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Biomedical subjects

A R Møller

Publications and source records attributed to A R Møller.

At least 19 recordsLinked to original sources
PubMed1995

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↗
PubMed1995

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↗
PubMed1995

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↗
PubMed1995

Contribution from crossed and uncrossed brainstem structures to the brainstem auditory evoked potentials: a study in humans.

The neural generators of the brainstem auditory evoked potentials (BAEPs) in humans are not completely known. Attempts to identify the anatomical location of the neural generators of the human BAEP based on the results of studies in animals commonly used in auditory experimentation have been difficult because of the considerable anatomical differences between the ascending auditory pathways in humans and animals. The authors of this study compared recordings obtained from different locations on the lateral side of the brainstem in six patients undergoing microvascular decompression surgery for a cranial nerve disorder affecting the fifth cranial nerve (i.e., trigeminal neuralgia). Ipsilateral click stimulation evoked prominent responses from the caudal aspect of the pons up to the junction between the pons and the midbrain, but all components of the responses with latencies shorter than 8 msec had smaller amplitudes when recorded at more rostral locations. Components with latencies in the range of peak V elicited by contralateral click stimulation had their largest amplitudes when recorded from the lateral brainstem at the level of the fourth cranial nerve (thus, close to the inferior colliculus). Earlier components of the contralateral responses (latencies in the range of the latency of peak III) had their largest amplitudes when recorded from the caudal lateral brainstem. The results of this study indicate that the part of the uncrossed auditory pathway that is located rostral to the cochlear nucleus contributes little to the farfield potentials (i.e., BAEP), and it is doubtful whether the contralateral response that can be recorded at the level of the cochlear nucleus contributes noticeably to the BAEP.

Acoustic Stimulation↗
PubMed1995

Microsurgical anatomy around the foramen of Luschka in relation to intraoperative recording of auditory evoked potentials from the cochlear nuclei.

Three cadaveric heads were dissected to investigate the microsurgical anatomy around the foramen of Luschka. It was found possible to place a recording electrode in proximity to the cochlear nuclei by inserting it in the lateral recess of the fourth ventricle through the foramen of Luschka. In operations of the cerebellopontine angle using the retromastoid approach, access to the foramen of Luschka and the lateral recess is obtained by retracting the biventral lobule of the cerebellum in a caudal-rostral direction under a caudal-rostral/medial field of vision. The craniectomy might need to be enlarged a few millimeters in the caudal direction. A wick electrode can be inserted in the lateral recess beneath the choroid plexus in a rostromedial direction and to a depth of approximately 3 to 5 mm from the foramen of Luschka without excessive retraction of the cerebellum. The optimum position for the recording electrode is in the triangle formed by the axis of the cochlear nerve and the glossopharyngeal nerve and by the lip of the foramen of Luschka. The caudal retromastoid approach is more suitable than the translabyrinthine technique for recording from the cochlear nuclei as well as for implantation of stimulating electrodes into the cochlear nuclei for use as hearing prostheses.

Cadaver↗
PubMed1994

Click-evoked responses from the cochlear nucleus: a study in human.

Recordings from the vicinity of the cochlear nucleus in 9 patients undergoing microvascular decompression operations to relieve hemifacial spasm, trigeminal neuralgia, tinnitus, and disabling positional vertigo were conducted by placing a monopolar electrode in the lateral recess of the fourth ventricle (through the foramen of Luschka), the floor of which is the dorsolateral surface of the dorsal cochlear nucleus. The click-evoked potentials recorded by such an electrode display a slow negative wave with a peak latency of about 6-7 msec on which several sharp peaks are superimposed. None of the peaks in the recordings from the vicinity of the cochlear nucleus coincided with any vertex-positive peaks of the brain-stem auditory evoked potentials. In recordings from the lateral aspect of the floor of the fourth ventricle near the cochlear nucleus 1 patient showed 2 positive peaks, the earliest of which had a latency close to that of peak II and the second of which had a latency close to the negative peak between peaks III and IV of the brain-stem auditory evoked potentials. There is a distinct negative peak in the responses recorded from the midline of the floor of the fourth ventricle, the latency of which is only slightly shorter than that of peak V of the brain-stem auditory evoked potentials, supporting earlier findings that the sharp tip of peak V of the brain-stem auditory evoked potentials is generated by the termination of the lateral lemniscus in the inferior colliculus.

Acoustic Stimulation↗
PubMed1994

Conduction pathways and generators of magnetic evoked spinal cord potentials: a study in monkeys.

Evoked spinal cord potentials (ESCPs) following transcranial magnetic stimulation were recorded from the spinal cord in monkeys anesthetized with ketamine. Isopotential maps of the earlier negative deflection of the magnetic ESCP (N1 wave) revealed a distribution of negative field potentials, the maximum of which were located within the medial dorsolateral funiculus, which corresponds to the dorsolateral corticospinal tracts. The N1 wave of the magnetic ESCP had the same latency as the D-wave of the electrical ESCP elicited by either direct cortical or transcranial electrical stimulation. We assumed that the N1 wave was generated by direct excitation of pyramidal axons. Isopotential maps of the waves that followed the N1 peak (waves N2, N3, N4, and N5) of the magnetic ESCP showed a negative field potential distribution, the maximum of which was at the ventromedial funiculus as well as within the medial dorsolateral funiculus. Later waves of magnetic ESCP were suggested to reflect not only the dorsal corticospinal tracts but also the ventromedial spinal cord function.

Action Potentials↗
PubMed1994

Neural conduction velocity of the human auditory nerve: bipolar recordings from the exposed intracranial portion of the eighth nerve during vestibular nerve section.

We measured the conduction velocity of the intracranial portion of the auditory nerve in 3 patients undergoing vestibular nerve section to treat Ménière's disease. The conduction velocity varied from patient to patient, with an average value of 15.1 m/sec. The latency of peak III of the brain-stem auditory evoked potentials (BAEPs) increased by an average of 0.5 msec as a result of exposure of the eighth nerve, and if that increase is assumed to affect the entire length of the auditory nerve (2.6 cm) evenly, then the corrected estimate of conduction velocity would be 22.0 m/sec. Estimates of conduction velocity based on the interpeak latencies of peaks I and II of the BAEP, assuming that peak II is generated by the mid-portion of the intracranial segment of the auditory nerve, yielded similar values of conduction velocities (about 20 m/sec).

Electroencephalography↗
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↗