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Biomedical subjects

A R Møller

Publications and source records attributed to A R Møller.

At least 55 records · Page 3Linked to original sources
PubMed1993

Late waves in the response recorded from the intracranial portion of the auditory nerve in humans.

We showed in previous studies that the click-evoked responses from the exposed eighth nerve in some patients contain quasi-periodic components that appear in the interval between 4 and 16 milliseconds after the click stimulus, and that the phase of these oscillatory components reverses when the click polarity is reversed. When the responses to clicks of opposite polarity are subtracted from each other, these late waves appear as a prolonged quasi-periodic oscillation with a frequency around 700 Hz. These late components appear more frequently in patients with high-frequency hearing losses than in patients with normal hearing. We have attributed these components to prolonged and in-phase oscillations of a large portion of the basilar membrane, possibly caused by the generation of standing waves on the basilar membrane. The results of the present study show that these oscillations correspond closely in both frequency and phase to the late oscillations that are seen in the cross-correlograms of the responses from the exposed eighth nerve to pseudorandom noise. The finding that similar quasi-periodic components can be retrieved from the responses from the exposed eighth nerve to both transient and continuous sounds is taken as an indication that the neural activity that these components represent reflects some general property of the cochlear frequency analyzer. We also found that the speech discrimination is not noticeably different in patients with such waves compared with what it is in patients with similar hearing loss who do not have such waves. This is taken as an indication that spectral analysis in the cochlea is less important in speech discrimination than previously assumed.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗
PubMed1993

Restoration of useful hearing after microvascular decompression of the cochlear nerve.

This report describes a patient with sudden sensorineural hearing loss who was found to have a megadolichoectasia vertebrobasilar system that appeared to be causing compression of the ipsilateral facial and vestibulocochlear nerves. The patient was treated conservatively for 4 months, during which time no hearing returned. He then underwent microvascular decompression of the affected nerves. At surgery, marked compression of the cranial nerves VII-VIII complex and the pons was observed. Postoperatively, the patient experienced a gradual return of useful hearing. We suggest that vascular compression may be a rare, but treatable, cause of sensorineural hearing loss.

Audiometry, Pure-Tone↗
PubMed1992

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.

Action Potentials↗
PubMed1992

Transcranial magnetic stimulation of the facial nerve: intraoperative study on the effect of stimulus parameters on the excitation site in man.

Magnetic stimulation (magStim) of the intracranial facial nerve is performed in clinical and research settings, but the activation site is a matter of controversy. Latencies of nasalis muscle responses to magStim were, therefore, compared with those obtained by direct electrical stimulation of the facial nerve (a) at the root exit zone (REZ); (b) at the porus of the facial canal; and (c) in the stylomastoid fossa during microvascular decompression operations in the cerebellopontine angle (CPA). Measurements of latencies of the nasalis muscle response, obtained while the stimulating coil was placed over the parieto-occipital area of the scalp, indicated that it was the labryinthine segment of the facial canal, 5 to 16 mm distal to the CPA, that was activated. This would be in agreement with studies of physical models reported in the literature that showed (a) the strength of the electrical current generated by a magnetic field is particularly high close to a nerve foramen; and (b) excitation to magStim is most likely to occur where the induced electrical field changes rapidly over distance, i.e., at anatomical boundaries between media of high and low specific resistance. These characteristics are found at the end of the labyrinthine segment of the facial canal, where the facial nerve leaves the low-resistance cerebrospinal fluid and enters the high-resistance petrous bone. The site of neural excitation is robust and unaffected by stimulus intensity and current direction within a wide range, or by large changes in location of the coil.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Compound action potentials recorded from the exposed eighth nerve in patients with intractable tinnitus.

Compound action potentials (CAP) were recorded directly from the exposed intracranial portion of the eighth nerve in 19 patients undergoing microvascular decompression (MVD) of the eighth nerve for intractable tinnitus. The waveform of the CAPs recorded in patients with tinnitus varied from normal to highly abnormal, but only in 1 patient were there distinct abnormalities in the waveform of the CAP that could not be attributed to the patient's hearing loss. The mean values of the latencies of the N1 and N2 peaks in the CAPs recorded from the exposed eighth nerve in patients with tinnitus and high-frequency hearing loss were virtually indistinguishable from the latencies obtained in patients with similar hearing loss but no tinnitus. There was no statistically significant difference between the latency of peak III in the brainstem auditory evoked potentials (BAEPs) in these two groups of patients, but the latency of peak V was slightly shorter (statistically significant) in the patients with tinnitus than it was in the patients without tinnitus.

Action Potentials↗
PubMed1992

Some forms of tinnitus may involve the extralemniscal auditory pathway.

It has previously been shown that the click-evoked responses recorded from the intracranial portion of the eighth nerve in patients with incapacitating tinnitus are not abnormal, nor is the latency of peak III of the click-evoked brainstem auditory-evoked potentials significantly altered; however, the latency of peak V is slightly (but significantly) shortened in comparison to that of patients with the same degree of hearing loss but no tinnitus. In this study the hypothesis that the extralemniscal auditory system is involved in the generation of tinnitus is tested. We made use of the fact that neurons of the extralemniscal auditory system also receive input from the somatosensory system, and that stimulation of the somatosensory system can influence the processing of auditory information in the extralemniscal system. In 4 of 26 patients with mild-to-severe tinnitus whose median nerve was stimulated electrically, the tinnitus increased noticeably during stimulation, in 6 the intensity of the tinnitus decreased noticeably, and in the remaining 16 there was no noticeable change in the tinnitus. In some of the patients the character of the tinnitus changed in a complex way. There were no significant differences in hearing thresholds in these three groups of patients. Electrical stimulation of the median nerve in 12 individuals with normal hearing who did not have tinnitus either had no effect on the loudness of sounds or it caused a slight increase in the loudness.

Auditory Pathways↗
PubMed1991

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.

Action Potentials↗
PubMed1991

The cranial nerve vascular compression syndrome: I. A review of treatment.

The author reviews current literature on microvascular decompression (MVD) for treatment of hemifacial spasm (HFS) and trigeminal neuralgia (TN), which shows that MVD is an effective treatment for these disorders. Although there are treatments for TN other than MVD that demonstrate a high rate of success, MVD is the only effective long-term treatment for HFS. MVD is also an effective treatment for glossopharyngeal neuralgia (GPN), and recently MVD has been shown to be an effective treatment for particular types of vertigo (disabling positional vertigo, DPV) and certain types of tinnitus.

Cranial Nerve Diseases↗
PubMed1991

The cranial nerve vascular compression syndrome: II. A review of pathophysiology.

The various hypotheses regarding the pathophysiologies of trigeminal neuralgia and hemifacial spasm are reviewed, and the results of recent physiological studies on the pathogenesis of hemifacial spasm are discussed. Evidence is presented that strongly supports the hypothesis that the symptoms and signs of hemifacial spasm are caused by hyperactivity in the facial motonucleus. Some of the contradictions regarding the prevalence of vascular conflicts in the cerebellopontine angle and the symptoms of vascular compression are discussed, and a hypothesis is presented that assumes that a suitable substrate must be present, in addition to vascular compression of the respective cranial nerve root, for the symptoms and signs of a cranial nerve vascular compression disorder to develop. Finally, it is discussed how this hypothesis can explain some of the differences between the disorders that can be cured by microvascular decompression of respective cranial nerves.

Cranial Nerve Diseases↗
PubMed1991

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.

Blinking↗
PubMed1991

Effect of high-frequency hearing loss on compound action potentials recorded from the intracranial portion of the human eighth nerve.

Compound action potentials (CAP) were recorded from the exposed intracranial portion of the eighth nerve to stimulation with click sounds in patients with sensorineural high-frequency hearing loss who underwent microvascular decompression (MVD) operations to treat trigeminal neuralgia (TN). In patients with normal hearing the CAP recorded in that way is characterized by a negative peak, preceded by a small positivity and followed by a positivity and sometimes a second negative peak. In patients with high-frequency hearing loss the CAP also usually had an initial sharp negative peak in response to clicks of high intensity (105 to 110 dB Pe SPL), similar to findings in patients with normal hearing, but in patients with high-frequency hearing loss the initial negative peak was often followed by a slow negative deflection. The latency of the initial negative peak in the CAP in patients with high-frequency hearing loss was longer than the latency of this peak in patients with normal hearing, but the difference in latencies of this peak to condensation and rarefaction clicks was small. When the stimulus intensity was lowered the amplitude of the initial peak decreased, and the CAP became dominated by a broad negative peak with a latency of 6 to 8 ms. In 11 of 15 patients with severe high-frequency hearing loss, a series of quasi-periodic waves was superimposed on the CAP. The frequency of these waves varied between 500 and 1200 Hz, and the waves could be detected between 6 and 16 ms after presentation of the click stimulus. These waves were usually present in the response to stimuli in the intensity range from 75 to 110 dB Pe SPL. Only 4 of 17 patients with normal hearing had similar waves.

Acoustic Stimulation↗
PubMed1991

Auditory nerve compound action potentials and brain stem auditory evoked potentials in patients with various degrees of hearing loss.

Click-evoked compound action potentials recorded in normal-hearing patients through a monopolar electrode placed on the intracranial portion of the eighth nerve were compared with the responses recorded in patients with high-frequency hearing loss or with high- and low-frequency hearing losses. That multiple peaks appear in the compound action potential in patients with hearing loss implies that click sounds elicit successive and separated volleys of neural excitation in the ascending auditory pathway, whereas click sounds in patients with normal hearing mainly give rise to a single volley of neural activity. This difference in the pattern of auditory nerve activity might explain why there are often multiple peaks in the brain stem auditory evoked potentials in patients with hearing loss and that the peaks are often less well-defined than peaks in patients with normal hearing.

Audiometry, Evoked Response↗
PubMed1991

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.

Brain Neoplasms↗
PubMed1991

Compound action potentials recorded from the intracranial portion of the auditory nerve in man: effects of stimulus intensity and polarity.

Compound action potentials (CAP) were recorded from the intracranial portion of the eighth nerve in patients with normal hearing who were undergoing neurosurgical operations for cranial nerve disorders (trigeminal neuralgia and hemifacial spasm). Brain-stem auditory-evoked potentials were recorded intraoperatively to ensure that no noticeable changes occurred in conduction in the auditory nerve as a result of surgical dissections. The CAP recorded from the middle portion of the exposed intracranial portion of the eighth nerve in response to clicks of high intensity (100-110 dB peak equivalent SPL, or pe SPL) had a triphasic shape, as is commonly seen in monopolar recordings from long nerves. A second negative peak (N2) could be identified in some patients. There was little difference in the waveform of the CAP in response to condensation and rarefaction clicks, and in some patients the waveform of the CAP remained the same over a range of stimulus intensities (from 105 to 75 dB pe SPL), whereas in others the negative peak of the CAP became much broader in response to stimuli with intensities of less than 85 dB. In some patients the N2 peak became dominant as the stimulus intensity was decreased. At low stimulus intensities, the response consisted of a single, broad negativity. The latency-intensity curves for the N1 peak had different slopes in different patients. In those individuals in whom there was a noticeable difference between the latency of the N1 peak in response to clicks of opposite polarity, the latency-intensity curves of the responses to rarefaction clicks were steeper than those of the responses to condensation clicks, and the latency of the N1 peak to condensation clicks became shorter than that to rarefaction clicks at intensities below 85-90 dB pe SPL. The latency-intensity curves for the N2 peak were usually less steep than those of the N1 peak, but in some patients the curves for these two peaks had similar slopes. The amplitude of the N1 peaks showed a steep increase in click intensities at 95 and 105 dB, and a much less steep course for intensities below 95 dB. The amplitudes of the N2 peak reached a plateau in the range 95-105 dB, and decreased more rapidly than the N1 peak below 95 dB.

Acoustic Stimulation↗
PubMed1990

Recordings from the facial nucleus in the rat: signs of abnormal facial muscle response.

On the basis of results of electrophysiological studies in patients undergoing microvascular decompression (MVD) operations to relieve hemifacial spasm (HFS), we have postulated that the abnormal muscle response characteristically found in patients with HFS is the result of irritation of the facial nerve by the blood vessel that is compressing the facial nerve near its exit from the brainstem in these patients. This abnormal muscle response is seen when one branch of the facial nerve is electrically stimulated and recordings are made from muscles that are innervated by other branches of the facial nerve. We further hypothesized that the facial nucleus is hyperactive in patients with HFS and that the spasm and the abnormal muscle response are results of a phenomenon known as "kindling". These hypotheses are supported by recent studies showing that chronic electrical stimulation of the facial nerve trunk in rats near the brainstem results in an abnormal muscle response that is similar to that seen in patients with HFS. In this paper, we present the results of recording from the facial motonucleus in rats that had been subjected to repeated electrical stimulation of the facial nerve. The results indicate that the abnormal muscle response in these rats was caused by changes in the function of the facial motonucleus. We interpret these results as showing that the physiological abnormalities that give rise to the signs of HFS in man are located in the facial motonucleus, and that the changes in the function of the nucleus are produced by chronic antidromic neutral activity resulting from close contact between a blood vessel and the facial nerve.

Animals↗
PubMed1990

Late components in the compound action potentials (CAP) recorded from the intracranial portion of the human eighth nerve.

The compound action potential (CAP) that can be recorded from the exposed intracranial portion of the eighth nerve in man to stimulation with broadband clicks of about 100 dB Pe SPL normally has an initial (small) positivity followed by a sharp negative peak with a latency of about 3 to 3.5 ms. The negative peak is usually followed by another positive-negative deflection with a latency of about 4 ms. Usually, no stimulus-related potential can be discerned at latencies longer than 5 ms. However, in a few patients we found a series of waves that occurred between 4 and 12 ms after the stimulation. The polarity of these waves reversed precisely (180 degrees phase shift) when the polarity of the sound was reversed. Thus, these waves appeared clearly when the responses to clicks of opposite polarity were subtracted. These late waves were quasiperiodic with intervals between 1 and 2 ms. The waveform and duration differed between patients, but were remarkably constant in each patient. The timing of these late peaks was nearly independent of the stimulus intensity in the range studied (between 105 and 70 dB Pe SPL); in this respect the late waves differ fundamentally from the initial peaks, which showed a monotone decrease in latency with increasing stimulus intensity over this intensity range. Although the origin of these late waves is not known, the similarities between these waves and stimulated otoacoustic emissions indicate that the late waves may be the result of active cochlear processes similar to those that produce the cochlear echo.

Acoustic Stimulation↗