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Biomedical subjects

A R Møller

Publications and source records attributed to A R Møller.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1995

Intra-operative neurophysiologic monitoring in neurosurgery: benefits, efficacy, and cost-effectiveness.

Intra-operative neurophysiologic monitoring is now a well established adjunct to many different kinds of operations in which neural tissue is being manipulated. Its main benefit is to reduce the incidence of permanent postoperative neurologic deficits, but there are also other advantages in using intra-operative monitoring, e.g., it helps to identify neural tissue that is not directly visible; in some cases it can identify the anatomic location of a pathology; and in a few operations it ensures that the therapeutic goal of the operation has been achieved before the operation is completed. The value of the techniques involved in intra-operative neurophysiologic monitoring differs from operation to operation, and surgeons with different degrees of experience in a particular operation may benefit by different degrees from the use of intra-operative monitoring.

Cost-Benefit Analysis↗
PubMed1994

Facial nerve demyelination and vascular compression are both needed to induce facial hyperactivity: a study in rats.

It is generally assumed that hemifacial spasm (HFS) is caused by vascular compression of the facial nerve at the root exit zone (REZ), but the mechanism for the development of HFS is not known. Evidence has been previously presented that the signs of HFS are caused by hyperactivity of the facial motonucleus that is caused by the irritation to the facial nerve from the vascular contact. This assumption has been supported by the finding that daily electrical stimulation of the facial nerve in the rat facilitates the development of an abnormal muscle response that is a characteristic sign of HFS in man and is an indication of an abnormal cross-transmission that makes it possible to elicit a contraction of muscles innervated by one branch of the facial nerve by electrically stimulating another branch of the facial nerve. In the present study we show that close contact between a peripheral branch of the facial nerve and an artery also facilitates the development of an abnormal muscle response, but only if the facial nerve has previously been slightly injured (by a chromic suture) at the location of the arterial contact. We also show that blocking neural conduction in the facial nerve proximal to the artificial vascular compression abolishes the abnormal muscle contraction, which supports the assumption that the anatomical location of cross-transmission that is causing the abnormal muscle response is central to the vascular compression, most likely in the facial motonucleus. These findings may explain why the facial nerve is only susceptible to vascular compression near its REZ, where an injury to its myelin is more likely to occur than where the nerve is covered with schwann cell myelin.

Animals↗
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↗
PubMed1994

Chronic vascular irritation of the facial nerve causes facial spasm in rats.

The abnormal muscle response, elicited by electrical stimulation of one branch of the facial nerve and recorded from muscles innervated by another branch, has been used previously as an objective sign of hemifacial spasm in the development of animal models of this disorder. In the present study we recorded spontaneous electromyographic activity from the orbicularis oculi muscle from both sides in rats in which a demyelination of the peripheral portion of the facial nerve and vascular contact had been made previously. The root mean square value of the electromyographic activity on the affected side was significantly larger than that on the unaffected side in all rats in which the vascular irritation had caused the abnormal muscle response to appear. The results support our earlier finding that vascular contact together with demyelination of the peripheral facial nerve can cause the development of signs of hemifacial spasm, including involuntary muscle contractions.

Animals↗
PubMed1994

Recordings from the facial motonucleus in rats with signs of hemifacial spasm.

We recorded evoked potentials from the facial motonucleus of rats in response to electrical stimulation of the temporal branch of the facial nerve in which chronic irritation from a blood vessel had caused the development of an abnormal muscle response. The abnormal muscle response that can be recorded from face muscles that are innervated by one branch of the facial nerve in response to electrical stimulation of a different branch is regarded to be a sign of hemifacial spasm. In the recordings from the motonucleus in rats that showed such an abnormal muscle response (model rats) there was a late component at a latency of about 5 msec, in addition to the early component with a latency of 1.5-2.5 msec that is also observed in normal rats. The latency of the electromyographic potentials recorded from the mentalis-orbicularis oris muscles in response to stimulation of the facial motonucleus was about 2 msec. The latency of the abnormal muscle response obtained from the mentalis muscle in the model rats was about 7 msec. This value is close to the sum of the conduction time from the motonucleus to the mentalis muscle (2 msec) and the latency of the late response from the motonucleus (5 msec). Similar results were obtained in rats in which the facial nerve had been chronically stimulated electrically and which had developed an abnormal muscle response. The results of this study further support the hypothesis that the hyperactivity of the facial motonucleus is the pathophysiology of hemifacial spasm.

Animals↗
PubMed1994

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.

Animals↗
PubMed1994

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.

Acoustic Stimulation↗
PubMed1993

Vascular decompression surgery for severe tinnitus: selection criteria and results.

Seventy-four patients were operated on within a period of 10 years to treat incapacitating tinnitus; 72 underwent microvascular decompression (MVD) of the intracranial portion of the auditory nerve, and 2 underwent section of the eighth nerve close to the brain stem. Of those who underwent MVD, 2 had no change in symptoms and later also underwent section of the eighth nerve near the brain stem. Two patients did not return for follow-up. Of the 72 remaining patients, 13 (18.1%) experienced total relief from tinnitus, 16 (22.2%) showed marked improvement, 8 (11.1%) showed slight improvement, 33 (45.8%) had no improvement, and 2 (2.8%) became worse. The patients who experienced total relief and those who showed marked improvement had experienced their tinnitus for an average of 2.9 years and 2.7 years, respectively; those who showed slight improvement and those who had no improvement had experienced their tinnitus for a longer time before the operation (mean, 5.2 and 7.9 years, respectively). Of the 72 patients who were operated on and followed, 32 were women. Of these, 54.8% experienced total relief from tinnitus or marked improvement, while only 29.3% of the men showed such relief or improvement. Selection of the patients for operation was mainly based on patient history and, to some extent, on auditory test results (brainstem auditory evoked potentials [BAEP], acoustic middle ear reflexes, and audiometric data).

Adolescent↗
PubMed1993

Abnormal response from the sternocleidomastoid muscle in patients with spasmodic torticollis: observations during microvascular decompression operations.

Electromyographic (EMG) recordings from patients undergoing microvascular decompression (MVD) operations to relieve spasmodic torticollis were studied. When EMG potentials were recorded from the sternocleidomastoid muscle in response to electrical stimulation of the spinal accessory nerve (SAN) at the neck, an abnormal (delayed) response was seen in 9 of 12 patients who had unilateral symptoms. In 5 patients with bilateral symptoms, no such delayed response was seen. We assume that this abnormal muscle response depends on an abnormal cross-transmission. Neural conduction time measurements, using electrical stimulation of the intracranial portion of the SAN, indicated that the location of this cross-transmission was more central than the vascular compression of the SAN. We hypothesize that this location might be in the motonucleus of the SAN. Similarities between these abnormal EMG findings in patients with spasmodic torticollis and those reported earlier in patients with hemifacial spasm (HFS) are presented.

Accessory Nerve↗
PubMed1993

Microvascular decompression of the eighth nerve in patients with disabling positional vertigo: selection criteria and operative results in 207 patients.

Two-hundred seven patients who were operated on consecutively between January 1983 and December 1990 to relieve disabling positional vertigo (DPV) using the microvascular decompression (MVD) procedure were studied. Selection of the patients for MVD operations was based on both case history and the results of otoneurological tests. Of the 177 patients with unilateral symptoms, 8 were excluded because of previous vestibular nerve section, and 6 did not return for follow-up; of the remaining 163 patients, 129 (79%) were free of symptoms or markedly improved following MVD, and none became worse. Thirty patients had symptoms and signs of bilateral DPV, and of these 1 was excluded because of previous vestibular nerve section and 3 because of multiple operations. Of the remaining 26 patients, 20 (77%) were free of symptoms or markedly improved following MVD. Eleven of these patients had more than 2 operations. The follow-up time was an average of 38 months, ranging from 3 months to 10 years. The cure rate (about 80%) of MVD for DPV is similar to that reported for MVD for trigeminal neuralgia and hemifacial spasm. The cure rate of MVD for DPV was not related to gender or to the duration of the symptoms. Following a total of 254 operations that these 207 patients underwent, 4 patients (1.6%) lost hearing and 4 (1.6%) suffered marked hearing loss. Three patients suffered temporary deficits of other cranial nerves. There were no other complications to these operations.

Adult↗
PubMed1993

Chronic electrical stimulation of the facial nerve causes signs of facial nucleus hyperactivity.

The proximal segment of the facial nerve in rats was stimulated electrically daily for a duration of 2-10 min. After 4-8 weeks of such stimulation, 12 of 18 rats developed abnormal muscle responses that could be demonstrated by recording the electromyographic response from lower face muscles (the mentalis muscle) while the temporal branch of the facial nerve was being stimulated electrically. This abnormal electromyographic response consists of activity that appears in the latency range 6.5-15 ms. In addition, these chronically stimulated rats developed signs of facial synkinesis on the side that had been chronically stimulated. This could be demonstrated by recording electromyographic activity when the blink reflex was being elicited by electrical stimulation of the ophthalmic nerve. Rats in which electrodes had been implanted but which had not been stimulated did not develop any abnormal electromyographic activity. The abnormal electromyographic activity that could be recorded in rats that had been stimulated chronically could not be recorded 4-8 weeks after the stimulation had been terminated. We interpret these results to indicate that chronic electrical stimulation of the facial nerve can render the facial motonucleus hyperactive, and that the signs of this hyperactivity (abnormal muscle response and synkinesis) are similar to those typically seen in patients with hemifacial spasm. We thus presume that these results support the hypothesis that it is the irritation of the facial nerve from a compressing blood vessel that causes the facial nucleus to become hyperactive in patients with hemifacial spasm.

Animals↗