Phenomenology and brain substrate
- T. D. Griffiths
-
Department of Neurology, Newcastle University,Newcastle-upon-Tyne and Wellcome Department of Cognitive Neurology, Institute
of Neurology, London, UK
- Dr T. D. Griffiths, Department of Physiological Sciences, Newcastle University Medical School, Newcastle-upon-Tyne NE2 4HH,
UK E-mail: t.d.griffiths@ncl.ac.uk
Summary
Six subjects with musical hallucinations following acquired deafness are described.
The subjects all experienced the condition
in the absence of any other features to suggest epilepsy or psychosis.
I propose a neuropsychological model for the condition
consistent with detailed observation of the subjects' phenomenology.
The model is based on spontaneous activity within a cognitive
module for the analysis of temporal pattern in segmented sound.
Functional imaging was carried out to test the hypothesis
that musical hallucinosis is due to activity within such a module, for which the neural substrate is a distributed network
distinct from the primary auditory cortex.
PET was carried out on the six subjects to identify
areas where brain activity
increased as a function of the severity of the
hallucination.
In a group analysis, no effect was demonstrated in the
primary
auditory cortices.
Clusters of correlated activity were demonstrated in the posterior temporal lobes, the right basal ganglia,
the cerebellum and the inferior frontal cortices.
This network is similar to that previously demonstrated during the normal
perception and imagery of patterned–segmented sound, and is consistent with the proposed neuropsychological and neural mechanism.
Introduction
Musical hallucinosis is a disorder
of complex sound processing. Subjects perceive complex sound in the form
of music in the
absence of an acoustic stimulus. As such, the
phenomenon might be regarded as an example of mental imagery, defined as
`mental
acts in which we seem to re-enact the experience of perceiving an object when the object is no longer available' (Halpern and Zatorre, 1999).
Mental imagery is, however, usually less vivid than actual perception, and is never attributed to an external process.
Musical hallucinosis may be associated with structural brain lesions, epilepsy or psychosis (for reviews, see Berrios, 1990;
Keshavan et al., 1992).
However, it is most commonly seen in subjects with moderate or severe acquired deafness, and as such it may represent
an auditory form of the Charles Bonnet syndrome.
This term is more commonly used to describe formed visual percepts in the
absence of visual stimulation in subjects with peripheral visual loss (ffytche et al., 1998).
This study addresses the basis for musical hallucinosis in six subjects with acquired deafness.
Musical hallucinosis is a disorder of the processing of the high-level pattern in sound.
Music comprises discrete sounds that
are characterized by fundamental properties such as pitch and onset time.
These sounds are built into a
high-level pattern
at the temporal level of hundreds of milliseconds.
Musical hallucinosis requires a mental representation of such a
high-level
pattern.
The mental representation might be based
on the same neural mechanism as that active during normal musical
perception,
although distinct mechanisms for musical perception
and imagery are also possible.
I use the term `high-level' to refer to
structure over and above that in the individual units; in this sense the term might equally be used to refer to tonal or atonal
Western music or African or Eastern music.
Previous studies suggest that the
processing of discrete sounds depends on a neural substrate different
from that used for
the processing of high-level patterns formed by
these sounds.
Several studies suggest that the processing of pitch is
related
to the function of the human primary auditory cortex in Heschl's gyrus (Zatorre, 1988; Pantev et al., 1989; Griffiths et al., 1998), whilst the onset time of auditory transients is accurately represented in the primary auditory cortex of animals (Phillips and Hall, 1990).
Stimulation of the primary auditory cortex at operation is associated with the perception of simple noises or tones (Penfield and Perot, 1963).
In contrast, the processing of musical patterns formed by individual sounds is related to a network of cortical areas distinct
from the primary auditory
cortex.
Melody is a pattern of sound pitches, whilst rhythm is a
pattern of the onset times and
durations of sounds.
Studies of melody perception
demonstrate a predominantly right-sided network that includes the planum
temporale and frontal cortex (Zatorre et al., 1994), whilst the involvement of the cerebellum and basal ganglia has been emphasized in studies of rhythmic processing (Penhune et al., 1998).
Stimulation of the superior temporal gyrus outside Heschl's gyrus at operation can be associated with the perception of
music (Penfield and Perot, 1963).
A study using atonal sequences without conventional rhythm (Griffiths et al., 1999a) suggests the possibility of a general role for superior temporal networks in the analysis of patterns in segmented sound,
rather than a specific role in the analysis of music.
This study is a test of the hypothesis that musical hallucinosis in subjects with acquired deafness is related to activity
within
the neural network for the perception of high-level pattern in sound.
The hypothesis makes predictions about the phenomenology
of, and the brain substrate for, musical
hallucinosis.
In terms of phenomenology, the hypothesis predicts that
subjects with
musical hallucinosis due to acquired
deafness will experience normal high-level sound patterns because of
activation of the
normal central perceptual mechanism.
In terms of
brain substrate, the hypothesis predicts that musical hallucinosis will
be
associated with activity in distributed networks, distinct from the primary auditory cortex, including the posterior superior
temporal cortex, frontal cortex and cerebellum.
I was particularly interested to examine
whether the planum temporale is active
during musical hallucinosis.
Several studies
suggest a general role for this area in the perception of
patterned–segmented
sound (Binder et al., 1996; Mummery et al., 1999).
Patients and methods
The subjects, all of whom were initially referred to neurologists with the exception
of Subject 5, who was initially referred for a psychiatric opinion.
All subjects gave informed consent to take part in this
study, which was conducted with the approval of the ethical committee of the National Hospital for Neurology and Neurosurgery
(London).
ENT symptoms/audiometry
All subjects had moderate or severe bilateral deafness, as assessed by pure-tone audiometry (Fig. 1).
All subjects suffered
progressive hearing loss.
No subject had a family history of deafness.
In Subject 2 the symptomatic onset occurred when the
subject was working as a tank crew member, whilst in Subject 5 there were two episodes of acute lateralized hearing loss following
head injuries.
The duration of symptomatic hearing loss varied between 5 and 40 years.
Subjects 4 and 5 experienced accompanying
tinnitus whilst Subjects 2 and 4 had experienced rotatory vertigo (related to head movement in Subject 2, and in only the early history
in Subject 4).
No subject experienced a syndrome to suggest Menière's disease (fluctuating deafness, fluctuating tinnitus, fluctuating vertigo or aural fullness).
Fig. 1
Pure-tone audiograms.
Case histories
The subjects perceived music in the absence of any musical stimulus.
Several of the subjects had initially thought that actual
music was playing, but all subjects subsequently attributed the experience to a problem with the
brain or the ears (the nature
of the percept did not change).
Apart from low mood
accompanying the experiences, which all of the subjects found
distressing,
no subject described any accompanying delusion.
There was no description of experiential features (Gloor, 1990) or generalized convulsions in any subject.
The abnormal auditory experiences were restricted to the musical domain in all
of the subjects except Subject 6, who also experienced auditory
hallucinations in the form of speech and environmental sounds.
All of the subjects described an experience of
continuous or near-continuous musical hallucinations and described
variation
in the severity of their symptoms over the course of the day (which was an inclusion criterion for the study).
There was no
historical suggestion in any of the subjects of any accompanying difficulty with the perception of music, speech or environmental
sound over and above that due to the deafness;
I did not feel that any of the subjects had an apperceptive auditory agnosia
(Griffiths et al., 1999b).
One of the subjects (Subject 1) had noticed a small decrease in symptoms with the consistent use of a hearing aid.
None
of the other subjects, all of whom had used
amplification devices, felt that these had any effect on the severity of
the experience.
Subject 1
This subject, with 5 years of symptomatic hearing loss, has been reported previously as a single case (Griffiths et al., 1997).
He had a history of <1 year of continuous musical hallucinations in the form of multiple singers singing familiar melodies
with indistinguishable lyrics.
The onset was abrupt and not related to any other symptoms. The songs included hymns and rugby
songs, and recent popular music.
Subject 2
This subject, with approximately 40 years of symptomatic hearing loss, had a history of 3 years of continuous musical hallucinations.
The onset was abrupt and was not accompanied by other neurological symptoms.
The songs included light operatic pieces, and
popular songs by artists including Shirley Bassey and Boyzone.
Subject 3
This subject, with 40 years of symptomatic hearing loss, had a history of 9 years of almost continuous musical hallucinations.
The onset was abrupt and not accompanied by other symptoms.
The experience would usually take the form of organ or piano music,
which might be accompanied by singers.
If
accompanied by singers, the lyrics would be distinguishable.
The songs
included
hymns, nursery rhymes and old popular songs.
Subject 4
This subject, with 23 years of symptomatic hearing loss, had a history
of more than 10 years of almost continuous musical
hallucinosis.
The onset of the hallucinations was
not abrupt.
The experience was different from that of the other subjects
in that she did not hear instruments or singers but
experienced musical hallucinations in which the individual notes had
the
quality of a buzzy pitch.
In psychoacoustic terms
her experience would be equivalent to hearing notes with pitch, where the
individual pitches were associated with band-pass noise with different passbands.
Her experience had evolved from almost continuous
tinnitus with similar characteristics to the buzzy pitches experienced as music.
She currently chooses not to listen to actual music
because it is so distorted at the level she needs to listen.
Subject 5
This subject, with more than 40 years of progressive deafness, had a history of 2 years of continual musical hallucinations
in the form of three or four male singers singing familiar songs with accompanying musical instruments.
The onset followed
shortly after a head injury, and was accompanied by hearing a
localized noise behind his head and experiencing a hot feeling
that rose up the back of his head on two occasions
only.
There were no accompanying experiential features or depression of
his conscious level.
The songs usually dated from
before the 1970s, when the patient lost interest in listening to music.
He finds the sound of actual music distorted.
Subject 6
This subject, with 15 years of progressive deafness, had a history of less than 3 years of continual musical hallucinations.
The onset of the events was coincident with an episode when she developed loss of vision, disorientation, perplexion, slurring
of her speech and unsteadiness of body; this is likely to have
been a posterior circulation vascular event.
She would hear
one or more singers and accompanying music in the
form of a piano or band.
Unlike the five other subjects, she also
experienced
environmental sound hallucinations and verbal
hallucinations.
The environmental sound hallucinations included wartime
planes
and sirens, and the sound of dogs barking and
children crying.
The verbal hallucinations included hearing indistinguishable
sounds similar to the murmuring of a crowd and the sound of her sisters talking to each other.
The voices never talked about
her or to her.
She also experienced palinacousis; she described several prolonged hallucinations in the form of hymns triggered
by listening to the television programme `Songs of Praise'.
Structural imaging
All subjects underwent structural
imaging using MRI (Subjects 1–5) or CT (Subject 6).
No subject
demonstrated loss of grey
or white matter volume. MRI of Subjects 2 and 4
demonstrated multiple areas of signal change in the deep white matter of
the
cerebral hemispheres consistent with small vessel disease (Subject 2, Fig. 2).
Subject 6 had a large arachnoid cyst in the
right occipital lobe (Fig. 2).
View larger version:
Fig. 2
Structural imaging of Subjects 2 and 6. MRI of Subject 2 (left) shows multiple vascular lesions in the hemispheric deep white matter. CT scan of Subject 6 (right) shows a large arachnoid cyst in the right occipital lobe.
Functional imaging
Functional imaging was carried out using PET to measure regional cerebral blood flow as a measure of local cerebral activity.
A parametric design was used to demonstrate areas of the brain where activity varied as a function of the reported severity
of the hallucinosis (Silbersweig et al., 1995; Griffiths et al., 1997).
For each subject, 12 PET scans were performed on a Siemens scanner with 3D acquisition using the intravenous oxygen 15
water bolus technique to estimate regional cerebral blood flow.
Twelve acquisitions were performed in two separate blocks
of six that were 12 h apart.
This was in order to maximize the differences in symptom severity corresponding to the scans.
Before the onset of each scan, the subjects were told that a scan was about to be carried out and asked to close their eyes.
At the end of each scan they were told that the scan had finished and asked to give a rating, between 1 and 7, of the severity
of musical symptoms during the scan.
A rating of 1 corresponded to no perception of music and 7 to the most severe experience
ever. Subjects also reported the features of the experience after each scan in response to structured questions, . There was no output task during the scan.
PET image processing and statistical analysis were carried out using statistical parametric mapping software (SPM99b, http://www.fil.ion.ucl.ac.uk/spm).
Scans were realigned and spatially normalized (Friston et al., 1995) to the standard stereotaxic space of Talairach and Tournoux (Talairach and Tournoux, 1988).
The data were smoothed with a Gaussian filter (filter width at half maximum, 16 mm).
Analysis of covariance was used to
correct for differences in global blood flow between the scans and to implement individual and group regression analyses to
find areas where blood flow increased with symptom severity.
The significance of this regression was assessed with the t statistic at each voxel.
These statistics (after transformation to a Z score) constitute a SPM{Z}.
Results
Systematic study of phenomenology
Systematic
interrogation of the subjects every 8 min over the course of the PET
experiment yielded the features reported .
All of the subjects showed variation in
the severity of the hallucinosis except for Subject 5, in whom the
severity
was fixed.
All subjects reported hearing normal patterns of pitch and rhythm that formed recognizable tunes consistent with
their listening experience and interests.
Only Subjects 1 and 2, who had the least severe hearing loss (~50 dB), experienced
contemporary tunes.
In a single scan for one subject, the reported experience was of music without a recognizable tune, although
it had similar characteristics to other pieces heard during scanning.
All of the subjects, except Subject 4, heard singers
during their imaging, with or without distinct lyrics. Four of the subjects heard distinct or indistinct instruments.
PET study to demonstrate areas of activity correlated with hallucinosis
Individual analyses were carried out on each of the six subjects except Subject 5, who failed to show
any variation in the
severity of the hallucinations over the course of
the experiment.
In Subjects 1–4, the analyses were carried out on
realigned,
normalized and smoothed data.
In Subject 6 the
analysis was carried out on realigned and smoothed data, because of the
markedly
abnormal brain structure.
The individual analyses
were carried out primarily to seek activation in the primary auditory cortex
in Heschl's gyrus (HG) (also called Tranverse temporal gyri) as a linear function of hallucinosis strength, taking HG as the a priori region of interest.
The centre of mass of HG from the probabilistic map of Penhune and colleagues (Penhune et al., 1996) (left coordinates –45, –20, 8; right coordinates 45, –15, 5) was used to define the centre of a spherical volume of interest
within HG of diameter 1 cm.
Within this volume, two subjects showed significant activation at the P < 0.05 voxel level with correction for the size of the volume of interest: Subject 2 for the left HG (P < 0.001 corrected voxel level) and Subject 3 for the right HG (P < 0.005 corrected voxel level).
Analysis was also carried out on the individual data sets to seek activation as a function
of hallucinosis strength in the planum temporale (PT) as a region of a priori interest.
The centre of mass of the PT from the probabilistic map of Westbury and colleagues (Westbury et al., 1999) (left coordinates –60, –30, 10; right coordinates 65, –30, 10) was used to define the centre of a spherical volume of interest
within the PT of diameter 1 cm.
Three subjects showed significant activation within this volume at the P < 0.05 voxel level with correction for the size of the volume of interest. Significant activation was demonstrated in the
three subjects as follows: Subject 1 (left PT, P < 0.05 corrected); Subject 2 (right PT, P < 0.05 corrected); Subject 3 (right PT, P < 0.005 corrected).
Group analysis was carried out for
Subjects 1–4 (Table 3 and Figs 3 and 4). Subject 5 was excluded from the
analysis because
of lack of variation in the severity of
hallucinosis, and Subject 6 was excluded from the analysis because of
markedly abnormal
brain structure.
The group analysis was carried out to demonstrate
the typical behaviour of the group. Formally, this represents
a fixed-effects analysis.
The four subjects'
similar experiences during scanning, age, handedness and musicality
justify such
an analysis. No activation as a function of
hallucinosis strength was demonstrated in HG on either side in the group
analysis.
Using the same volume-of-interest method for HG as
in the individual analyses, no activation was shown at the P < 0.05 level with correction for the size of the volume.
Using the same method for PT as in the individual analyses, significant
activation as a function of hallucinosis strength was shown in the left and right plana temporale (left P < 0.005, right P < 0.05, corrected voxel level).
The activation in each planum temporale (Fig. 4) formed part of a cluster extending on to
the lateral surface of the posterior
superior temporal gyrus, as shown in Fig. 3. In the whole-brain
analysis, without taking
any prior hypotheses into account
(Table 3 and Figs 3 and 4), significant clusters of activation were
demonstrated in the
right basal ganglia and right frontal operculum,
the posterior temporal lobes (especially the right), both lobes of the
cerebellum,
the left deep sylvian cortex and the left frontal
lobe.
Functional imaging (areas of significant
activation as a linear function of hallucinosis intensity): group
analysis for Subjects
1–4
View larger version:
Fig. 3
Functional imaging (correlated activity with hallucination
strength surface reading). PET group analysis for Subjects 1–4
showing areas where regional cerebral blood
flow increased as a linear function of hallucinosis intensity.
The
functional
data shown were thresholded at the P < 0.001 (uncorrected) voxel level and rendered on to an MRI surface template with the same degree of smoothing as the PET
data.
View larger version:
Fig. 4
Functional imaging. (Top)
PET group analysis for Subjects 1–4 showing areas where regional
cerebral blood flow increased as a linear function of hallucinosis
intensity (no sound stimulus).
The data shown
were rendered on to an axial section of the mean T1-weighted MRI for the four subjects. (Bottom) For comparison, data for the activation during the normal perception of patterned–segmented sound in nine normal subjects
(Griffiths et al., 1999a) are shown superimposed on an axial section at the same level.
Both sections are at the vertical level z = 0 mm. A line at y = –30 mm corresponds to the anteroposterior maximum for the planum temporale (Westbury et al., 1999).
Notice the bilateral activation in the region of the planum temporale in both analyses.
Discussion
In this study I observed the detailed phenomenology of musical hallucinosis in six patients with acquired deafness.
The subjects
all had musical hallucinations that occurred after the onset of deafness in the absence of features to suggest
psychosis or
epilepsy.
Based on the phenomenology, I will argue
for a model for the production of musical hallucinations in such patients
based on activity within a common mechanism for the perception of pattern in segmented sound.
The functional imaging data
suggest a neural substrate for this common mechanism.
Model
Figure 5 shows a model for the normal and
abnormal perception of patterned–segmented sound.
This is a cognitive
neuropsychological
model (Ellis and Young, 1988) based on modular psychological mechanisms, although I will also argue for the likely neural substrate for its implementation.
Fig. 5
The processes occurring during the normal perception of pattern in segmented sound. (Bottom)
The proposed basis for musical hallucinations, due to spontaneous activity in the module for the perception and imagery
of pattern in segmented sound.
During normal listening to patterned–segmented sounds such as music, the auditory input is processed by two perceptual mechanisms,
operating in a hierarchical fashion (Fig. 5, top).
The perceptual mechanism for individual sounds operates before that for
the perception of the pattern formed by these
sounds.
After the pattern has been perceived, it is encoded into memory.
The
model is based on a single module being active
during both the perception and the imagery of patterned sound.
In
acquired
deafness there is impoverished normal input to this module.
I propose that this allows spontaneous activity within the module
(Fig. 5, bottom).
I also propose that the recognition system for patterned sound can interact strongly and reciprocally with
the perception/imagery module in the absence
of normal processing activity in the latter.
This may produce positive
feedback,
represented by the bold arrows in both directions
in the lower part of Fig. 5, between the perception/imagery module and
encoding/recognition
modules.
The model predicts first that musical hallucinosis due to acquired deafness will be associated with the perception of normal
temporal patterns within segmented sound that are consistent with the
subject's previous experience.
This is the case in all
six subjects observed. In the model, this is the
result of the interaction between the perception/imagery and recognition
modules, the latter accessing patterns encoded
during previous listening experience.
All of the subjects experienced
music
that had been heard before they developed severe
deafness, and it is notable that Subjects 1 and 2, who had experienced
more
contemporary music, have less severe hearing loss than the others.
In the subjects with the most marked hearing loss (Subjects
4 and 5), there was a disparity between the normal experience of old tunes during hallucinosis and the distorted perception
of actual music;
this is entirely consistent with the model.
Subject 4 is of particular interest with respect to her
normal
perception of temporal pattern during hallucinosis.
She perceives normal temporal patterns of pitch, although the
individual
pitches are not associated with normal musical notes.
This is consistent with distinct mechanisms for the processing of the
features of individual sounds compared with the
processing of higher-level patterns formed by these sounds.
Essentially, I
am arguing in her case that abnormal activity in
the module for the perception of individual sounds can have a normal
higher-order
structure imposed by the perception/imagery module.
Some studies of tinnitus (Lockwood et al., 1998) suggest low-level activity in the individual sound module (which, I have argued, is the primary auditory cortex), whereas
others suggest more distributed high-level processing (Giraud et al., 1999).
This difference might reflect whether the tinnitus has associated high-level temporal or spatial structure associated with it.
Secondly, the model allows for the `triggering' of activity in the perception/imagery module by the impoverished auditory
input.
For some sounds the low signal-to-noise ratio in such input might lead to misperception and misrecognition of certain
incoming sounds as music followed by mental `amplification' due to the
positive feedback loop between the perception/imagery
and recognition modules.
The model also allows for
the triggering of activity in the perception/imagery module by any
abnormal
activity from the module for the perception of
individual sounds.
Gordon has particularly stressed the possible
contribution
of early parts of the auditory pathway to musical hallucinations (Gordon, 1994).
I would point out here only that the proposed model does not require the ascending auditory system to represent a true
musical pattern to produce the phenomenon of musical hallucinosis.
Triggered activity would also provide a mechanism for the
phenomenon of palinacousis seen in Subject 6.
Two questions arise immediately from the model.
First, the model is based on the processing of patterned sound rather than
music per se.
The question arises of why
the subjects do not usually perceive other forms of patterned–segmented
sound, such as speech.
Speech, like music, contains a high-level structure
at the level of hundreds of milliseconds, called prosody or the `melody
of language' (Monrad-Krohn, 1947).
Speech, unlike music, is also characterized by spectral and temporal complexity within
the segmented sounds (in terms of
temporal structure, at the level of milliseconds
and tens of milliseconds).
The production of verbal hallucinosis in this
model would therefore require additional abnormal
activity in the module for the perception of individual sounds, as well
as in that for the perception of higher-order
pattern.
This is possible within
the model, although less likely.
Only one of
the six subjects in this study also suffered verbal
hallucinations in the form of spoken speech, although in 41 of the 72
scans observed the subjects perceived speech with accentuated pattern or prosody in the form of singing.
Previous studies
in a broader population, including subjects with psychiatric disorders, epilepsy and structural lesions (Berrios, 1990), have also reported verbal hallucinations in subjects with musical hallucinations.
As in the present study, associated auditory
verbal hallucinations in the form of spoken speech
were found only in a minority of subjects.
A second question is why all
subjects with acquired deafness of the degree shown by these subjects do not experience musical hallucinosis, if this is due
to the activity of a normal module cut off from its normal input?
This might reflect differences between subjects in a threshold
for spontaneous or triggered activity within the perception/imagery module.
Model implementation
In terms of the neural mechanisms that might underlie this model, I argued earlier that the perception of the features of
individual sounds involved neural mechanisms at or close to the primary auditory
cortex in HG, whilst the perception of higher
order patterns formed by such sounds involved more
widely distributed mechanisms, including the planum temporale.
A
prediction
of the model is therefore that increasing intensity
of hallucinosis with increasing spontaneous activity in the module for
pattern perception will be associated with increasing activation in a network distinct from HG, including the planum temporale.
The group analysis has demonstrated that the typical behaviour of the group is to show such increasing activation with increasing
hallucinosis strength in the planum temporale.
The typical behaviour of the group is not to show such activation in HG, although
it was shown in one or other HG in two of the individual analyses.
A striking feature of this study is the similarity of the activation produced by musical hallucinosis when there is perception
without input and the perception of actual patterned–segmented sound in controls (Fig. 4).
This is consistent with the proposed
model. However, the perception of actual patterned–segmented sound also leads invariably to activation in the primary auditory
cortex, something that has not been demonstrated in
this study of hallucinosis.
The analysis of hallucinating patients is
not consistent with the primary auditory
cortex being a sufficient substrate for higher-order pattern
perception.
The model
in Fig. 5 does not make strong predictions about
activation in the module for the perception of individual sounds in
hallucinosis,
but this could occur with descending excitation from the pattern-perception module to the
module for the perception of individual
sounds.
If this were the mechanism, the present
data suggest that such feedback activation is not universal.
Activation in a cortical network including the right planum temporale has been shown in previous studies of the basis of musical
perception (Zatorre et al., 1994).
Moreover, studies of musical imagery have demonstrated a network similar to that for perception (Zatorre et al., 1996; Halpern and Zatorre, 1999),
which supports the common mechanism for musical perception and imagery
proposed in this model.
This network includes predominantly
the right auditory association cortex (including the planum temporale) and the right and left frontal cortices.
The model I propose is based on activity within a module for the perception and imagery of pattern within segmented sound
rather than music per se.
Imaging studies that incorporate a task which demands imagery of simple auditory patterns (Rao et al., 1997; Penhune et al., 1998) have also demonstrated activation of the right planum temporale in the absence of activity in the primary auditory cortex.
This is consistent with the activation of the planum temporale in the current study being a mechanism for the perception and
imagery of patterned–segmented sound, the primary auditory cortex having an obligatory role in perception only.
The role of central lesions
The role of central lesions in producing musical hallucinations has been the subject of controversy. Although gross structural
lesions in the brainstem or either hemisphere can be associated with musical hallucinosis (Tanabe et al., 1986; Paquier et al., 1992; Inzelberg et al., 1993; Murata et al., 1994) such lesions are not seen in most patients with this condition.
In the present study, one subject had a large structural
anomaly (arachnoid cyst), of uncertain relevance, in addition to a major-territory vascular event.
Two other subjects had
multiple vascular lesions affecting the white matter, whilst two others had vascular risk factors (in addition to age) without
demonstrated lesions on MRI.}
Central vascular lesions might be the additional factor that distinguishes subjects with musical hallucinosis from subjects
with the same degree of deafness without hallucinosis.
Several mechanisms are possible.
First, it is possible that diffuse
vascular disease might lead to a degree of disconnection between the primary auditory and association cortices.
In such a
way the input to the perception/imagery module might be more diminished in the group with vascular disease.
A second possibility
is that a vascular lesion or lesions within the network for the perception and imagery of segmented sound alters the threshold
for spontaneous activity within this network.
I favour the second mechanism, as the distributed nature of the network would
make it more likely to be affected by a stochastic process such as small vessel disease.
Moreover, the second mechanism involves
a network that includes deep brain structures, which are more likely to be affected by small vessel disease than the superior
temporal cortex.
For either mechanism, vascular disease would act as a factor to augment the suggested process in the model
dependent on peripheral deafness.
Such vascular disease would not be an adequate explanation in itself.
Conclusion
I have proposed a model for the production of musical hallucinations in subjects with acquired
deafness in the absence of
psychosis or epilepsy.
This model is based on
spontaneous activity in a module usually involved in the normal
perception of
pattern in segmented sounds.
Functional imaging
data support the hypothesis that such a module is physically realized in
a
distributed cortical network distinct from the
primary auditory cortices.
All of the subjects considered here found the experience of musical hallucinations distressing and requested treatment.
Only
one subject benefited from any treatment, in the form of improved amplification.
I recommend that subjects within this group
are assessed by an audiology service to decide if improved amplification may be of benefit, but in general the prognosis for
improving the condition is poor.
Acknowledgments
I wish to thank the patients, many of whom travelled long distances to undergo detailed assessment and scanning, the referring
clinicians (R. Brenner, D. Burn, M. Jackson, J. Palace, S. Pereira, P. Reading, J. Spillane, B. Toone, R. Wise), members of
the Neurootology
Department, National Hospital for Neurology, Queen Square and the
Department of Audiology, Kings College
Hospital for carrying out the audiograms, the
radiographers at the Wellcome Department of Cognitive Neurology for
expert technical
assistance, and R. S. J. Frackowiak for helpful
comments. I am supported by the Wellcome Trust (UK).
- © Oxford University Press 2000
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fuente: "Brain "
Es
por ello muy importante determinar cuál es el origen de esos ruidos
molestos ya que existe la Norma IRAM 4062/73, titulada "Ruidos molestos
al vecindario. Método de medición y clasificación",
que se refiere a la determinación de los niveles de ruido de cualquier
origen (excepto el del tránsito) capaces de provocar molestias a los
vecinos. Esta norma abarca el aspecto de la medición y de la clasificación.
