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HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY II 



ORIGIN OF PYRAMIDAL TRACT 



That the pyramidal tract arises entirely from corti- 

 cal neurons is now established in man (6ij and 

 monkey (76), in which hemispherectomy causes com- 

 plete degeneration of longitudinally descending axons 

 in the pyramid. Delineation of specific cortical areas 

 contributing axons to the pyramid has been the goal 

 of many anatomical investigators using retrograde 

 and secondary degeneration techniques. These studies 

 have been summarized by Tower (103) and Lassek 

 (59, 60). The giant pyramid-shaped cells of Betz, 

 particularly prominent in the fifth layer of the pre- 

 central gyrus, undergo unmistakable chromatolytic 

 changes and atrophy following interruption of the 

 pyramid (47, 63, 64, 91 , in). Contrary to oft-repeated 

 statements in unsophisticated textbooks, however, it 

 is perfectly clear that the large, pyramid-shaped cells 

 account for only about 2 to 3 per cent of the axons in 

 the bulbar pyramids. In man, Lassek (56) counted 

 only 34,000 giant pyramid-shaped cells with cross- 

 section areas ranging from 900 to 4100 n-; whereas 

 the bulbar pyramid contains about i million axons 

 (62). In the monkey, a similar ratio obtains, 18,845 

 cells (600 to 3000 ij.-) to 500,000 fibers (57). If the 

 reasonable assumption that large cell bodies give rise 

 to large axons is accepted, it may be supposed that 

 the large Betz cells are the parents of the 30,000 

 myelinated pyramidal axons, which range in diameter 

 from 9 to 22 ;u (62). The much more numerous small 

 myelinated pyramidal axons (almost 90 per cent are 

 less than 4 fi in diameter) and the unmyelinated 

 axons (which comprise roughly 40 per cent of the 

 total) must arise from smaller, less distinctive cortical 

 elements. The density of giant Betz cells varies in the 

 different topographical sul:)divisions of area 4, 75 per 

 cent being found in that for the leg, 17.9 per cent in 

 that for the arm and 6.6 per cent in that for the face 



(56). 



Pyramidal axons arise largely from cells in the 

 internal lamina (74). In single-unit recording of 

 cortical cells of cats, Patton & Towe (unpublished 

 oiiservations) found corticopyramidal units (identified 

 by their ability to follow high-frequency antidromic 

 pyramidal stimulation) in all layers except I and II, 

 but the greatest density was in layers V and VI. 

 Seventy-one such cells were distributed as follows: 

 layer III (depth, 500 to 870 /x), 6; layer IV (870 to 

 1070 n), 6; layer V (1070 to 1370 /j.), 24; and layer 

 VI (1370 to 1900 n), 35.* There was no significant 



** Depth ranges for indi\iduai layers are mean \'alncs taken 

 from frozen sections of arm somatosensory area I; paraffin sec- 

 tions shrink too much for accurate measurement (67). 



correlation between the relative size of a unit (as 

 estimated from the bulb-to-cortex conduction time) 

 and its apparent depth location. Depth location in 

 cortical unit analysis is, of course, subject to some in- 

 accuracies, which are discussed at length below. 



The contributions of different cytoarchitectural 

 areas to the pyramid have been investigated inten- 

 sively. Lassek (58) found that ablation of area 4 

 caused degeneration of 27 to 40 per cent of the pyram- 

 idal axons in monkeys. Virtually all of the largest 

 myelinated pyramidal axons degenerated. Haggqvist 

 (42) found only a 20 per cent loss after such lesions. 

 It is not clear that the cortical lesions in these studies 

 included the entire supplementary motor area on the 

 mesial surface (113). Fiber counts have not been 

 made following combined lesions of areas 4 and 6, 

 but Welch & Kennard (108) noted that pyramidal 

 degeneration was incomplete. About half the pyrami- 

 dal fibers degenerate after combined pre- and post- 

 central ablation (58), and Pcele (83) noticed py- 

 ramidal degeneration (Marchi and Weigert stains) 

 following lesions of areas i, 2, 3, 5 and 7. In cats, 

 degeneration studies with Glees' silver method sug- 

 gests pyramidal contributions from the temporal and 

 occipital cortex (104), a finding so surprising that it 

 should be further investigated. In summary, it tnay 

 be said that degeneration studies of different sorts 

 and by different investigators give a confused picture 

 with contradictory elements, but all agree that the 

 classical motor cortex of area 4 is not the sole source 

 of pyramidal fibers. 



.Studies in which electrical recording is used to 

 localize pyramidal origins generally reveal a somewhat 

 more restricted cortical pattern. Since the presence of 

 a D wave in cortically evoked pyramidal discharges 

 indicates that corticospinal neurons lie within the 

 effective radius of the stimulating electrodes, mapping 

 the cortical regions froin which D waves can be evoked 

 might be expected to yield a picture of the areal 

 origin of corticospinal projections. Because effective 

 stimulus radius depends on stimulus strength, such 

 maps err, if at all, in the direction of overextensive- 

 ness. In cats, Patton & Roscoe (unpublished observa- 

 tions), using this method, found two distinct projection 

 zones. The first includes the anterior sigmoid gyrus 

 and that part of the posterior sigmoid gyrus corre- 

 sponding to the leg and arm subdivisions of somato- 

 sensory area I. The second is in the anterior ecto- 

 sylvian gyrus and is roughly coextensive with the arm 

 and leg subdivisions of somatosensory area II. An 

 isthmus of cortex, either silent or yielding only I 

 activity, extends over part of the coronal gyrus be- 

 tween the two projection areas and corresponds to the 



