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In 1909, Rudolf Bálint described optic ataxia within
the context of a more general parietal syndrome that also included
psychic paralysis of gaze, and emispatial neglect. The post-mortem
exam of his case revealed a bilateral softening of the parietal
lobe.
As Bálint refers, optic ataxia impaired his patients
daily activities, since, while cutting a slice of meat
which he held with a fork in his left hand,
would search
for it outside the plate with the knife in his right hand,
or
while lighting a cigarette he often lit the
middle and not the end. Bálint pointed out the
systematic nature of this disorder, which was evident in the
patients behaviour when searching in space. Thus,
when asked to grasp a presented object with his right hand,
he would miss it regularly, and would find it only when his
hand knocked against it
.
The term optic ataxia was introduced in analogy to tabetic ataxia,
which is characterized by a lack of proprioceptive control of
movement. It was meant to describe a disorder of hand reaching
movements that, in Bálints view, was specifically
dependent on a defective visual control. The patient, in fact,
correctly performed all movements when these were guided by
somatosensory information, as when the right hand reached to
different parts of his own body. With eyes closed, he could
perfectly imitate with the right hand passive postures imposed
to his left hand, thus excluding the possibility of apraxic
disorders. Crucial to this interpretation was the observation
that
all movements performed defectively with the
right hand were executed perfectly or with very little error
with the left hand, which excluded the possibility of
a disorder of visual attention.
Thus, Optic ataxia is characterized by an impaired visual control
of the direction of arm reaching to visual targets, and is accompanied
by defective hand orientation and grip formation as well. In
humans, optic ataxia is associated to lesions of the superior
parietal lobule (SPL), that also affect visually guided saccades.
In the last 10 years, anatomical and physiological studies of
the SPL have shed new light on the role of parietal cortex in
the control of combined eye-hand movements to visual targets,
and on the underlying distributed network linking parietal to
frontal cortex. A main emerging functional feature of SPL neurons
seems their capacity to combine in a spatially congruent fashion
different directional eye and hand related information, those
that any coding scheme so far proposed considers essential for
the composition of motor commands for reaching. This integration
occurs within the global tuning field (GTF) of parietal neurons,
is context-dependent, and involves eye and hand information
that share same directional properties. Depending on task demands,
this integration of signals can result in the representation
of different reference frames for coordinated eye-hand movements.
The dynamic operations occurring within the GTFs might depend,
at least in part, on the reciprocal sets of association connections
linking the superior parietal lobule and the premotor areas
of the frontal lobe. From this picture, the SPL emerges both
as a main source of visual input to the frontal cortex, and
as a key structure for visuomotor integration based on re-entrant
signalling, therefore, as a crucial node in the visual control
of movement.
It is our hypothesis that in parietal patients the directional
errors that characterize reaching are consequence of the breakdown
of the combination of directional eye and hand information within
the GTFs of parietal neurons. In these patients, the spatial
match among information about target location, eye and hand
position, and movement direction would be prevented, so as to
impair visually-guided eye-hand movements. This breakdown could
be, al least in part, dependent on the failure of a re-entrant
fronto-parietal signalling, an obvious consequence of the degeneration
of the cortico-cortical systems linking parietal and frontal
cortex. Cortico-cortical connections are in fact essential for
shaping the dynamic properties of cortical neurons.
Publication
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