Is there a place for microvascular decompression?
Explore the source record for details and available documents.
Cerebrovascular Disorders↗
Biomedical subjects
A R Møller
Publications and source records attributed to A R Møller.
Neurophysiologic basis for cochlear and auditory brainstem implants.
The physiologic basis for cochlear and brainstem implants is discussed. It is concluded that the success of cochlear implants may be explained by assuming that the auditory system can adequately discriminate complex sounds, such as speech sounds, on the basis of their temporal structure when that is encoded in a few separate frequency bands to offer moderate separation of spectral components. The most important roles of the cochlea seems to be to prepare complex sounds for temporal analysis and to create separate channels through which information in different frequency bands is transmitted separately to higher nervous centers for decoding of temporal information. It is then pertinent to ask how many channels are needed. Because speech discrimination is very important, it is probably sufficient to use enough channels to separate formants from each other.
Brain Stem↗
Symptoms and signs caused by neural plasticity.
Plastic changes in the central nervous system are associated with hyperactivity, hypersensitivity, and spread of activity including activation of brain regions that are not typically involved. Symptoms and signs such as neuropathic pain and tinnitus and hyperactive disorders such as muscle spasm and synkinesis may result from such changes in function. Plastic changes that cause symptoms of diseases can be initiated by novel stimulations, overstimulation, or deprivation of input and the induced changes in the function of central nervous system structures may persist and aggravate after these events have ceased if the condition is not reversed. Disorders that are caused by neural plasticity are potentially reversible with treatment. However, the absence of morphologic abnormalities makes diagnosis of these conditions difficult and their treatment has been hampered by lack of understanding of their pathophysiology. Here the role of neural plasticity in the pathophysiology of several disorders is reviewed.
Animals↗
Diagnosis of acoustic tumors.
Explore the source record for details and available documents.
Cochlear Nerve↗
Vascular compression of cranial nerves: II: pathophysiology.
The pathophysiology of trigeminal neuralgia, hemifacial spasm and other disorders that can be cured by microvascular decompression of cranial nerves, is reviewed and different hypotheses about its pathophysiology are discussed. It is found that the pathophysiology of these disorders is complex and other factors than vascular compression are necessary to cause symptoms. While the efficacy of the microvascular decompression (MVD) operation is indisputable, it is questionable if the symptoms and signs of these disorders are caused by abnormal neural activity in the respective cranial nerves that result from the compression from a blood vessel. Instead, studies point to hyperactivity and hyperexcitability of the respective nuclei as a cause of the symptoms and signs of these disorders. Results of several studies indicate that irritation of the cranial nerve in question from close contact with a blood vessel may promote such development, and it seems necessary that other factors in addition to the vascular contact must be present in order that such a condition develops.
Cerebellopontine Angle↗
Neural mechanisms of BAEP.
Explore the source record for details and available documents.
Auditory Pathways↗
Delayed hearing loss after microvascular decompression of the trigeminal nerve.
OBJECTIVE: The development of sudden postoperative hearing loss as a complication of microvascular decompression (MVD) operations in the cerebellopontine angle has already been reported. A sudden hearing loss of vascular origin may also occur hours or days after such operations, but even in such cases an improvement of hearing over the following weeks is possible. Here we report on a gradual deterioration of hearing over a period of two weeks after MVD which has not been described in the literature up to now. CLINICAL PRESENTATION: A MVD operation was performed twice on a 36 year old patient with trigeminal neuralgia. After the second operation the patient developed a slight hearing impairment 3 days postoperatively which increased over a period of two weeks and ended up with total deafness. The course of intra-operative brainstem auditory evoked potentials and postoperative audiograms is documented. CONCLUSION: Because of gradual development of the delayed hearing loss, we conclude that postoperative tissue scarring may be the underlying pathology.
Adult↗
Correlation between latency and amplitude of peak V in the brainstem auditory evoked potentials: intraoperative recordings in microvascular decompression operations.
Intraoperative prolongation of the latency and decrement of the amplitude of peak V of brainstem auditory evoked potentials (BAEP) were studied in 38 microvascular decompression operations in which prolongation of the latency of peak V exceeded 1.0 msec. Postoperative hearing tests of all patients were compared with their preoperative hearing tests. Postoperative hearing loss was unrelated to the maximum prolongation of latency, but the amplitude decreased to lower values in patients with postoperative hearing loss compared to patients whose postoperative hearing was unchanged (P < 0.05). Twelve (32%) of 38 patients whose latency of peak V was prolonged more than 1.0 msec and 11 (61%) of 18 patients whose amplitude of peak V decreased more than 40% during the operations had decreased hearing postoperatively. In all patients, a prolongation of the latency of peak V was always accompanied by a decrease in the amplitude of peak V. The decrement of the amplitude was greater in the patients with decreased postoperative hearing thresholds than in the patients with unchanged postoperative hearing thresholds. The results of this study indicate that it would be valuable to monitor changes in the amplitude of peak V of BAEP in addition to monitoring the latency of peak V during operations where the VIIIth cranial nerve is manipulated.
Adult↗
Vascular compression of cranial nerves. I. History of the microvascular decompression operation.
The development of the microvascular decompression (MVD) operation is reviewed. It is stressed that a few innovative neurosurgeons discovered the role of vascular compression of cranial nerves V and VII in trigeminal neuralgia (TGN) and hemifacial spasm (HFS) and developed an operation, later to be known as the MVD operation. While the understanding of the pathophysiology of these disorders has improved, the surgical procedure has undergone little change since Gardner described the operation about 1960.
Cerebrovascular Circulation↗
Temporal integration of pain from electrical stimulation of the skin.
The threshold of sensation and the threshold of pain in response to electrical stimulation (impulses of 1 msec duration) of the skin on the forearm or hand in individuals without pain were compared with the thresholds of individuals with chronic pain in the range 1 to 100 pulses per second repetition rate. The threshold of sensation in patients without pain was little affected by the repetition rate of the stimulation within the range studied, and the threshold for pain decreased exponentially with increasing repetition rate. In individuals with chronic pain the threshold of sensation was similar to that of individuals without pain over the entire range of stimulus repetition rates studied, but the threshold of pain in patients with pain was lower and less affected by the stimulus rate than it was in the individuals without pain, thus closer to the threshold of sensation.
Adult↗
Similarities between chronic pain and tinnitus.
OBJECTIVE: The aim of this study is to review hypotheses about the mechanisms of chronic pain and to compare them with that of tinnitus. Hypotheses about the pathophysiology of severe tinnitus and chronic pain have been of mainly two kinds: one of which claims that pathology located in the periphery (the ear for tinnitus, and peripheral nerves for pain) can explain the symptoms, while the other claims that the symptoms are caused by changes in the function of nuclei of the central nervous system. DATA SOURCES: A search of the literature from the past 35 years was used. CONCLUSIONS: There is considerable evidence that both chronic pain and some forms of tinnitus are caused by changes in the central nervous system and that the anatomic location of the physiologic abnormality causing the symptoms of chronic pain and some forms of tinnitus is not the same location to which the symptoms are referred, i.e., the ear for tinnitus and the location of injury for pain. Such changes in the central nervous system may have been induced by peripheral processes such as tissue damage, but the changes can persist a long time after complete healing of a peripheral lesion. Different forms of tinnitus may respond to different treatments as is the case for chronic pain. If the different forms of tinnitus cannot be separated, then the results of studies of the efficacy of different kinds of drugs may be misleading.
Chronic Disease↗
Evidence of neuronal plasticity within the inferior colliculus after noise exposure: a study of evoked potentials in the rat.
Recent investigations have implicated that the central nervous system has a role in the changes that occur in auditory function following acoustic trauma caused by noise exposure. These investigations indicate that the inferior colliculus may be the primary anatomical location in the ascending auditory pathway where noise-induced neuronal plasticity occurs, thereby resulting in changes in the neuronal processing of auditory information. In the present investigation, we show that the amplitudes of all peaks in the click-evoked response from the external nucleus of the inferior colliculus decrease during a 30 min exposure to a tone (104 dB sound pressure level (SPL) at 4 kHz and 8 kHz). After tone exposure, the amplitudes of two of the peaks of the response from the external nucleus of the inferior colliculus that reflect the input from more caudal structures slowly returned to baseline levels, whereas the amplitudes of the two peaks reflecting neuronal activity in the inferior colliculus increased above baseline levels and remained at the increased levels for at least 90 min following exposure to the tone. We also show that exposure to a 4 kHz tone at 104 dB SPL causes changes in the neuronal processing of tonebursts in the form of changes in the temporal integration function for one of the peaks of the response from the external nucleus of the inferior colliculus that originates in the inferior colliculus. Before tone exposure the amplitude of this peak decreased with increasing stimulus duration, but after tone exposure the amplitude of this peak was independent of the duration of the toneburst stimulus. We interpret these changes as evidence that noise exposure (tone exposure) causes changes in the excitability of the inferior colliculus that are not seen in more caudal structures, and these changes are probably a result of a change in the balance between inhibition and excitation in the inferior colliculus.
Acoustic Stimulation↗
Contralateral evoked brainstem auditory potentials as an indicator of intraoperative brainstem manipulation in cerebellopontine angle tumors.
Brainstem auditory evoked potentials (BAEP) were studied during operations to remove acoustic tumors using the retromastoid approach. BAEP were elicited from the side contralateral to the tumor, and changes in the latencies of peaks III and V of the BAEP were compared with changes in cardiovascular parameters throughout the operation. When the changes in the determined cardiovascular parameters were related to surgical manipulations, the related changes in the latencies of peaks III and V of the BAEP were more consistent than the changes in the cardiovascular parameters and they tended to occur earlier than the changes noted in the cardiovascular parameters.
Adult↗
Monitoring auditory function during operations to remove acoustic tumors.
The use of auditory evoked potentials in the preservation of hearing is reviewed, and the feasibility of using brainstem auditory evoked potentials, electrocochleography, and compound action potentials directly recorded from the eighth nerve is discussed. The method of recording directly from the surface of the cochlear nucleus using an electrode placed in the lateral recess of the fourth ventricle is described, and the advantages of its use are demonstrated.
Audiometry, Evoked Response↗
Effects of (-)-baclofen, clonazepam, and diazepam on tone exposure-induced hyperexcitability of the inferior colliculus in the rat: possible therapeutic implications for pharmacological management of tinnitus and hyperacusis.
Recent investigations in the authors' laboratory have shown that acute tone exposure (4 kHz continuous tone, 104 dB sound pressure level (SPL), 30-min duration) induces increases in the amplitude of click-evoked potentials in the inferior colliculus (IC). These increases have been attributed to a decrease in GABAA-mediated inhibition on IC neurons. In the present study, we examined the effects of three compounds (diazepam, clonazepam, and (-)-baclofen) that are known to enhance GABAergic inhibition on these tone exposure-induced increases and on changes in temporal integration in the IC. (-)-Baclofen was the only one of the three compounds tested that reversed in a dose-dependent manner the effects of tone exposure on both the amplitude of the click-evoked potentials recorded from the IC and on measures of the changes in temporal integration based on these potentials. Diazepam and clonazepam exhibited remarkably different effects on the click-evoked potentials recorded from the surface of the IC. Diazepam caused a dose-dependent decrease in one of the components of the IC potentials that reflects postsynaptic activity in the IC, whereas clonazepam caused a dose-dependent decrease in a peak that reflects input to the IC from the superior olivary complex (SOC). At dosages up to 40 mg/kg, neither diazepam nor clonazepam reversed the changes in temporal integration in the IC that were induced by the tone exposure; diazepam caused a small, but statistically significant, enhancement of the effects of tone exposure on this function. The results of this study show that (-)-baclofen is a potent modulator of both the excitability of neurons in the ascending auditory pathway and the processing of auditory information by IC neurons. The finding of the present study that two benzodiazepines (clonazepam and diazepam) have remarkably different effects on evoked potentials, which reflects both input to the IC and postsynaptic events in the IC neurons, suggests heterogenicity of the GABAA receptor from one structure to another in the ascending auditory pathway. We suggest that (-)-baclofen may be clinically useful in treating disorders of the auditory system that are caused by plasticity in the ascending auditory pathway.
Acoustic Stimulation↗
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.
Animals↗
Transcranial magnetic stimulation of the trigeminal nerve: intraoperative study on stimulation characteristics in man.
We studied responses from the masseter and nasalis muscles following magnetic stimulation (magStim) and compared these responses with those obtained by direct electrical stimulation of the trigeminal (NV) and facial (NVII) nerve near the root exit zone during microvascular decompression operations of NVII. We found that (1) magStim threshold to excite the nerve is high for NV and low for NVII; (2) excitation of all motor fibers is impossible for NV, and easy for NVII; (3) optimal coil placement is critical for NV, but not critical for NVII; and (4) between and within subjects, the excitation site is variable on NV, but stable on NVII. We estimated that the anatomical location of magStim to be either within or outside the cerebrospinal fluid for NV, and to be in the labyrinthine segment of the facial canal for NVII. Physical models explain and clinical lesion models support these differences found between NV and NVII.
Adult↗
Effects of L-baclofen and D-baclofen on the auditory system: a study of click-evoked potentials from the inferior colliculus in the rat.
The drug baclofen is a potential treatment for severe tinnitus, but its action in relieving tinnitus is not known. Baclofen is available as an approved drug only in racemic form with about equal content of the two enantiomers. In the present paper we show that L-baclofen causes a considerable (40.7%) suppression of the amplitude of the second peak in the click-evoked response from the cochlear nucleus. Bipolar recordings from the external nucleus of the inferior colliculus showed that L-baclofen caused a reduction in the amplitude of three or four distinct peaks in this response. D-Baclofen had no detectable effect on the response from the cochlear nucleus, and had only a slight effect on one component of the response from the external nucleus of the inferior colliculus. The demonstrated effect of L-baclofen on excitation in the ascending auditory pathway indicates that this drug may be a potential treatment for hyperactive auditory disorders such as tinnitus and hyperacusis.
Animals↗