title: Diagonistic dyspraxia. Clinical characteristics, responsible lesion and possible underlying mechanism.
abstract: 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 grasping phenomena. The abnormal movements of the left hand consisted of (i) antagonistic movements to the right; (ii) non-antagonistic, irrelevant movements to the right; (iii) symmetric movements to the right in which the left hand sometimes preceded the right, and (iv) occasional inability to move at will during a bimanual task. From these observations and a review of previous publications, we propose that, in most right-handed subjects; diagonistic dyspraxia could be defined as abnormal motor behaviour of the left hand activated by voluntary movements of the right hand. Motor phenomena similar to diagonistic dyspraxia but attributable to impulsive groping movements induced by medial frontal lobe pathology should be excluded from diagonistic dyspraxia. Comparison of MRIs of the three patients with those of five patients who developed no diagonistic dyspraxia following an infarction of the corpus callosum, with or without medial hemispheric involvement, revealed that damage to the ventral part of the posterior end of the body of the corpus callosum was crucial for the development of diagonistic dyspraxia. Since the commissural fibres between the superior parietal lobules pass through the caudal part of the body of the corpus callosum, and also since there is accumulating evidence that the human superior parietal lobule is concerned with selection of movement based on the integration of visual and/or somatosensory information, we infer that diagonistic dyspraxia is produced by a disconnection of the right superior parietal lobule from the left which is dominant for volitional control of movement in most right-handed subjects.
authors.affiliation: Department of Neurology, Jichi Medical School, Tochigi, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Tanaka
authors.forename: A
authors.initials: A
authors.lastname: Yoshida
authors.forename: N
authors.initials: N
authors.lastname: Kawahata
authors.forename: R
authors.initials: R
authors.lastname: Hashimoto
authors.forename: T
authors.initials: T
authors.lastname: Obayashi
mesh_terms: D001072:Apraxias / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology*; D002544:Cerebral Infarction / Q000150:complications; D003337:Corpus Callosum / Q000098:blood supply / Q000503:physiopathology; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D010296:Parietal Lobe / Q000098:blood supply / Q000503:physiopathology