Biomedical subjects

Aage Møller

Publications and source records attributed to Aage Møller.

3 recordsLinked to original sources

PubMed2005

Pulsatile tinnitus and the intrameatal vascular loop: why do we not hear our carotids?

OBJECTIVE: Pulsatile tinnitus is characterized by hearing the heart beat or respiration in one or both ears. In 15% of patients with pulsatile tinnitus, no cause can be found. Other investigators have suggested that a vascular loop entering the internal auditory meatus can be another cause of arterial, pulse synchronous tinnitus. If so, we should constantly hear the arterial pulsations of the carotid arteries passing through the petrous bone. METHODS: Using magnetic resonance imaging, 17 patients with unilateral pulsatile tinnitus and 46 with non-pulsatile tinnitus were analyzed for the presence of a vascular loop entering into the internal acoustic meatus. Four temporal bones were sectioned to find structural differences between the internal acoustic meatus and the pericarotid area. Four patients with intrameatal vascular loops and ipsilateral pulsatile tinnitus underwent surgery by Teflon interpositioning between the loop and the cochlea. RESULTS: In unilateral pulsatile tinnitus, a statistically highly significant amount of intrameatal vascular loops was noted in comparison to non-pulsatile tinnitus. A well-developed pericarotid venous plexus was found histologically. Three of the four patients who underwent surgery were initially tinnitus free, but pulsations recurred after 3 months in one patient. CONCLUSION: Vascular loops in the internal auditory canal may generate pulsatile tinnitus. It may be treated by placing Teflon between the cochlea and the intrameatal vascular loop. One then does not hear the pulsation of the carotids due to a dampening effect of a pericarotid venous plexus.

Adolescent↗

PubMed2004

Magnetic and electrical stimulation of the auditory cortex for intractable tinnitus. Case report.

Tinnitus is a distressing symptom that affects up to 15% of the population for whom no satisfactory treatment exists. The authors present a novel surgical approach for the treatment of intractable tinnitus, based on cortical stimulation of the auditory cortex. Tinnitus can be considered an auditory phantom phenomenon similar to deafferentation pain, which is observed in the somatosensory system. Tinnitus is accompanied by a change in the tonotopic map of the auditory cortex. Furthermore, there is a highly positive association between the subjective intensity of the tinnitus and the amount of shift in tinnitus frequency in the auditory cortex, that is, the amount of cortical reorganization. This cortical reorganization can be demonstrated by functional magnetic resonance (fMR) imaging. Transcranial magnetic stimulation (TMS) is a noninvasive method of activating or deactivating focal areas of the human brain. Linked to a navigation system that is guided by fMR images of the auditory system, TMS can suppress areas of cortical plasticity. If it is successful in suppressing a patient's tinnitus, this focal and temporary effect can be perpetualized by implanting a cortical electrode. A neuronavigation-based auditory fMR imaging-guided TMS session was performed in a patient who suffered from tinnitus due to a cochlear nerve lesion. Complete suppression of the tinnitus was obtained. At a later time an extradural electrode was implanted with the guidance of auditory fMR imaging navigation. Postoperatively, the patient's tinnitus disappeared and remains absent 10 months later. Focal extradural electrical stimulation of the primary auditory cortex at the area of cortical plasticity is capable of suppressing contralateral tinnitus completely. Transcranial magnetic stimulation may be an ideal method for noninvasive studies of surgical candidates in whom stimulating electrodes might be implanted for tinnitus suppression.

Adult↗

PubMed2002

Is the root entry/exit zone important in microvascular compression syndromes?

OBJECTIVE: Microvascular compression syndromes such as trigeminal neuralgia, hemifacial spasm, and disabling positional vertigo involve an artery or vein compressing a cranial nerve. A cranial nerve is composed of a central nervous system (CNS) segment and a peripheral nervous system (PNS) segment separated by the root entry/exit zone (REZ). Although vascular compression can occur at any point along the cranial nerve, it has been generally assumed that only vascular contact at the REZ of the affected cranial nerve can cause symptoms. On the basis of personal surgical experience, we propose that vascular compression of the CNS segment alone causes symptoms. This has important repercussions for the future diagnosis and treatment of microvascular compression syndromes, especially the cochleovestibular compression syndrome. METHODS: For the anatomic study, four autopsy specimens and one surgical biopsy specimen of the vestibulocochlear nerve were microscopically and ultramicroscopically analyzed for structural differences between the CNS and PNS segments. For the clinical study, five patients with the clinical picture of cochleovestibular compression syndrome were treated by microsurgical decompression at the level of the CNS segment and not the REZ. One patient underwent reoperation for recurrent symptoms 4 years later, and a 4-mm vestibular neurectomy was performed at that stage. We performed an epidemiological analysis to demonstrate that the known incidences of trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia are related to the length of their respective CNS segments. RESULTS: Histological differences between the PNS and CNS segments suggest that the PNS segment is more resistant to compression. This was confirmed by neurophysiological data from intraoperative monitoring in posterior fossa surgery and experimental studies. We found a clear epidemiological correlation between the length of the CNS segment, which differed among cranial nerves, and the incidence of the microvascular compression syndrome. Successful decompression of the CNS segment in patients without compression at the REZ of the vestibulocochlear nerve for disabling positional vertigo provides clinical support for this hypothesis. CONCLUSION: The evidence we present supports the hypothesis that vascular compression syndromes arise from vascular contact along the CNS segment of the cranial nerves.

Blood Vessels↗