The
"Mechanics of Instinct" in Putting:
The Neurophysiological Paradigm for Applied Research
Geoff
Mangum
The
PuttingZone
http://puttingzone.com
[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.]
***
INTRODUCTION
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.);
-
neuromuscular
re-education;
-
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.
D.
Biofeedback.
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.
Conclusion
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.
References
Abrahams J. (2001),
First prize: putting under stress, Golf Mag. 43(3): 94-96.
Abbruzzese G,
Marchese R, Buccolieri1 V, Gasparetto B and Trompetto C (2001). Abnormalities
of sensorimotor integration in focal dystonia - A transcranial magnetic
stimulation study, Brain, 124(3): 537-545 (Abstract).
Adler C.H. (1999).
Botulinum toxin treatment of movement disorders. In: Gilman, S., Goldstein,
G.W., Waxman, S.G., eds. Neurobase (Book on CD-ROM). 3d ed.
San Diego: Arbor Publishing.
Adler CH (2000).
Strategies for controlling dystonia: Overview of therapies that may
alleviate symptoms. Postgraduate
Med 108(5).
American Psychiatric Assoc. (1994), Diagnostic and Statistical Manual
of Mental Disorders. Washington, DC: APA, 4th ed.
Andreassi, J.
(2000). Psychophysiology: Human Behavior and Physiological Response.
Mahwah, NJ: Lawrence Erlbaum Assocs.
Andrews, G.,
Crino, R., Hunt, C., Lampe, L., and Page, A. (1994). The Treatment
of Anxiety Disorders. Cambridge: Cambridge University Press.
Anthony M (2001).
Eliminating the yips, Dec., www.asiapacificamateurgolfers.com.
Archer, G. (1969).
The putting stroke that won me the Masters, Golf Dig. June
1969: 36-40.
Armour T (1967).
The ABCs of golf. New York: Simon and Schuster.
AtNeurology (2001).
Movement
disorders resources.
Austin, J. (1999).
Zen and the Brain: Toward an Understanding of Meditation and Consciousness.
Cambridge, MA: MIT Press.
Bach-y-Rita,
P, Collins, C. and Hyde, J., eds. (1971). The Control of Eye Movements.
NY: Academic Press.
Ballesteros,
S. and Andrisani, J. (1988). Natural Golf. NY: Atheneum.
Bahill, A. and
LaRitz, T. (1984). Why can't batters keep their eyes on the ball?
Am. Scientist. 72(3): 249-253.
Bara-Jimenez
W, Shelton; P, Hallett M (2000). Spatial discrimination is abnormal
in focal hand dystonia, Neurology 55(12):1869-73 (Abstract).
Barbeito, R.
(1981). Sighting dominance: an explanation based on the processing
of visual direction in tests of sighting dominance. Vision Res.
21: 855-860.
Basar, E. (1999).
Brain Function and Oscillations, Volume II: Integrative Brain Function.
Neurophysiology and Cognitive Processes. Berlin: Springer-Verlag.
Becker, W. (1989).
Metrics, in Wurtz, R. and Goldberg, M., eds., The Neurobiology
of Saccadic Eye Movements. Amsterdam: Elsevier, pp. 13-67.
Benson, H. (1975).
The Relaxation Response. NY: Morrow.
Berthoz, A. (2000).
The Brain's Sense of Movement. Trans. Giselle Weiss. Cambridge:
Harvard
Berthoz, A.,
Graf, W. and Vidal. P. (1992). The Head-Neck Sensory Motor System.
NY: Oxford Univ. Press.
Blais J, Chapman
ER, Link E et al. (1993). Botulinum neurotoxin A selectively cleaves
the synaptic protien SNAP-25. Nature 1365: 160-163.
Blakeslee, T.
(1980). The Right Brain. NY: Berkeley Books.
Bordens, K. and
Abbott, B. (1991). Research Design and Methods: A Process Approach.
2nd ed. Mountain View, CA: Mayfield Pub. Co.
Boros J (1968).
Three ways to banish your putting jitters, Golf Dig. 19(10):
27-29.
Burchiel KJ,
(1995). Thalamotomy for movement disorders, Neurosurg Clin N Am
6:55-71.
Burgess, N.,
Jeffrey, K. and O'Keefe, J., eds. (1999). The Hippocampal and Parietal
Foundations of Spatial Cognition. Oxford: Oxford Univ. Press.
Byl NN, McKenzie
A, Nagarajan SS (2000). Differences in somatosensory hand organization
in a healthy flutist and a flutist with focal hand dystonia: a case
report, J Hand Therapy 13(4): 302-9 (Abstract).
Carpenter, R.
(1977). Movements of the Eyes. London: Pion.
Carter, R. (1998).
Mapping the Mind. Berkeley: Univ. of Cal. Press.
Casper, B. and
Barkow, A. (1980). The Good Sense of Golf. Englewood Cliffs,
NJ: Prentice-Hall.
Caviness JN (2000).
Hyperkinetic movement disorders: A four-article symposium. Postgraduate
Med 108(5).
Charles, B. and
Ganem, R. (1965). Left-Handed Golf. Englewood Cliffs, NJ: Prentice-Hall.
Cohen, L. (1961).
Role of eye and neck proprioceptive mechanisms in body orientation
and motor coordination. J. Neurophysiology. 24: 1-11.
Cohn PJ (2001).
Tips for beating the yips, peaksports.com.
Cohn, P. and
Winters, R. (1995). The Mental Art of Putting: Using Your Mind
to Putt Your Best. South Bend, IN: Diamond Communications.
Coria F, Blanco
Martin AI, Rivas Vilas MD (2000). Pseudodystonic hand posturing contralateral
to a metastasis of the parietal association cortex, Neurologia
15(8): 362-5 (Abstract).
Cox, R. (1990).
Sport Psychology: Concepts and Applications. 2nd ed. Dubuque,
IA: William C. Brown.
Craig, C., Delay,
D., Grealy, M. and Lee, D. (2000). Guiding the swing in golf putting.
Nature. 405(6784): 295-296.
Crenshaw, B.
(1977). Don't putt like me: the Tour"s best putter tells why
his way is not for you. Golf Mag. 19(5): 62-63
Crews, DJ (2001).
Faculty page, Dept of Sports Exercise, Arizona State University, Tempe,
AZ, asu.edu/~crewsd/.
Crews D., and
Landers D. (1993). Electroencephalographic measures of attentional
patterns prior to the golf putt, Med. Sci. Sports & Exercise
25: 116-26.
Damarjian, N.
(1993). Effects of heart rate deceleration biofeedback training on
golf putting performance. Eugene, OR: Univ. of Ore. (unpublished thesis).
Davis M. (1992).
The role of the amygdala in fear and anxiety. Ann. Rev. Neurosci.
15: 353-75.
DeGunther, R.
(1996). The Art and Science of Putting. Indianapolis, IN:
Masters Press.
Dystonia Medical
Research Foundation (2001), www.dystonia-foundation.org/.
Eccles, J. (1989).
Evolution of the Brain: Creation of the Self. London: Routledge.
Epstein, W. and
Rogers, S, eds. (1995). Perception of Space and Motion. NY:
Academic Press.
Evidente VGH
(2000). Understanding essential tremor: Differential diagnosis and
options for treatment. Postgraduate
Med 108(5).
Faldo, N. and
Simmons, R. (1995). A Swing for Life. NY: Viking Press.
Farnsworth, C.
(1997). See It and Sink it Mastering Putting through Peak
Visual Performance. NY: Harper Collins.
Faxon, B.
and Anderson, L. (1995). Sink more long putts. Golf Mag. Jan.
1995: 56-57.
Foston, P., ed.
(1992). The Encyclopedia of Golf Techniques. Philadelphia:
Courage Books.
Frith, C. , and
Friston, K. (1997). Studying brain function with neuroimaging, in
Rugg, M., ed., Cognitive Neuroscience. Cambridge, MA: MIT Press,
pp. 169-196.
Gazzaniga, M.
and LeDoux, J. (1978). The Integrated Mind. NY: Plenum
Press.
Georgopoulos,
A. (1997). Voluntary movements: computational principles and neural
mechanisms, in Rugg, M., ed., Cognitive Neuroscience. Cambridge,
MA: MIT Press, pp. 131-18.
Goldman-Rakic,
P, and Chafee, M. (1994). Feedback processing in prefrontal-parietal
circuits during memory-guided saccades. Soc. for Neurosci. Abstracts.
20: 808.
Golf Digest (1995).
Primer 1995: putting. Golf Dig. 46(2), 76-78.
Golf Digest (1973).
The yips -- putter's enemy no. 1, in Golf Digest's Handbook of
Putting (NY), 163-167.
Golf World (1949).
Jitter-putt jive, Golf World July 13, 1949; 3(5): 1.
Gollin, E. (1981).
Developmental Plasticity: Behavioral and Biological
Aspects of Variations in Development. NY: Academic Press.
Greenough, W.
and Juraska, J. (1986). Developmental Neuropsychobiology. Orlando:
Academic Press.
Gray J. and McNaughton
N. (2000). The Neuropsychology of Anxiety. 2nd ed. Oxford:
Oxford Univ. Press.
Gregory, R.
(1987). Saccades, in The Oxford Companion to the Mind. Oxford:
Oxford Univ. Press, p. 693.
Hadley M (1996).
Endocrinology. Upper Sadle River, NJ: Prentice Hall, 4th
ed.
Hallett M (1998).
The neurophysiology of dystonia, Arch Neurol 55(5): 601-3 (Abstract).
Held, R. (1965).
Plasticity in sensory-motor systems. Sci. Am. 213(5):
84-88, 91-94.
Hershenson, M.
(1999). Visual Space Perception. Cambridge, MA: MIT Press.
Hobson DE (2001),
Botulinum treatment: A review of it's therapeutic role in movement
disorders, Canadian Movement Disorder Group, http://www.cmdg.org/medicati/botox/botox.htm.
Hochberg FH,
Harris SU, Blattert TR (1990). Occupational hand cramps: professional
disorders of motor control, Hand Clin 6(3):417-28 (Abstract).
Howard, I. and
Templeton, W. (1966). Human Spatial Orientation. NY: John Wiley
and Sons.
Hubel, D. (1988).
Eye, Brain, and Vision. NY: Sci. Am. Library.
Iaccino, J. (1993).
Left Brain -- Right Brain Differences: Inquiries, Evidence,
New Approaches. Hillsdale, NJ: Lawrence Erlbaum Assocs.
Ibanez V, Sadato
N, Karp B, Deiber MP, Hallett M (1999). Deficient activation of the
motor cortical network in patients with writer's cramp, Neurology
53(1): 96-105 (Abstract).
Irwin, H.
(1980). Play Better Golf. NY: Octopus Books.
Jankovic J, Hallett
M, eds. (1994). Therapy with Botulinum Toxin. New York: Marcel
Dekker.
Jeannerod, M.
(1997). The Cognitive Neuroscience of Action. Oxford:
Blackwell Publishers.
Johnston, C.
and Pirozzolo, F., eds. (1988). The Neuropsychology of Eye Movements.
Hillsdale, NJ: Lawrence Erlbaum Assocs.
Kaluzne, S. and
Piparo, T. (1999). Master the Art and Science of Putting:
Training the Eyes, Mind, and Body. Winston-Salem, NC: Sports
Performance Centers of Am.
Kandel, E., Schwartz,
J. and Jessell, T., eds. (2000). Principles of Neural Science (4th
ed.). NY: Elsevier.
Kelly PJ (2001).
Stereotactic
thalamotomies, NYU Med School.
Kolb , B., and
Wishaw, I. (1985). Fundamentals of Human Neuropsychology. NY:
W.H. Freeman and Co.
Lampert, L. (1998).
The Pro's Edge: Vision Training for Golf. Boca Raton,
FL: Saturn Press.
Landers, D.,
Petruzzello, S., Salazar, W., Crews, D., Kubitz, K., Gannon, T. and
Myungwoo, H. (1990). The influence of electrocortical feedback on
performance of pre-elite archers. Med. & Sci. in Sports &
Exercise. 23(1): 123-129.
Lanman, J., Bizzi,
E. and Allum, J. (1978). The coordination of eye and head movements
during smooth pursuit. Brain Res. 153(1): 39-53.
Latash, M. (1998).
Neurophysiological Basis of Movement. Champaign, IL:
Human Kinetics.
Leadbetter D,
Huggan J. (1993). David Leadbetter's Faults and Fixes. NY:
Harper and Row.
LeDoux, J. (1992).
Emotion and the amygdala, in The Amygdala: Neurobiological
Aspects of Emotion, Memory and Mental Dysfunction (ed. J.P. Agglegton).
NY: Wiley-Liss, pp. 339-51.
LeDoux, J. (1996).
The Emotional Brain. NY: Simon and Schuster.
Leonard, C. (1998).
The Neuroscience of Human Movement. St. Louis, MO: Mosby-Year
Book.
Liepert J, Hallett
M, Samii A, Oddo D, Celnik P, Cohen LG, Wassermann EM (2000). Motor
cortex excitability in patients with cerebellar degeneration, Clin
Neurophysiol 111(7):1157-64 (Abstract).
Linder, D., Lutz,
R., Crews, D., and Lochbaum, M. (1998). Who chokes and when? situational
and dispositional factors under pressure, in Farrally, M.R. and Cochran,
A.J., eds., Science and Golf III: Proceedings of the 1998
World Scientific Congress On Golf, pp. 158-65. St. Andrews, Scotland.
Llinas, R. (2001).
I of the Vortex: From Neurons to Self. Cambridge, MA: MIT Press.
Locke, B. (1953).
Bobby Locke on Golf. London: Country Life Ltd.
Longhurst H.
(1978). The yips - once you've had 'em, you've got 'em, in The
best of Henry Longhurst. NY: Golf Digest Book.
Maas, E., Heubner,
W. Seidman, S. and Leigh, R. (1989). Behavior of human horizontal
vestibular-ocular rteflex in response to high-acceleration stimuli.
Brain Res. 499(1): 153-156.
Mackenzie, M.
and Delinger, K. (1990). Golf: The Mind Game. NY: Dell Pub.
Co.
MacLean, P. (1990).
The Triune Brain in Evolution. NY: Plenum Press.
Magill, R. (1993).
Motor Learning: Concepts and Applications. 4th ed. Madison,
WI: William C. Brown.
Mann, C. and
Morrow, M. (1997). Effects of eye and head position on horizontal
and vertical smooth pursuit. Investigative Opthalmology & Visual
Sci. 38(3): 773.
Mayo Clinic (2000).
Yips: more than a putting problem, www.mayo.edu.
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