Gait and Parkinson's Disease - A Conceptual Model:        part 2 of 3


A Proposed Model For PD Gait

In PD I would propose that the underlying cause of the majority of gait
problems is impairment in the visual processing of motion data. =

Specifically, this impairment is an inability to properly process motion,=

which falls below a certain velocity, and small changes in the velocity o=
f
motion i.e. acceleration and deceleration.   This may in turn manifest
itself as (or be a consequence of) an impairment in depth perception (dat=
a
which originates at greater distances from the observer will appear to
exhibit lower velocity optical flow and lower rate of expansion).  This
impairment is the underlying pathology of all gait problems associated wi=
th
PD although the presence of what I call the T-factor can make some of the=
se
gait problems even more malignant and will be discussed shortly.  This
impairment spans a range of gait problems ranging from the dopamine
deficient state (e.g. akinesia) to those of the fully medicated state (e.=
g.
dyskinesia).  Indeed, I would suggest that akinesia and dyskinesia are
manifestations of the same underlying visual pathology.  The difference i=
s
the former is being expressed in the absence of dopamine and the latter i=
n
the presence of dopamine. This theory is based on the discovery that
visually accelerating optical flow above a certain minimal threshold can
overcome akinesia, festination, freezing and dyskinetic gait.   There are=

numerous ways to create environments where optical flow is accelerated. =

For example walking on a moving sidewalk, roller-skating, bicycling or an=
y
of a number of total immersion virtual reality scenarios.  PD subjects wh=
o
exhibit ambulatory dyskinesia will frequently speed up their gait (i.e.
accelerate their optical flow) to facilitate the suppression of dyskineti=
c
gait.  Also, note that running overcomes dyskinesia for the same reason. =
 =

And finally walking over regularly spaced objects, the classic scenario
described in kinesia paradoxa, also serves to accelerate optical flow.   =
In
fact it is not the "objectness" of walking over an array of objects which=

enables gait but rather their role as reference markers on the real world=

whose apparent motion serves to augment the visibility  of optical flow a=
s
we walk over them.  This is analogous to watching the dashed lines on a
highway "move towards us"  as we drive over them thereby enhancing the
visibility of optical flow.

When undermedicated this visual pathology is perceived as an inability to=

generate the required weight-bearing stride length for a particular gait
the environment requires at any given time.  When undermedicated the only=

available externally cued stride length (if any) is the very small 2-3"
stride length associated with festinating gait.  In order to enable gait
which accelerates from a standstill to cruising speed one must be able to=

process optical expansion (the perception that objects appear to enlarge =
as
we approach them) at low velocities and through small changes in velocity=
=2E =

Since this ability is compromised in PD, gait initiation problems occur
because stride lengths fall short of the demands of the environment.   Fo=
r
the same reason the self-cueing automatic gait program, (though undamaged=
)
is inaccessible, in spite of the fact that the environment is potentially=

compatible with its performance. This is because conscious stride lengths=

(if any) do not approach the stride length parameters necessary to create=

the template to switch it on.  Even if the automatic gait package were
accessed, it would break down because the same pathology exists in the
peripheral processing of data which is essential for sustaining the
automatic gait package.  In the absence of normal peripheral processing
peripherally perceived data will seem inconsistent with what the brain
would expect relative to the motor activity it is performing.  Thus, the
automatic motor program cannot be sustained, and the result is the freezi=
ng
associated with a state of undermedication. =


Consistent with this hypothesis is the observation that activities, which=

result in accelerated or augmented optical flow immediately, suppress
dyskinesia.  Examples include bicycling, skating, skateboarding, skiing
(including riding on a chair lift), running, walking on a moving sidewalk=
=2E
In summary, conscious externally cued gait (e.g. when trying to initiate
gait) requires the perception of the expansion component of optical flow =
or
augmented centrally perceived optical flow of virtual motion.  In its
absence the result is akinesia.  =


The PD subject is often thought of as being more dependent than normals o=
n
visual feedback of the self-perception of motion for initiating and
sustaining ambulation.  I would suggest that this dependency on optical
flow is the same in normal and PD subjects.  What differs is the ability =
to
perceive it. Normally, when gait is internally cued we monitor the optica=
l
flow of the environment  (virtual motion) visually but below the level of=

conscious awareness, in a manner similar to the way we can monitor the
subtle motion of being in a boat on the ocean i.e. below the level of
conscious awareness.  (Nevertheless, such sensory input can impact on our=

motor skills - e.g. motion sickness).  Freezing is the pathological
inability to sustain unconscious, automatic gait in spite of the
environment being compatible with automatic gait and the subject's
intention to achieve it.  Freezing occurs when there is insufficient,
erroneous, or misinterpreted visual perception of the optical flow
generated by ambulation.    Once frozen the subject is forced to change t=
o
an externally cued gait.  But very often this same pathology manifests
itself as an inability to produce an initiating stride of adequate length=

to conform to the demands of the environment.  This is what I would call
gait initiation problems which can be defined as the inability to produce=

an initiating stride of adequate length to conform to the demands of the
environment - a failure to meet one's conscious expectations of stride
length.  Consider the following analogy.  You are stopped at a red light =
at
an intersection on a steep incline.  The parked car to your right begins =
to
back up.  You "see" this peripherally but initially your brain perceives
this as apparent (not real) motion and concludes that you are moving
forward.  The resulting conflict between what the brain is predicting
should happen based on the motor program it is running (foot on the brake=
) =

and the accompanying visual feedback results in a kind of reflexive
slamming on the brakes. The brain cannot produce motor activity, which is=

inconsistent with predicted visual feedback. Sustaining unconscious,
automatic gait requires the processing of virtual motion (optical flow)
which is generally perceived via peripheral vision.   Whenever peripheral=

optical flow disappears or appears to disappear freezing results.  For
example, doorways frequently induce freezing in PD subjects, but I would
argue it is not the doorway but rather the opaque walls around the doorwa=
y
which precipitate freezing by obstructing one's ability to perceive optic=
al
flow.   =


If one is already in motion and the environment requires a change in
velocity the result would be festination in the presence of a  need to
decelerate and freezing if acceleration is required.   Festination occurs=

whenever we resist an accelerating force imposed on us by the environment=

(for example, going downhill or maneuvering around an obstacle in our pat=
h)
and our maximum externally cued stride length is on the order of  2 to 3
inches.    To stop (i.e. neutralize the force of acceleration, and a cent=
er
of gravity displaced forward beyond the fall point) requires that one tak=
e
many of these small steps in a very short period of time to avoid a fall.=
  =

 If the environment compels one to accelerate, one must elongate one's
stride within the same time interval as previous strides.    With only a =
2
or 3 inch externally cued stride available this becomes an impossible
maneuver and results in freezing.  Taking a step requires a deliberate
forward displacement of one's center of gravity, which puts one in peril =
of
falling.  The perceived availability of a subsequent stride of adequate
length to catch up to this displaced center of gravity and save us from
falling is what gives us the confidence to place ourselves in this
unbalanced position.  Conversely if one perceives an inability to extend
the leg (either far enough or quickly enough) the fear of falling inhibit=
s
the attempt at ambulation.   Note how getting up from a chair requires a
similar displacement of one's center of gravity.  The perceived inability=

to adequately extend the leg to catch oneself results in consistent
undershooting of the forward propulsion needed to get up from the chair
(except in the presence of the weightbearing pathologic tone - see
"T-factor" discussion to follow).   Akinetic subjects have little
difficulty negotiating stairs.  Again, this is because walking up/down
stairs is really walking with greatly reduced forward displacement of one=
's
center of gravity and as a result it is ambulating with minimal stride
length (assuming stride length is defined as the length of a stride in th=
e
horizontal axis).  Also, walking backwards is often possible when akineti=
c.
 This is a consequence of human anatomy.  Anatomically, walking backwards=

can take place without posterior displacement of one' s center of gravity=
=2E =


Motion, both real and virtual, can be perceived centrally or peripherally=
=2E =

 Virtual motion can be perceived without conscious attention and this is
the basis by which unattended, automatic gait is sustained.  When motion =
is
perceived the brain makes a best guess determination based on experience
(i.e.  sensory conditioning) whether that motion is real or virtual.  The=

ability to distinguish these two categories of motion is essential to the=

normal performance of gait.  Under certain circumstances real motion can =
be
perceived as virtual motion or vice versa.  Indeed, such perceptive
"mistakes" can be the basis of both gait pathology and therapeutic device=
s.
Sensory conditioning has taught us which characteristics of perceived
motion are most reliable indicators of whether that perceived motion shou=
ld
be functionally interpreted as real or virtual motion.   Motion perceived=

as real can define or select a gait motor package.   Motion perceived as
virtual sustains the performance and influences the quality of performanc=
e
of that motor program.   Dyskinetic gait is an example of what happens wh=
en
the brain tries to perform an automatic gait package in the presence of
impaired perception or processing of virtual motion.

The visual perception of self-motion requires the perception of virtual
motion to be perceived.  The characteristics of the perception of
self-motion (e.g. is the motion fluid or disjointed)  are a visual
reflection of the characteristics of the motor program being performed.  =

As long as this reflection is consistent with what experience has
conditioned us to expect then performance of the motor package is normal.=
 =

If this visual reflection is at odds with what experience has taught us i=
s
the appropriate feedback then this conflict must be resolved either by
adjusting the performance of the motor program to conform to the feedback=

or if this is physically impossible the program stops.   This is why
monitoring the environment through the viewfinder of a video camera with
image stabilization technology suppresses dyskinetic gait.
 =

PD subjects with dyskinetic gait often have a diminished awareness of the=

degree of their dyskinesia.   I would suggest that this is because their
motor behavior is in compliance with their aberrant perceptions.  It is
only when their motor behavior is more grossly abnormal that they become
more fully aware of the degree of variance from the norm (perhaps via oth=
er
modes of sensory feedback such as proprioception or plantar tactile
feedback).   An analogous situation might be the person who is moderately=

intoxicated and insists that his behavior has been unaffected.  =


In spite of normal motor function the manner in which this perceived moti=
on
behaves is also a function of how it is referenced to the subject.  In th=
e
absence of pathology apparent motion of a subject walking at constant spe=
ed
will appear to be of constant velocity if it is monitored peripherally.  =
In
the presence of reference markers on the floor, apparent motion can be
tracked in the central field of view.   Looking at an outstretched hand
while walking (head referencing) results in apparent motion which exhibit=
s
constant velocity (the head moves with constant velocity in gait) whereas=

if one looks at one's feet apparent motion starts,  accelerates,
decelerates and stops as each foot goes through the swing and stance phas=
e
of gait.  Both behavior patterns, though different, are normal and expect=
ed
with normal gait.  Deviation from expected behavior of this apparent moti=
on
can be a consequence of many and varied causes (for example, orthopedic
problems, alcohol intoxication, environmental forces).    This model
proposes that in PD there is an impairment in seeing or processing low
velocity motion or small changes in velocity of motion.   If this is the
case then one would predict different gait behavior when apparent motion =
is
head referenced (for example walking while looking at outstretched hands
(where apparent motion velocity is constant) versus walking while looking=

at ones feet (where apparent motion varies and motion would be perceived
abnormally).   Indeed, masking of feet and head referencing apparent moti=
on
ameliorates dyskinetic gait.  =



End of part 2

































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