Falsi�cations of Hamero�-Penrose Orch OR

Model of Consciousness and Novel Avenues for

Development of Quantum Mind Theory

Danko Dimchev Georgiev

November 17, 2006

Laboratory of Molecular Pharmacology, Faculty of Pharmaceutical Sciences,Kanazawa University Graduate School of Natural Science and Technology,Kakuma-machi, Kanazawa, Ishikawa 920-1192, JAPAN,E-mail: dankomed@yahoo.com

Abstract

In this paper we try to make a clear distinction between quantum mys-ticism and quantum mind theory. Quackery always accompanies scienceespecially in controversial and still under development areas and sincethe quantum mind theory is a science youngster it must clearly demar-cate itself from the great stu� of pseudo-science currently patronized bythe term �quantum mind�. Quantum theory has attracted a big deal ofattention and opened new avenues for building up a physical theory ofmind because its principles and experimental foundations are as strangeas the phenomenon of consciousness itself. Yet, the unwarranted recourseto paranormal phenomena as supporting the quantum mind theory plusthe extremely bad biological mismodeling of brain physiology lead to greatscepticism about the viability of the approach. We give as an example theHamero�-Penrose Orch OR model with a list of twenty four problems notbeing repaired for a whole decade after the birth of the model in 1996.In the exposition we have tried not only to pesent critique of the spotted�aws, but to provide novel possibilities towards creation of neuroscienti�cquantum model of mind that incorporates all the available data from thebasic disciplines (biochemistry, cell physiology, etc.) up to the clinical ob-servations (neurology, neurosurgery, molecular psychiatry, etc.). Thus ina concise fashion we outline what can be done scienti�cally to improve theQ-mind theory and start a research programme (in Lakatos sense) thatis independent on the particular �aws in some of the existing Q-mindmodels.

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1 Split-brain

Hamero� overestimates the role of dendro-dendritic processing and the role ofgap junctions between neighbouring dendrites as the main mechanism for co-herence between cortical neurons, producing entangled quantum coherent �su-perneuron�. He wrongly believes that dendritic microtubules somehow a�ectthe axonal hillock potential and after that the axonal �ring follows the well-known classical deterministic behaviour as described by the Hodgkin-Huxleyequation. Thus Hamero� claims that in dendritic microtubules occur the quan-tum events associated with consciousness and after that axons manifest purelyclassical nonconscious activity. It is believed that

�consciousness occurs primarily in dendrites, with axons servingto execute and communicate results of conscious dendritic processes�(Woolf and Hamero�, 2001, p.474).

The main theoretical grounding of such extreme position is the �nding thatsome cortical neurons do not have axons.

�Some cortical neurons have no axons, and extensive dendriticactivity may occur without causing spikes. Excitatory postsynap-tic potentials below spike threshold (historically considered noise bymany neuroscientists) oscillate coherently in the γ range across wideregions of brain. Although it is widely assumed to be so, initiationof axonal spikes is not necessarily the raison d'etre of dendrites.�(Hamero�, 2006a, p. 403).

1.1 Remark

Classical experiments with split-brain human subjects showed that axons incorpus callosum are necessary for �united mind� and cutting them by surgerydisintegrates the conscious activities of the two cerebral hemispheres producingprodigious Jekyll-Hyde syndrome. After cutting the axons of corpus callosumin the brain there are two minds each one being completely unaware of other'smind existence, and each mind taking control over the opposite half of the body.For this discovery Roger Sperry actually took the Nobel Prize in 1981.

Roger Sperry and Ronald Myers discovered the split-brain e�ect in the early1960s. Myers (1955) showed that when the cat had its optic chiasm and corpuscallosum severed, two independent learning centers were established - one ineach hemisphere of the cat's brain. If the cat had its right eye open and its lefteye covered and learned to make a simple conditioned response, it was unableto make the same response when the right eye was covered and the left eye wasopen. It was as if the learning was unable to be communicated to the otherside of the brain; thus, it was obvious that information available to one sideremained o�-limits to the other.

Roger Sperry and Michael Gazzaniga (Gazzaniga and Sperry, 1967; Sperryand Gazzaniga, 1967; Sperry et al., 1969) began a series of studies of split-brain

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humans, patients who had had the corpus callosum severed as a therapeuticprocedure, and the observations of these clinical patients have formed the basisfor a number of signi�cant ideas concerning brain function.

The World War II veteran (known in the scienti�c literature as W.J.) hadundergone surgery to alleviate his epileptic seizures. After the surgery W.J.easily named and described colours, letters, and other information �ashed brie�yto the right side of his visual �eld; therefore, W.J.'s left hemisphere neededno help handling basic tasks requiring verbal responses. Then the scientists�ashed items in W.J.'s left visual �eld and waited for the responses of his righthemisphere. As the anxious investigators looked on, W.J. acted as though hehad suddenly gone blind. He insisted that he could not see bursts of light,boldface letters, or anything else presented to him. Yet his left hand, under thecontrol of his right hemisphere, pushed down on a telegraph key each time avisual stimulus appeared, just as the scientists had instructed him to do.

In later series of experiments it was shown that the right hemishere has itsown mind and can communicate regardless of the fact that it has no control ofthe speech center located in the left hemisphere and therefore is deprived fromthe priviledge to speak.

In his Nobel Lecture Roger Sperry (1981) concluded that after commissuro-tomy:

�each of the disconnected hemispheres, not only the left, has itsown higher gnostic functions. Each hemisphere in the lateralizedtesting procedures appeared to be using its own percepts, mental im-ages, associations and ideas. As in the split-brain animal studies,each could be shown to have its own learning processes and its ownseparate chain of memories, all of course, essentially inaccessible toconscious experience of the other hemisphere�.

That is after commissurotomy the human brain hosts not one but two minds!Here we want to raise the extremely important point - the binding problem

cannot be solved by classical communication of information (Georgiev, 2003a;Mashour, 2004). Indeed Hamero� (2006a, 2006b) correctly postulates quantumcoherence to explain the conscious binding. The conscious mind feels itself asa single unit, it is a holistic entity and does not equal to two persons commu-nicating with each other. You and your friend may communicate and exchangeinformation, but you and your friend do not collectively feel as being one globalmind. In non-split-brain humans the two hemispheres do not equal to twoseparate minds that communicate like you and your friend. In normal state(non-split-brain humans) there is a �binding� that unites the two hemispheresso that their experience is united into a single experience. So if quantum coher-ence is postulated to solve the binding problem, then axons must also convey thequantum coherent states. Therefore axons cannot only classically �execute andcommunicate results� as if between you and your friend, axons provably uniteconsciousness, and if this is achieved by quantum coherence then they must atany rate extend the quantum coherent states. The observation that some corti-cal neurons do not have axons must not be erroneously interpreted in a way that

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�axons and axonal microtubules are unconscious classical relay/output pathwaysonly�. This is incompatible with the split-brain data.

Additionally we might argue against axonal classicality. The extremely lowreliability of terminal button exocytosis of 0.15-0.30 leads either to chaos, orreduces enourmously the computational power of brain via need of classicalerror correction codes, as will be discussed in a subsequent paragraph.

2 Gap junction tuneling and decoherence

Hamero� wrongly believes that gap junctions can sustain coherence betweencortical neurons for time of 25 ms. The acclaimed model requires electrons de-rived from mitochondria, then tunnelled though gap junctions, and transmittedto microtubules via so called dendritic lamellar bodies (DLBs). The coherentstates of microtubules extend in both neurons and glial cells.

2.1 Remark

Gap junctions electrotonically couple neighbouring neurons, and they are hex-americ channels composed of subunits called connexins, or recently describednovel proteins called pannexins. There is extensive ion �ow, and small moleculetransfer through gap junctions such as Ca2+, adenosine triphosphate (ATP), ormetabolites. Gap junction hemi-channels are also used for non-SNARE depen-dent release of neuromediators such as glutamate in developing brain. Hamero�strictly agrees that ion superposition across plasma membrane is impossible asnoted by Max Tegmark (1999) where he calculates time till decoherence to beonly 10−23 s. But ions �owing through gap junction will decohere the sys-tem in the same decoherence time. Conservatively done numerical estimate byGeorgiev (2002) gives decoherence time τdec ≤ 10−9 s.

Another critical issue - the molecular biology is completely messed up. DLBsare found only in the main branch of dendrite. They have never been observedin the dendritic spines that communicate with gap junctions. De Zeeuw et al.(1995) clearly show that DLBs are found tens of micrometers away from theactual gap junction couplings, and that there is only �correlation� between theexistence of gap junctions and existence of DLBs in sense that DLBs might beinvolved in the biosynthesis of gap junctions, but there is no direct structurallink between these.

And last, but not least, the tiny astrocytic/glial projections really couplewith neurons through gap junctions, but the connexin proteins are mainly Cx43,while neuronal type is Cx36. Even if this is not a big problem, the obviousproblem is that the tiny glial projections are lacking microtubules but are �lledwith actin �laments. Therefore there seems to be a big morphological di�er-ence between the cellular projections coupled through gap junctions - neuronalprojections have mainly microtubule-based cytoskeleton, while glial projectionshave almost exclusively actin-based cytoskeleton lacking microtubules.

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3 The dendritic lamellar bodies

Hamero� severely mismodels the actual gap junction coupling between neuronssuggesting a highly �ctious structural construction with mitochondrion and den-dritic lamellar body (DLB).

�The dendritic lamellar bodies are tethered to small cytoskele-tal proteins anchored to microtubules, and it is suggested that themitochondria within the bodies provide free electrons for tunneling,forming a tunneling diode pair or Josephson junction between cells�(Hamero� et al., 2002, p.163).

3.1 Remark

The described by De Zeeuw et al. (1995) dendritic lamellar bodies are locatedin dendrites and are possibly derived from smooth endoplasmatic reticulum orGolgi apparatus. DLBs are composed of stack of cysternae that lack ribosomes.In some cases DLBs are attached to mitochondrion. There is however big mis-understanding when it comes to the links with gap junctions. The DLBs arelocated always in bulbous parts of the main dendrite and the correlation betweenDLBs and gap junctions was suggested by the fact that antibody for gap junc-tion protein cross-labels the DLBs. Thus De Zeeuw and co-workers concludedthat DLBs are somehow involved in the synthesis of gap junctions (De Zeeuwet al., 1995, p. 1602). Also the DLBs are not located in the dendritic spines,which contain the gap junctions, therefore the distance between DLBs and gapjunctions is several micrometers. Another striking comment by De Zeeuw andcoworkers is that the bulbous structure of the dendrite that contains the DLBdoes not contain neither microtubules, nor neuro�laments! This is explicitlystated so that readers are not lead into delusion - DLBs should be involved inthe synthesis of gap junctions, but there is not structural link between DLBsand gap junctions. The �correlation� is based on biogenesis of gap junctions.The original �gure with the original caption on the DLB morphology is providedon the next �gure.

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Figure 1. Drawing of a serial reconstruction of a portion of a dendrite con-taining a DLB. The bulbous appendage with the DLB does not contain a gapjunction while the dendritic spine originating from that dendrite does. Notealso that the appendage with the DLB does not contain any microtubules orneuro�laments, whereas the dendrite that gives rise to this appendage does con-tain these neuronal elements (original caption by De Zeeuw et al., 1995).

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We conclude that one of the main reasons for choosing gap junction tun-neling, instead of coherence through the synaptic cleft, is the extremely shortdistance between the neuronal membranes at the gap junctions that is just 4nm. However the imaginary construction done by Hamero� extends tens ofmicrometers and completely destroys the idea of suitable distance for electrontunneling. The decoherence time of gap junctions has been already discussedabove.

4 Glial role in consciousness

Hamero� believes that glial cells should be involved in consciousness becausethey number will increase the computational power of brain, and since glial cellsare coupled with neurons via gap junctions.

4.1 Remark

In many neurologic disorders (syringomielia, epilepsia, etc.), there is a death ofneurons and concomitant growth of glial cells. But glial cells cannot compensatefor neuronal loss.

The involvement of glial cells in cognitive processes as memory storage de-vices has been suggested in the dawn of neuroscience and has been continuouslyfuelled with �new data� by researchers of astrocyte biology (Ng et al., 1992;Temburni and Jacob, 2001). Today the evidence is that glial cells are onlytrophic cells for the very capricious neuronal cells, which need extremely nar-row range of physiological parameters for their proper function. Small deviationsin glucose concentrations, pH, ionic concentrations, etc., are not tolerated byneurons, and although neurons do not die, unconsciousness follows in tens ofseconds. Of course glial cells are subject to the common molecular transductionpathways but every cell in the body is involved in some form of processing ofclassical information. Every physical change in the cell is a form of classical�memory trace� for past events so for the unexperienced researcher who has notfaced seriously with the problem of consciousness it is easy to confuse the clas-sical �memory traces� that result from irreversible processes, with the �cognitivememory storage�. Indeed the engrams of consciousness should be physical, butit is impossible to localize a physical change in brain and then claim that this isnecessarily a �cognitive memory trace�. So far it has been observed that injuryof neurons leads immediately to cognitive memory loss, while the initial stagesof autoimmune diseases against glial cells (e.g. multiple sclerosis) are not as-socaited with serious cognitive loss. The cognitive de�cits appear later in theevolution of the disease when the neurons are also damaged. Therefore thereis evidence that neurons solely are responsible for consciousness and cognitivefunction, while glial cells are only trophic and protective cells.

Extending of consciousness through other cell types such as glial cells, �-broblasts, even connective tissue, blood vessels, immune cells, etc. is of no realpurpose for solving the enigma of consciousness. To add more problems and to

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make more hypotheses than necessary is too bizarre, and against the aestheticnotion for a theory to be as simple as possible, but not simpler than needed!Neuronal morphology and biology is so complicated and many times richer indetails than glial biology that it is �insult to neurons� to make their function inhosting consciousness shared by glial cells as well.

5 Subjective time �ow and gravitational ORs

Roger Penrose speculated that the psychological arrow of time, should be cou-pled with the cosmological time arrow, and that possibly our consciousness andthe �felling of passing time� could be born by the occurring gravitational objec-tive reductions (ORs).

5.1 Remark

It was reported by Georgiev (2003b) and already known from neurological prac-tice, that there are human subjects (e.g. after stroke, or other neurologicaldisorders) that su�er from time agnosia - they cannot consciously realize thetime �ow, nor can judge duration of time intervals. It has been argued thatthese patients do not feel passage of time, and numerous psychophysiologicalexperiments have con�rmed the known by everybody fact that the same objec-tive time interval, subjectively can be experienced as �too fast� or �too slow�depending on the situation, the company, and other factors. Thus the existenceof patients with time agnosia clearly shows the possibility for a subject to beconscious, without having associated feeling of time �ow. Therefore if ORs (pro-ducing �objective time �ow�) are responsible for consciousness, they cannot bealso cause for subjective feeling of time �ow. Otherwise time agnosia would bea priori impossible, which is not the case.

However a much more general concept should be stressed upon. Georgiev(2004) have pointed out that the spatial extention of the brain does not produce�feeling of 3 dimensions�, and this can be generalized by the statement thatthe physical characteristics of the brain (mass, temperature, ..., etc.) do notproduce associated �feeling of mass�, �feeling of temperature�, ..., etc. Thus itis conceptually �awed to suppose that objective passage of time itself shouldproduce subjective feeling of passing time.

The suggestion that ORs produce the fundamental consciousness is discussedin a separate paragraph, where we disagree that fundamentalism and emergen-tism as approaches towards consciousness should be used together.

6 Microtubule's 25 ms �coherent freezing�

One of the most frustrating features of the Orch OR model is the fact thatmicrotubules should be coherent for 25 ms in order to perform their cognitive

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function. Every Orch OR event needs microtubule isolation from the cellu-lar environment to prevent decoherence for 25 ms. This putative isolation ispostulated to occur via acting gelation.

6.1 Remark

All protein enzymatic/catalytic function occur at dynamic timescale of 10-15picoseconds and this fast dynamics should have survival value in order the bio-logical complexity within the cell to be e�ectively organized against the destruc-tive action of the thermodynamics arrow, which implies increase of entropy intime. Therefore the proteins within cells must be fast enough to counteract theincrease of entropy (at the expense of metabolic energy), so that all entropicerrors in function be repaired/corrected, all waste products be eliminated, etc.

Microtubules have certain enzymatic functions through their C-terminal tailsin controlling the MAP attachment sites, and kinesin walk. Why then micro-tubules and tubulin do not use the fast picosecond dynamics done by all pro-teins? Classical (irreversible) events like attachment/detachment, motor proteincontrol, reaction catalysis, need necessarily collapse of the wavefunction, in orderthe state to become irreversible. If the state is quantum coherent, then every-thing is reversible, everything is in superposition and indeed no �real� time �owhas occurred, because there are multiple space-times in superposition. There-fore no �output� by the microtubules could be achieved without collapse of thewavefunction. In order to have �output� from microtubules an objective time�ow (irreversible evolution) is needed, so ORs must occur in picoseconds.

Illustration of the di�erence between the quantum coherence and the irre-versible time �ow composed of discrete events (collapses, or ORs) could be themovie analogy - in the quantum coherent case, you have just one picture withmany superposed images one over the other, so no time �ow occurs, while inthe irreversible classical time �ow you can watch a movie in which every cadreis replaced by another one in time, there is both motion and time �ow, thepictures are dynamic, not still.

Emerges the embarrassing question - why if all proteins in the cell counteractthe increase in entropy (i.e. the �cellular movie is going on�), the microtubulesfor that time are �frozen� in motionless coherent picture. After microtubulesdecide to �unfreeze� and �give order� to the cellular protein interior at such longmillisecond intervals could they really be able to organize the cellular functions?Isn't it better if the microtubules control everything at picosecond time scale,as well as produce conscious events in 10-15 picoseconds?

The psychophysiological question, �If we are indeed 100 GHz quantum pro-cessors why we do not feel that our conscious �ow is so fast?�, is answered byGeorgiev (2003b) in extremely fascinating fashion - we do not feel that ourconscious �ow is so fast because our conscious steps do not produce associatedexperience of time �ow at all. The evidence from patients su�ering time agnosiasuggests that consciousness occurs without co-producing a subjective feeling oftime.

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7 Photon capturing in retina

Hamero� and co-workers (St. Hilaire et al., 2001) suggested that coherent statesof photons in retina could be transmitted to the brain cortex, and that micro-tubules could capture photons directly. Indeed this is one of the 20 testableOrch OR predictions proposed by Hamero�.

7.1 Remark

Color blindness is result from defect of opsin genes in retinal neurons (retinalcones), and there is extensive evidence that visual image processing occurs inthe layers of the retina at the level of amacrine, and bipolar cells. Particularimportance in neurophysiology is paid to the phenomenon of lateral inhibitionthat is responsible for the e�ect of sharpening (i.e. increasing the contrast of)the boundaries of percepted objects. This e�ect is responsible for the feelingof travelling rabbit on the skin of your forarm under discrete skin stimulation,and is implicated in the function of all analysators (sense organs); for detailswe refer the reader to the excellent exposition of that matter by von Bekeshy(1961) in his Nobel lecture on hearing.

Therefore if the visual pictures enter the brain cortex in the form of electricimpulses it is impossible the quantum information (coherent states) of photonsto be delivered to the brain cortex. The fact that visual information entersthe brain cortex in the form of electric excitations has been used by Dobelle(2002) to input through implanted electrodes in the visual cortex of a blindman captured by camera visual information. Thus if the visual informationis to be classically processed by the lateral inhibition mechanism at the levelof neuronal membrane generated electric excitations, the idea of Hamero� andco-workers is theoretically doomed to failure from the very beginning. IndeedSt. Hillaire (2003) in a personal communcation confessed that the predicted byGeorgiev (2002b) failure of the whole experiment indeed did occur.

8 Microtubule A-lattice in brain cortex

Based on modelling of microtubules as ferroelectric lattices done by Tuszynskiand co-workers, Hamero� suggested that possible good prediction of Orch ORis to bet on existence of A-lattice microtubules in brain cortex, compared to theB-lattice microtubules observed elsewhere in vivo. This is also one of the 20testable Orch OR predictions proposed by Hamero�.

8.1 Remark

The ferroelectric model has no any biological advantage, and is also insen-sitive for local electric �elds. What is more B-lattice for microtubules wasproved/observed directly by freeze fracture electron microscopy both for in vitroassembled microtubules and for microtubules isolated from various brain regions

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(Kikkawa et al., 1994). So far there is no observed case of in vivo microtubuleswith A-lattice.

Indeed the tubulin lattice of microtubules was found to be irrelevant forthe recently proposed information processing by the C-terminal tubulin tailsoperating in an interplay with the local electromagnetic �eld (Georgiev et al.,2004, Georgiev and Glazebrook, 2006).

9 Is tubulin bound GTP �pumping� possible?

Hamero� and co-workers (Hagan et al., 2002) insisted that indeed GTP cycleof tubulin bound nucleotides might support a �pumping process� whose energymight be used for microtubules in order to achieve Fröchlich type of coherence.

9.1 Remark

It has been shown that α-tubulin bound GTP never hydrolyzes in assembledmicrotubule, while β-tubulin bound GTP hydrolyzes to GTP soon after theincorporation in the microtubule wall. After that the successive α-tubulin sub-unit occludes the preceding β-tubulin nucleotide binding pocket and neitherexchange of GDP for GTP, nor phosphorylation of the β-tubulin bound GDPis possible. Therefore tubulin bound GTP pumping cycle cannot occur in sta-ble microtubules (Georgiev, 2003c). Alternatives for energy supply should befound (see speci�c proposals in Georgiev et al., 2004; Georgiev and Glazebrook,2006a).

10 Bionic vision and Dobelle's breakthrough

In Hamero�-Penrose Orch OR the microtubules are suggested to be screenedfrom external electromagnetic �elds.

10.1 Remark

In an breakthrough neurosurgical operation Dobelle (2002) was able to implantelectrodes directly in the visual cortex of a blind man, who lost his vision asa result of accident. The electrodes were connected to a bionic camera thattransmitted the visual image in the form of electric pulses. Each electric pulsecreated sensation of bright spot called �phosphene� and the totality of such�phosphenes� creates the visual input. Thus the blind man called Jerry, wasable to navigate in unknown environment such as the subway, with the use ofthe bionic vision.

Dobelle's achievements are based on classical work of Pen�eld who showedthat electric stimulation of the brain cortex is able alone to elicit consciousexperience. This is in agreement with all the current medical knowledge fromclinical neurology, where the sensory information is delivered to the cortex inthe form of electric impulses through thalamus.

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Hamero�-Penrose Orch OR theory has the big shortcoming of supposing thatmicrotubules are insensitive for the local electric �eld. We believe the possiblequantum model of microtubules that should account for consciousness shouldbene�t from microtubule sensitivity to local electromagnetic �elds. This issuewas addressed in a pioneering work of Georgiev (2003d) that was re�ned intoa QFT model with electromagnetic sine-Gordon solitons coupled with the C-terminal tubulin tails projecting out of the microtubules; see Georgiev (2004a),Georgiev et al. (2004), and Georgiev and Glazebrook (2006a) for detailed dis-cussion on the topic.

11 Output at the axonal hillock

Hamero� believes that dendritic microtubules solely are responsible for con-scious Orch OR events, and that the output of the microtubule gravitational ORevent is to a�ect somehow by unknown mechanism the axonal hillock potential.After that the Hogkin-Huxley dynamics of the axon is classical (deterministic)and the communication with other neurons is ensured.

11.1 Remark

One of the major concerns is that each axon ends up with about 10 000 synapsesfor a cortical neuron. The probability for exocytosis and neuromediator releaseat each terminal button (hence reliability of synaptic transmission) is only 0.15−0.30. Therefore it seems that if there is no subneuronal control of the synapticrelease at random only about 3 000 of the synapses of the cortical neuron will��re�, while 7 000 of them will be �silent�. Thus it is not clear how the Orch ORwill prevent the huge chaos as expected due to synaptic failures.

12 Machine-brain interfaces and thought control

of robot arm

Hamero�-Penrose Orch OR model completely leaves out the possibility for mi-crotubules to control the process of neuromediator release except indirectlythrough control of axonal spiking. If the microtubules indeed controlled onlythe axonal hillock potential (by yet unknown mechanism!) then for each axonalterminal you would better bet that the exocytosis will not occur (you have 70%chance to guess) instead of relying on neuromediator release (the chance is only30%). Since neuromediator release is followed by predictable postsynaptic elec-tric activity of dendritic tree, it seems that within Orch OR the microtubulescannot control the pattern of electric excitations of the cortical neurons (thatis because the randomness introduced by synaptic failures is disastrous, and, inorder to be avoided, a subneuronal control is needed).

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12.1 Remark

Carmena et al. (2003) in a breakthrough neurosurgery have implanted elec-trodes in the monkey's cortex that measure the cortical neuron potentials, andthen send them to computer that processes the measured data by a certain soft-ware program. According to the measured electric excitations of the corticalneurons, the computer deterministically controls a robot arm. The amazingthing is that monkeys in time were able to learn how to move �by thought� therobot arm for their own purpose. After all the connected computer was just atransmission device operating in fully deterministic manner, in the same waythe transmission of a car is navigated. You don't need to know how exactly allmachinery of your car works, you only need to know that it operates determin-istically and what you have to learn is what kind of commands you must outputin order to control the car. In the case of monkeys this happens by try-and-errormechanism. What is particularly amazing is that in the beggining the monkeysmoved the robot arm with associated movement of their arms, however in timethe parasitic movement of the monkey arms disappeared.

Recently the experiment has been proved successful in humans. Thoughtcontrol of computer linked to the brain cortex of paraplegic human throughmachine-brain interface has been achieved by Hochberg et al. (2006) and themethod remains the only possibility to restore the independence for humanswith paralysis.

What is the important conclusion from such experiments? Of course theypoint towards the essential place where your mind outputs its orders - namelythe consciousness is able to control the neuronal excitations! This could hap-pen if the mind controls exocytosis at synapses and thus neuromediator release.Following exocytosis the excitation of the postsynaptic dendrite is considered adeterministic event as a result of neuromediator binding to postsynaptic ligandgated ion channels. Since microtubules cannot control directly the function ofthe voltage-gated ion channels (the channels are voltage-gated, not microtubule-gated!), they should control them indirectly - through control of the release ofneurotransmitters (synaptic exocytosis). Particular support for the suggestedinterpretation (for mind control of electric excitations via control of the exocy-tosis) is the observation that in time the monkeys can eliminate the parasiticmotion of their arms. This means that the electric excitation is there to becaptured by the electrodes, yet when the electric signal arrives at the termi-nal buttons of the pyramidal tract (axons that output the motor informationfrom the cortex to the α-motoneurons in the spinal cord), it does not releaseneuromediator.

13 Axonal processing of information

Hamero� is silent on the possibility for axo-axonal gap junction couplings with200 Hz activity that ensure axonal couplings and possibilities for induction ofaxonal spike in gap junction coupled silent axon with smaller diameter than

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the �ring one. Indeed in Orch OR all this is not relevant because axons arenot involved in conscious processes. Mentioning of 200 Hz gap junction activ-ity within Orch OR will be somehow contrasting with the 40 Hz gap junctionactivity proposed by Hamero�.

13.1 Remark

It seems unfair to have contraposition dendritic vs. axonal microtubules, den-dritic vs. axonal computation. We think that none of these extreme points ofview stressing on priority of only one type of neurites is acceptable. Indeed thereis undisputable evidence for axons to �integrate mind�, and for the split-brainstudies Roger Sperry took Nobel Prize in 1981. So both dendrites and axonsshould be involved in cognitive processes.

Another frustrating observation is the logical mess - in Orch OR the den-dritic microtubules are accounting solely for consciousness, while the axonalmicrotubules are not endorsed with the priviledge to be conscious. But whysuch unjustice - these are parts of a same neuron, and exclusion of axonal mi-crotubules from mind processes decreases the mind computational power? Onthe other hand glial cells are involved in conscious activity (in order to increasethe computational power of mind!), but they are completely di�erent cell typethat has the primary duty to ensure the trophic needs of neurons. Orch OR inits current form is a bad cell biology with nothing positive for the model exceptthe fact that is completely scandal.

14 Synaptic failures and neuromediator release

The probability for exocytosis at a CNS synapse varies in the range 0.15-0.30.The randomness/chaos from such a �lottery� is enormous number. For a smallneuron with only 1 000 synapses of which 30% �re and 70% are silent therandomness is 1 to 10263. This means that there are 10263 possibilities for thedecision which 300 synapses from the total 1000 will �re. If the exocytosis isnot subneuronally controlled then any of these 10263 possibilities will have equalchance to occur, and the chaos in the brain function seems to take disastrousdimensions. We also have stressed that Orch OR cannot resolve the problemwith synaptic failures because it insists on microtubule output at the axonalhillock, hence no e�ect on synaptic boutons.

14.1 Remark

One can repair the above problem with synaptic failures assuming that thepresynaptic cytoskeleton is performing quantum computation, as recently advo-cated by Georgiev, 2002c and reviewed in Georgiev et al. (2004), Georgiev andGlazebrook (2006a).

If one does not like the idea for presynaptic cytoskeleton controlling theexocytosis there remains the �ugly� classical possibility to assume a classical

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error correction code that enormously decreases the computational activity ofbrain. In such an �ugly scenario� not every synapse should be considered as a�bit� but a group of say 10 or 15 synapses will constitute a �bit�. In this case itwould be enough only one of those 10-15 synapses to �re in order for the wholebit to have value 1. This can be achieved if all these synapses end only on a singlepostsynaptic neuron and there is the requirement that the postsynaptic spines ofthose synapses be coupled with classical OR-gates. Such possibility is extremely�ugly� from biological perspective and seems to contradict the fact that dendriticspines perform all kind of computational gates including AND-gates, which arehardly to be implemented if this huge error correction code was operating. Theseclassical error correction codes seem to be in contradiction with the precisesubneuronal (molecular) control of individual sysnapses, that have their ownmemory through enzyme sequestration like CaMKII, local ribosome and mRNAclustering and local protein synthesis under active spines.

15 G-proteins and MAP-2 phosphorylation

One of the main conjectures by Woolf and Hamero� (2001) is that the dendriticmicrotubules input the information coming from extracortical neurons in theform of neuromediator pulses with the help of G-protein coupled cascades thata�ect the MAP-2 phosphorylation status. One of their estimates is that the timeneeded for such a process is 250-500 milliseconds and this should be comparableto each conscious step.

15.1 Remark

The G-protein e�ects are much slower (utilize greater timescales) than the directelectric depolarizations. While it means that the onset of the G-protein couplede�ects is delayed, it also means that the decay of the e�ect is protracted in time.Therefore once triggered such a G-protein cascade needs a longer time to beturned o�. The main principle is that the G-protein after its activation triggerssecond order and third order messengers in the form of kinases or phosphatasesthat amplify the signal in a form of chain reaction! Hereafter it will be di�cultfor the chain reaction to be turned o�. The electric excitations in contrast havefaster dynamics and can be dissipated (�turned o��) for shorter time.

In Orch OR seems that there is some problem with the interpretation of theclassical Pen�eld results that showed clearly that electric current itself is evokingconscious experience when applied to the brain cortex (Pen�eld, 1954a; 1954b;1955). Also it is not seen direct link between Orch OR and the applicationsof Pen�eld's discovery by Dobelle (2002) who implanted directly the electrodesconnected with bionic camera in order to recover the vision in blind humansubject after neurosurgery.

Although the Hamero�-Woolf's scheme is based on the dual action of neu-romediator, namely to activate both ion channels and G-protein coupled recep-tors, in the case of direct electric input to the cortex it is necessary explanation

15

how the electric current itself induces conscious experience. But if this pieceneeds to be integrated in the theory then it seems that Hamero�-Woolf's the-ory in its current form is incomplete because it ignores (does not explain) howthe electric currents (generated by ion channels when activated by neuromedi-ator) are inputted to microtubules. There is also additional problem with theHamero�-Tuszynski proposal for screening/isolation of microtubules against ex-ternal electric �elds (Hamero� and Tuszynski, 2003) because direct input willbe impossible.

16 Microtubule screening by the C-terminal tails

Hamero� and Tuszynski (2003) propose extremely bizarre screening of micro-tubules against external electric �elds by double Debye layers organized by theC-terminal tubulin tail (CTT) presence. The main idea is that CTTs �shield�the microtubule against external electric �elds. The suggestion however is basedon misapplication of Debye-Hückel theory of charge screening in electrolyte.

16.1 Remark

If microtubules are responsible for consciousness but are insensitive to the elec-tric excitations of neurons, then the Pen�eld's and Dobelle's experimental re-sults proving the role of electric processes as direct input resources of consciousexperience would be left outside the theory of quantum consciousness.

Second much more important result stems from the main mathematicalderivation of the Debye-Hückel theory itself. It is approximation in a modelin which is assumed Boltzmann distribution of ions in the solution and one ofthe critical steps is the electric neutrality of the electrolyte (see detailed exposi-tion in Georgiev and Glazebrook, 2006b). Since during electric excitations theion �ow across dendritic membrane is electrogenic, the electrolyte of the cytosolis no more electroneutral and the Debye-Hückel approximation might not bevalid, and it is not at all evident why microtubules should be insensitive forexternal electric �eld as generated by the electric excitations. Indeed the elec-trosensitivity of microtubules could be modelled exactly through the CTTs thatHamero� wrongly believes are responsible to shielding. If neuronal electric exci-tations are modelled within quantum �eld theory (QFT) as proposed by Jibu etal. (1994, 1996), Jibu and Yasue (1997), it can be shown that electromagneticsine-Gordon solitons could propagate within the neuronal cytosol (Abdalla etal., 2001), and these solitons could be coupled with conformational change inthe CTTs (Georgiev and Glazberook, 2006a).

17 Freud and subconsciousness

One of the main ingredients of Hamero�'s Orch OR is the emergence of con-scious processes out of subconscious ones. The quantum coherence leads tosubconsciousness, while the Orch OR event is a conscious occasion. Hamero�'s

16

attempt is to somehow inbuild in the Q-mind model the Freudian psychoanalysisand Freudian scheme for the structure of human psyche being Ego (conscious)+ Id (subconscious) + Superego (conscious).

17.1 Remark

Freudian psychoanalysis (Freud, 1899; 1901; 1905a; 1905b; 1913; 1914; 1920;1923; 1927) has been a subject of extensive critique, and it was shown thatpsychoanalysis hardly can be called a science; see Popper (1982) and the de-marcation criterion. There is nothing that is forbidden from occurrence inpsychoanalysis, and amazingly the analysis done by the psychoanalyst hardlycould be subject to any counter-argument or revision. Typical example couldbe if you do not agree with the conclusions of your psychoanalyst that you haveEdip's complex (�subconscious desire to make sex with your own mother�), yourargumentation will be taken as evidence that your �subconsciousness is resistingthe actual realization by you that you have this sexual complex�, and the psy-choanalyst will never assume that your denial maybe is evidence that his theoryis wrong. Freudian theory is thus immunized against any form of critique, be-cause it does not forbid anything, and could explain everything concerning thefunctioning of the human psyche.

There has been extensive biological work to show that �subconsciousness� isresult of extracortical neural substrates such as thalamus. Therefore the modernbiological approach is that �subconsciousness� is brain activity outside your con-sciousness, while your consciousness is solely result of your brain cortex activity(classical or quantum one). However in the modern neurobiological approachtowards psychoanalysis the term �subconsciousness� is already unnecessary, mis-leading, and �dangerous�. Simply this is not qualitatively di�erent state fromconsciousness. �Freudian subconsciousness� in modern terms is �extracorticalneuronal activity� therefore no qualitative transitions from subconscious to con-scious activities should take place in your cortex. The cortex is either conscious,or unconscious (e.g. during anesthesia), and extracortical neuronal impulses be-come conscious when they enter the cortex. Thus Freudian state transition fromsubconscious mind state into conscious mind state is no more necessary. Themind is always conscious (tautologically), and only the physical signal carrier ofinformation undergoes dynamics i.e. it is outside or within the mind.

Example of extracortical activity may be neuronal impulse entering fromthe periphery towards the spinal cord that will trigger sensation of pain whenit reaches the brain cortex. This entering pain impulse may be blocked withlocal anesthetic (spinal anesthesia) before it goes to the brain cortex. So spinalanesthesia acts by making all pain impulses remain outside the brain cortex -i.e. they are blocked somewhere on their way from the body to the brain cortex,and this block happens at the level of spinal cord neurons. You don't experiencethese pain impulses, but nevertheless they may a�ect the body functions.

Block of sensory impulses can be done higher in the sensory pathways atthe level of thalamic neurons, or the communiation of thalamic neurons withbrain cortex. For example radiatio optica is composed from axons of thalamic

17

neurons that enter the visual cortex. If they are cut, despite of the fact thatyour eyes �see� the visual image, and your thalamus as well �sees� the image, youare not consciously aware of that because your brain cortex i.e. visual cortexcannot input this visual information. But your thalamus is center for triggeringvarious vegetative responses, so the �thalamic seeing� could lead to extracorti-cal/unconscious triggering of vegetative responses or other re�exes like blinkingof the eyes (this is wrongly called �subconscious� in Freudian psychoanalysis).

Our conclusion is that there is no any need of accounting for �subconscious�processes in the (quantum) physical theory of mind. Any such process if being a�real� process and thus having e�ect on bodily functions, could have �extracorti-cal� neural modelling. So postulating a consciousness being at the fundamentallevel of Universe at the quantum level, does not need neither associated �fun-damental subconsciousness�, nor any threshold for consciousness to occur. Thisis consistent with the evolutionary approach suggested by prof. Chris C. King(1989, 1991, 1996, 1997, 2003a, 2003b, 2004) for the early prebiotic evolution ofmolecules in the primary ocean on Earth. In this scenario every molecule man-ifests a form of �free will� in quantum transactions in the primary ocean, andthe whole process of evolution of life, now can be seen as a growing complex-ity of conscious choices (panpsychism). Of course the quantum states of singlemolecules cannot be as rich as macroscopic quantum states realized in brain.So in a sense the experience is always there, but its complexity evolves withevolving life systems that could have harvested mechanisms to sustain macro-scopic quantum coherence entangling billions of protein molecules in the cellularcytoskeletons of millions neurons.

18 Emergent vs. fundamental experience

In Orch OR model there is bizarre mixture of �fundamental consciousness� that�emerges� at OR events. The whole approach is over-complicated for the sakeof satisfying some old and mainly non-scienti�c Freudian concepts.

18.1 Remark

We suggest a direct fundamental experience/consciousness manifested by quan-tum systems. Thus we think of the quantum events/collapses as �decisions� doneby the experiencing quantum system, not as �events producing consciousness�.In this new framework the OR event will be �decision making�, not �experiencecreating� event. If consciousness is irreducible phenomenon at the quantumlevel there is no need for it to �emerge� from �subconsciousness� which is apseudo-scienti�c Freudian concept.

19 Thalamo-cortical 40 Hz

Hamero�'s Orch OR is based on the idea that thalamocotical 40-80 Hz activityis somehow responsible for consciousness.

18

19.1 Remark

We agree that the β-EEG is a good indicator of consciousness, and that thecorrelation between β-EEG and consciousness is reliable enough to serve moni-toring function in controlling the depth of anesthesia, etc. However we do notsee why thalamus should be involved in conscious experience, nor why if expe-rience is a fundamental ingreadient of relaity should be created by any �form ofactivity�.

Indeed if quantum coherence is responsible for �conscious binding of ex-perience� then it does not matter whether the sensory stimulus is present inthalamus, or in cortex. The whole system manifests quantum wholeness andthe sensory stimulus should be already present in the conscious experience. Thiswas the fundamental preliminary argument raised by Georgiev (2002b) againstthe possibility for coherent sates in retina, that are simultaneously coherent withthe brain cortex, as responsible for vision. If this were the case, then the neuralimpulses will be useless to carry information to the cortex. Indeed already atthe very moment your retina has detected the photon, due to quantum coher-ence and conscious binding between the retina and the brain cortex you musthave experienced the visual information. Otherwise if there is no such quan-tum coherence between the retina and the brain cortex, there is no mechanismto account for coherent transfer of the state of the photon seen by the retina.All quantum teleportation schemes need both quantum and classical channel.Without quantum Einstein-Podolsky-Rosen channel (existent quantum coher-ence) there is no possibility for quantum teleportation of unknown quantumstate, such as the state of the incoming photon. And last, if you deny to usethe quantum coherence for binding of experience, then why to use a quantumapproach towards consciousness at �rst place.

If the quantum coherence is responsible for �binding of conscious experience�one can conclude similarly that thalamus is not involved in consciousness be-cause the sensory impulses must be realized already when they enter in thethalamus, and not later when they are delivered to the brain cortex. For ex-ample in the surgical severing of radiatio optica the brain cortex �sees nothing�,and you are not consciously aware of the visual information, but the thalamus is�seeing� the visual image. Therefore since cortico-thalamic connections/axonsare not severed, and you can imagine that other thalamic areas are not sev-ered - so they deliver sensory information to the brain cortex, there should bestill possible �binding� of the perceived by the thalamus information with theperceived by the cortex information, via the quantum coherence mechanism.

Solution of all these problems outlined above as imposed by facts from theclinical neurology, can be found only if one also believes the conclusion of clinicalneurology that only and solely the brain cortex is responsible for your conscious-ness (at least this is the main theory in European post-communist countries,and in Russia; Western science is most tolerable and has allowed for variousattempts to involve extracortical regions in conscious awareness, yet all this isself-controversial and we do not see any use of it). So if the brain cortex issolely responsible for consciousness and the quantum coherence is maintained

19

and shared only between brain cortical neurons, then there will be no prob-lems with the hypothesis that quantum coherence leads to �conscious bindingof various experiences�.

Remains to be explained the correlation between the 40 Hz thalamocorticalactivity (β-EEG) and consciousness. Well, the obvious thing is that sensoryinformation from the surrounding environment is delivered always through tha-lamus, except for olfaction. Therefore when consciousness is waken up it willneed sensory input from thalamus. To have consciousness only without anyexternal sensory information is useless because all normal activities are inter-esting, only when done in communication with the external world. But it ispossible to be conscious, and not to be interested in external sensory informa-tion. For example mediating tibetian budhists may try to isolate themselvesfrom the surrounding sensory input. In this case communication of conscious-ness residing within the brain cortex with thalamus is not necessary and slowerwaves are measured. So our explanation is somehow inverted. Consciousnessis the cause for β-EEG through interaction with thalamus in order to deliversensory information. The β-EEG is not responsible for consciousness but resultfrom the interaction of your consciousness with the environment. Our thesisis con�rmed by the fact that mediation or other conscious experiences mighthappen without β-EEG.

We conclude that 40 Hz as the needed objective time for a conscious step tooccur is wrong and useless prediction! All evidence is against. Also this openspossibility for consciousness to be 100 GHz phenomenon, as proved originally byGeorgiev (2003b). This is an amazing proof since Q-mind theory with 100 GHzquantum consciousness will not lead to psychophysiological paradoxes. Now theroad for Q-mind theories is open down to smaller time intervals needed for co-herence/ time until decoherence, and the original objections by Tegmark (1999)and others, for brain being �hot, wet and noisy�, are meaningless. The necessaryBose-Einstein condensation can be achieved for 10-15 ps that is the timescale ofprotein dynamics/catalysis solely by means of energy pumping (Georgiev andGlazebrook, 2006a).

20 The actin gel-sol cycles

The actin gel sol cylces in Orch OR serve the function to shield the coherentmicrotubules for 25 milliseconds.

20.1 Remark

The fact that NMDA receptor triggered actin dynamics (contraction, polymer-ization/depolymerization) is responsible for change in dendritic spine shape isobserved by special video-microscopic technique. This has great e�ect in synap-tic transmission, and the generated postsynaptic potentials. However we donot see any purpose this to be relevant to microtubule shielding. Actually thespine is �lled with sca�old protein cytoskeleton, and microtubules from di�erent

20

spines couple only indirectly by these sca�ols proteins. So actin �laments andother sca�old proteins may be quantum coherent link between microtubules ofneighboring neurons. Indeed there is no theoretical possibility for interaction ofmicrotubules between neighbouring neurons without any sca�old protein beingthe link between the microtubules. In Orch OR such �linkage� was supposed tooccur by gap junctions, but the ionic �ows through gap junctions lead to prob-lems with decoherence in Orch OR scheme. In recent work we were able to showthat the synaptic environment is beter for microtubule coupling between neigh-bouring neurons, plus there is ensured direct ouput on neuromediator release,thus solving the problem of control of the electric excitations, and the synapticfailure problem. See Georgiev (2002a), Georgiev et al. (2004), Georgiev andGlazebrook (2006a).

If the actin is �shield� then it cannot be used for mediating of coherence.However the evidence is that in muscle contraction actin uses quantum coherence(Hatori et al., 2001). Yet the mechanism in muscle contraction as well as themechanism in spine contraction is the same - just myosin/actin action.

Also the microtubule insensitivity to local electromagnetic �eld is bad forthe theory, and indeed after the revision of the dynamic timescale of conscious-ness being 10-15 ps, the proposed within Orch OR actin gel-sol cycling will beunnecessary to account for microtubule shielding.

21 Libet's �delayed experience�

Stuart Hamero� suggests that the described by Libet back-referral of time mustimply that consciousness uses quantum coherence - during the quantum coherentperiod indeed the future and past co-exist together and future events mighta�ect the outcome of past events.

21.1 Remark

As noted by Pockett (2002) it is always easier to read the conclusions of thearticles and to skip the boring reading of the technical part that describes theactual setup of the experiment. However if one struggles to understand theprinciples underlying the brain function then a careful study of the data isneeded. Here we brie�y summarize some of the most quoted results by Libetand point out obvious �aws in the interpretation of the experimental data.

As a grounding fact of most of the Libet's conclusions is taken the obser-vation that direct stimulation of the brain cortex with electric current elicitsconscious sensation only some time after the start of the electric current. It wasshown that the electric current I must have some threshold magnitude I0. IfI < I0 the electric current may be continued for a long time without elicitingany conscious sensation. If I = I0 the conscious sensation occurs approximately500 ms after the start of the electric stimulation, and if I > I0 the conscioussensation occurs faster than 500 ms in such a fashion that higher current elicitedconscious sensation faster. With the used higher intensities of the currents the

21

minimal period for duration of the current that elicited conscious report wasapproximately 200 ms. Libet interprets the I0 as �normal� stimulus and thensuggests that consciousness occurs with delay of 500 ms. There is nothing �nor-mal� however in opening the skull of a human and delivering electric impulsesto his brain with electrodes dipped in saline. Also Libet completely forgetsabout neuronal fascilitation - there is possibility for electric excitations to sumover time, so that subthreshold agitations �nally result in a spike. From such aperspective it is highly plausible that at the beggining of the electric train withI0 the subthreshold currents summated, so that only after 500 ms some rele-vant to induce conscious experience neuronal activity has been induced by theelectrode. There seems nothing to be explained here, as all this is well knownis modern neuroscience.

Based on misunderstanding of this �rst series of experimental data, Libet andcolleagues perform a second experiment that is maybe the most quoted in thescienti�c literature experiment. A patient is deliverred an electric stimulus withcurrent I0 for duration of 500 ms, while at the same time a suprathreshold skinstimulus on his hand is delivered 200 ms after the onset of the electric current I0

delivered to his somatosensory cortex. It was reported that the hand stimulusis experienced before the sensation that resulted from the electrode stimulation.Libet then concludes that this is surprizing because the skin stimulus wouldhave been experienced with delay of 500 ms that summed up with the 200 msdelay from the onset of the current I0 gives us delay of 700 ms. This predictionfails however Libet does not consider it as evidence that his pet hypothesis fordelay in consciousness of 500 ms is false, but ridiculously claims that a novelexplanation is needed (i.e. back-referral of time). Of course that taking intoaccount that there is no any such delay in consciousness, the skin signal willneed only about 80 ms to reach the brain cortex, so if the onset of the current I0

is labelled as t0 then it follows that the experience of the skin stimulus will beat time t0+ 280 ms, while the direct current delivered to the cortex will evokeconscious experience only after some fascilitation takes place at time t0+ 500ms. Our prediction does not fail, so there is no whatsoever reason to searchfor exotic explanations such as Libet's hypothesis based on misunderstandingof neurobiology.

Alas, as it often happens in science despite of the fact that Libet's work waspioneering (indeed it is irrelevant to our dicussion!) he became victim of his �pettheory�. It is not so rare in science that researchers prove experimentally theirexpectactions, or if the experimental data does not �t exactly their expectationsthey misinterpret it i.e. interpret it in �novel� (exotic) way, so that in the endthe expectations are con�rmed.

And last, a note should be added on the meaning of the term �back-referralof time�, that should be understood within the framework proposed of Libet- consciousness occurs with delay of 500 ms after the neural mechanism thatgenerate it, however the consciousness ��lls up the gap� by (illusory) assum-ing that it has triggered itself the neural mechanisms (thus consciousness isepiphenomenon here). Other possible interpretations of the term �back-referralof time� such as in Klein (2002) are not necessarily incompatible with our views,

22

but they have completely di�erent meaning from the one discussed here.Our conclusion is that quantum mind theories does not need to speci�cally

resort to Libet's experiments as something extraordinary.

22 Bierman's �presponse�

Stuart Hamero� provides Bierman's presponse as an experimental evidence forquantum mind theories and Orch OR.

22.1 Remark

The reported unconscious presponce by Bierman and Radin (1997, 1999) isindeed a mixture of bad statistical manipulation of experimental data plusmisunderstanding of neurophysiology. Brie�y described the experiment is asfollows: subjects are shown in a random fashion pictures divided into threegroups: (i) neutral pictures, (ii) fear-inducing pictures and (iii) photos withhighly pornographic content. The pictures were shown randomly to a subjectand the activity of various brain areas was monitored by fMRI. Then it wasshown that the neural arousal as detected by fMRI just before the appearanceof the highly pornographic pictures is higher than the nerural arousal beforethe other two sets of pictures. Biermann interprets this data as evidence forunconscious fortune-telling called �presponse�.

Indeed except for the fact that Bierman felt perverted pleasure to show inhis lecture slides �examples� of the pornographic pictures he had presented tohis test-subjects thus shocking the auditory, there is nothing else special to bediscussed. Severe statistical errors in the manipulation of the data were reportedindependently by Georgiev (2003f) and Jiri Wackermann (2002) pointing outthe possibility that the observed arousal before the pictures with pornographiccontent might be explained with the gambler fallacy e�ect. If this is accountedfor in the statistical analysis, the observed �presponse� will be washed out as anartefact of the bad mathematics used by Biermann.

Below we provide for illustration a nice story suggested by Wackermann(2002) and for full mathematical tackling of the problem we refer the curiousreader to Wackermann's paper also.

�Stephen feels a special a�ection for Phyllis: each Saturday evening he phonesher to invite her for a dinner. She is not much impressed by Stephen's person,but she does not want to injure his feelings, so she invented a convenient strat-egy. Whenever Stephen phones, she rolls fair dice to determine her response. Ifthe die shows �6�, she accepts the invitation; in case of any other outcome, from�1� through �5�, she �nds a socially acceptable excuse to decline.

Stephen also has his secret habits. On Friday he obtains his weekly pocketmoney from his father, a constant amount of $10. If Phyllis declines to go fora dinner, he saves the money in a shoe box for the next occasion. If she accepts

23

his invitation, he takes the cash from the box and expends all the money for thedinner with Phyllis.

Stephen's father is fairly scared about his son's unfortunate passion, and se-cretly keeps track of Stephen's cash reserves. On each Saturday the dad notesthe state of Stephen's deposit, and then he observes Stephen's going or not goingout. In this way, the father obtains a bi-variate data series which, for example,may look like this:

cash [$] 10 20 30 10 20 30 40 10 20 · · ·dinner no no yes no no no yes no yes · · ·

Having collected enough data points, he submits the data to a simple analysis:he calculates the average state of Stephen's funds separately across successful andfailed invitations, and �nds that the average money sum on accepted invitationswas signi�cantly higher than on rejected invitations! Stephen's father is facingan interpretation problem. Given that Steve did not tell Phyllis anything abouthis money saving habits, something de�nitely anomalous seems to be happening.Does Phyllis possess an fortune-telling ability? Was she perhaps scanning bytelepathy Stephen's dinners funds? Stephen's father has a moral problem, too.Should he tell his son what he has found, or not? And, if so, what is he goingto tell him?�

The example provided by Wackermann is crystally clear - di�erent prede-termined behaviors may lead to �pseudo-telepathy� artefacts. Noone will takeseriously in the above scenario that Phyllis can forsee the future. Yet, exactlysuch kind of statistical errors are reported uncritically by various researchers assupport to psi-phenomena.

23 �Shielding� in Orch OR

Hamero� suggests that the possible water lasing by superradiance in and aroundmicrotubules could have the function of a shield against environmental decoher-ence.

23.1 Remark

One of the important questions in the Q-mind models is to explain how neuronscan sustain long-ranged quantum coherence in their interiors. Jibu et al. (1994,1996) have suggested that water molecules manifest lasing e�ect known as su-perradiance. The dynamical timescale of this process however is 10−14 s, andmight be too fast in order to have some impact on much slower protein dynamicsthrough which all cellular functions are realized (timescale of 10−11 s). Jibu andYasue (1997) have shown that there is a possibility for �energy pumping� of thewater lasing process which will prolong the coherence time above the timescaleof thermal �uctuations (10−13 s). That is why Georgiev and Glazebrook (2006a)have further explored the possibility for �energy pumping� in which the water

24

lasing is attained for 10-15 ps. In this case travelling electromagnetic pulsesin the form of sine-Gordon solitons might a�ect the enzymatic function of theC-terminal tubulin tails of microtubules. The model describes the interactionbetween the electromagnetic �eld within neurons and the cytoskeleton that iswhy it is easily accomodating all the results found by Pen�eld, Dobelle, andothers, concerning the role of electric �elds and currents in eliciting consciousexperiences.

Gilmore and McKenzie (2005) have shown that any quantum coherent pro-cess taking part in a biomolecule will su�er a signi�cant decoherence from thesurrounding dipole disorder of the solvent molecules. That is why it seems im-possible to be realized a quantum theory of brain function without includingin the model coherent ordering of water molecules. In other words a quan-tum coherent process within a biomolecule cannot last for signi�cant biologicaltimescale if the biomolecule is coupled with equilibrium thermal bath.

However is there any rational argument that will force us to model the neu-ronal interior as electrolyte solution at thermodynamic equilibrium? Certainlynot only such argument does not exist, but it is quite the opposite - the neuronalinterior is a system far from equilibrium!

Biological systems are systems that evolve far from equilibrium. This iswell known in biophysics and indeed the continuous supply of metabolic energyis what keeps the organized neuronal interior. Yet, under such circumstancesFröchlich type of Bose-Einstein condensates could form. Laser functioning isa typical example of quantum coherent process realized at room temperature.Thus coupling of the microtubules or any other protein molecule residing withinthe neuronal interior with equilibrium thermal bath will be severe biological mis-modelling. Most physicists trying to �disprove� Q-mind, do exactly this viciouscircle reasoning - they couple the quantum system of interest with an equilib-rium thermal bath, and prove what they want to prove (i.e. Q-mind is notfeasible in vivo?!). Yet, properly pointing out that the neuronal interior is asystem far from equilibrium, should invalidate all kind of such �awed critiques.So far, biophysical modelling for neuronal cytosol as system far from equilib-rium suggests that Fröhlich type of Bose-Einstein condensation occurs for 10-15picoseconds, a timescale that is su�cient to account for long-range quantumcorrelations between the enzymatic function of neuronal proteins (Georgiev andGlazebrook, 2006a).

Therefore in the current Orch OR model Hamero� wrongly suggests thatthere is an equilibrium thermal bath near the microtubule, so that the micro-tubule needs to be shielded. Indeed this is a severe mismodelling also. Onceaccepting the �awed argument that (i) the neuronal interior is �thermal bath�then one should start to invent (ii) various additional mismodels in order tocounteract the wrong supposition (i). Our conclusion is that Q-mind modelscannot be properly developped if one does not clarify and resolve this confusion.The supply of metabolic energy makes the neuronal interior a system far fromequilibrium and further no shielding mechanisms are needed. What one needs isa proper understanding of the quantum behaviour of systems far from equilib-rium, and this should be done with advanced mathematics, not by philosphical

25

arguments. A pioneering work in that direction was done already by Fröhlich(1968, 1975, 1984, 1986).

24 Where act the anesthetics?

Hamero� suggests that the main action of volatile anesthetics (as well as anes-thetic gases) is to cause unconsciousness via binding to the hydrophobic pocketsof tubulins. Also Hamero� argues that volatile anesthetics are the most perfectagents to produce unconsciousness that we currently have.

24.1 Remark

The model suggested by Hamero� is certainly interesting, however it is toosimplistic to be used as a general approach towards anesthesia. In the followingwe will raise two particular issues that need to be considered.

The volatile anesthetics have numerous molecular targets: the core SNAREcomplex, two pore domain potassium channels, calcium and sodium voltagegated ion channels, gap junction hexamers, GABAA receptors, etc. Therefore itis arguable that microtubules are the primary target that leads to unconscious-ness. In this way it is experimentally impossible to �nd out the primary targetof volatile anesthetics without comparisson with the e�ects of other more selec-tive drugs that have less number of molecular targets. Here is where the role ofintravenous anesthetics should be considered i.e. almost all known intravenousanesthetics realize their anesthetic action through activation of GABAA recep-tors (with the exception of NMDA receptor agents such as ketamine that lead to�dissociative anesthesia� - a condition manifested with hallucinations, amnesia,and unpleasant post-anesthetic recovery, hence not deserving to be correctlytermed �anesthesia�). Thus, it seems that the key towards understanding anes-thetic action must involve the GABAergic neuromediation as one of the majormechanisms for producing unconsciousness.

The second issue we would like to stress upon, is the fact that volatile anes-thetics are far from being the perfect anesthetics as argued by Hamero�. Indeedthe induction is anesthesia is slow (currently intravenous induction is preferred),the e�ect within brain is diverse (multiple molecular targets as listed above),and as a consequence the recovery from anesthesia is delayed and associatedwith unpleasant experiences. Vomitting, nausea, and disorientation are oftenseen in the early post-anesthetic period, even after perfectly performed volatileanesthetic anesthesia. All this is avoided with the usage of intravenous anesthe-sia, and a particularly close to perfect anesthetic agent is propofol (except thatit is relatively expensive). Propofol should be the primary choice in all caseswhere there is no contraindications for its usage (such as accompanying heartdisease, newborn child, etc.), yet, the range of applicability of propofol is grow-ing and if the anesthetist is experienced propofol could be used even in caseswhere the contraindication is relative. Compared to volatile anesthetics, thetime needed for propofol induction in anesthesia is rapid (roughly equal to the

26

circulation time from the place of injection to brain), and the recovery is alsorapid (in most cases associated with pleasant experiences, possibly mediatedby dopamine receptors). It seems that GABAergic mechanism is very close tothe physiologic mechanism generating unconsciousness during sleep, hence us-age of selective GABAAagents predictably leads to better anesthesia comparedto volatile anesthetic anesthesia (agents with diverse molecular targets one ofwhich is the GABAAreceptor). Despite of the fact that our notes are sketchy,the key argument is that hardly one could point out solely the microtubule asthe main target for producing unconsciousness.

Outlook

As stated in the beginning of this paper the purpose of the current work is tooutline a research programme that will put the Q-mind theory on stable scienti�cgrounds. Unfortunately at the present time a lot of pseudo-scienti�c concepts arepatronized under the name �quantum mind� and this has negative e�ect on thedevelopment of the very idea of �quantum e�ects in brain as explanation of somefeatures of consciousness such as nonlocality and noncomputable evolution�.

References

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[2] Bierman DJ, Radin DI. 1997. Anomalous anticipatory response on random-ized future conditions. Perceptual and Motor Skills 84: 689-690.

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