A Simulated Hallucination Mechanism Compared to Hallucination Brain Response Studies
John J. McMurtrey, [a] Copyright 2007, May 3, 2007
Co-authorship is negotiable towards professional publication in an NLM indexed journal, Email- Johnmcmurt@aol.com
Donations toward future research are gratefully appreciated at http://www.slavery.org.uk/FutureResearch.htm
The substantiation for a simulated hallucination mechanism is compared to brain response findings during hallucination in review. A technology for simulating auditory hallucination has had development that is based on the microwave hearing effect. The microwave hearing effect produces auditory responses consistent with many observations of brain activation occurring during hallucination. Some studies regarded as of hallucination indicate brain responses from the more initial auditory pathway that particularly support a microwave hearing mechanism. Further research is advocated for definitive differential diagnosis of simulated hallucination.
Anatomical features of the auditory pathway of interest to microwave hearing begin with the cochlea within which hair cells transduce sound into neural impulses that are transmitted through the vestibulocochlear nerve. The cochlear nerve arises from the vestibulocochlear nerve for transmission to the cochlear nuclear complex at the brainstem pontomedullary junction.  Neural fibers from the dorsal cochlear nucleus project [b] predominately [c] to the lateral lemniscus of the contralateral brainstem.  Axons from the ventral cochlear nucleus project through the trapezoid body to the ipsilateral and contralateral superior olivary complex. 28 This parallel route in the auditory pathway is mainly devoted to sound localization, and also joins the lateral lemniscus, which proceeds to the inferior colliculus. The above brainstem neural pathways contribute to the Auditory Brainstem Response recorded from surface electrodes.  The inferior colliculus connects brainstem auditory centers to the medial geniculate body in the posterior thalamus from which the rather disperse acoustic radiation projects to the primary auditory cortex. 
Actual sound response of the microwave hearing effect is recorded from implantable microphones known as hydrophones when placed within the heads of animals,   as well as in model equivalents of muscle  and brain.  The physical effect is the basis for developing microwave-induced thermoacoustic tomography, which generates ultrasound frequencies within tissues,    and the hearing effect can be produced by appropriately pulsed Magnetic Resonance Imaging radio frequency coils.  The most accepted physical mechanism for microwave hearing is rapid thermoelastic expansion causing sound waves, 6 which activates the cochlea, but the middle ear is not involved. 8
Microwaves pulsed for the hearing effect produce electrophysiologic response at various levels of the hearing pathway of animals including: the cochlear round window,    eighth cranial nerve, [d]   cochlear nucleus,   inferior colliculus,  medial geniculate body,  and auditory cortex.  Rat blood flow increases significantly in the temporal cortex, and the medial geniculate body with microwave hearing exposure.  Hearing effect pulsed microwave exposure increases rat brain glucose metabolism by [14C] 2-deoxy-D-glucose with particular auditory pathway prominence in the cochlear nucleus, the superior olivary complex, the inferior colliculus, and medial geniculate body.  Microwave hearing exposure decreases animal cortical auditory evoked potential amplitudes with increased latency.   The microwave hearing effect also produces an auditory brainstem response,   which can be decreased by interfering sound. 40
Studies of Brain Response on Hallucination
The functional imaging decrease in auditory cortex response to sound
while hallucinations occur suggests shared brain pathways. 
 Delayed auditory event response is observed
during hallucination by both electroencephalography (EEG)
and magnetoencephalography,  which resembles the interfering sound response.  Hallucination causes the auditory electrophysiologic N100 to decrease in amplitude with delay of response, which implicates a shared pathway with sound.  Simultaneous auditory cortex activity occurs in each hemisphere during hallucination as demonstrated by EEG coherent response.  Auditory Brainstem Response (ABR) abnormalities of increased peak latency and missing peaks are especially associated with hallucinating schizophrenics   without particular hearing impairment, and are frequent findings in some patients of studies not immediately assessing hallucination,      yet normal ABR reversion may occur on symptom improvement. 
Numerous functional imaging studies during hallucination confirm activation of the primary auditory cortex,        or the superior temporal gyrus (STG)    that contains the auditory cortex. Of further hallucination studies diverging somewhat in results, one reports posterior STG activity not including the auditory cortex,  and two found the STG not activated,   yet no imaging technique is a snapshot of neural activity instantaneous to patient signaling of hallucination. [e] Subcortical functional imaging of the rest of the auditory pathway by commonly utilized methods is difficult. The acoustic radiation is somewhat disperse for functional observation, 30 and large blood vessel pulsation obscures resolution in the brainstem with this effect applying as well to the medial geniculate body,  which both have connection for the auditory pathway by the inferior colliculus. One study of hallucination noted activity in the region of the colliculi while stipulating problematic brain stem localization, 79 and another study detected activity within the inferior colliculus while ascribing detection to imaging without scanner noise. 74
Numerous investigations of the microwave hearing mechanism well demonstrate actual auditory activity, which fully predicts those brain response findings that hallucination resembles effects produced by sound. Many studies confirm primary auditory cortex activation on hallucination, and particularly the finding of increased activity in the vicinity of the colliculi, 79 or of the inferior colliculus 74 support a microwave hearing mechanism of simulated hallucination. Auditory Brainstem Response (ABR) abnormalities are especially apparent in hallucinating patients 61 62 with some evidence that such abnormality does resolve, 68 which is predicted by direct microwave hearing auditory activation. Increased ABR wave latency found in ‘hallucinating’ patients are also reported for simple broadband noise coincident with the sound producing the ABR in normal subjects.  Other isolated ABR abnormalities of missing peaks in hallucinating patients correspond to forward masking effects of sound presented just prior to normal ABR testing. The solitary wave V of the ABR from one ‘hallucinating’ patient 61 matches the results on forward masking in normal subjects, where the additional sound precedes the ABR stimulus by milliseconds, and is of the same frequency.  The missing ABR wave I in another ‘hallucinator’ 62 can result from loudness and stimulus rate effects  as well as frequency quality of additional sound maskers  just prior to the ABR of normal subjects. Simulated hallucination at the time of ABR testing could explain all ABR abnormalities observed. [f] Therefore microwave hearing studies particularly correspond for observations during hallucination in temporal cortex, and some studies directly indicate activation of the initial portions of the sensory pathway that occurs in hearing by sound or microwaves.
The ABR is a common present clinical measurement,  which could be altered for patient signaling of ‘hearing voices,’ without sound presented or with such to replicate the ‘hallucination’ associated abnormalities in previous studies. There are existing studies of normal ABR responses to speech sounds,  or different frequencies  with which any results might be compared. The functional Magnetic Resonance Imaging (fMRI) observation identifying inferior colliculus activity with ‘hallucination’ utilized ear plugs decreasing scanner noise effects, which obscures further hallucination induced activation in the auditory pathway. No other fMRI hallucination studies utilized the various scanner noise attenuation methods, and none utilized cardiac gating [g]  that are necessary to optimize observation of subcortical auditory pathway response in hearing studies for which protocols are available.   Another clinical technique that may detect such occult cochlear activation is otoacoustic emission,  with expected differences between emissions that are spontaneous or evoked,  and differences in noise evoked emissions from transient evoked emissions described.  Further definition of any subcortical hearing pathway involvement in hallucination must be undertaken, and any additional substantiation would strongly support technologic assault.
Only a few of the functional imaging studies of direct hallucination activity observe activation within Broca’s area. 74 75 80 These few Broca’s area activity reports have fostered the hypothesis that hallucination occurs by inner speech misattribution,  since the area is involved in producing inner speech without vocalization.   However some Broca’s area activity on hearing words,   for statements,   and with activity increases for subjectively significant,  or emotional words  particularly those unpleasantly arousing,  mitigates considerably Broca’s area activity per se as evidence of involvement in producing hallucination, since hallucination frequently involves all conditions.  Furthermore, Broca’s area during hallucinations does not correspond for EEG coherent activity between the hemispheres, but electrodes over each auditory cortex exhibit coherent response. 60
Brodman’s Areas (BA) 41 and 42 comprise the primary auditory cortex. These areas during inner speech are reported as actually deactivated in BA 41, 104 without observed activation in normals 97    or schizophrenics,   and only show some partial activation during very fast repetition (in BA 42), which is lesser in schizophrenics.  Therefore the endogenous hallucination hypothesis with any empirical evidence does not well correlate with the majority of inner speech observations.
Besides the issue of primary auditory cortex activation, subcortical hearing pathway activation while ‘hearing voices’ is particularly inconsistent with the inner speech model. Though the inner speech model of hallucination is entirely logical, and endogenous hallucination does apparently exist, the discrepancies point out the fact that in terms of a known pathway this model is entirely theoretical, especially as compared to the defined auditory pathway that is the mechanism of microwave hearing. Many patients attempt effective complaint of remote voice transmission, but are neutralized with their civil rights abrogated by shunting into the medical community who deem stigmatizing diagnoses based on uninformed dogma. There are considerable rationale to suspect schizophrenia diagnoses, particularly of the paranoid type as presumptive.  Considering that some evidence implicates subcortical auditory activation in ‘hallucination,’ both ethics and the scientific method make investigation of a microwave hearing mechanism imperative. Defining initial auditory pathway activation consistent with sound is fully expected as a differential criterion in diagnosing simulated hallucination.
Acknowledgements: Thanks are given to God for inspiration and Dr. Allen Barker for his suggestions.
[b] Through the commissure of Probst.
[c] This discussion describes the preponderant pattern of neural projection, as 90 % of the total brainstem auditory pathway is contralateral, yet there are ipsilateral projections as well according to Moore, 1985. Smaller projections from the dorsal cochlear nucleus to the superior olivary complex as well as synapses of less or undefined auditory nuclear origin to nuclei within main tracts of the lateral lemniscus and trapezoid body are also omitted here.
[d] The eighth cranial nerve is the vestibulocochlear nerve.
[e] There are methodological issues for capturing brain response, particularly to short hallucinatory episodes. In van de Ven et al. 2005, the estimation of time that a hallucination episode must last for adequate functional Magnetic Resonance Imaging capture of brain responses is 10 seconds, and some time constraint applies to the tomographic mechanics of Positron Emission Tomography as well.
[f] In Lindstrom et al, 1987, one patient with an abnormal ABR denied hallucination. Whatever the truth of this denial, there is certainly enough literature on patient non-compliance to acknowledge that Parkinsonian and extrapayramidal dyskinetic adverse effects particularly of typical anti-psychotics predominantly prescribed at the time of this study are obnoxious enough for some patients to deny such an obvious positive symptom for fear of increased dosage exacerbating these side effects.
[g] Cardiac gating restricts the timing of imaging to only at a certain point in the cardiac cycle for minimization of blood vessel pulsation effects on image quality.
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