Top-Down versus Bottom-Up Golf Science
The World Scientific Congress on Golf is holding its Fifth Congress this week in Arizona. One of the three themes for research is "the Golfer". Unfortunately, the leadership of the WSCG has been ignoring the massive collection of real science about the golfer available in the neuroscience literature detailing how the brain and body actually works. Ignoring this top-down knowledge while purporting to engage in original bottom-up empirical research is not exactly the best approach.
Studying the golfer's brain and body from the bottom up without top-down guidance and understanding from existing science is, frankly, amateur science. This bottom-up approach gives the impression of "empirical" research exploring uncharted territory for "new discoveries." What in fact it represents is a deliberate ignoring of existing science so that the pretense of "original work" is maintained.
For example, the first Mayo Clinic "sports medicine" team (actually, conventional sports researchers Aynsly Smith, Debbie Crews and others) that purported to study the "yips" in golf did not research the neurophysiological basis of the yips and was apparently unaware of its own Mayo Clinic experts in movement dystonias (Dr Charles Adler and others). This first team's effort was largely a waste of time. After the addition of the Mayo expert in the neurology of movement disorders, the "yips" study went in a new direction with better guidance from the top down of existing neuroscience. How a team studying a problem that is widely understood to have a neurological etiology can proceed in the ignorance of the extensive existing neuroscience of dystonias is a question with an obvious answer: not well.
Similarly, the so-called "quiet eye" study by Joan Vickers, the editor of the journal Sports Vision, purports to "discover" a pattern of gazing during putting (and other sports) as exemplified by "expert" or "elite" golfers (actually, a small number of ready-to-hand college students with low handicaps). This study shows no evidence of awareness of the neuroscience of visuospatial targeting, to wit, how the brain uses vision to comprehend the relationship of objects and locations in the environment for purposes of body action in reference to the object or location. This top-down knowledge of visuospatial targeting is readily available, massively extensive, and patently applicable to the problem under study, but is completely ignored in the "quiet eye" study. Fundamentally, vision for action is a separate system from vision for detail or identification of objects, and is closely integrated with body postures and movements, so that merely tracking eyeball movements without also tracking head and neck movements (mediating brain knowledge of retinal and eyeball signals with body postures) is similar to reading only the Japanese-language instructions for using a computer when the English-language instructions are on the facing page. The related top-down knowledge of what real putting greats have done with gaze in history is also not surveyed, and no attempt is made to reality-check the behaviors of the college students against golfers like Arnold Palmer, Bobby Locke, Bob Charles, and many others.
In the Golf Magazine version of the "quiet eye" article, as opposed to the journal version, college students have "morphed" into "expert golfers" and Debbie Crews purports to explain how golfers can attain the "quiet eye" by understanding what is occurring in the brain and how to best dispose the brain to the "quiet eye." This attempt is utterly devoid of any top-down guidance from the available neuroscience and lapses hopelessly into the empty jargon of "new age" concepts like "balancing" the brain's hemispheres.
When will golf science get serious? If you are in this realm and you wish to comprehend and study the human brain and body of the golfer in action, please do not pretend that medical researchers have not devoted decades to studying and writing about these issues with literally billions of dollars in funding from Congress since the early 1990s. The work is readily available via Medline and sooner or later, golf science will have to catch up and square up with this massive collection of knowledge. Anything else is mere pretense of science that misleads golfers and wastes time and effort getting to a substantive and helpful understanding of how the human brain and body function in golf.
The following article is from 2003:
The "Mechanics of Instinct" in Putting:
The Neurophysiological Paradigm for Applied Research
[ABSTRACT: The present study is an examination of the neurophysiology of putting as revealed in recent studies of putting. At this time in the history of putting science, a new paradigm is emerging that focuses upon the human actor in terms of the perceptual and movement processes of brain and body. Early research initiatives lack a thorough grounding in the rapidly advancing field of neuroscience, and such a sound theoretical foundation is essential to efficient and meaningful progress in this promising approach to putting science. The study examines in detail neurophysiologolcal investigations into putting visual processes and putting pressures. The study probes the theoretical limitations of these studies, and proposes future lines of research.]
Over the past thirty years, the golf science of putting has been dominated by physics and engineering, an approach that focused upon impact dynamics and putter materials science and design. Presently, a new paradigm is emerging dominated by the neurophysiology of the human actor. The old paradigm posited the "robotic" ideal as the guiding model for putting excellence, and explored the parameters of general competence and optimal performance in terms of surface conditions, equipment physics, and biomechanics (DeGunther, 1996; Pelz, 1986; Pelz, 2000). This approach has given us a clearer understanding of the conditions and boundaries within which putting phenomena must be studied (e.g., biomechanical motion, ball-putter physics, ball-green physics, and ball-hole physics), but has generally left unexplored the perceptual and motor processes of targeting and stroke movement. Within this realm of the human actor, the most important research currently is taking place.
The neurophysiological approach seeks to give scientific definition to processes of the human body during the physical, mental, and emotional context of putting performance. The quarry of this approach is a deeper, widely applicable understanding of how best to engage in the action of putting, from targeting perceptions to stroke movement planning and execution. In a phrase, the new paradigm looks to the inner workings of the human mind and body to investigate the "Mechanics of Instinct" and explore the full integration of perceptual, emotional, cognitive, and motor processes in the action of putting. This new paradigm promises to build upon the old and to dominate the ensuing thirty or more years in putting science and perhaps will succeed in advancing the "black art" of putting to a new level of competency and expertise where the old "robotic" paradigm has fallen short.
The new paradigm reflects a coalescence of traditional psychology and sports science and non-traditional mind-body integration techniques within the realm of neurophysiology. This new paradigm, however, requires theoretical clarification at its foundational base. Early research efforts in this area have focused upon the clinical and behavioral neurophysiology of golfers during putting (Craig et al., 2000; Crews et al., 1991; Crews et al., 1993; Vickers, 1992; Linder et al., 1998; Abrahams, 2000). These studies have generated valuable and interesting empirical data, but generally lack a coordinated theoretical approach to the underlying neuroscience of brain functioning. The resulting studies present data in conflict with related studies and provide only a weak basis for deduction of important observations about how to putt or how to teach putting. To the extent golf is a science, it is a preeminently applied science. Current research explorations risk being stranded upon the shore of Voodoo Island without careful attention to the science as it may be applied by golfers and golf instructors.
This paper presents a brief general overview of neuroscience, and then proceeds to a critical examination of two key areas for neurophysiological research in putting: visual processes and choking under pressure. The purpose is to suggest that the theoretical limitations of much current research restrict the utility of the science and generally infuse the field with inefficiencies and redundancies that could be avoided with a clarified theoretical base. This paper concludes by outlining a number of lines of research suggested by the present boundaries of neuroscience as applied in the context of putting action.
I. Overview of Modern Neuroscience
The 1990s were designated by the US Congress as "the Decade of the Brain" in recognition of the tremendous strides achieved in neuroscience in recent years. While clearly a great deal remains unknown and even unexplored about the functioning of the human brain, the years since 1980 have witnessed an explosion in our knowledge about the organization and processes of the brain. This great expansion of knowledge has taken place mainly at the neurophysiological level, relating neural processes to physiological processes. Out of this body of research has emerged a consensus view of the brain that is represented in the following "big ideas":
1. Human brains are a result of primate evolutionary developments. Human brains are a result of primate evolutionary developments and retain primitive components and functions overlaid with more recent and sophisticated structures and processes (Eccles, 1989; MacLean, 1990). The homo sapiens brain is a descendant of its evolutionary predecessors. In general, animal brains have advanced by modification of preceding structures and processes rather than by abandonment or wholesale replacement. As a result, the human brain can be considered a layered organ, with older, more primitive structures and functions overlaid with more adaptive and complex features (the so-called "Triune Brain"). As advanced biological adaptations freed up primitive capacities and made possible a higher brain-mass ratio, some specialized structural features of the human brain became possible, such as language and symbolic reasoning. The human brain, then, is a composite of primitive and advanced components, with some overlapping of function. In particular, the human emotional system retains many features in common with animals, albeit subject to the restraints of self and society via the inhibitory controls of the frontal lobe. In addition, certain features of the human visual system, such as motion detection of threat or prey, coexist to complement more advanced visual processing. Because of this evolutionary relatedness of the human and other animal brains, the experimental study of animals (especially rats, cats, and monkeys) frequently supplies the bedrock knowledge about brain function that must be interpreted and applied to the human brain by taking into account known structural and processing differences.
2. Brain function depends upon synaptic signaling via neurotransmitter and neuroendocrine chemistry. Brain function depends upon synaptic signaling via neurotransmitter and neuroendocrine chemistry, and hence upon neural pathways, connections, and interactions (Kandel, Schwartz and Jessell, 2000; Shepherd, 1990). The central nervous system, including the brain and spinal cord, is essentially a complex network of interconnected neurons that process sensory input and output physical or cognitive behavior. Environmental inputs are electromagnetic radiation, chemical, sound waves, and mechanical contact. These sources of information about the world are converted by out sensory organs into electrical signals that course along each neuron. But between neurons, at the inter-neuron junction, there is a minute gap, and transmission of the signal across this gap is accomplished by release of neurotransmitter or neuropeptide molecules that diffuse across the gap to be received by receptor molecules specifically structured to capture and react with a given transmitter. The nature of this neurotransmitter process, combined with the structural typology of the neural cells and circuits, determines the sort of processing the environmental signals receive inside the brain. Some transmitter molecules are "excitatory" and tend to elicit an electrical firing of the receptor neuron, thus passing the signal along in the circuit. Other neurotransmitters, however, are "inhibitory" and tend to suppress the firing of the receptor neuron. Much of modern neuroscience is concerned with the detailed mapping of the connections in the human brain and with the functioning of the neurotransmitter system. For this purpose, anatomical studies post-mortem provide the most direct evidence of connecting patterns. Certain techniques for tracing neuronal pathways in vivo and neuropharmacological studies are also relied upon.
3. Brain activity requires the metabolism of glucose from the blood supply. Gluscose in the blood supplies the metabolic energy for brain functioning. The human brain consumes approximately 20% of the glucose in the blood stream, even though it typically constitutes no more than about one-fiftieth of the body mass (ten times more than proportionate to mass). This glucose metabolism and the related blood flow to active brain sites can be monitored by neuro-imaging techniques to yield functional data about brain processes with good temporal and spatial resolution (e.g., Positron Emission Tomography, or PET scans). (Andreassi, 2000; Kandel, Schwartz and Jessell, 2000).
4. Brain development proceeds in stages of proliferation and pruning, resulting in considerable individual variation in capacities and preferred modes. Brain development proceeds in stages of proliferation and pruning during early childhood and continuing through adolescence, resulting in considerable individual variation in capacities and preferred modes (Edelman, 1988; Thompson, 1993). Embryonic and peri-natal development of brain tissue and structures proceeds at a phenomenal rate. Shortly around birth, the total neuronal population is largely established and in place, but the ensuing years of childhood define the patterns of connections of inchoate brain modules. These early years of development are characterized by a proliferation of neural connections as the brain learns about and adapts to its environment. Eye teaming and binocular vision, language comprehension and expression, and walking, for example, develop only after birth. At the conclusion of early childhood, this proliferation is "pruned" to eliminate those connections and circuits that have not been favored by adaptive use. In a sense, each individual anatomically-normal brain "develops" after birth not unlike the photochemical process in photography, whereby light photons of different colors and intensities falling upon the light-reactive chemical of the film result in the image. During the years of puberty, a secondary although muted proliferation-pruning cycle occurs, and the adult brain is typically not fully clear of these systemic changes until somewhere between 18 and 21 years.
5. The brain is plastic and its structures adapt to injury and as a result of learning.The brain is "plastic" and its structures capable of adapting to injury and as a result of learning (Gollin, 1981; Greenough and Juraska, 1986; Held, 1965). "Plasticity" refers to the capacity of the neural structures of the brain to adapt to environmental stimuli, aging process, and insults. Whether the human brain can "regenerate" neurons in adult life stages is a matter of current study, but it is clear that the brain has the capacity to adapt to functional deficits and to rearrange its patterns of connections to generate alternative pathways and to accommodate newly learned patterns. For example, the cortical structures that represents finger sensation are normally distinct for each finger, but after amputation of an inner, this structural circuitry can become reorganized such that adjacent fingers encroach upon the absent finger"s neural territory. Similarly, in some case of stroke in which vascular accident inside the brain destroys neural circuitry in a localized region, the individual can sometimes generate new pathways to restore function either partially or totally. And learning, defined as the establishment of long-lasting neural pathways associating stimuli and responses, is a form of plasticity. The amount of time to lay down these long-lasting patterns, or to modify or extinguish existing patterns, depends upon the conditions of learning such as motivation, rewards, practice regime, and similar factors.
6. The brain processes information both serially and in parallel. Serial (or one-thing-at-a-time) processing is the characteristic mode for thinking or internal self-talk and other cognitive functions, but other processes are carried out in parallel (many-parts-of-a-whole-in-many-locations). Many aspects of visual cognition are carried out in parallel. Those activities that are serial in nature typically have limited "workspace" or mental resources available. Consequently, attempting to carry out multiple tasks simultaneously can often outstrip available resources and lead to degradation of function. This is especially the case with visual attention. (Gazzaniga and LeDoux, 1978; Shepherd, 1990).
7. The brain has specific modules and structures for specific functions. In over 90% of humans, the language functions of hearing and comprehending spoken or written words and generating spoken or written words and sentences is localized in the temporal lobe of the left hemisphere. In the broader sense, logic, analysis, and symbolic thought are localized in this so-called "dominant" hemisphere. Strokes with brain damage confined to the right hemisphere seldom affect language functions per se. Naturally, auditory processing is close to verbal centers of the brain. The so-called "nondominant" hemisphere contains specialized centers for spatial awareness, musical and intonational appreciation, and more global intuitive processes. Visual processes begin in the retinas and proceed through the optic nerve to the thalamus inside the brain (lateral geniculate nucleus, LGN, and superior colliculus, SC), and then to the occipital lobe at the back of the head to the primary visual area (PVA, V1, or V17) -- also called the striate cortex. The striate cortex carries out analysis of fundamental visual features like edges, corners, colors, contrast, and intensities. From here, visual signals are passed to the extra-striate cortical areas, V18 and V19, where the features are seen as forms in relation. Tertiary processing then proceeds into the multimodal association areas, where forms are recognized as familiar objects and given contextual meaning and value. Body knowledge, or the sense of position and state of body parts in relation, general orientation in the external environment, and balance, is principally the function of the parietal lobe and it"s somatosensory cortex. Proprioceptive receptors in the skin, muscles, and joints signal this part of the brain about the state of the body in space, either statically or dynamically. In addition, vestibular sensory organs in the inner ear (semicircular canals and uticles) signal the state of orientation in gravity and accelerated motion changes of position of the head in space. (Gazzaniga and LeDoux, 1978; Kandel, Schwartz and Jessell, 2000; Ornstein, 1997).
8. The brain has specific modules and structures for specific functions (audition, vision, language, movement, and so on), and certain functional processes and modes are dominated by structures in one or the other hemisphere, but behavior expresses inter-hemispheric integration. The human brain has developed specializations beyond the other primates, especially language. Most humans have language functions concentrated in the left hemisphere, and the areas of brain devoted to language have forced other functions to pool in the opposite hemisphere. This is especially the case with movement and spatial awareness. The hemispheres are connected by "bridges" of nerve cabling that connect cooperative modules of the brain in opposite hemispheres and that otherwise coordinate total brain functioning. During the 1970s and 1980s, it was very trendy to speak about the capacities of the hemispheres as if they acted with complete independence, but in fact the normal adult brain is always a matter of both hemispeheres contributing to interaction with the world. Even so, localized specialization of function has important consequences for optimizing sports performance. (Gazzaniga and LeDoux, 1978; Iaccino, 1993; Kandel, Schwartz and Jessell, 2000; Ornstein, 1997).
9. Motor movement in voluntary goal-directed action expresses the integration of sensory, cognitive, and emotional processes in the context of habituated patterns of movement. The basic unit of brain function is action. The human brain, and indeed the brain of all animals, is the controlling organ by which the actor interacts with the world, by perception of threat or opportunity for survival and the adaptive behaviors available in response. Thinking and emotion should be the mere handmaidens of action. And action is movement. Golf putting, then, is primarily action in the context of the human repetoire of movements. (Jeannerod, 1997; Latash, 1998; LeDoux, 1992; LeDoux, 1996; Leonard, 1998).
10. Identification and understanding of brain processes relies upon a complementary consort of investigative techniques, including neuro-imaging (EEG, PET, fMRI, MEG), lesion studies, animal experiments, anatomical and histological studies, and other approaches. The normal adult brain contains over 100 Billion nerve cells, each with an average of 1,000 connections to other cells. The possible brain pathways is far more numerable in a single brain than all the atoms in the universe. The history of studying the brain makes it abundantly clear that modern science has only begun to learn the complexity of the brain. This history shows that neuroscientists must rely upon a wide array of techniques and strategies in order to tease out these subtle complexities and to gain an accurate overall understanding of processes and relations between processes. No one technique or approach is adequate alone, and can only add to our understanding when its unique contribution of data is interpreted against a background of data from other sources. (Frith and Friston, 1997; Kolb and Wishaw, 1985).
With these broad tenets of neuroscience in mind, what follows is a critique of current neurophysiological studies of golf putting for the purpose of illuminating more efficient and valuable research initiatives.
II. Critique of Current Neurophysiological Research in Putting
A. Visual Processes
Much is said about the eyes in putting. Various optometrists (Farnsworth, 1997; Piparo and Kaluzne, 1999) and sports vision experts (Lampert, 1998) have written technically about visual processes in putting, golf instructors have commented repeatedly about the proper positioning of the eyes in relation to the ball in the setup (e.g., Golf Digest, 1995), golf psychologists have suggested patterns of eye usage supposedly enhancing attentional resource allocation and targeting perceptions (Cohn and Winters, 1995; Rotella and Cullen, 2001), and some sports science studies have investigated various targeting techniques concerning patterns of eye usage in putting (e.g., Steinberg, Frehlich and Tennant, 1995). Actual neurophysiological studies, however, are rare.
1. The Vickers Gaze Control Study.
Dr. Joan Vickers at the University of Calgary has investigated gaze control in putting (Vickers, 1992). Using eye-tracking equipment, Dr. Vickers has obtained gaze data from a sample of twelve golfers during putting, and compared gaze patterns in a low-handicap group (range 0-8) versus those in a high-handicap group (range 10-16). The gaze pattern of the better putters featured "express saccades" from the ball at address to the target in close temporal proximity to initiation of the putt stroke, plus a fixation of the ball during the stroke and the surface beneath the ball immediately after impact. Poorer golfers also exhibited saccadic gazes, but used with less economy and routinization. A "saccade" is a quick, ballistic shift of the eyes from one position in their orbits to another position, independent of head motion (Gregory, 1987). To the extent her analysis necessitates a theoretical discussion of neuroscience, Dr. Vickers refers to the general neurophysiological literature of eye movements and the Vestibulo-Ocular Reflex (VOR) explaining saccadic gaze shifts (either with or without simultaneous head movements). She speculates that the better golfers have learned through experience to use a pattern of gaze shifts that minimizes degradation of distance cues in comparison to other golfers, and that the fixation of the gaze on the ball and then on the surface immediately after impact reflects a superior approach to hand-eye coordination yielding a more accurate stroke for line.
This work is subject to criticism on the following grounds: 1) the study does not take into account other, arguably superior patterns of gaze control in putting derived strictly from theoretical considerations from the controlling neurophysiology; 2) the suggestion that the group of better golfers represents use of an "optimal" gaze pattern is dubious at best, especially when considered in the light of putting lore from great putters in history; and 3) the speculation concerning the relation of gaze pattern to distance cues lacks significant analysis of the relevant neurophysiology of targeting.
a. Dead-eye gaze.
An arguably superior form of gaze control in targeting is a fixed, straight-ahead gaze moved targetward along a line across the surface solely by head rotation by neck muscles. The theory is that spatial analysis for voluntary goal-directed movement (targeting) is only partially a matter of vision and is more importantly the relating by vision, vestibular processes, and proprioceptive body-sense of the state and location of the body in relation to the target for purposes of generating an effective stroke that rolls the ball into the hole (Jeannerod, 1997). The dead-eye gaze pattern generates visual and other spatial-analysis cues in a complementary, synergistic fashion that takes advantage of the underlying neurophysiological processes more effectively than the "common" saccadic gaze pattern in targeting. In addition, the pattern eliminates variable signaling during targeting occasioned by the brain having to account for shifting eye positions as well as variable head motions (Bach-y-Rita et al., 1971; Howard and Templeton, 1966; Senders et al., 1978; Wurtz and Goldberg, 1989). Finally, as a general proposition of perceptual accuracy, orthogonal or cardinal positions generate more accurate perceptions of reality than "in-between" positions (e.g., straight-ahead versus askance, erect versus tilted), especially in a culture dominated by rectilinearity (Howard and Templeton, 1966).
This "dead-eye" pattern maintains a steady relation between the eyes and the head at all times in the gaze to the target. This pattern generates coincident and therefore presumably reinforcing signals relating the body to the target in space: plane of vision in the vertical plane of the putt; head-turn axis of rotation orthogonal to the plane of the putt; visual cues during turning motion of head time-locked to neck-muscle proprioception; two eyes have separate fields of vision consistently related in a Ferris wheel pattern of verticality. This gaze yields a rich assortment of perceptual cues about target location with a consistency, regularity, and veridicality that is not attainable by the gaze described in the Vickers study, purely as a matter of the relevant neurophysiology.
The Vickers study did not control or account for head position or head motion by putters. A photograph of a golfer wearing the eye-tracking gear in his setup (119) strongly suggests golfers in the study used a typical head position characterized by eyes inside the ball (not vertically above the ball) and head tilted up from horizontal with the gaze directed downward out of the face instead of straight ahead out of the face. One can argue that the pattern of gaze control exhibited by the studied population is simply a "default" pattern forced by static setup positioning of the head and eyes in relation to the ball, line, and target, and the ensuing head movements and eye shifts targetward from this initial positioning. From these considerations, the saccadic gazes used by both high and low handicap golfers in the Vickers study are the normal, unreflective pattern that accompanies the setup position. Indeed, Vickers states that the saccadic gaze is "the most common" way of directing the gaze toward a target (118) and notes, "In skills such as putting, a subject is not aware of the moving of the eyes as being separate from moving the head, shoulder, trunk, or other muscle systems." (121) This is undoubtedly the case with sub-optimal gaze control, but is far from the case with optimal routines.
In order to employ a fixed-gaze pattern with minimal changes and variation, it is necessary to suppress the VOR. The VOR allows foveal fixation after a saccadic shift while the head catches up in its face-on reorienting (Johnston and Pirizzolo, 1988). Without VOR suppression, even a setup with gaze in the vertical plane of the putt straight out of the face will produce a series of saccadic jumps along the line of the putt during the head turn. While this may well be preferable to the express-saccade "default" pattern, a fixed-gaze pattern is better still, since it eliminates the gaze shifts in the targeting calculus and allows the bulk of relevant signaling to proceed from the proprioceptive signals of the neck muscles in the head turn. The suppression of the VOR consists essentially in delinking visual attention during the head turn so that foveal vision is prevented from fixating upon locations of interest (Bahill and LaRitz, 1984; Carpenter, 1977; Maas et al., 1989; Pelisson et al., 1988). It is the fixation of foveal sight on specific locations that necessitates saccadic shifts to begin with, and saccadic shifts bring into play the VOR. The delinking is done by concentrating on the linearity of the optic flow during the turn, instead of focusing attention on specific features on the surface. In this way, the accommodation process whereby the lens adjust to focus foveal vision on a location of interest is not engaged by the specific noticeable features of the surface along the line to the target. Vision "hovers" and "glides" with "soft focus," as it were, slightly above the surface from ball to target, and accommodation and foveal focus do not occur until the target is centered in the visual field by the head turn, at which point visual attention focuses on the target itself and the lenses adjust to the distance.
This sort of gaze pattern is identical to the smooth-tracking gaze Vickers notes in low-handicap golfers as they watch the roll of the ball proceed to the target after impact. Smooth pursuit eye movement maintains foveal gaze on a moving target (Lanman, Bizzi and Allum, 1978; Mann and Morrow, 1997). Smooth tracking can be done with fixed head or moving head. In putting, this would typically be smooth tracking of the roll of the ball with the eyes moving faster than the head until the ball attains a certain distance and then the head motion closes the gap and head orientation becomes coincident with gaze direction. This move involves the VOR, as the gaze fixation and head motion are not coincident until the end (if then). However, a smooth tracking of the roll of the ball with a fixed gaze throughout and with gaze coincident with head orientation, so that only the head is moving in the pursuit, would not involve the VOR (Misslich, Tweed and Vilis, 1996). In other words, a fixed-gaze smooth pursuit of a rolling ball is the same as a dead-eye gaze in targeting. More specifically, by imagining the roll of a perfect putt across the surface to the hole, and then engaging in fixed-gaze smooth pursuit of this imaginary rolling ball, saccadic shifts are minimized during targeting and the VOR is not engaged. The result of this simple visualization technique is an enhanced gaze pattern that eliminates complexity and variation in neural signaling and that works synergistically with more fundamental spatial targeting processes from proprioceptive cues.
The notion that the proprioceptive cues in the neck turn are superior to visual cues to location is counter-intuitive and requires elaboration. In relation to the body at address, location may be spoken of as distance and direction, but from a neurophysiological perspective such a location is most likely registered in an integrated fashion and not as a composite of analytical vectors and scalars. The target is "there," not 11.5 feet away in the two-o"clock direction. The brain is built for action, and simulation of action (Llinas, 2001). A target is not simply an object or location of interest; it is an object to act upon or react to (Jeannerod, 1997). A coffee mug is an object to grasp and lift by the handle. A slot machine is made to fit a coin into. A putter is something to use to stroke a ball into a hole. In this sense, targeting at address is acquiring the knowledge of the body"s positions and the relation of the body and ball to the target so that the effective stroke can be made. The neck-turn feeds the motor movement system with these action-oriented signals in a well-timed manner and such signals are more closely related to the impending limb movement than are visual cues (Berthoz, Graf and Vidal, 1992; Cohen, 1961; Richmond and Abrahams, 1979)
When the dead-eye gaze pattern is used, the neck turn establishes a plate in the neck that interfaces the still shoulderframe with the turning head. The turn itself is characterized by angular amplitude and by the smoothness and pacing of the turn. The simulation of the perfect roll by visualization, combined with the smooth pursuit gaze for targeting, fixes the smoothness and pace of the turn in quite a natural and experientially valid manner. The distance of the scan along the surface from ball to target fixes the angular amplitude of the turn. This angular amplitude corresponds exactly to distance, so that for a given person using this sort of pattern, a ten-foot putt is always exactly the same degree of turn, and a twenty-two-foot putt also always has a corresponding angle of turn. Consequently, over the course of practice and playing, the repetitive use of this gaze pattern engrains a consistent, repeating, veridical registry that correlates neck-turn with distance. Moreover, the "plate" in the neck turn mirrors or prefigures an identical "plate" in the shoulderframe-head interface during a shoulder stroke, in which the head is fixed still while the shoulderframe pivots about the same axis. Because of this, the dead-eye gaze in targeting not only locates the target as described; it does so in a fashion that"teaches" the body how to perform an efficacious shoulderframe motion by prefiguring a pace and an orientation of the motion. One of the main jobs that gaze control should have is to avoid detracting from the effectiveness of these proprioceptive cues. The express-saccade pattern proceeds without regard to neck-shoulder orientation and without regard to the timing or pace of the turn; typically, the pace of the head turn is significantly out of synchronization with the planned stroke motion, and this disjunction likely degrades good timing in the stroke.
b. Optimal Gaze Patterns among Golfers.
The group of golfers studied by Vickers did not include any PGA Tour professionals. Even so, the suggestion is clear that low-handicap golfers represent an "elite" model of optimal performance. (This notion is usually explicit in the case of studies of touring pros.) Do touring pros use the same pattern as that found by Dr. Vickers? If so, does that mean the pattern is optimal? Data from the history of golf suggest that the vast majority of golfers of today (including touring pros) use a similar gaze control pattern to that in the Vickers study, but that this was not formerly and is not now uniformly the case. The best putters of yesterday and today have been careful to use a gaze straight out of the face. While this alone does not guarantee a targeting pattern without saccades, it does tend to minimize saccades in favor of a more veridical perceptual process. One can argue that even these top putters have ample room for improvement in their targeting skills.
A survey of top putters from the history of professional golf would include the following players as exemplifying consistent excellence in putting: Bobby Locke, Billy Casper, Bob Rosburg, Bob Charles, George Archer, Hale Irwin, Arnold Palmer in his heyday (up to about 1970), Seve Ballesteros, Nick Faldo (up to at least 1996), Dave Stockton, and Brad Faxon. All of these players consistently setup with eyes directly over the ball and gaze straight out of the face (Archer, 1969; Ballesteros. 1988; Casper, 1980; Charles, 1965; Faldo, 1995; Faxon and Anderson, 1995; Irwin, 1980; Locke, 1953; Palmer and Doberreiner, 1986; Rosburg, 1964; Stockton and Barkow, 1996). In contrast, Ben Crenshaw sets up with eyes inside, forehead up, and gaze directed down the cheeks (Foston, 1992). The Crenshaw pattern has been emulated by Phil Mickelson and others (Mickelson 1997), and is evident in the setup of Tiger Woods and numerous pros on tour today. (For comparisons of setup positions, see the collection of photos at http://puttingzone.com/setup.html) While Crenshaw is regarded as one of the best modern putters on a year-in and year-out basis, he himself has warned others not to emulate his setup (Crenshaw, 1977), and both Mickelson and Woods have shown great streakiness and inconsistency in their putting, mixing stretches of brilliance with doldrums of slumping. In addition, Crenshaw"s personal pattern of targeting has always featured the so-called "Million-dollar look," where he raises his head out of the setup position, faces the target, and assesses target location from this upright gaze before returning to his setup. This evidence from history does not support the proposition that express-saccade targeting is an optimal gaze control pattern.
c. Saccadic Gazes and Distance Cues.
Dr. Vickers speculates that distance cues degrade more rapidly than "location" cues. It is probably true that different neural processes are engaged in the motor planning and execution with respect to force and "direction" of voluntary movement, but in the sensorimotor cortex where spatial mapping combines sensory cues for the purpose of intended, goal-directed action, there is no evidence for separate processing of distance and "direction" in this manner. The visual system yields many different sorts of cues to distance, including apparent image size versus known actual size; angle of regard of the eyes upward or downward; perspective; occlusion; motion parallax; eye-vergence proprioception; and binocular disparity and depth perception (ineffective beyond about twenty feet) (Hershenson, 1999). These "distance" cues are obtained at various times while on the green, not necessarily only during the putting routine itself. In fact, a professional golfer studies the greens he faces on Tour in order to be readily familiar with their shape, size, contour, and other features. This knowledge can be committed to long-term memory, probably in the hippocampus, and available for utilization in targeting during play, including distance awareness (Burgess, Jeffrey and O"Keefe, 1999). Moreover, the building up of a veridical awareness of distance in the context of putting is not something that begins and ends neatly, prior to assuming the address position. And kinetic senses of distance gained from walking about and visualizing or imaging walking to the target, rolling a ball to the target, or otherwise interacting with the target, are cues that become integrated with visual cues (Epstein and Rogers, 1995; Jeannerod, 1997; Paillard, 1991).
The unstated notion in the Vickers study is that the distance cue is generated (somehow, unspecified) and then begins to decay. This is also the notion behind the suggestion of golf psychologists to "refresh" awareness of target location with a last quick look at the target just prior to initiating the stroke (Cohen and Winters, 1995). The other unstated assumption by Vickers is that the visual process of gazing to the target does not add to the perception of distance or is not part of the process of building up a veridical awareness of the distance. The unstated notion of the cited golf psychologists is that a simple image of the target gained by a quick look somehow "refreshes" target awareness, which then sets about decaying again. An alternative explanation of the Vickers data is that many golfers do in fact learn that target awareness decays rapidly (not simply distance cues per se) and that express saccades are better than non-express saccades simply because the stroke is started more quickly. Even so, this does not show that an alternative pattern of gaze in targeting would not continue to build the target awareness up to the initiation of the stroke by means more potent and efficacious for the putt than a simple image refreshment. The dead-eye gaze builds target awareness and relates body position to the intended stroke movement right up to the time the stroke is initiated.
In summary, the saccadic system is probably not the best way to locate a target for purposes of acting with respect to that target. The saccadic system depends upon spatial and somatosensory mapping in the superior colliculus (SC) (Sparks, 1991), with some concurrent feedback processing in prefrontal-parietal circuitry (Goldman-Rakic and Chafee, 1994). The SC is an evolutionary holdover in the visual system, and is a direct descendant of the system that allows a frog to notice movement of a fly in the periphery and dart his tongue out and catch it. The SC has its utility for threats and opportunities for survival, but it is best used in reference to an object in motion that enters visual awareness, to redirect foveal gaze for purposes of quick identification of friend or foe. In addition, the accuracy of the saccadic system is questionable, in that almost all saccades fail to direct foveal vision directly onto the target and must be supplemented by corrective saccades thereafter. In putting, the target does not move and identification of threat or opportunity is not at issue. The efficacy of the saccadic system, then, depends primarily upon returning the gaze position to a remembered location as represented in the SC (Zivotofsky, Rottach and Leigh, 1996). The saccadic system thus spends the perceptual capital of the SC (remembered location), and not the more accurate and action-pertinent mapping in the somatosensory cortex that guides motor movement. And in any event, alternative gaze patterns such as the dead-eye gaze compile perceptual capital in the somatosensory cortex for purposes of action in putting.
The Vickers study is a careful observation of the gaze patterns of some golfers, and suggests that better golfers typically use a gaze pattern of express saccades in a well-defined routine whereas less-skilled golfers have less well-defined visual routines. The neurophysiology underlying visual processes and especially targeting processes for voluntary goal-directed action strongly suggests that the gaze pattern in use by the better golfer under study is not optimal or indeed necessarily efficacious for performance. Research designed in light of known neurophysiological processes could profitably investigate how targeting for goal-directed action is optimally accomplished, and in that context seek to investigate what sort of visual processes optimize targeting effectiveness.
B. Anxiety and the Yips - The Mayo Clinic
1. The Mayo Study - Basic Criticisms.
A movement disorder long known to interfere with putting, the "yips" affect between one-fourth and one-half of all mature golfers (Smith et al., 2000). The Sports Medicine Center of the Mayo Clinic (MCSMC) in Rochester, Minnesota, is heading up a multidisciplinary team studying the yips in golf (Smith et al., 2000; Mayo Clinic, 2000). The study focuses on anxiety and neuromuscular movement disorders that have wide applicability to other sports. Previous researchers have classified yips as an occupational focal hand dystonia, a type of movement disorder apparently caused by degeneration of neural circuitry following decades of the same hand movement. The Mayo Clinic team departs from earlier researchers by assigning a prominent role in the etiology of the yips to psychological rather than neurological factors. They have also opted for a behavioral definition of yips that does not distinguish between the contributions of anxiety and dystonia. The team may therefore have difficulty identifying effective therapy.
The study team does not distinguish by clear clinical criteria between neuromuscular movement disorders and neuropsychological processes responsible for anxiety deficits in sports performance. Relying on 1,031 responses to a detailed questionnaire from skilled, low-handicap Minnesota golfers, plus a small pilot study of the physiology of seven respondents during putting, the team investigated anxiety and putting performance. The team's preliminary report concluded that the yips consist of a continuum of disorders from the psychology of choking at one extreme to a strictly neurological deficit (occupational focal hand dystonia) at the other. The team believes that the majority of afflicted golfers suffer from a mixed psycho-neurological form of the yips between these extremes (Smith et al., 2000). Studies of additional golfers are planned for the World Golf Village in St Augustine, Florida (Mayo Clinic, 2001). The working definition of the "yips" used by the MCSMC unfortunately confounds anxiety and neuromuscular deficits by relying upon behavioral rather than clinical characteristics.
While admittedly psychological stress can cause performance detriments, including poor putting, it begs the analysis of the yips to define stress-induced as part of the yips phenomenon and then conclude that the yips span a continuum from psychologically-induced to neurologically-induced deficits. Similarly, while it may be true that psychologically-induced stress may exacerbate an underlying neurological condition, this simply amplifies the need to dissociate the psychological from the neurological processes. This confounding of underlying processes reduces the search for a cure or even a deep understanding of the phenomena and their interrelations to an ad hoc trial-and-error approach to treating symptoms. Such a trial-and-error approach, moreover, must necessarily be individualized for the unique combination of psyhoclogical and neurologic dysfuctions of a specific subject and his or her unique responsiveness to the trial treatment. While this may make for laudable medical practice, it is doubtful that it is a sound scientific procedure for illuminating the neurophysiology.
The principal criticism of the Mayo Clinic approach is failure to separate anxiety and dystonia according to clinical criteria. The underlying neurophysiological processes of anxiety and dystonia are distinctly different (Gray and McNaughton, 2000; Hallett, 1998). Anxiety is generally categorized as a normal psychological state that may extend into pathological forms (with well-recognized physiological signs such as cardioacceleration, forced breathing, and mind blanking) (American Psychiatric Assoc., 1994), but focal hand dystonia is a neurological dysfunction with specific neurophysiological abnormalities (Hallett, 1998). Instead of clinical criteria for anxiety or dystonia, the Mayo Clinic team uses self-reporting of behavioral characteristics of the yips. The team uses four criteria to assess whether subjects are affected:
the golfer was previously a good putter, so the condition is acquired;
the yips are episodic (considered to be consistent with dystonia);
the yips have prompted the golfer to change putting technique in search of relief; and
the change in technique yielded at least temporary improvement in performance (Smith et al., 2000).
Golfers are then rated according to how many criteria they self-report. Only 200 respondents gave sufficient information to be rated. Of these 136 (68%) met 3 or 4 of the criteria. Actual physiological data during putting was gathered only from seven respondents, measuring heart rate (ECG), grip force (GF), and muscle activation patterns (EMG). Of these, only four self-reported as yips-affected, but the criteria rating was not reported for these subjects. The four affected golfers exhibited higher heart rates, grip force, and EMG excitation than non-affected golfers. While the data allow dissociation of these four golfers from non-affected golfers in terms of the physiological signs, the physiological data fail to discriminate between effects due to anxiety versus neuromuscular dysfunction.
The criteria for defining which golfers are yips-affected conflate anxiety and dystonia by focusing on yips behavioral rather than the distinct clinical signs and symptoms of anxiety and dystonia. The team's working definition of the yips in these terms of behavior effectively precludes separating out the contributions of the two from a neurophysiological perspective. It should be possible to identify golfers suffering solely from anxiety-related performance deficits and golfers suffering solely from neuromuscular-related deficits unattended by anxiety, with appropriate clinical symptomatology.
The underlying neuroscience of anxierty-related and neurogenic performance dysfunction in putting suggests a different, more promising approach to a study of the yips.
2. Neuroscience of Occupational Focal Hand Dystonia.
These earlier putting studies are in line with modern neuroscience, in which occupational focal hand dystonia is only imperfectly understood (Hochberg et al., 1990; Wake Forest Neurosurgery, 2001), but is no longer considered to be psychological in origin (e.g., Abbruzzese et al., 2001; Adler, 2000; Hallett, 1998; Hochberg et al., 1990; Sheehy and Marsden, 1982). Classed as a movement disorder along with Parkinson's Disease, cortico-basal degeneration (CBD), and various forms of spasticity (Dystonia Medical Research Foundation, 2001; We Move, 2001), focal hand dystonia has been linked with:
sensorimotor degradation of hand-finger neurons in the sensory cortex (blurring of the fine sensory discrimination of finger and hand proprioception underlying movement control) (Abbruzzese et al., 2001; Byl et al., 2000);
basal ganglia dysfunction in the "release" of prepotent motor programs by inhibition of inhibition (Ibanez et al., 1999; Reilly et al., 1992);
disturbed levels of sensorimotor cortical excitation (Coria et al., 2000; Reilly et al., 1992; Tinazzi et al., 1999; Toro et al., 2000);
and imbalanced forearm muscle inhibition patterns (Nakashima et al., 1989).
The emerging picture is of a complex loop of brain centers integrating perception, emotion, and movement that is subject to disruption at varying points with resulting movement deficits that can be quite similar. For example, vestibular dysfunction contributes to spasmodic torticollis (a related dystonia; Munchau et al., 2001); cervical spinal lesions can produce dystonia-like deficits in hand movements without involvement of cerebral circuits (Uncini et al., 1994); and cerebellar degeneration results in excess cortical activation in motor control (Liepert et al., 2000). Focal hand dystonia is considered mostly intractable, but limited relief can be gained from periodic injections of the hand muscles with botulinum toxin A (Naumann and Karlheinz, 1997; Poungvarin et al., 1995). In addition, brain surgery with thalamotomies (lesioning of the basal-cortico motor control loop at a point in the thalamus) has been effective (Kelly, 2001; Mempel et al., 1986). Drug treatments have generally been disappointing (Adler, 2000).
3. Neuroscience of Anxiety Disorders.
The American Psychiatric Association recognizes four broad classes of anxiety disorders: panic, phobia, obsessive-compulsive, and generalized anxiety disorders (American Psychiatric Assoc., 1994). Golfers tend to speak very broadly of "pressure," "stress," "anxiety," "fear," and similar terms without careful definitions. "Anxiety" is too often used to cover a wide variety of mental and neuropsychological states. In particular, current neuroscience distinguishes "defensive avoidance" in the amygdala circuitry from "defensive approach" in the septo-hippocampal circuitry. The former is related to fear, panic, phobia, and flight behavior, and the latter to generalized anxiety and dread or "anticipatory frustration" (Gray and McNaughton, 2000; LeDoux, 1992; LeDoux, 1996 ). These dissociations of the underlying neurology and the forms of anxiety-related responses represents a more complex view of the traditional "fight-flight" reaction in light of recent neuroscience.
The therapeutic efficacy of anti-anxiety psychopharmaceuticals (anxiolytics such as beta-blockers and tranquilizers) depends upon these underlying structural differences (Gray and McNaughton, 2000). For example, the amygdala system mediates fear and phobia and generates panic and flight behavior, whereas the septo-hippocampal network mediates dread and anticipatory frustration and generates hesitation and vacillation behaviors. While the amygdala system responds to panicolytic drugs with relief of behavioral signs, it is not directly responsive to anxiolytic drugs. The septo-hippocampal system, on the other hand, is responsive to anxiolytics but not to panicolytics. Classical anxiolytics include ethanol, barbiturates, and benzodiazepines, but their side effects mask locating the affected neural structures . The new class of anxiolytics developed in the last decade, especially busiprone, has the advantage of working to reduce anxiety without the side effects of the benzodiazepines or the addictive toxicity of ethanol and barbiturates. Clinical observation of the efficacy of this new class of drugs allows much clearer identification of the neural structures mediating anxiety. (Gray and McNaughton, 2000).
The neurophysiology of the so-called stress response is naturally closely connected with the fear-anxiety mechanisms in the amygdala and hippocampal circuitry. The autonomic fight-flight response in the sympathetic nervous system is the stress-induced mechanism whereby the adrenal gland readies the body's muscular, cardiovascular, immune, and nervous systems for aggression, escape, and possible injury under conditions of real or imagined threat or danger (Hadley, 1996; Stanford and Salmon, 1993; West 1990). Two neural subsystems activate this stress response: the anterior pituitary adrenal cortex system (elevating blood levels of glucocorticoids, which forms the most common physiological measure of stress) and the hypothalmic-adrenal medulla system (elevating blood levels of epinephrine and norepinephrine) (Pinel, 1997; Shier et al., 1999). In both cases, the adrenal systems are activated by signals from the hypothalamus, which in turn is initially recruited by the amygdala (Davis, 1992). The form of anxiety mediated by the hippocampal circuitry also activates the hypothalmic-adrenal system (probably via the amygdala), but does so in a manner inhibiting and moderating the behavioral outputs of the stress response (Gray and McNaughton, 2000). The behavioral basis, then, for detecting whether the underlying neurology is principally fear-based (amygdala) or anxiety-based (hippocampal) is a matter of intensity of physiologic reaction. Consequently, the outward behavioral signs of the stress response may appear similar for differing underlying neural mechanisms, but pharmacological treatments have different effects depending on the differing mechanisms (Gray and McNaughton, 2000).
Reports of yips behavior, including the dread of failure facing short putts (e.g., Longhurst, 1973), are more consistent with the septo-hippocampal system of anxiety from anticipatory failure than the panic-phobic behavior of the amygdala system. The septo-hippocampal system appears to mediate situations where the person is acting with conflicting goals and motives, such as the need to attempt a short putt to complete play on the hole versus dread of embarrassment at missing the putt. This is categorically different from the fear and phobic reactions that necessitate escape behavior without conflicting motivation. Assuming the septo-hippocampal system underlies yips anxiety, then the interference with motor programs is believed to have its telling effect via hippocampal neural projections to the basal ganglia (Gray and McNaughton, 2000). This common basal-ganglia connection between anxiety and dystonia may well support an overlapping of motor deficit symptoms, but the issue remains to be examined. Again, notwithstanding similarities in outward behavioral signs, the underlying neural mechanisms are distinct, and identification of appropriate treatments requires clinical tracking of these mechanisms.
In addition, anxiety-sponsored behaviors may exhibit a progressive course that simulates the progression of a neuromuscular disorder. Recurrence or intensification of yips behavior is a potentially confusing and unreliable indicator of the neuropathology. There is evidence that the anxiety response of the septo-hippocampal system becomes conditioned to repeated exposures to stimuli, reacting more strongly over time with a reduced threshold for activating stimuli. (Gray and McNaughton, 2000). Similarly, the "fight-flight" reaction, whereby release of adrenaline heightens arousal, adapts to repeated exposure to the stressful stimulus by producing greater release of adrenaline (Xie and McComb, 1998). Hence, an intensification of the anxiety-sponsored motor deficits can occur without regard to neuromuscular dysfunction. While on the one hand this observation suggests that yips behavior from anxiety may be as potent and outwardly similar as that derived from dystonia, on the other hand it underscores the need for non-behavioral signs to separate the phenomena.
4. The Question of Therapy or Cure.
The Mayo Clinic study does not attempt analysis of treatment or cure for its description of yips behaviors. Instead, the team lists possible interventions for future study, including:
compensatory golf techniques (long putters, fat grips, grip style or position change, grip pressure adjustment, "sidesaddle" putting, reliance upon non-dominant hand, reliance upon shoulders rather than hands for stroke, etc.);
sports psychology cognitive strategies;
thought-control (e.g., meditation, mindfulness, positive self-talk, self-hypnosis, neurolinguistic programming); and
anxiolytic pharmacology (beta-blockers and tranquilizers).
Curiously, the Mayo Clinic apparently does not discuss periodic botulinum toxin injections in hand muscles " the principal treatment for hand dystonia " most likely on the premise that golfers would not wish to endure the sequelae of transient hand weakness for the sake of golf.
Treatment programs aimed at a cure must be tied to a specific diagnosis of the underlying psycho- or neurophysiology (Andrews et al., 1994). Because of the diverse and complex neurophysiological processes encompassed by anxiety and dystonia, disentangling the separate processes that underlie performance deficits collectively known as the yips is a necessary first step in identifying effective treatment. In the absence of a known etiology for a condition, curative therapeutics are not available and textbook medical practice defaults to treatment of symptoms in a conservative, individualized, managed approach. This is typically on a trial-and-error basis. This is the current posture of the MCSMC team in its investigation of the yips. Treatment protocols must be individualized and will not likely have wide application for sufferers of the yips in general (Adler, 2000). The Mayo Clinic study affords a detailed look at the current understanding of the yips among golfers and golf scientists. However, the phenomena under examination must be observed separately by well-crafted experimental protocols for a deeper understanding of the controlling neurophysiological processes. Without this deeper understanding, effective therapy will likely remain elusive.
C. Anxiety and Choking in Putting - ASU's Debbie Crews
Choking is generally understood to refer to anxiety-sponsored increases in arousal level that lead to performance deficit, typically associated with failure in informal situations or in high-pressure competition. The 1996 experience of Greg Norman at the Masters in losing a final-round six-shot lead to Nick Faldo prompted the NBC program Dateline to bankroll a study of choking in golf by Dr Debra Crews and others (Linder et al., 1998). The initial study consisted principally in taking a State-Trait Anxiety Inventory of golfers under simulated pressure. Ten college-student golfers with an average of 5.2 years of golfing experience and a mean scoring average of 90.1 strokes were tested. (Subsequently, Dr. Crews obtained EEG readings and prepared a composite image of golfer brains showing chokers and non-chokers.) The task was a trial of 20 five-foot putts for baseline, followed by a second trial of 20 putts on condition that the golfers who improved won $300 while golfers who performed worse than baseline would have to pay $100. Five did better, and five did worse (Linder et al., 1998; Abrahams, 2001).
The 1998 report simply concluded that anxiety was associated with performance decrement, and experience with pressure helps. (Linder et al., 1998) In the separate EEG study, Dr Crews compared EEG images of golfers in the trial and concluded that successful golfers had increased cortical activity just like unsuccessful golfers, but the activation was spread evenly over both hemisphere of the brain, whereas activation for unsuccessful golfers concentrated in the left (dominant) hemisphere (Abrahams, 2001). Dr Crews interpreted the increased left-brain EEG activity as anxiety-related and interpreted the successful golfer's brain pattern under pressure as the consequence of employment of right-brain processes that were better suited to "handle" the added pressure. In keeping with this analysis of handling pressure, Dr Crews teaches "right-brain" golf by encouraging golfers to use imagery, relaxation techniques, and target focus as ways to promote right-brain activation and therefore hemispheric balance.
The main difficulty with this research is there is no scientific analysis of so-called "right-brain" golf techniques. The connection between EEG composite imagery of golfers under pressure and golf techniques claimed to ameliorate performance decrement under pressure is simply not attempted. The notion of "balance" in hemispheric activation, additionally, is a very nebulous notion, without operational or functional meaning.
III. Suggested Lines of Future Research
A. Integration of Targeting with Stroke Movement.
The key neurophysiological phenomenon for golf putting is the relationship between targeting and stroke movement. Optimal putting technique will most likely be founded upon the integration of targeting with movement control. In the brain, the somatosensory mapping of the body in space, for purposes of voluntary goal-directed action with reference to a target in the environment, nourishes and guides the motor processes of movement planning and execution. This is evident in the movement planning process called "neuronal population vector surveying" in the operational choosing of voluntary limb movement direction. In effect, the accuracy and potency of the targeting determines the effectiveness of movement towards the goal (e.g., Georgopoulos, 1997). Future neurophysiological studies should be used to assess untrained versus trained movement accuracy in putting, and identify strategies and techniques for reducing error and for learning optimal techniques.
B. Eye Dominance.
Of course, the isolated subjects of targeting and movement control are intrinsically important and should be examined independently. For example, patterns of eye dominance clearly relate to the nature of targeting routines (Barbeito, 1981; Hubel, 1988), but there have been no reported neurophysiological studies addressing eye dominance in targeting or the special problems of cross-dominant golfers like Jack Nicklaus (left-eye dominant but right-handed in putting). How eye dominance functions in sighting a target, as opposed to observing the surface contour or assessing distance) and the effect of different patterns of eye usage in sighting on the accuracy, potency, and durability of targeting perceptions should be investigated.
C. Distance Perceptions and Force Calibration.
There are essentially two different approaches to distance control in putting: force control via muscle contraction regulation (the "hit" model), and pendulum-like stroke (the "hitless" model). These two approaches exist normally in combination and only rarely in pure form, but in principle are separable. The neurophysiological processes underlying these two approaches are radically distinct. The "hit" model would appear to depend upon processes located in the sensorimotor cortex to assess and calibrate muscle control in agonist-antagonist pairs. The "hitless" model depends upon targeting associations with backstroke amplitude, and relies upon (relatively) relaxed and inactive muscles during the downstroke. Both model rely upon cerebellar timing processes for the smoothness and the timing control of the action. These two distance-control models in putting should be investigated further to assess the relative efficacy of the different neurophysiological processes.
Current neurophysiological studies of putting enhancement are limited to suggestions that EEG biofeedback (also called neurofeedback or neurotherapy) can enhance putting performance. A study of the use of EEG biofeedback in archery by ASU's Dr. Daniel Landers and others found that not only does "correct" EEG biofeedback enhance performance, but "incorrect" biofeedback results in performance decrements (Landers et al., 1990). The definition of "correct" or "incorrect" biofeedback apparently varies with the sport and its techniques, with right-handed archery differing substantially from two-handed golf putting. A 1993 study by Damarjian on heartrate deceleration biofeedback in putting found no difference in performance among control, tonic, or phasic biofeedback protocols, and suggested the need for further research, especially concerning the transfer and retention of biofeedback training protocols. (Damarjian, 1993). This paint-by-numbers approach to mimicking supposed superior physiological or neurophysiological "states" as defined by EEG or EKG readings is a decidely "blunt" approach. The golfer is given no guidance about a "skill" that promotes these "states," and the evidence supporting the claim that the "states" are correlated with "superior" performance is of the relative sort. In sum, this approach sheds little light on optimal "states" or how the golfer should go about achieving them. Biofeedback would be better used in a more comprehensive, top-down approach to the neurophysiology of putting skills (targeting, timing, stroke movement, psychological controls), to learn something about how optimal putting works. For example, a golfer highly skilled in specific targeting techniques could be compared to a novice golfer in terms of EEG, and then the same highly skilled golfer compared to a mid-level golfer. If the targeting skills are first defined in terms of the correlated neurophysiology that one would expect from a deep understanding of neuroscience, we could learn something useful about the skills themselves.
E. NLP and Hypnosis.
Numerous golf psychologists of today have incorporated neuro-linguistic programming (NLP) into their golf instruction, including putting (e.g., Mackenzie and Delinger, 1990). However, NLP is essentially a form of self-hypnosis, and is more akin to traditional psychological mind-control techniques than to any neurophysiologically-based approach to performance. Nonetheless, NLP and more traditional hypnotic techniques should be examined for their effect on anxiety, arousal, motivation, focus, and other important performance traits in putting.
F. Music and Rhythm Entrainment.
The human brain is subject to entrainment by internal and external oscillations, whether by the cycles of daylight and night or by the rhythmic soundwaves of entrancing music (Moore-Ede, Sulzman and Fuller, 1982; Southard and Miracle, 1993). Byron Nelson is reputed to have credited his victorious final round in the Masters with the happenstance encounter with a lady performing Strauss" Blue Danube Waltz on the piano the morning before his teetime, and he is said to have played the tune in his head throughout the day, crediting his performance with the beneficial effects of the tune. Regardless of any specific tempo that may be considered as optimal in a golfer"s putting, the performance can likely be kept close to the desired tempo with the use of music as a training protocol. Music therapy is a recognized technique for anxiety control and even pain alleviation in the medical establishment (Moritz, 1997; Storr, 1992; Unkefer, 1990). Future lines of research might investigate the neurophysiological response to certain types of music during putting practice, especially stress-relaxation levels, arousal, perceptual acuity, attention, and concentrated focus.
G. The Gamma Wave.
According to Rodolfo Llinas of the NYU Medical School, the brain is primarily an organ for movement, and movement requires timing precision (Llinas, 2001). His studies have found a 40 Hz oscillation from the inferior olive in the brain stem that effectively regulates cerebellar control of movement timing. Perhaps coincidentally, the disparate processes of the cortex appear to be organized by a cortical oscillation of neurons in the 40 Hz range (36 to 44 Hz). The so-called gamma wave is considered in neuropsychology to represent a brain state of focused arousal, most likely associated with specific neuronal processes (Andreassi, 2000; Basar, 1999; Traub, Jefferys and Whittington, 1999). Prior studies have shown that biofeedback is effective in training evocation of the 40 Hz wave (Sheer, 1989). This same EEG pattern has been observed in the attentional patterns prior to the golf putt, and the 40 Hz wave was observed to decrease in the left (dominant) hemisphere of right-handed golfers prior to initiating the putting stroke (Crews and Landers, 1993).. Crews and Landers suggested follow-up studies of the gamma wave in putting, especially putting competition, where the decrease in focused arousal may not occur (Crews and Landers, 1993). Similarly, the notion of entrainment of a 40 Hz brain state, either with biofeedback training or external frequency stimuli, should prove valuable.
H. Meditation and Other Mind-Body Integration Techniques.
Neuroscience researcher Dr. James Austin at the Colorado Health Science Center has studied the neurophysiology of zen meditative states, and has charted the close relation between cardio-pulmonary control techniques and induced states of consciousness (Austin, 1999). A great deal of research into the neurophysiology of meditative states, including zen and yoga, was begun in the 1970s and continues today (Newberg and D"Aquili, 2001; Ornstein, 1972). Clearly, such practices are integrally related to standard western "relaxation" techniques (e.g., Benson, 1975; Cohn and Winters, 1995). These techniques for mind-body integration should be examined from the perspective of neurophysiology for their benefit in putting targeting and stroke control enhancement.
The neurophysiological paradigm of putting promises to provide rich and useful information about efficacious techniques for optimal performance. Such an approach, with a clarified theoretical basis as guide for research endeavors, is capable of explaining how golfers with widely differing techniques of setup and stroke can nonetheless attain comparable levels of excellence: the neurophysiological processes important in performance may be enhanced or degraded by these physical techniques, but the real job of putting is not visible to the outward eye. Putting happens between the ears. And neurophysiological research can also identify those physical behaviors that support and enhance innate perceptual and movement processes, so that what happens between the ears and on the green can advance towards the optimum.
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