Y. Tanaka et al., DIAGONISTIC DYSPRAXIA - CLINICAL CHARACTERISTICS, RESPONSIBLE LESION AND POSSIBLE UNDERLYING MECHANISM, Brain, 119, 1996, pp. 859-873
We present three patients who showed, in addition to signs of callosal
interruption, a variety of abnormal motor behaviour of the left hand
dissociated from conscious volition, in the absence of pathological gr
asping phenomena. The abnormal movements of the left hand consisted of
(i) antagonistic movements to the right; (ii) non-antagonistic, irrel
evant movements to the right; (iii) symmetric movements to the right i
n which the left hand sometimes preceded the right, and (iv) occasiona
l inability to move at will during a bimanual task. From these observa
tions and a review of previous publications, we propose that, in most
right-handed subjects, diagonistic dyspraxia could be defined as abnor
mal motor behaviour of the left hand activated by voluntary movements
of the right hand. Motor phenomena similar to diagonistic dyspraxia bu
t attributable to impulsive groping movements induced by medial fronta
l lobe pathology should be excluded from diagonistic dyspraxia. Compar
ison of MRIs of the three patients with those of five patients who dev
eloped no diagonistic dyspraxia following an infarction of the corpus
callosum, with or without medial hemispheric involvement, revealed tha
t damage to the ventral part of the posterior end of the body of the c
orpus callosum was crucial for the development of diagonistic dyspraxi
a. Since the commissural fibers between the superior parietal lobules
pass through the caudal part of the body of the corpus callosum, and a
lso since there is accumulating evidence that the human superior parie
tal lobule is concerned with selection of movement based on the integr
ation of visual and/or somatosensory information, we infer that diagon
istic dyspraxia is produced by a disconnection of the right superior p
arietal lobule from the left which is dominant for volitional control
of movement in most right-handed subjects.