Year 6, Number 25, July 2004

Fuctional studies of the human auditory cortex, auditory memory and musical hallucinations.

Article N° AJ25-2

Marcos Goycoolea MD MS PhD*, Ismael Mena MD**, Sonia Neubauer MD**.
Departments of Otorhinolaringology* and Nuclear Medicine**. Clínica Las Condes. Santiago Chile.

Correspondence:

Marcos Goycoolea MD
Department of Otorhinolaringology, Clinica Las Condes. Santiago, Chile E-mail: mgoycool@mi.cl

Cita/Reference:
Goycoolea, Marcos; Mena, Ismael; Neubauer, Sonia. Fuctional studies of the human auditory cortex, auditory memory and musical hallucinations. Alasbimn Journal 6(25): July 2004. Article N° AJ25-2.

 

 

 

Abstract


Objectives. 1. To determine which areas of the cerebral cortex are activated stimulating the left ear with pure tones, and what type of stimulation occurs (eg. excitatory or inhibitory) in these different areas. 2. To use this information as an initial step to develop a normal functional data base for future studies. 3. To try to determine if there is a biological substrate to the process of recalling previous auditory perceptions and if possible, suggest a locus for auditory memory.

Method. Brain perfusion single photon emission computerized tomography (SPECT) evaluation was conducted: 1-2) Using auditory stimulation with pure tones in 4 volunteers with normal hearing. 3) In a patient with bilateral profound hearing loss who had auditory perception of previous musical experiences; while injected with Tc99m HMPAO while she was having the sensation of hearing a well known melody.

Results. Both in the patient with auditory hallucinations and the normal controls -stimulated with pure tones- there was a statistically significant increase in perfusion in Brodmann's area 39, more intense on the right side (right to left p < 0.05). With a lesser intensity there was activation in the adjacent area 40 and there was intense activation also in the executive frontal cortex areas 6, 8, 9, and 10 of Brodmann. There was also activation of area 7 of Brodmann; an audio-visual association area; more marked on the right side in the patient and the normal stimulated controls. In the subcortical structures there was also marked activation in the patient with hallucinations in both lentiform nuclei, thalamus and caudate nuclei also more intense in the right hemisphere, 5, 4.7 and 4.2 S.D. above the mean respectively and 5, 3.3, and 3 S.D. above the normal mean in the left hemisphere respectively. Similar findings were observed in normal controls.

Conclusions. After auditory stimulation with pure tones in the left ear of normal female volunteers, there is bilateral activation of area 39 of Brodmann, more intense in the contralateral (right) side. There is activation of both frontal executive areas without lateralization. Simultaneously, while area 39 of Brodmann was being activated, the temporal lobe was being inhibited. This seemingly not previously reported functional observation is suggestive that also inhibitory and not only excitatory relays play a role in the auditory pathways. The central activity in our patient (without external auditory stimuli) -who was tested while having musical hallucinations- was a mirror image of that of our normal stimulated volunteers. It is suggested that the trigger role of the inner ear -if any- could conceivably be inhibitory, desinhibitory and not necessarily purely excitatory. Based on our observations the trigger effect in our patient, could occur via the left ear. Finally, our functional studies are suggestive that auditory memory for musical perceptions could be seemingly located in the right area 39 of Brodmann.


Key words. Auditory cortex, Auditory memory, Musical hallucinations, Musical perception, HMPAO, Brain SPECT.

 

 

 

Introduction


It is well established that the mechanical energy of sound waves which is amplified by the external and middle ears is transformed into electrical stimuli by the hair cells in the inner ear. This energy is transmitted by the ganglion cells and reaches the temporal lobe -through a number of ipsi and contralateral relays of excitatory and inhibitory stimuli - where functional neuronal groups interpret such impulses (Huxley 1928, Saunders 1997, Hudspeth 2000). However, there is paucity of information regarding the functional distribution and processing of these acoustic stimuli in the brain (Griffiths 2004) and there is no normal functional data base available. The question also arises if we are capable of storing this information in the form of auditory memory and if there is a cortical representation where this coded information is stored.

Having the sensation of listening to previous auditory perceptions, particularly of well known songs, has been previously described in patients with sensorineural hearing loss (Goycoolea 1994, Griffiths 2000, Tanriverdi 2001). It has also been reported in patients with inner ear disease in whom these musical perceptions have been precipitated by the administration of stimulant drugs or by the withdrawal of a sedative agent (Paquier 1992, Gilbert 1993, Gordon 1994). To our knowledge, to date, there are no definite studies available that would identify the cortical area involved in the generation of these musical perceptions.

In this study, single photon emission computerized tomography (SPECT) evaluation was conducted: A. Using auditory stimulation with pure tones in 4 volunteers with normal hearing. B. In a patient with bilateral profound hearing loss who had auditory perception of previous musical experiences, injected with Tc99m HMPAO while she was having the sensation of hearing a well known melody.
The purpose of this study is three fold:

  1. To determine which areas of the cerebral cortex are activated stimulating the left ear with pure tones, and what type of stimulation occurs (e.g. excitatory or inhibitory) in these different areas.
  2. To use this information as an initial step to develop a normal functional data base for future studies.
  3. To try to determine if there is a biological substrate to the process of recalling previous auditory perceptions and if possible, suggest a locus for auditory memory.

 

 

 

Material and methods


This study was submitted to and approved by the Ethics Committee of Clínica Las Condes.

A. Four normal right handed healthy female volunteers with normal hearing

-ages 21 to 55 (Table 1) - were included in this study. All subjects had a personal interview, gave written consent and filled out a health questionnaire before the study. Exclusion criteria included pregnancy, breast feeding, history of head trauma, neurologic, psychiatric or metabolic disorders, and previous consumption of psychotropic drugs or other drugs with potential effect on the central nervous system.

Table 1.

Patient
Age
date of testing

VB

43
03/30/04

JP

22
04/06/04

KN

21
04/06/04

HG

55
05/12/04

Age distribution of healthy female volunteers for brain SPECT
Under auditory stimulation.

During the personal interview the health questionnaire was completed and the subjects were informed of the purposes of the study and the methodology that was going to be used. In addition, they were informed about risks and radiation exposure during the study.

Following this, their hearing was tested (pure tone audiogram and speech discrimination) in a sound proof room. In addition, Carhart tone decay (Carhart 1957) and loudness intolerance were tested at 2 KHz. Exclusion criteria included abnormal audiogram, positive tone decay and loudness intolerance. The purpose of this evaluation was to establish that the subjects could not only hear a pure tone at 2 KHz, but that they could hear it comfortably and without tone decay.

Ten minutes prior to testing, the volunteers were premedicated with 500 mg oral potassium perchlorate and their right antecubital vein was canulated. In a sound proof, dimmed light room a pure tone was delivered at 50 dB above threshold during two minutes in the left ear by means of A G16 Grason-Stadler audiometer with head phones. Simultaneously 25mCi (925 mBq) of Tc99m - hexametyl-propylenamine-oxime (HMPAO) (Ceretec; Nycomed Amersham plc, Amersham, England) were injected intravenously with bolus technique. The subjects were instructed to concentrate on listening to the sound delivered through the headphones and to sit as motionless as possible. At the end of the two-minute period the volunteers were asked to confirm that they had heard the tone during the whole duration of the test. Sixty to ninety minutes after the injection, the neuroSPECT images were gathered on a double head Siemens - ECAM, with LEHR collimators (Mena 2004).


NeuroSPECT Image Processing (Mena 2004).

The acquisition is tridimensionally reconstructed by back projection and a Butterworth filter 4.25 is used. Non-useful information was excluded by means of an elliptic mask. We performed oblique reorientation for transaxial, coronal and sagital planes with a volume zoom of 35%. The reconstructed tridimensional raw images are transferred in an Interfile format to a personal computer in order to reprocess, quantify and normalize their volume.

a) Normalization of HMPAO brain uptake.

The computer performs an analysis of voxel by voxel brain uptake of HMPAO. The results are normalized and expressed as percentage of maximal uptake observed in the brain for cortical and also for basal ganglia analysis. The results are normalized to the maximum in the brain and displayed by means of a color scale that defines as normal the values between a range of 72% ± 5 in gray color; values above the normal mean, in red, pink and white color for values 2, 3 and 4 standard deviations above the normal mean; values below 60% (larger than 2 standard deviations below normal mean) expressed in light blue, 55% of maximum in dark blue and below 50% in green representing 2, 3 and 4 standard deviations below the normal mean.

b) Volume Normalization

We use the technique of Talairach (Mena 2004) (NEUROGAM, SEGAMI Corp. Maryland USA) for volume normalization. We reorient the tridimensional volume of the brain using standard procedure for the Neurogam software. With this information, the Talairach technique renders the brain volume into a normalized volume and allows therefore, a voxel by voxel comparison of the HMPAO uptake in the brain cortex with normal data bases, corrected also volumetrically, of young normal individuals aged 18 to 45 years and also for adults > 45 years. In this tridimensional image, we define a new color scale that represents in red, pink and white color values 2, 3 and 4 standard deviations above the normal mean respectively. Values below 60% (larger than 2 standard deviations below normal mean) are expressed in color light blue, 55% of maximum in color dark blue and below 50% in color green, corresponding to 2, 3 and 4 standard deviations below the normal mean respectively. (Segami Corp., Maryland, USA).

In order to define with high reproducibility the exact localization of areas of hyperperfusion observed in our patient with hallucinations and their normal controls, we produced a template of 11 areas of Brodmann in each cortical hemisphere by means of the program CORELDRAW 8. We used the Brodmann areas as reference for clinical and experimental functional cerebral and pathological reported information. All these Brodmann areas are projected automatically by the computer on the left and right lateral and both para-sagittal images of the three dimensional images of the brain. The projection of this template is automatic and therefore the reproducibility of the results is 100%. Fig. 6.

Analysis of Basal Ganglia Uptake of Tc99m HMPAO.

The same acquisitions used to analyze cortical uptake distribution of HMPAO Tc99m were used for further evaluation of basal Ganglia uptake. For this purpose, images were corrected in first place for attenuation by Chang's first order method (Mena 2004) (attenuation coefficient µ=0.09cm-1). Uptake in the basal Ganglia was normalized to maximal uptake in the brain, images were displayed with the ± 2 Standard Deviations color scale and later on compared against the matched normal database, expressing the results in standard deviations above and below the normal mean.

Statistical analysis

A voxel by voxel comparative analysis with a normal age matched control group was performed and cortical perfusion values were expressed as Standard Deviation (SD) above or below the normal mean for this age group. ROIs were defined by cortical Brodmann Areas and our system determined the maximal perfusion level in each region of interest (ROI). We considered as abnormally increased perfusion only with maximal perfusion values above 2 SD of the normal mean perfusion. For each of 15 ROIs studied, we calculated the mean of the standard deviations of this sample. We considered that the absolute SD was a continuous variable, and therefore we applied an unpaired Student t test for the intracomparison of pairs of ipsilateral ROIs in each study group. Note: The interpreter was unaware of what volunteer or which ear was being evaluated.


B. Testing of a patient.

Clinical history.

70 year old right handed female who consulted in January 2004.
She had normal hearing (documented with audiograms in September 1999 - (Audiogram Figure 1) until October 1999 when she developed right sided profound sensorineural hearing loss (Audiogram Figure 2) associated with vestibular symptoms. Her vestibular symptoms gradually subsided but her hearing did not recover. In November 2003 she developed sudden left sided profound sensorineural hearing loss (Audiogram Figure 3) from which she did not recover. Her loss was such that hearing aids did not help her.

Audiogram Figures:

   

 Fig. 1. September 1999. Previous to her hearing loss.

   

 Fig. 2. October 1999 and March 2000 after her first hearing loss.

   

 Fig. 3. November 2003; after her second hearing loss.

She underwent at that time complete hematologic workup which was negative. Imagenologic evaluation included Chest X rays, CAT scan (brain and mastoids) that were normal. Magnetic resonance imaging (with gadolinium) revealed only a small lacunar lesion in the head of the left caudate nucleus.

The patient had been otherwise healthy. She had had a hysterectomy. She had no thyroid, hematologic, immunologic, allergic, metabolic, or psychiatric (personal or familial) history, and was taking no medications. She had no otologic history of infection, trauma, noise or ototoxic drug exposure.

Following her second episode of hearing loss she started to hear familiar songs and, occasionally, familiar voices.

After a complete standard cochlear implant preoperative evaluation, she underwent a successful right sided cochlear implantation (Nucleus 24 Contour device) on 12 March 2004.

Her pure tones are currently normal (Audiogram Figure 4) and she is in the rehabilitation process of cochlear implantation.

   

 Fig. 4. May 2004 after her cochlear implant.


The cochlear implant has not changed her listening to familiar music.

A SPECT examination was conducted with intravenous injection of Tc 99m HMPAO while she was having the sensation of listening a traditional and well-known local song entitled "Caballito Blanco."

The SPECT study was conducted in the same manner as in the 4 volunteers, but without external auditory stimulation.

 

 

 

Results


Auditory hallucinations

During perception of auditory hallucinations the patient presented a significant increase of function in area 39 of Brodmann in the right hemisphere, with a maximal function at 4.7 Standard Deviations (S.D.) above the normal mean uptake of HMPAO in the cerebral cortex. Fig. 5. However, in the left hemisphere there was a lesser increase at 2.8 S.D. above the normal mean. In area 40, that projects on the left hemisphere in the Wernicke area, the increased functional change was milder, namely 2 and 1.9 S.D. above normal for right and left hemispheres respectively. Fig. 6. Furthermore, in the frontal cortex there was a marked increase of function in the executive cortex, namely areas 6, 8, 9, and 10 of Brodmann. In the right hemisphere maximal values were 2.4, 2, 3.5, and 4.0 S.D. above the normal mean; while the respective values in the left hemisphere were 2, 2.3, 3.8, and 4.0. In the temporal lobes, however, there was a diminution of function with a mean uptake of HMPAO in areas 21, 22 and 38 of -1.4, -0.9, and -0.4 in the right hemisphere. Similar results were recorded for the left hemisphere. Please see Table 2

Table 2

-
Standard Dev. Above Normal Mean
Maximun perfusion
Controls
Hallucinations
Putamen - Left.roi
Putamen - Right.roi
Thalamus - Left.roi
Thalamus - Right.roi
Caudate Nucleus - Left.roi
Caudate Nucleus - Right.roi
4.03 ± 0.46
3.75 ± 1.01
2.90 ± 0.26
3.28 ± 0.56
2.10 ± 0.39
2.13 ±0.87
5
5
3,3
4,7
3
4,2
Area 6 - Left.roi
Area 6 - Right.roi
Area 7 - Left.roi
Area 7 - Right.roi
Area 8 - Left.roi
Area 8 - Right.roi
Area 9 - Left.roi
Area 9 - Right.roi
Area 10 - Left.roi
Area 10 - Right.roi
Area 39 - Left.roi
Area 39 - Right.roi
Area 40 - Left.roi
Area 40 - Right.roi
2.63 ± 1.70
3.28 ± 1.70
3.48 ± 1.41
3.83 ± 0.74
3.10 ± 1.86
3.88 ± 1.87
3.98 ± 1.86
3.73 ± 2.11
3.85 ± 1.81
3.95 ± 1.97
2.95 ± 0.60
3.95 ± 0.37
2.15 ± 0.97
3.38 ± 1.41
2
2,4
3
3,9
2,3
2
3,8
3,5
4
4,1
2,8
4,7
1,9
2
 
-
( ) Standard Dev. Below Normal Mean
Maximun perfusion
Controls
Hallucinations
Area 21 - Left.roi
Area 21 - Right.roi
Area 22 - Left.roi
Area 22 - Right.roi
Area 38 - Left.roi
Area 38 - Right.roi
(3.45) ± 1.11
(2.35) ± 0.37
(3.75) ± 1.08
(3.08) ± 1.31
(3.45) ± 0.53
(3.18) ± 1.28
-2,2
-2,7
-2,4
-2,5
-2,6
-1,9
0
0
0

 

Figure 5. NeuroSPECT HMPAO cortical function during Auditory Hallucinations.
3D images of the brain in 70 years old woman . Color gray depicts normal brain perfusion ( mean ± 2 SD. Colors red, pink and white denote areas increased at 2, 3 and 4 S:D. above the normal mean respectively. Colors light blue, dark blue and green denote diminution of perfusion at 2, 3 and 4 SD below the normal mean respectively. There is a strong activation of right posterior parietal, both frontal lobes, weak left posterior parietal and mild diminution of function in lateral temporal lobes, Increased visual cortex is a normal finding.


Figure 6. During Auditory Hallucinations there is increased function in Right area 39 and 40, also in area 10 and 9 in the frontal cortex and diminution of function in area 21 of the temporal lobe.

Normal controls

In the normal controls during auditory activation in the sound proof room a similar phenomenon was detected. In area 39 there was an increase in perfusion with a maximum of 3.9 S.D. above the normal mean in the right hemisphere and in the left area 39 there was an increase of only 2.9 S.D. (p < 0.05).Fig 7 and 8. Please see Table 3. In area 40 of Brodmann 3.3 and 2.1 in the right and left hemispheres respectively. In the frontal executive cortex there was an increase in the right areas 6, 8, 9, and 10 of 3.2, 3.8, 3.7 and 3.9 S.D. above the normal mean while the matching values in the left areas 6, 8, 9 and 10 were 2.6, 3.1, 3.9 and 3.8 respectively. The inhibition of function in temporal lobes was suggested by a Minimum Perfusion results in the right temporal lobe; areas 21, 22 and 38 of -2.3, -3.0 and -3.2 and in the left areas 21, 22 and 38 there were similar results. Please see Table 2.

Figure 7. Normal Control. Auditory Experimental Activation.
There is marked increased function in Right temporal-parietal area, both frontal lobes, and diminution of function in lateral temporal lobes and cyngulate gyri.


Figure 8.  Same control. Areas of  .

We can conclude that in both the patient with auditory hallucinations and the normal controls activated with pure tones, there was a marked hyperperfusion in the right area 39 of Brodmann (Figure 6 and 8) statistically significant (p < 0.05) as compared with the left area 39 (Table 3). With a lesser intensity there was activation in the adjacent area 40 and there was intense activation also in the executive frontal cortex; areas 6, 8, 9 and 10 of Brodmann. There was also activation of area 7 of Brodmann. This is an audio-visual association area more intense in the right area 7 and the left area 7 in the patient with hallucinations and the normal controls of 3.9 and 3 S.D. above the normal mean and of 3.8 and 3.5 in the normal controls respectively. (Table 2).

Table 3.

CONTROLS
Statistical significance Maximum

-
LEFT.ROI
RIGHT.ROI
Area 39
3,5
4,1
-
3,6
4,1
-
2,5
4,2
-
2,2
3,4
p Value
0,045709839
-
-
-
LEFT.ROI
RIGHT.ROI
Area 40
2,9
4,3
-
2,8
2,9
-
2,1
4,7
-
0,8
1,6
p Value
0,202468709
-

In the sub cortical structures there was also marked activation in the patient with hallucinations in both lentiform nucleus, thalamus and caudate nucleus also more intense in the right hemisphere 5, 4.7 and 4.2 S.D. above the normal mean respectively and 5, 3.3 and 3 S.D. above the normal mean in the left hemisphere respectively. Similar findings were observed in the normal controls. Please see Table 2.

 

 

 

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.

 

 

 

References


Carhart R. Clinical determination of abnormal auditory adaptation. Archives of Otolaryngology 65:32-40, 1957.

Corkin S. Amaral DG. González RG.Johnson KA. Hyman TB. H.M.'s medial temporal lobe lesion: findings from magnetic resonante imaging. The Journal of Neuroscience 17(10): 3964-3979, 1997.

Gardner EP. Martin JH. Codificación de la información sensorial. In: Principios de Neurociencia. (Kandel ER. Schwarz JH. Jessel TH. Eds.) Mc Graw-Hill-Interamericana, Madrid 2000. pp.411-429.

Gilbert GJ. Pentoxifylline-induced musical hallucinations. Neurology 43:1621-1622, 1993.

Gilbert GJ. Musical hallucinations. Reply from the autor. Neurology 44:986, 1994.

Gordon AG. Musical hallucinations (correspondence). Neurology 44:986, 1994.

Goycoolea MV. Cárdenas JL. Pérez M. Martínez G. Poblete R. Does an auditory memory exist? Clinical case suggestive that it does. Presented at the Collegium Otorhinolaringologicum AS. Meeting. Cascais, Portugal 4 September 1994 (Proceedings).

Griffiths TD. Musical hallucinosis in acquired deafness. Phenomenology and brain substrate. Brain 123:2065-2076, 2000.

Griffiths TD. Warren JD. Scott SK. Nelken I. King AJ. Cortical processing of complex sound: a way forward? Trends in Neuroscience 27:181-185, 2004.

Hudspeth AJ. Audición. In: Principios de Neurociencia (Kandel ER. Schwartz JH. Jessel TH. Eds) Mc Graw-Hill-Interamericana. Madrid 2000. pp.590-613.

Huxley A. Point Counterpoint. Literary Guild of America. 32-35, 1928.

Mena I, Villanueva-Meyer J
Cerebral blood flow and cortical activation response in normal subjects and Alzheimer type dementia. Bulletin of Clinical Neurosciences 55:89-90, 1990

Mena, I. Correa R., Nader A., Boehme V.. Bipolar affective disorders: Assessment of functional brain changes by means of Tc99m HMPAO NeuroSPECT. Alasbimn Journal 6(23): January 2004
http://www2.alasbimnjournal.cl/alasbimn/CDA/sec_b/0,1206,SCID%253D6213,00.html

Milner B, Squire LR, Kandel E. Cognitive neuroscience and the study of memory. Neuron 20:445-468, 1998.

Paquier P. Transient musical hallucinations of central origin; a review and clinical study. J Neurol Neurosurg Psychiatry 55:1069-1073, 1992.

Penfield W, Perot P. The brain's record of auditory and visual experience. Brain 86:595-694, 1963.

Saunders J. Erulkar S. Neurophysiology of the auditory system. In Bases of Hearing Science. Durrant JD. Lovrinic JH. Eds. Williams and Wilkins Co. Baltimore 1977. pp.110-137.

Tillman TW. Special hearing tests in otoneurologic diagnosis. Archives of Otolaryngology 89:51-56, 1969.

Tanrivedi N. Akif Sayilgan M. Ozcurumez G. Musical hallucinations associated with abruptly developed bilateral loss of hearing. Acta Psychiatr Scand 103:153-155, 2001.

 

 

 

Acknowledgements


Our special thanks to our Audiologists Raquel Levy, Josefina Ernst and Viviana Orellana; especially to Raquel Levy who coordinated with enthusiasm and professionalism. We also want to thank Luz Navarrete, librarian of Clínica Las Condes for her efforts and success in doing extensive literature searches and obtaining reference articles.

 

 

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