324 S. Simpson,. 



relationship between the motor and sensory paralysis on the affected 

 side of the body, and that therefore the motor cortex cannot be the 

 sole seat of tactile sensation as advocated by Munk [7\ Mott [8] and 

 others, but that this must be sought for in some other part of the 

 cortex. The transient sensory disturbances that often follow motor 

 cortical lesions, may, as pointed out by Schäfer [5], be due to slight 

 unavoidable injury to other parts of the hemisphere, or to altered 

 vascular conditions produced by the operation, and when these con- 

 ditions return to the normal the sensory paralysis passes off while the 

 motor remains. They may, however, have a more far reaching cause 

 as is shown by the fact that they are often accompanied by hemi- 

 anopsia. This has been recorded by Mott [-i], and by Ferrier and 

 Turner [5], and has recently been emphasized by Hitzig [10]. 



2. Anatomical. Briefly stated, as a result of complete left motor 

 cortical lesions in tlie cat, dog and monkey, in addition to degene- 

 ration of the main pyramidal tract in the internal capsule, crusta, 

 pyramidal bundles of pons, and anterior pyramid in the medulla ob- 

 longata on the left side, and in the crossed pyramidal tract of the 

 spinal cord on the right side, fine or terminal degeneration was pre- 

 sent in the optic thalamus, substantia nigra, grey matter of the ante- 

 rior corpus quadrigeminum and of the nuclei pontis on the left side, 

 and in the grey matter at the base of the posterior horn in the cer- 

 vical and lumbar enlargements of the spinal cord on the right side. 

 A few fibres could be traced from the degenerated tract into the 

 optic thalamus and substantia nigra, and numerous fibres were found 

 to pass from the degenerated crusta to the anterior corpus quadri- 

 geminum of the same side where they appear to end, while a few cross 

 the middle line in the roof of the aqueduct to the anterior corpus of 

 the opposite side. These fibres to the ant. corp. quad, were only 

 found in the cat. No degenerated fibres could be made out passing 

 to any of the cranial motor nuclei and no fine degeneration was found 

 in these nuclei or in any portion of the central grey matter ai-ound 

 the Sylvian aqueduct, or in the floor of the 4*^ ventricle. In the 

 medulla oblongata above the crossing of the ])yramids a few fibi-es 

 could be traced from the degenerated pyi-aniid foi' a short distance 



