Parkinson's disease and dementia

Wakayama concerning our study of a sensory level on the trunk in lower lateral brainstem lesions. Hayakawa’s report3 on the claseification of the sensory impairment dealt with the side of the face that was affected when there was involvement of the entire contralateral trunk and limbs. Hayakawa’s type 1 (with ipsilateral facial involvement) is the same sensory defect as in typical Wallenberg’s syndrome. ?Lpe 2 (with contralateral facial involvement) is the complete unilateral sensory defect such as that usually seen in supratentorial lesions, and type 3 (with bilateral facial involvement) corresponds to our case 9. His careful clinical observations and speculations on localization of the lesions according to the type of sensory defect were noteworthy. The main focus of our report, however, was the existence of a sensory level on the trunk that was not shown in any of Hayakawa’s cases. Hemisensory defects in our 3 canes and in the 1 case of Kase et al involved the face, arm, and trunk, with the lower border demarcated at a sensory level (termed “unilateral” pattern in our study). The sensory defect had an ususual distribution and is apparently distinct from Hayakawa’s type 2 or 4, which Dr. Wakayama referred to as the unilateral type. Furthermore, by use of MRI, we were able to precisely localize the lesions and confirm the clinicoanatomic correlation of the sensory defect. Hayakawa showed no anatomic verification by either autopsy or radiologic findinge. We were aware of Dr. Wakayama’s work‘ in this field as well as that of Hata et al,6 and chose not to comment on their work because, again, there were no descriptions of a sensory level on the trunk. We have provided the evidence that such a sensory level appeared as the result of the partial disruption of the lateral spinothalamic tract by MRI. To our knowledge, no similar studies have been reported heretofore.