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Discussion
Functional (hemodynamic) auditory responses of the cortex can be clinically evaluated using SPECT and silent functional magnetic resonance imaging (Yetkin 2004). We elected SPECT with Tc99m-HMPAO as tracer because: 1. HMPAO is a lipophilic tracer which in its optical configuration d-l diffuses through the blood brain barrier with ease and has a very high extraction rate. Once inside the brain tissue, after 2 minutes, it changes to the optical form meso which is hydrophilic and becomes trapped in it. The same thing happens to the circulating HMPAO, therefore, once trapped it does not traverse towards the brain (Mena 1990). This allowed us to deliver pure tones in optimal conditions in a sound proof room. Thus, the SPECT images obtained with HMPAO correspond to the brain perfusion at the time of administration (plus 2 minutes) even if the tomographic study is done hours later. In our study, SPECT was done within one hour of injection.
2. We intend to use our database for our systematic studies in cochlear implant patients. Our interest includes areas such as information regarding which ear to implant, the potential need for additional auditory stimulation in the contralateral ear, and long term follow up and evaluation of neural plasticity. Cochlear implants have a magnet that precludes MRI studies in implanted patients. They would need a surgical procedure in order to remove the magnet and then another one to replace it after the study is completed. Magnet removal is not necessary in SPECT studies.
3. Furthermore, the results of HMPAO Neurospect are expressed statistically after comparison to an age matched normal database. This is not available with fMRI. In addition, fMRI only shows changes related to stimuli in a given patient, ignoring the expected normal response.
Receptors have perceptive adaptation, that is to say, after constant continuous stimulation; the intensity of activation decreases and the sensation is lost (Gardner 2000). This occurs in different degrees in normal individuals and in patients with retrocochlear disease (Tillman 1969).
Our normal volunteers were tested for tone decay. After delivery of pure tones, they were asked if they were still hearing the tone at the end of the two minutes. Our purpose was to decrease the perceptive adaptation factor. Finally, we made sure that the tones delivered were comfortable to the listener, in order to avoid any "gating" effect of the efferent system over the receptor (Pedemonte and Velluti 1984), and the lights were dimmed so that additional stimuli could be avoided.
Evidences of cortical storage of such information comes in part from patients with bilateral lesions of association areas of the temporal lobe who have no long term memory (Milner 1998), suggesting that long term memory requires a functional temporal lobe (Corkin 1997).
Evidences also come from electrical stimulation of different parts of the brain in patients subjected to epilepsy surgery with local anesthesia. In this manner, Penfield (1963) obtained the recall of previous auditory perceptions in many patients by stimulating in the neighborhood of the auditory cortex.
A third type of evidence comes from patients that experience the sensation of previous auditory perceptions, particularly musical experiences. In 1994 we reported the case of a 56 year old woman who had a history of right sided sudden sensorineural hearing loss, who, after having a sudden loss in the second (left) ear -12 years later- started having auditory perceptions of previously known songs (Goycoolea 1994). Perception of previous musical experiences in patients with hearing loss have also been reported by Griffiths (2000) -6 cases- and Tanriverdi (2001) -1 case-.
In addition, Gordon (1994) quoted 14 and Gilbert (1993) 3 cases of patients with ear disease (hearing loss) that had musical auditory perceptions; in the great majority of cases precipitated either by the administration of stimulants or suppression of sedative medications. In all these cases there is one constant, and that is that there is an inner ear involvement in musical perceptions, therefore, that inner ear dysfunction seems to be a pre requisite for them to occur. There has been some argument as to this occurring via a peripheral or central mechanism (Gordon and Gilbert 1994). Our impression is that although it is central in origin, it is essential to have a trigger that is represented by the inner ear. However, this trigger could also conceivably involve inhibitory or desinhibitory and not necessarily only excitatory stimuli. This does not mean that in other musical auditory perception syndromes different triggers (other than the inner ear) could operate.
It is also of interest to mention that both our current and previously reported patient (Goycoolea 1994) had sudden right sided sensorineural hearing loss after which they had no musical auditory perceptions, and these occurred once sudden sensorineural hearing loss occurred in the second ear (left).
Our results suggest that after auditory stimulation with pure tones in the left ear of normal female volunteers, there is bilateral activation of area 39 of Brodmann, with more activation in the contralateral (right) side. In addition, there is activation of both frontal executive areas without lateralization. It is also of interest to note that simultaneously, while area 39 of Brodmann is being activated by the auditory stimuli, the temporal lobe is being deactivated. This observation - seemingly not previously reported with functional auditory cortex response studies- is suggestive that also inhibitory and not only excitatory relays play a role in the auditory pathways. The functional significance of this phenomenon has still to be defined and a larger data base of normal controls (unpublished data) is needed. In brief, our observations after auditory stimulation in normal volunteers are supportive of the concept that sound energy transmitted by the ganglion cells reaches the temporal lobe -through a number of ipsi and contralateral relays of excitatory and inhibitory stimuli- where functional neuronal groups interpret such impulses (Saunders 1997, Hudspeth 2000). Moreover, they also suggest degrees of ipsi and contralaterality and location for the functional neuronal groups in charge of interpretation.
Our patient was tested while having musical hallucinations, that is to say while having spontaneous central auditory cortex activity. It is of utmost interest to observe that when spontaneous (without external auditory stimuli) auditory central activity -in the form of musical hallucinations- occurs in area 39 of Brodmann; the activation process is a mirror image of that of stimulated (left ear stimulation) normal volunteers. The trigger role of the inner ear receptor -if any- in providing inhibitory, desinhibitory and/or excitatory stimuli for musical hallucinations to occur remains to be evaluated. Moreover, based on our observations in our normal volunteers, it is likely that if the inner ear plays a role it would do so -in this clinical case- via the left ear.
Finally, our functional studies are suggestive that storage of previous musical perceptions (auditory memory) could be seemingly located in the right area 39 of Brodmann.
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