and the cross-correlation functions both had a series of peaks. The two functions had a similar morphology. The latency of the peaks in the cross-correlation showed less dependence on sound intensity than did the latency of the peaks in the compound action potentials.

Evidence of decreased GABAergic influence on temporal integration in the inferior colliculus following acute noise exposure: a study of evoked potentials in the rat.

Many investigations have shown that modulation of sensory input, either by over stimulation or sensory deprivation, can cause a reorganization of structures located high in the central nervous system (CNS). Although most of these studies had focused on studying changes in the function and tonotopic organization of the sensory cortex, recent evidence has suggested that plastic changes in specific subcortical nuclei of sensory systems may also occur in response to modulation of sensory input, and may be partially responsible for changes reflected at the level of the cortex. In the present study we investigated the effects of noise exposure (4-kHz continuous tone at 104 dB sound pressure level (SPL) for 30 min duration) on the processing of auditory information at the level of the inferior colliculus (IC). We studied how evoked potentials recorded from the surface of the IC changed as a function of the duration of the tone bursts used as stimuli. We measured the amplitude of a peak that is generated postsynaptically in the IC in response to tone bursts between 1 and 6 ms duration. In animals that were not exposed to the tone, the amplitude of this peak decreased with increasing stimulus duration, but after tone exposure, the decrease in the amplitude of this peak was significantly less than in the animals not exposed to the tone. A microinjection of the GABAA antagonist, bicucullene, into the IC in the animals not exposed to the tone caused the amplitude of the peak to be less dependent on tone burst duration, which indicates that the decrease in the amplitude of this component of the response from the IC with increasing stimulus duration is a result of GABAA mediated inhibition on IC neurons. The tone exposure caused a similar decrease in amplitude of this component of the response from the IC, thus indicating that noise exposure reduced the GABAA mediated component of this function. This is supported by the finding that microinjections of bicucullene into the IC of noise-exposed animals did not significantly change the relationship between the amplitude of this peak and the stimulus duration.

Transcranial magnetic stimulation excites the labyrinthine segment of the facial nerve: an intraoperative electrophysiological study in man.

The site where transcranial magnetic stimulation (magStim) depolarizes the facial nerve was investigated in 6 patients who underwent surgery of the cerebellopontine angle (CPA). The facial nerve was stimulated (1) magnetically prior to craniotomy, (2) electrically near the brainstem (elREZ), (3) at the exit from the CPA into the facial canal (elPorus), and (4) in the stylomastoid fossa (elStylo). The range of latency differences (delta) of compound muscle action potentials (CMAPs) recorded from the ipsilateral mentalis muscle were as follows: delta elREZ-magStim: +0.5 to +1.1 ms (P less than or equal to 0.03, Wilcoxon test); delta elPorus-magStim: +0.2 to +0.5 ms (P less than or equal to 0.03); delta elStylo-magStim: +0.8 to +1.0 ms (P less than or equal to 0.03). On the basis of anatomical data and a facial nerve conduction velocity of 33-46 m/s in these patients, it was concluded that transcranial magnetic stimuli depolarized the facial nerve at a location 10-15 mm distal to its entrance into the facial canal. This corresponds to the end of the labyrinthine segment of the facial nerve, i.e. the transit zone where the nerve ceases to be surrounded by cerebrospinal fluid (CSF) with its high electrical conductivity and enters the high-resistance tissue of the petrous bone.

The excitation site of the trigeminal nerve to transcranial magnetic stimulation varies and lies proximal or distal to the foramen ovale: an intraoperative electrophysiological study in man.

The excitation site of the trigeminal nerve using transcranial magnetic stimulation (magStim) was analyzed in 5 patients in whom the trigeminal nerve was surgically exposed in the posterior fossa during microvascular decompression of the facial nerve for hemifacial spasm. The trigeminal nerve was stimulated (1) magnetically immediately prior to craniotomy, and (2) electrically near the root exit zone (elREZ) of the nerve from the brainstem. Mean latency differences (delta) of masseter compound muscle action potentials (CMAPs) (delta elREZ minus magStim) were 0.7 (range: +0.3 to +1.3) ms (P less than or equal to 0.05, Wilcoxon-test). From these results, an analysis of anatomical data, and using a trigeminal nerve conduction velocity (NCV) of 50 m/s as reported in the literature, the following conclusions were drawn: the excitation site to magStim (1) is variable among individuals, (2) is located 3.4 (1.6-6.5) cm distal to the trigeminal REZ, and (3) which corresponds to segments of the nerve that are located either within or outside the cerebrospinal fluid (CSF), either proximal or distal to the foramen ovale. These findings are in contrast to those we obtained in a previous study of the facial nerve in which the excitation site was found to be constant among subjects and restricted to the location on the nerve where it exists the high conductivity CSF to enter the high-resistance petrous bone.

Interaction between the blink reflex and the abnormal muscle response in patients with hemifacial spasm: results of intraoperative recordings.

Patients with hemifacial spasm (HFS) have an abnormal muscle response (AMR) that can be elicited by stimulating one branch of the facial nerve and recording electromyographically from muscles innervated by other branches of the facial nerve. In addition, the R1 component of the blink reflex can be elicited from the affected side in patients with HFS who are undergoing microvascular decompression (MVD) operations under inhalation anesthesia. A synkinetic component of the blink reflex response that corresponds to the R1 component can be recorded from the mentalis muscle. In the present study we show that the blink reflex elicited by electrical stimulation of the supraorbital nerve can suppress the AMR elicited by electrical stimulation of the temporal branch of the facial nerve in patients with HFS when the interval between stimulation of the supraorbital nerve and stimulation of the temporal branch of the facial nerve (interstimulus interval, ISI) is such that the blink reflex response would appear later than the AMR if they had been elicited independently. Within a short range of ISIs the two responses suppress each other partially or totally. We find evidence that the suppression of the AMR is the result of an interaction in the facial motonucleus. We believe that the results of the present study support the hypothesis that the facial motonucleus is hyperactive in patients with HFS, and we suggest that the AMR is a result of backfiring from the facial motonucleus and that it may thus be an exaggerated F-response.

Blink reflex in patients with hemifacial spasm. Observations during microvascular decompression operations.

The blink reflex cannot normally be elicited during surgical anesthesia using inhalation anesthetics. However, in patients with hemifacial spasm (HFS) the early component of the reflex response (R1) can be elicited on the affected side but not on the unaffected side during such anesthesia. The electromyographic (EMG) response from the mentalis muscle to stimulation of the supraorbital nerve was recorded during microvascular decompression (MVD) of the facial nerve to relieve HFS and compared to the response from the same muscle to stimulation of the zygomatic branch of the facial nerve in four patients. During the operation before the facial nerve was decompressed, contractions in both the orbicularis oculi and the mentalis muscles could be elicited by stimulation of the supraorbital nerve (mean latencies 12.2 +/- 1.9 and 12.9 +/- 2.0 ms, respectively). When the facial nerve had been decompressed the blink reflex could no longer be elicited, and there was no response from the mentalis muscle to stimulation of the zygomatic branch of the facial nerve. Compound action potentials (CAP) recorded from the 7th cranial nerve in response to stimulation of the supraorbital nerve had latencies of 7.5 ms +/- 1.4 ms to the negative peak.

Brainstem auditory-evoked potentials.

Brainstem auditory-evoked potentials (BAEPs) are generated in the ear and brainstem nuclei of the ascending auditory pathways following a transient acoustic stimulus. Because they can be recorded noninvasively in humans, BAEPs have a number of clinical and research applications. This paper reviews the properties of BAEPs, with particular emphasis on those characteristics that are relevant to the acquisition and analysis of the responses. Theories of the neural origins of the responses are reviewed. The dependence of the responses on the stimulus waveform and the problem of stimulus artifact are considered. Then, origins of the background noise are discussed, and the use of linear filtering and methods of artifact detection to improve the signal-to-noise ratio are reviewed. Finally, the problem of identifying parameters to quantify the responses is considered. The definition of response components in terms of response peaks and data on intra- and intersubject variability are reviewed, and the use of algorithms to measure parameters is discussed.

Avulsion rupture of the internal auditory artery during operations in the cerebellopontine angle: a study in monkeys.

The effect of manipulations in the cerebellopontine (CP) angle on the cochlear nerve was studied in 12 rhesus monkeys to elucidate how surgical procedures in the CP angle may affect the peripheral auditory system. Brain stem auditory evoked potentials and compound action potentials from the cochlear nerve were recorded throughout the experiments and were studied to determine the level of injury to the cochlear nerve. After the manipulations, the animals were perfused with fixatives and their temporal bones were removed and examined histologically. The monkeys showed electrophysiological changes similar to those observed in humans as a result of surgical manipulations in the CP angle. Avulsions of the internal auditory artery and cochlear nerve fibers at the area cribrosa were the most common histological findings. The auditory evoked potentials were suddenly and irreversibly lost during the manipulations in 3 monkeys, and hemorrhagic foci were identified histologically in these animals at the fundus of the internal auditory canal (the area cribrosa). No morphological changes at locations other than the area cribrosa were identified in these 3 monkeys. The results of this study indicate that injury to the internal auditory artery at the area cribrosa may play an important role in the abrupt loss of hearing experienced by some patients while they are undergoing operations in the CP angle. This study also led to speculation regarding the possible existence of collateral circulation to the cochlea as a factor in injury to the internal auditory artery during acoustic neurinoma operations.

Microvascular decompression in hemifacial spasm: intraoperative electrophysiological observations.

Facial muscle responses in patients with hemifacial spasm undergoing microvascular decompression operations were recorded. Two peripheral branches of the facial nerve were stimulated and the electrical responses of muscles innervated by these branches were studied to see how the lateral spread of activity that is known to be present in these patients was affected by decompressing the facial nerve. In some of the patients the hemifacial spasm ceased when the dura mater was opened, in some it ceased when the arachnoid was opened, and in others the spasm persisted until the offending vessel was dissected away from the nerve. The lateral spread of activity elicited by antidromic stimulation of a branch of the facial nerve was less affected by opening of the dura mater or arachnoid: it usually persisted until the blood vessel that had been compressing the facial nerve was removed and reappeared when the vessel that had been compressing the facial nerve was allowed to slip back onto the nerve. This seems to indicate that microvascular decompression of the facial nerve is effective in alleviating hemifacial spasm because it removes the actual cause of the disorder rather than simply causing local injury to the nerve as a result of the procedure.

Does intraoperative monitoring of auditory evoked potentials reduce incidence of hearing loss as a complication of microvascular decompression of cranial nerves?

During a 14-month period, 129 individuals underwent 140 operations for microvascular decompression to relieve hemifacial spasm, disabling positional vertigo, tinnitus, or trigeminal neuralgia at our institution. Seven patients were operated upon twice on the same side and 4 were operated upon on both sides at different times. In each case, the brainstem auditory evoked potentials were monitored intraoperatively by the same neurophysiologist. In 75 of these operations, compound action potentials were also recorded from the exposed 8th nerve. Comparison of speech discrimination scores before the operation and at the time of discharge showed that at discharge, discrimination had decreased in 7 patients by 15% or more and increased in 4 patients by 15% or more, in 2 patients by as much as 52%. Essentially similar results were obtained when preoperative speech discrimination scores were compared with results obtained from the 87 patients who returned for a follow-up visit between 3 and 6 months after discharge. Only one patient lost hearing (during a second operation to relieve hemifacial spasm). Another patient (also operated upon to relieve hemifacial spasm) suffered noticeable hearing loss postoperatively, but had recovered nearly normal hearing by 4 months after the operation. Nine patients had an average elevation of the hearing threshold for pure tones in the speech frequency range (500 to 2000 Hz) of 11 dB or more at 4 to 5 days after the operation; 8 of these had fluid in their middle ears that most likely contributed to the hearing loss. Threshold elevations occurred at 4000 Hz and 8000 Hz in 19 and 29 ears, respectively.

Recordings from human dorsal column nuclei using stimulation of the lower limb.

Responses from the surface of the dorsal column nuclei and the dorsal surface of the spinal cord were recorded using monopolar electrodes after stimulation of the lower limbs (common peroneal nerve at the knee and posterior tibial nerve at the ankle) in patients undergoing neurosurgical operations for spasmodic torticollis. Those responses were smaller in amplitude than responses to stimulation of the upper limbs (median nerve at the wrist), and the waveforms differed. The negative deflection that is prominent in the response to stimulation of the upper limbs is more variable, broader, and relatively smaller in amplitude than the response to upper limb stimulation. Another difference between responses to upper and lower limb stimulation was that multiple peaks were superimposed on the initial response to stimulation of the lower limbs, but were not as consistently seen in the responses to upper limb stimulation. The negative peak in the response from the dorsal column nuclei to lower limb stimulation was of about the same latency as the P27 peak in the far-field response (somatosensory evoked potential) to stimulation of the peroneal nerve.

Preservation of hearing in operations on acoustic tumors: an alternative to recording brain stem auditory evoked potentials.

The monitoring of auditory function by recording brain stem auditory evoked potentials in patients undergoing removal of acoustic tumors is hampered by the small amplitude of the brain stem auditory evoked potentials. Because several thousands of responses must be added, it takes several minutes to obtain an interpretable record. Recordings done directly from the exposed eighth nerve have much higher amplitudes, and, therefore, interpretable responses can be obtained after only a few responses have been added. However, it is difficult to place the recording electrode in an optimal position and the electrode may interfere with the removal of the tumor. In this report, we show that evoked potentials from the cochlear nucleus, which can be recorded by placing an electrode in the lateral recess of the fourth ventricle, have a large amplitude, and that the electrode placed in this way does not interfere with the removal of the tumor. This way of monitoring, therefore, yields interpretable responses within 15 to 20 seconds, or less, and makes it possible to detect injuries to the entire intracranial portion of the eighth nerve, just as brain stem auditory evoked potentials do, but 20 to 50 times faster.

Auditory neurophysiology.

The anatomy and the physiology of the ear and the auditory system are reviewed. The differences between the anatomy and physiology in humans and animals commonly used in auditory research are discussed. The clinical importance of brainstem auditory evoked potentials and their neural generators are discussed as well as the anatomy and physiology of the acoustic middle ear reflex. The possible clinical relevance of the extralemniscal auditory system is also addressed.

Cochlear nerve injuries caused by cerebellopontine angle manipulations. An electrophysiological and morphological study in dogs.

Changes in the response from the cochlear nerve in dogs resulting from cerebellopontine angle (CPA) manipulations were correlated with histological changes in the nerve. The aim of this study was to determine the mechanisms underlying hearing deficits incurred as a result of manipulations in the CPA. Compound action potentials (CAP) were recorded from the cochlear nerve in response to click stimulation before, during, and after cerebellar and eighth nerve retractions were performed under anesthesia. The retractions were carried out to elicit different degrees of change in the latency and waveform of the CAP. About 30 minutes after completion of the manipulations, the dogs were perfused with a fixative and their cochlear nerves and brain stems were prepared for histological studies. The results showed that retraction of the eighth nerve caused a disintegration of the myelin sheath, and there were multiple and extensive foci of petechial hemorrhage and thromboses of the vasa nervorum of the cochlear nerve. In two dogs in which retraction was carried to a point at which the N2 peak of the CAP was abruptly obliterated, there was a separation of the central and peripheral myelin junction (Obersteiner-Redlich (OR) zone) and bleeding from the vasa nervorum at the OR zone. In the dogs in which the changes in the CAP had almost recovered before fixative perfusion, there were petechial hemorrhages within the cochlear nerve trunk, thus showing that improvement of electrophysiological responses may not always correlate with the absence of morphological changes.

Monitoring facial EMG responses during microvascular decompression operations for hemifacial spasm.

Facial electromyographic (EMG) responses were monitored intraoperatively in 67 patients with hemifacial spasm who were operated on consecutively by microvascular decompression of the facial nerve near its exit from the brain stem. At the beginning of the operation, electrical stimulation of the temporal or the zygomatic branch of the facial nerve gave rise to a burst of EMG activity (autoexcitation) and spontaneous EMG activity (spasm) that could be recorded from the mentalis muscle in all patients. In some patients, the spontaneous activity and the autoexcitation disappeared after the dura was incised or when the arachnoid was opened, but stimulation of the temporal branch of the facial nerve caused electrically recordable activity in the mentalis muscle (lateral spread) with a latency of about 10 msec that lasted until the facial nerve was decompressed in all but one patient, in whom it disappeared when the arachnoidal membrane was opened. When the facial nerve was decompressed, this lateral spread of antidromic activity disappeared totally in 44 cases, in 16 it was much reduced, and in seven it was present at the end of the operation at about the same strength as before craniectomy. In four of these last seven patients there was still very little improvement of the spasm 2 to 6 months after the operation; these four patients underwent reoperation. In two of the remaining three patients, the spasm was absent at the 3- and 7-month follow-up examination, respectively, and one had mild spasm. Of the 16 patients in whom the lateral spread response was decreased as a result of the decompression but was still present at the end of the operation, 14 had no spasm and two underwent reoperation and had mild spasm at the last examination. Of the 44 patients in whom the lateral spread response disappeared totally, 42 were free from spasm and two had occasional mild spasm at 6 and 13 months, respectively, after the operation. Monitoring of facial EMG responses is now used routinely by the authors during operations to relieve hemifacial spasm, and is performed simultaneously with monitoring of auditory function for the purpose of preserving hearing. The usefulness of monitoring both brain-stem auditory evoked potentials recorded from electrodes placed on the scalp and compound action potentials recorded directly from the eighth cranial nerve is evaluated.

Preservation of facial function during removal of acoustic neuromas. Use of monopolar constant-voltage stimulation and EMG.

The authors describe a modification in the way the facial nerve is stimulated electrically during operations to remove medium and large-sized (greater than 2 cm) acoustic tumors. This consists of monopolar stimulation with low internal impedance. Proper use of this modified stimulation technique together with acoustic monitoring of the electromyographic responses of facial muscles helps to preserve facial nerve function in patients undergoing these operations, and also decreases the duration of the operation.