6 . Dr. R W. Mott. Microscopic Changes in the [Feb. 21, 



Both these conditions are the outcome of the destruction of the posterior 

 spinal ganglion cells. But this destruction must also have led to destruction 

 of the peripheral branch of the T-shaped process of the ganglion cells, and 

 this would give rise to a sensory polyneuritis. Unfortunately, I have not 

 had forwarded to me any of the nerves to examine. However, the com- 

 paratively normal appearance of the anterior roots, and the very complete 

 destruction of many of the sensory roots, together with the well-marked 

 sclerosis of the posterior columns, would suggest that this animal may have 

 suffered with a sensory paralysis of the hind limbs analogous to tabes 

 dorsalis, rather than a polyneuritis. An argument in favour of this 

 hypothesis is that in severe alcoholic and other forms of polyneuritis the 

 motor anterior horn cells usually show characteristic degenerative changes 

 which are not seen in the spinal cord of this animal. Now it has been 

 shown by numerous authorities, but especially in a very systematic manner 

 by Head and Campbell, that herpes zoster is caused by an inflammation of 

 the posterior spinal ganglia, the seat of the eruption depending upon the 

 particular segmental ganglion or ganglia affected. It is therefore reasonable 

 to associate the eruption of the characteristic cutaneous plaques with the 

 inflammatory irritation of the ganglia as they become successively affected 

 by the noxious agent. 



Both Lingard and Laveran remark upon the curious nature of the 

 eruption : the former believes it to be an angio-neurotic oedema which 

 occurs in the form of circular plaques, as if a ring had been introduced 

 under the skin. They remark that although trypanosomes can only be 

 found in the blood with difficulty, yet they are always present in the fluid 

 which can be drawn from a plaque. Lingard concludes therefore that 

 embolism by trypanosomes is the cause, but if there is an angio-neurotic 

 oedema occasioned by the irritation of the posterior spinal ganglia, then 

 it is possible that in the blood or the inflammatory exudation the trypano- 

 somes may find suitable conditions for multiplying by fission. The theory 

 which I have advanced for the origin of the rash finds some support, more- 

 over, in experiment, for Dr. Bayliss has shown that stimulation of the 

 posterior roots produces vaso-dilation. Again, these plaques often leave 

 patches of leucoplacia which may be due to neurotrophic causes associated 

 with the destruction of numbers of the spinal ganglion cell neurotrophic 

 centres. 



In chronic trypanosome infections by T. Oambiense, even before the 

 lethargy occurs, outbursts of irritative papules or other skin eruptions occur, 

 and they might be accounted for by irritation of the neurotrophic centres in 

 the spinal ganglia. The changes in the ganglia are never so intense as in 



