502 F. H. PIKE 
motor neurones. Concerning the truth of this latter statement, 
I must confess to a deep and enduring skepticism. Complica- 
tions arise in such a scheme. If we follow out the types of move- 
ment that are present in various representatives of the verte- 
brate phylum, we find that even in such forms as the chimaeroid 
fishes in which higher motor neurones, as we know them in 
mammals, are lacking, clonic as well as tonic movements are 
possible. Moreover, in such forms, there is no sustained rigidity 
of the skeletal muscles: even without the supposed inhibitory 
action of the pyramidal fibers, the lower motor neurones do not 
normally develop any activity which results in a prolonged 
spastic condition of the muscles. If in the higher type of ani- 
mals the pyramidal fibers exert an inhibitory influence, it seems 
equally clear that in the course of the evolution of vertebrates a 
change has occurred in the lower motor neurones, resulting in 
the development of some activity which must be inhibited. 
One must therefore admit a change in the function of the lower 
motor neurones in phylogenetic development if the hypothesis of 
the tonic inhibitory action of the pyramidal fibers is to be sub- 
stantiated. Such a change in the function of the lower motor 
neurones seems improbable. It appears simpler to assume that 
as evolution has progressed there has been a separation in the 
types of movement represented by higher and lower motor 
neurones; and that in the higher animals, when the higher 
motor neurones are injured or destroyed, there may be a change 
in the amount of energy passing through—a quantitative but 
not a qualitative change—in the function of the lower motor 
neurones. As Dejerine (714) shows, man is the only form in 
which a permanent spasticity of the skeletal muscles results 
from. a purely cortical lesion. Goltz’s decerebrated dog, in which 
although decerebration was not complete, no part of the motor 
area remained, did not exhibit any permanent spasticity. Com- 
plete decerebration in a dog is followed, usually within an hour, 
by marked decerebrate rigidity (Sherrington). The particular 
nerve cells which it is necessary to rupture in order to produce 
permanent spasticity have a different anatomical location in 
man as compared with the dog. Some change in the anatomical 
