Computerized Physiologic Blind Spot Mapping
The Next Generation . . .
Free *Bonus Blind Spot Mapping System - (See "Free Blind Spot" Box Right Below)
The Hariett Hall Syndrome



Deception, Fraud and Misrepresentation:


The Harriet Hall Syndrome


By: Frederick Carrick, DC, PhD


I have just read the article “Blind spots, Brain Maps, and Backaches: A New Chiropractic Delusion” by Harriet A. Hall, published in the November/December 2004 issue of the SKEPTICAL INQUIRER.  The article might have been more appropriately titled “Deception, Fraud and Misrepresentation: The Harriet Hall Syndrome”. Hall’s article would have the reader believe that she had spoken to me about my research or that she had actually discussed it with me. In fact she never desired to discuss my work at all.


Since the airing of the PBS Television documentary about my work “Waking up the Brain: Amazing Adjustments” in 2000, I have I received hundreds of emails per week, some from professionals and other interested individuals.  I attempt to answer as many inquiries as I can but time constraints prohibit a 100% response. The PBS documentary film featured my approach to the treatment of a variety of neurological disorders after other methods of treatment had failed.  PBS interviewed patients from around the country and featured them in a very passionate emission that created a great deal of interest and inquiry.


Harriett Hall sent me a series of emails regarding my research. I suggested that she contact me by telephone (I have a toll free number) so that I might respond to any question she might have.  She refused!  Hall’s emails were compilations of bizarre thoughts culminating with insulting notes from both her and a magician friend, James Randi.  The correspondence was so bizarre, rude and offensive that I refused to be insulted or coerced by the inquiry and forwarded it to the legal council for the American Chiropractic Association for review.


For individuals who have read Harriett Hall’s article, it should soon be obvious that it was not a typical or rational response to science, but rather a very caustic attempt to distort my work personally and also to tarnish the credibility of an entire profession by inference.  My response to her article is not written for Harriett Hall but hopefully for those inquiring minds that are seeking truth and are inquisitive enough to be objective.


Hall begins and ends her article with a trip down the rabbit hole.  Quite appropriately, The "Alice in Wonderland syndrome” includes an array of symptoms which can be confused with psychosis or drug intoxication (1).  When reviewing the intentional misrepresentations that Hall makes throughout her article it is not so difficult to envision her in the rabbit hole, quite confused and perhaps psychotic.  Whatever Ms. Hall’ agenda, the reader will soon discern between fact and delusion.


As difficult as it is, I will overlook the fact that she attempts to link my work with some unidentified advertisement by a chiropractor and another website ( unrelated to my work or person but designed to cast aspersions on my integrity.  She starts her article with blatant misrepresentation of my research.  Hall states, “It demonstrated that chiropractic manipulation of the proper side of the neck could shrink the enlarged blind spot; if you manipulated the wrong side, nothing happened. “  Hall is hoping that no one will take time to read the research that demonstrated that Manipulation of the neck on one side was associated with a decrease in the blind spot whereas manipulation of the neck on the other side was associated with an increase of the blind spot.  Both of these findings were found to be of strong statistical significance (p<.001) (2). 


Why would Hall misrepresent?  Why would she state something that is not true?  Any interested person can do a Medline search of the indexed literature and read the abstracts of my paper (Changes in Brain Function after Manipulation of the Cervical Spine, Journal of Manipulative and Physiological Therapeutics, Volume 20, Number 8, October 1997) that state things completely opposite to Hall’s representation. Is she incapable of reading a scientific paper?  Hall’s motive in her purposeful deception appears to be an attempt to bash chiropractors, plain and simple, rather than an intellectual critique of my article. Her article starts with a fabricated distortion of my work.   This response is to provide the reader with an exposé of a host of more purposeful misrepresentations to be found and one does not have to take a trip down a rabbit hole to find them.


Hall suggests that she “could not get this PhD scientist to admit that reproducibility did not equate with validity”.  

Nonsense: first of all and to clarify a significant point, I did not discuss this subject with her.  If she would have taken up my offer to talk to her she might have understood a little more about validity and reproducibility in medicine.  Validity refers to measuring something that we intend to measure accurately.  Content validity is measuring everything we intend to measure. As far as construct validity, it is established when one test has a meaningful relationship with the concept of why you are testing in the first place (based on some theory or construct that the test is supposed to measure a competency or competencies.)  Reliability comes into play when over a period of several occurrences, your measurement device replicates itself consistently (3). 


Let us take a further look at Hall’s twisted representation of reality.  She states that “Ophthalmologists use sophisticated equipment; Carrick’s test uses a paper and pencil” I am very experienced in the utilization of a variety of perimetry systems, particularly the Haag-Streit Octopus and the Humphrey systems.  These are the gold standards in automated computerized perimetry alluded to by Hall as being sophisticated.  Of all of the equipment in our laboratories, the perimetry system is the least expensive, with a new Haag-Streit Octopus 301 selling for approximately $12,000.  The majority of the electrodiagnostic equipment utilized in our laboratory is considerably more expensive.


What Hall does not say is that the “sophisticated equipment” is merely an automated methodology of doing what manual perimetry (used in this research) does.  Manual perimetry has always been the gold standard and the validation of automated computerized systems is subject to reproducibility of what we can find with good quality manual perimetry.  We have the equipment Hall talks about but preferred to use the manual methods for a variety of reasons.  Had she asked I would have been glad to tell her.  Had she been experienced in this area there would be no need to inquire.


When using the automated systems it takes significant technician time when compared to the manual perimetry measurements.   Patients get bored with the automated tests whereas they tolerate the manual perimetry of the blind spot well.  In the study quoted by Hall, we were interested only in the blind spot and not in the entire visual field.  The accuracy of manual perimetry, its reproducibility and the fact that it is the gold standard to which automated perimetry is compared contributed to the rationale for using the test and for validating its use in this experiment.   This research used multi-blinded examiners such that subjects had repeated testing of the blind spots.  Our choice was one based upon accuracy of the instrument, patient comfort and reliability of the outcomes.


The statistical analysis of our data confirmed the validity of the test, even though such tests have been validated for centuries.  In other words, we have done nothing new here as Hall suggests.  Perimetry is the systematic measurement of visual field function (the total area where objects can be seen in the peripheral vision while the eye is focused on a central point). The two most commonly used types of perimetry are Goldmann kinetic perimetry and threshold static automated perimetry. A visual field test (perimetry) will detect loss of peripheral vision and provide a map of that loss which will be helpful in diagnosing the cause of the loss. Highly trained blinded perimetrists were utilized in all portions of this study.  They were qualified to employ manual techniques and computer-driven automated techniques (Humphrey and Octopus perimetry).  Manual perimetry has been used since 1855 when Von Graefe built on the work of Helmholtz and introduced it into clinical medicine (4).


Hall would have the reader believe that my study is the only study which links manipulation to visual system changes when she states: “I later found out this one article was the only thing in print on the subject”.  What irresponsible reporting. Hall perhaps thought  and possibly even hoped that her readership might not be sophisticated enough to uncover her distortion of truth.  Did she think that readers would not be aware of medical literature that states things quite different than her?  The limited references at the end of her article would clearly demonstrate Hall’s lack of ability to search the literature and recognize the vast array of information on this topic literally exploding in the referenced journals.  Ocular symptoms in cervical (neck) osteochondrosis has been discussed in the literature (5) as has the treatment of the loss of vision caused by cervical spondylosis utilizing combined traditional Chinese and western medicine approaches (6). Changes in the organ of vision has been described in cervical osteochondrosis (7)  and the identification of cervical visual disturbances and its manipulative treatment is appreciated (8).


Improvement in vision with spinal manipulation was first observed in the early 1970s and reports of the phenomenon appeared in the 1980s in the popular press and at scientific meetings, but it was not until the mid-1990s that general discussion of the potential value of this knowledge occurred(9).  Gorman demonstrated the value of quantitative static perimetry in the research and practice of spinal manipulation, by reference to the recovery of uniocular loss of vision (10).  He further discussed a case of a patient who demonstrated that spinal injuries may cause both cortical and ocular visual loss that was ameliorated by manipulative care (11).


Improvement in optic nerve function before and after spinal manipulation has been demonstrated by computerized static perimetry (12), the same sophisticated instrumentation that Hall alludes to.   The use of computerized static perimetry to measure the cerebral effects of spinal manipulation has increased our knowledge of how chiropractic works (13).  In fact, Chiropractors have been encouraged to test patients by wall perimetry with examination of the visual fields using kinetic or static perimetry techniques before spinal manipulation therapy (14) and not by me.


The recovery of constricted fields of vision with spinal manipulation has now been discussed with greater frequency in the literature (15). Detection of patients with visual field loss is to be expected if the practitioner examines the patient’s visual fields (6).  Our study revealed this conclusively, although it was not our original observation as suggested by Hall.


Changes in visual function immediately related to spinal manipulation indicates that spinal manipulation may have an effect on brain function (16).  Stephens and Gorman used computerized static perimetry changes (the “sophisticated tests” alluded to by Hall) to measure the cerebral effects of spinal manipulation which they observed to result in a measurable rise in visual sensitivity (17). They recommended the use of computerized static perimetry changes to measure the cerebral effects of spinal manipulation. 


The recovery of optic nerve function after chiropractic spinal manipulation adds to previous accounts of progressive and expeditious recovery of optic nerve function in association with spinal manipulation therapy (18).  Even a patient with severely reduced visual fields arising from terminal glaucomatous retinal damage has been treated successfully by spinal manipulation after failure of all other medical modes of treatment (19).  There is also a developmental association of cervical spine, heart and eye abnormalities (20). 


Hall suggests that she knows what the blind spot is.  She states that the “blind spots are approximately equal in size because the optic nerves are equal in size”.  Well, what is it, approximately equal or equal?  Approximately equal, means that they are different, and in fact, they are.  Does Hall think that the most minimally discerning reader will believe her proposition that the optic nerves on both sides of the body are exactly equal in size when virtually all other structures are not exact mirror images of each other? In my extensive experience involving dissection of the human brain, never have I seen one with the left and right sides being equal.  The same is true for optic nerves that are different in size from right to left.


The size of the right blind spot is different from the size of the left blind spot when measured with the Octopus instrument (Hall’s “Sophisticated Instrumentation”) (21). Lest'ak established the size of the blind spot for the right visual field to be 14.6 degrees +/- 0.86 up to 18.6 degrees +/- 1.5 laterally from the place of fixation and 1.4 degrees +/- 2.2 up to 4.9 degrees +/- 3.5 under the horizontal line.  The established size for the left visual field was 13.2 degrees +/- 1.5 up to 16.1 degrees +/- 2.5 laterally from the place of fixation and 2 degrees +/- 3 up to 4.9 degrees +/- 3 under horizontal line.


The prominent nasal part of the optic disc appears less 'blind' than the shallow temporal part, probably because of more intensive light scattering by the prominent nasal part of the disc (22).  Changes in the size of a mapped blind spot after any type of treatment (manipulation included) would be due to either a change in the anatomical size of the optic disc or a change in the brain representation of it.  Since manipulation in our study did not do anything to the size of the optic disc it would be illogical to promote an argument that it did.  The brain representation of the blind spot is well known and understood by today’s brain scientists.  It is more appropriate to suggest that the changes in the size of the blind spot are due to changes in brain function than a change in anatomical dimensions (which do not change with manipulation).


The effects of spinal manual therapy (SMT) results in a combination of findings supporting the proposal that SMT may, at least initially, exert part of its influence via activation of structures in the mesencephalon (top of the brainstem associated with vision) (23).  The feedback effect on the cervical spine is also recognized in visual disorders and especially when vision is decreased such as in darkness (24).  Although there is no retinal input within the blind spot, it is filled with the same visual attributes as its surround. Earlier studies have shown that neural responses are evoked at the retinotopic (eye) representation of the blind spot in the primary visual cortex (V1-brain) when perceptual filling-in of a surface or completion of a bar occurs. (25).


Locations of the visual field have highest interpoint correlation with neighboring points and with distant points in areas corresponding to the distribution of the retinal nerve fiber layer. The quantification of interpoint correlations may be useful in the design and interpretation of visual field tests in patients with glaucoma (26).  Neurons in the V1 (primary visual cortex-brain) region representing the blind spot encode information essential for perceptual filling-in at the blind spot (27).  Although no visual inputs arise from the blind spot, the same visual attribute there as in the visual field surrounding the blind spot is perceived because of this remarkable perceptual filling-in a hole corresponding to the blind spot is not perceived, even when one eye is closed (28) due to brain function.


Now let us revisit Hall’s “Sophisticated Equipment”.  We work with this equipment every day and are very experienced in when, why and how to use it.  In our experiment there was no need to utilize it as manual perimetry was considered to be better for what we wished to measure (blind spots and not whole visual fields).  This “Sophisticated Equipment” is not without its own faults.  For instance, subjects can imitate enlarged blind spots with automated, computed perimetry (29).  Conventional automated perimeters usually work with a given set of grids and thus are normally not adapted to individual conditions. This fact restricts efficiency of this method not only for any single examination but also for follow-up studies (30).


Hall asserts, “Carrick did not seem to notice that he had found something no other observer had ever found”.  While it would be pleasant to imagine that I was the first to observe what countless others have, I cannot accept the credit here.  Quite simply, Hall purposefully distorts reality.   While increases in the sizes of blind spots are well known in certain pathological cases (described and ruled out by examination in our study) an increased in blind spot size is also recognized without pathology. For example, enlargement of the blind spot occurred in some subjects when central visual fields were investigated by automated static perimetry (“Sophisticated Equipment” using programs 30-2 and 30-1 of the Humphrey Field Analyzer), in a group of healthy myopic individuals (31).


An enlargement of the blind spot can occur with widespread visual field loss which is not explained by fundus changes (32).  This asymmetry can be explained by nasotemporal asymmetries that have been described in anatomical studies of the visual system in primates and humans. In part, the representation of the monocular crescent of the temporal hemifield of either eye, which exists only in the crossed projection, may explain this. In addition, within the binocular field, there is a biased crossed projection of nasal retinal ganglion cells that drive the contralateral ocular dominance columns in V1 (brain).   Again we come back to a brain based explanation that Hall is incapable of understanding.  Worse than her inabilities to embrace current medical literature, she distorts that which she reads to make it “fit” into the storyline of her time spent in Wonderland.


Asymmetric activation patterns occur in the visual cortices (brains) of normal humans with the contralateral hemisphere activated more strongly and to a greater spatial extent than the ipsilateral hemisphere when either eye is stimulated and the blind spot representation in the ipsilateral visual cortex may contribute to the observed asymmetries (33).  The paired cortical representations of the monocular blind spot can be demonstrated by functional MRI in the primary cortical visual area V1 (34).  Those of us that are involved in brain research realize that the blind spot is perceived in the brain and we utilize a variety of techniques to visualize it. 


The cortical region V1 corresponding to the blind spot greatly prefers stimulation of the ipsilateral eye to that of the blind-spot eye with a monocular blind-spot representation activated when ipsilateral stimulation becomes perceptually dominant and suppressed when the blind-spot grating stimulation becomes dominant (35).  The human natural blind spot is usually filled in based on contextual information such that when two sufficiently different images are presented to the two eyes, observers typically perceive an alternation between the two images suggesting that the filled information in the area of the blind spot does contribute to the rivalry process (36).  The visual blind spot is treated by early perceptual processing as a region of reduced or absent information such that many perceptual effects observed in blind spot completion are similar in detail to the amodally perceived completion of partly occluded objects viewed somewhat peripherally (37).


The brain does not objectively reflect outer reality, but rather what is necessary in order to survive and adapt to the environment such that the eye's blind spot reflects the brain's capacity to invent information producing occurrences which in reality have never happened, in such a way that, for the brain, convenient reality and objective reality are two very different things (38).  Measurement of the blind spot may depict objective measurements dependant upon the convenient reality of brain perception.  The sizes of the blind spot are expected to be different when measured and subjected to mathematical analysis.  Hall confuses the blind spot size with the size of the optic disc and even these do not have a probability of having exactly the same quantity of nerve fibers contributing to the bundle making up the optic nerve.  Dichoptic lateral interactions occur in the region of the visual field of one eye that corresponds to the physiological blind spot in the other eye.  The presence of these dichoptic interactions in a region lacking direct retinal afferents from one eye is consistent with the proposition that long-range horizontal connections of the primary visual cortex mediate these interactions (39).


Let us look at a statement from Hall’s wonderland parade.  “If current medical science is right, nothing in the neck should have any effect on the size of the optic nerve where it enters the retina”.  That is precisely what we stated in our paper.  Since the blind spot changes in size and neck manipulation does not have a probability of affecting the size of the optic disc, the changes are most probably explained by brain functional perception.  The size of the blind spot is a component of a greater or lesser filling in effect.  Hall purposefully introduces a concept from my paper in a fashion that would suggest that it is not our concept.  This type of purposeful deception by Hall continues throughout her article and clearly demonstrates an agenda which conflicts with the basis of scientific investigation.


Hall continues to attempt to mislead the reader.  She states “Never mind the fact that medical science has never found any anatomical connections that would allow for that (neck manipulation and brain functional changes), or any rationale that would explain it.”  Hall suggests that her lack of knowledge of medical science is representative of the totality of that which comprises such science.  Such statements are patently absurd and represent purposeful misrepresentation.  Input from spinal anatomy and the neurological pathways affecting brain function are well represented in the medical literature. 


Spinothalamic (major pathway from spinal cord to thalamus) input is directed mostly to the ventral posterior complex of the thalamus and cells just caudal to it. In addition, the patches of spinothalamic terminations intermingle and partly overlap with the cerebellothalamic (pathways from the cerebellum to the thalamus) pathways. (40).  The thalamus is the major sensory integration area in the brain and receives information not only from spinal segments but from areas associated with vision and hearing as well. 


The thalamus receives a distinct set of spinal projections principally from the cervical (neck) level (41).  Intrathalamic neuronal activity is responsible for brain activation of a variety of sensory modalities including vision and hearing as well as the somesthetic sensations.  I proposed that since the manipulations resulted in changes in the size of the perceived blind spot (yes, bigger and smaller) without changes to the size of the optic disc that it was probable that the mechanism was due to thalamic integration.


Serial activation of the human spinocerebellum (area of the cerebellum associated with spinal function) following peripheral nerve stimulation suggests that that muscle afferent inputs are the source of cerebellar activation (42).  It is obvious that manipulation of the neck involves some distortion of the length of muscles with changes in the receptor potential of these receptors and resulting cerebellar and thus brain activation.  The adult motor cortex adapts following cervical spinal cord injury. The nature of the adaptation and the underlying biological mechanisms responsible for this change illustrate the relationship between spinal anatomy and brain function (43).


The acceleration forces infringing the cervical spine (neck) in whiplash injury are frequently associated with multiple cerebral (brain) symptoms.   A brain single-photon emission computed tomography (SPECT) study can demonstrates perfusion abnormalities in patients with chronic whiplash syndrome and the combination of these studies with neurocognitive and neurobehavioral tests may be useful in identifying a subgroup of patients having organic brain lesions (44).  The general public is well aware that doctors of chiropractic are commonly consulted in cases of whiplash.  Ipsilaterally blurred vision is a commonly accompanying phenomena to cervicogenic headache and can be precipitated in all patients by head movements or by pressure at specific points in the neck (45).


The peak latency of the earliest cortical negativity (N1) (brain activation associated with the first negative wave) was found to be the most consistent and easily measured parameter of cortical evoked potentials in healthy individuals following stimulation of peripheral nerves providing reference values for neurophysiological evaluation of patients with cervical spine disorders (46).


In the upper cervical spinal segments, neurons in the medial part of lamina VI give rise to uncrossed spinocerebellar axons, whereas the central cervical nucleus (CCN) and neurons in laminae VII and VIII give rise to crossed spinocerebellar axons suggesting that the medial lamina VI group and the CCN in the upper cervical segments project to the different areas of the cerebellar nuclei and are concerned with different functions (47).  In any event, the human cerebellum is bombarded by information from segments in the upper neck.  These segments are the same as those that were manipulated in my study.


The internal representation of space involves the integration of different sensory inputs-visual, somatosensory/proprioceptive, vestibular-yielding reference frames which are not based on individual peripheral sensory codes, being organized instead in ego-centered and object- or environment-centered coordinates (48).  Somatosensory/proprioceptive refers to the information from body parts and joints.  The neck has the richest supply of such receptors.


The visual cortex is used to study structural and functional plasticity regulated by experience with thalamic projections to the visual cortex, and neuronal connectivity in the visual cortex itself (49).  When we refer to functional plasticity we are talking about the changes that occur in brain function as a consequence of a variety of events.  The relationship between the thalamus and the visual cortex are well known and discussed in my article.  As well as our studies involving human kind there is much evidence in animal studies.  For example, neurons in the main cuneate nucleus MCN of the rat project directly to the cerebellum and transmit predominantly dynamic information from joint and cutaneous receptors that are likely to be normally activated as a result of limb movements (50).


The visual map in the mind needs to be co-located with reality and is primarily plotted by the posterior parietal lobes, which interact with the frontal lobes to choose the object of interest. Neck and extraocular muscle proprioceptors are probably responsible for maintaining this co-location when the head and eyes move with respect to the body, and synchronous input from both eyes is needed for correct localisation of moving targets. Recognition of what is being looked at is brought about by comparing the visual input with the "image libraries" in the temporal lobes. Once an object is recognized, its choice is mediated by parietal and frontal lobe tissue. The parietal lobes determine the visual coordinates and plan the visually guided movement of the limbs to pick it up, and the frontal lobes participate in making the choice. The connection between the occipital lobes and the parietal lobes is known as the dorsal stream, and the connection between the occipital lobes and the temporal lobes, comprises the ventral stream. Both disorders of neck and extraocular muscle proprioception, and disorders leading to asynchronous input along the two optic nerves are peripheral causes of impaired visually guided movement, while bilateral damage to the parietal lobes can result in central impairment of visually guided movement, or optic ataxia. Damage to the temporal lobes can result in impaired recognition, problems with route finding and poor visual memory. Spontaneous activity in the temporal lobes can result in formed visual hallucinations, in patients with impaired central visual function, particularly the elderly. Deficits in cognitive visual function can occur in different combinations in both children and adults (51).


Hall talks about her blind grandfather who threw a basketball through a hoop.  When asked to do it again she relates that he replied, “Nope, I don’t want to break a perfect record.  Well this grandfather popped 2,000 baskets in a row in this research that involved test and retest all under strict blinded controlled study parameters.  The only benefit the reader has from Hall’s grandfather’s predicament is the knowledge that this gentleman was blessed to be unable to read his Granddaughter’s distortion of what I reported. 


Now let us address the million dollar prize from the James Randi Educational Foundation.  James Randi has an international reputation as a magician and escape artist, He is very entertaining, and I have seen him and enjoyed his performance.  His Foundation offers a one-million-dollar prize to anyone who can show, under proper observing conditions, evidence of any paranormal, supernatural, or occult power or event.  I do not consider my work in the field of brain function to be associated with the paranormal, supernatural or occult powers.  In fact, I take exception at any suggestion that it could be related.  I looked at the Amazing Randi’s Foundation site.  I am not interested in attending that party.  I forwarded his “invitation” to the legal council of the American Chiropractic Association.  It was perhaps the most insulting thing that I have ever read and I do not desire to do anything with this man or his foundation.


Hall suggests, “unexpected results must be always confirmed in another lab”.  That is a fundamental premise of scientific investigation and as a scientific investigator I agree with that premise. Furthermore the quality of papers published in the indexed medical literature demands and promotes just that approach.  Any accredited institution might have their Institutional Review Board entertain a proposal to replicate my experiments in an independent fashion.  I suggested this to both Harriet Hall and Mr. Randi.  While they were not interested in research done in accredited institutions under the direction of an appropriate Institutional Review Board, others were.  In fact, investigators in England conducted research in accordance with the University of Surrey’s ethics procedures. N. Daubeny replicated my study as part of a Master of Science Thesis.


The search for truth and its unbiased reporting are the ultimate goals of conducting scientific research. The intentional misrepresentation of data, such as in Hall’s article, is a form of fraud or deception. Accuracy and authenticity in data reporting are first and foremost a matter of individual integrity, and are crucial to the preservation of academic credibility, the protection of future patients, and the public's trust in the medical research enterprise (52).


Fraud is defined as an intentional deception or misrepresentation that the individual or entity makes knowing that the misrepresentation could result in some unauthorized benefit to the individual, the entity, or some other party (53).  Hall is a chiropractic basher who has intentionally misrepresented an article published in the indexed literature.  She misstates the conclusions of the paper and falsely links a variety of bizarre unrelated situations to enhance her position and to mislead the public.


Deception is the deliberate misrepresentation of facts through words or actions in order to make a person believe that which is not true. The forms deception can take include explicit lying, deception by implication, and deception by omission of information that people need to make decisions in their own regard (54).  In numerous incidences, the news coverage of medical research has incited unjustified optimism or fear. The medical literature provides an archive of the scientific community's condemnation of these misleading reports, but little is known about how they are judged by newsmakers (55).  In order to prevent false expectations, submissions to the press such as Hall’s ought to be based on firm evidence and as is usual with publications in professional journals, editors of the press should scrutinize the claims made by authors, and, in addition, the general public should be educated on the diagnostic process and the assessment of treatment efficacy (56).


Important asymmetries between self-perception and social perception arise from the simple fact that other people's actions, judgments, and priorities sometimes differ from one's own. This leads people not only to make more dispositional inferences about others than about themselves but also to see others as more susceptible to a host of cognitive and motivational biases.  Certainly Hall’s biases serve self-enhancement motives, exacerbated furthermore, by her tendency to attach greater credence to her own introspections about potential influences on judgment and behavior than she attaches to similar introspections by others.  Evidence, new and old, of this asymmetry and its underlying causes in relation to other psychological phenomena and to interpersonal and intergroup conflict have been thoroughly studied (57).


Hall tends to believe that her own judgments are less prone to bias than those of others, in part because she tends to rely on introspection for evidence of bias in herself but on her lay theories in assessing bias in others. Hall tends to believe that her own personal connection to a given issue is a source of accuracy and enlightenment but that such personal connections in the case of others who hold different views are a source of bias (58).


It is a critically important distinction to note that my 1997 article did not suggest nor allude to a clinical application of my findings, to do so would have been counter to any scientific interpretation.  My paper is published in the indexed scientific literature in a quality peer reviewed journal.  The publication of a scientific paper in a quality journal provides society with an opportunity to respond to and comment on the strengths and weaknesses of the paper.  While there are always strengths and weaknesses in scientific reporting, it is by this mechanism that our knowledge can increase.  Hall’s comments involve purposeful manipulation of my findings which does nothing to contribute to science. 


My intent in this response is not to refute or rebut Harriett Hall, but rather to enable those who seek unbiased scientific investigation to have the opportunity to have references and the advantage of my thoughts without distortion.  It is unfortunate that this discussion could not have taken place in a scientific forum with proper protcols and honorable intention to advance science and knowledge rather than to advance a personal or organizational agenda.


The Alice in Wonderland syndrome (AIWS), as described by Todd in 1955, denotes a variety of self-experienced disturbances which may co-occur with depersonalization, derealization and visual illusions. (59).   There are many of us in science that do not want to play with rabbits or entertain million dollar prizes from magicians.  Harriet Hall may be living in Alice’s world or a world of Deception, Fraud and Misrepresentation.  She should be ashamed, for herself and the community she has humiliated.




1.         Cau C. [The Alice in Wonderland syndrome]. Minerva Med 1999;90(10):397-401.

2.         Carrick FR. Changes in brain function after manipulation of the cervical spine. J Manipulative Physiol Ther 1997;20(8):529-45.

3.         Braun HI, Wainer H, Educational Testing Service. Test validity. Hillsdale, N.J.: L. Erlbaum Associates; 1988.

4.         Hoffmann-Axthelm W, Wollensak J. [In memory of Albrecht von Graefe's 150th birthday (author's transl)]. Klin Monatsbl Augenheilkd 1978;172(5):645-56.

5.         Krylova LM, Klocheva EG. [Ocular symptoms in cervical osteochondrosis and vegetative disorders]. Vestn Oftalmol 1978(6):25-7.

6.         Zhang CJ. [Treatment of loss of vision caused by cervical spondylosis with combined traditional Chinese and western medicine: report of 4 cases (author's transl)]. Zhonghua Wai Ke Za Zhi 1979;17(6):437-8.

7.         Lysenko TA, Kuz'mina AP, Kolesnikova MA. [Changes in the organ of vision in cervical osteochondrosis]. Oftalmol Zh 1980;35(5):298-9.

8.         Zhang CJ, Wang Y, Lu WQ, et al. Study on cervical visual disturbance and its manipulative treatment. J Tradit Chin Med 1984;4(3):205-10.

9.         Bilton D, Stephens D, Gorman F. Tunnel vision information: a paradox of ethics, economics, politics and science. J Manipulative Physiol Ther 1998;21(7):468-78.

10.       Gorman RF. Automated static perimetry in chiropractic. J Manipulative Physiol Ther 1993;16(7):481-7.

11.       Gorman RF. Monocular visual loss after closed head trauma: immediate resolution associated with spinal manipulation. J Manipulative Physiol Ther 1995;18(5):308-14.

12.       Gorman RF. The treatment of presumptive optic nerve ischemia by spinal manipulation. J Manipulative Physiol Ther 1995;18(3):172-7.

13.       Gorman RF. Monocular scotomata and spinal manipulation: the step phenomenon. J Manipulative Physiol Ther 1996;19(5):344-9.

14.       Stephens D, Bilton D, Pollard H, Gorman F. Wall perimetry in chiropractic. J Manipulative Physiol Ther 1998;21(1):32-6.

15.       Stephens D, Gorman F. The association between visual incompetence and spinal derangement: an instructive case history. J Manipulative Physiol Ther 1997;20(5):343-50.

16.       Stephens D, Gorman F, Bilton D. The step phenomenon in the recovery of vision with spinal manipulation: a report on two 13-yr-olds treated together. J Manipulative Physiol Ther 1997;20(9):628-33.

17.       Stephens D, Gorman RF. Does 'normal' vision improve with spinal manipulation? J Manipulative Physiol Ther 1996;19(6):415-8.

18.       Stephens D, Pollard H, Bilton D, Thomson P, Gorman F. Bilateral simultaneous optic nerve dysfunction after periorbital trauma: recovery of vision in association with with chiropractic spinal manipulation therapy. J Manipulative Physiol Ther 1999;22(9):615-21.

19.       Wingfield BR, Gorman RF. Treatment of severe glaucomatous visual field deficit by chiropractic spinal manipulative therapy: a prospective case study and discussion. J Manipulative Physiol Ther 2000;23(6):428-34.

20.       Awan KJ. Association of ocular, cervical, and cardiac malformations. Ann Ophthalmol 1977;9(8):1001-11.

21.       Lest'ak J. [Mariotte's spot]. Cesk Oftalmol 1993;49(6):394-8.

22.       Meyer JH, Guhlmann M, Funk J. Blind spot size depends on the optic disc topography: a study using SLO controlled scotometry and the Heidelberg retina tomograph. Br J Ophthalmol 1997;81(5):355-9.

23.       Sterling M, Jull G, Wright A. Cervical mobilisation: concurrent effects on pain, sympathetic nervous system activity and motor activity. Man Ther 2001;6(2):72-81.

24.       Braun R, Breil M. [Vision disorders in darkness and the feedback effect on the cervical spine]. Z Arztl Fortbild (Jena) 1973;67(14):732-5.

25.       Matsumoto M, Komatsu H. Neural Responses in the Macaque V1 to Bar Stimuli with Various Length Presented on the Blind Spot. J Neurophysiol 2005.

26.       Gonzalez de la Rosa M, Gonzalez-Hernandez M, Abraldes M, Azuara-Blanco A. Quantification of interpoint topographic correlations of threshold values in glaucomatous visual fields. J Glaucoma 2002;11(1):30-4.

27.       Komatsu H, Kinoshita M, Murakami I. Neural responses in the primary visual cortex of the monkey during perceptual filling-in at the blind spot. Neurosci Res 2002;44(3):231-6.

28.       Murakami I, Komatsu H, Kinoshita M. Perceptual filling-in at the scotoma following a monocular retinal lesion in the monkey. Vis Neurosci 1997;14(1):89-101.

29.       Thompson JC, Kosmorsky GS, Ellis BD. Field of dreamers and dreamed-up fields: functional and fake perimetry. Ophthalmology 1996;103(1):117-25.

30.       Schiefer U, Stercken-Sorrenti G, Dietrich TJ, Friedrich M, Benda N. [Fundus-oriented perimetry. Evaluation of a new visual field examination method for detecting angioscotoma]. Klin Monatsbl Augenheilkd 1996;209(2-3):62-71.

31.       Rudnicka AR, Edgar DF. Automated static perimetry in myopes with peripapillary crescents--Part II. Ophthalmic Physiol Opt 1996;16(5):416-29.

32.       Holz FG, Kim RY, Schwartz SD, et al. Acute zonal occult outer retinopathy (AZOOR) associated with multifocal choroidopathy. Eye 1994;8 (Pt 1):77-83.

33.       Toosy AT, Werring DJ, Plant GT, Bullmore ET, Miller DH, Thompson AJ. Asymmetrical activation of human visual cortex demonstrated by functional MRI with monocular stimulation. Neuroimage 2001;14(3):632-41.

34.       Tootell RB, Hadjikhani NK, Vanduffel W, et al. Functional analysis of primary visual cortex (V1) in humans. Proc Natl Acad Sci U S A 1998;95(3):811-7.

35.       Tong F, Engel SA. Interocular rivalry revealed in the human cortical blind-spot representation. Nature 2001;411(6834):195-9.

36.       Alajbegovic A, Resic H, Merhemic Z, Rasic S, Bratic M. [The vertigo syndrome, magnetic resonance and magnetic angiography of the head in patients on a chronic hemodialysis program]. Med Arh 2001;55(4):227-9.

37.       Durgin FH, Tripathy SP, Levi DM. On the filling in of the visual blind spot: some rules of thumb. Perception 1995;24(7):827-40.

38.       Vila FJ. [Our brain deceives us]. An R Acad Nac Med (Madr) 1999;116(2):463-74; discussion 75-82.

39.       Tripathy SP, Levi DM. Looking behind a pathological blind spot in human retina. Vision Res 1999;39(11):1917-25.

40.       Stepniewska I, Sakai ST, Qi HX, Kaas JH. Somatosensory input to the ventrolateral thalamic region in the macaque monkey: potential substrate for parkinsonian tremor. J Comp Neurol 2003;455(3):378-95.

41.       Shaw VE, Mitrofanis J. Lamination of spinal cells projecting to the zona incerta of rats. J Neurocytol 2001;30(8):695-704.

42.       Hashimoto I, Kimura T, Tanosaki M, Iguchi Y, Sekihara K. Muscle afferent inputs from the hand activate human cerebellum sequentially through parallel and climbing fiber systems. Clin Neurophysiol 2003;114(11):2107-17.

43.       Mikulis DJ, Jurkiewicz MT, McIlroy WE, et al. Adaptation in the motor cortex following cervical spinal cord injury. Neurology 2002;58(5):794-801.

44.       Lorberboym M, Gilad R, Gorin V, Sadeh M, Lampl Y. Late whiplash syndrome: correlation of brain SPECT with neuropsychological tests and P300 event-related potential. J Trauma 2002;52(3):521-6.

45.       Fredriksen TA, Hovdal H, Sjaastad O. "Cervicogenic headache": clinical manifestation. Cephalalgia 1987;7(2):147-60.

46.       Kwast-Rabben O, Libelius R, Heikkila H. Somatosensory evoked potentials following stimulation of digital nerves. Muscle Nerve 2002;26(4):533-8.

47.       Matsushita M, Xiong G. Uncrossed and crossed projections from the upper cervical spinal cord to the cerebellar nuclei in the rat, studied by anterograde axonal tracing. J Comp Neurol 2001;432(1):101-18.

48.       Bottini G, Karnath HO, Vallar G, et al. Cerebral representations for egocentric space: Functional-anatomical evidence from caloric vestibular stimulation and neck vibration. Brain 2001;124(Pt 6):1182-96.

49.       Bence M, Levelt CN. Structural plasticity in the developing visual system. Prog Brain Res 2005;147:125-39.

50.       Cerminara NL, Makarabhirom K, Rawson JA. Somatosensory properties of cuneocerebellar neurones in the main cuneate nucleus of the rat. Cerebellum 2003;2(2):131-45.

51.       Dutton GN. Cognitive vision, its disorders and differential diagnosis in adults and children: knowing where and what things are. Eye 2003;17(3):289-304.

52.       Marco CA, Larkin GL. Research ethics: ethical issues of data reporting and the quest for authenticity. Acad Emerg Med 2000;7(6):691-4.

53.       Leonardo JA. Health care fraud: a critical challenge. Manag Care Q 1996;4(1):67-79.

54.       Deception. ACOG Committee opinion: Committee on Ethics number 87--November 1990. Int J Gynaecol Obstet 1992;37(1):63-4.

55.       Cooper CP, Yukimura D. Science writers' reactions to a medical "breakthrough" story. Soc Sci Med 2002;54(12):1887-96.

56.       Vermeulen M. ['Another breakthrough': general news reports raise false hopes]. Ned Tijdschr Geneeskd 2000;144(39):1879-82.

57.       Pronin E, Gilovich T, Ross L. Objectivity in the eye of the beholder: divergent perceptions of bias in self versus others. Psychol Rev 2004;111(3):781-99.

58.       Ehrlinger J, Gilovich T, Ross L. Peering Into the Bias Blind Spot: People's Assessments of Bias in Themselves and Others. Pers Soc Psychol Bull 2005;31(5):680-92.

59.       Podoll K, Ebel H, Robinson D, Nicola U. [Obligatory and facultative symptoms of the Alice in wonderland syndrome]. Minerva Med 2002;93(4):287-93.



_____________________________________________________________________________   -   Int'l Phone: 530.949.1353