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Regarding the recent postings relative to gait I felt compelled to get my
2-cents in.....

There are, I would suggest, two distinct categories of freezing.   One which
generally occurs while in the "off" state and is visually mediated and another
which occurs in the "on"  state and is mediated by what I term the "T" factor
(more later).

There are also two categories of gait.  One I call automatic gait and can be
performed without conscious attention - it is the kind of walking one performs
while strolling down an obstacle-free, level country lane.  One can, for example
easily carry on a conversation with a friend while performing automatic gait.
The second category of gait is what I call "externally cued" gait - i.e. the
environment cues the gait.  Fording a stream by  stepping on randomly protruding
rocks is an example of externally cued gaiit.   Automatically cued gait can also
be called internally cued gait because each succeeding step is cued by the
previous one, independent of the environment as long as the environment remains
compatible with automatic gait.   The most important parameter required for
sustaining this self-cuing automatic gait  is stride length.   As long as the
stride length exceeds a certain minimal threshhold, internally cued automatic
gait is sustained.   When the environment imposes a situation that requires a
reduction in stride length below this minimal stride length threshhold we must
shift from internally cued automatic gait to externally cued, conscious gait.

In PD with associated gait pathology, the pathology is such that automatic gait
can indeed be performed but is very difficult to access (i.e. initiate) and
vulnerable to breaking down,  but internally cued gait  (where the environment
dictiates varying stride length gaits below the minimal threshhold
stridelength), cannot be accessed because in PD with associated gait pathology,
we have only two stride lengths available, 1.  the minimal threshhold stride
length asssociated with automatic gait and 2. the very, very short stride length
associated with festinaing gait  (or in some cases no stride length at all).

Turning or quick maneuvering is an environmentally dictated event which imposes
the necessity to attenuate one's stride length.  Thus, if one is walking along
(automatic gait) and someone approaches there is a need to manuever which
requires a shortened stridelength which in PD is not available which results in
freezing.

Sustaining automatic gait is dependent upon the reliable processing of
dependable peripheral data.  If such data is absent  (e.g. walking down long
corridors with nothing on the walls)  or if such data cannot be seen  (e.g.
approaching a doorway  framed by walls on either side which prevent one from
seeing peripherally upstream) or if the data is misinterpreted (e.g. you are in
your car, stopped at an intersection and the parked car visible peripherally
begins to back up) freezing will occur.

T-factor mediated freezing  occurs as a consequence of a disturbance in the
dynamic balance or interaction of excitatory and inhibitory neurotransmitters.
It occurs in the presence or absence of therapeutic dopamine levels.  It also
results in an akinesia or freezing which is not vision mediated.  I'll save this
for a future discussion.

Regards.

tom