PRODUCED BY ATROPIA IN COLD-BLOODED ANIMALS. 471 



ments of all the extremities; but a somewhat severe excitation of the head, as by 

 a smart tap, was followed by pretty strong spasm of the anterior extremities, and 

 of the chest muscles, and by violent tetanus of the two posterior extremities, the 

 latter lasting for four seconds. 



On the same day — at twenty-five hours after the administration — stimulation 

 caused increase of the tonic spasm of the muscles anterior to the ligature, and, 

 simultaneously, sudden and rigid contraction of the muscles posterior to it — in 

 fact, a general tetanic convulsion — the latter lasting for seven seconds. These 

 convulsions could readily be excited by moderate stimulation of the skin of any 

 region — below the ligature (non-poisoned regions) as well as above it. 



On the third day — at forty-four hours after the administration — it was impos- 

 sible to excite tetaniG spasm in the non-poisoned regions. At forty-six hours, the 

 posterior extremities were slightly rigid, and soon afterwards stimulation of the 

 sacral nerves did not produce in them any movement whatever; but violent 

 spasm could still be excited in the anterior extremities, and in the other poisoned 

 regions.* 



The evidence contained in these experiments is sufficient to exclude the 

 muscles and the afferent and the efferent nerves from being held to be directly 

 concerned in the production of the spasmodic and convulsive symptoms of atropia. 

 In each experiment, certain regions of considerable extent were protected from the 

 direct influence of the poison, and yet freely participated in the spasmodic and 

 tetanic effects, thereby proving that these effects were not caused by a direct action 

 of atropia on either muscles or efferent nerves. The evidence that excludes the 

 afferent nerves is quite as satisfactory ; for in each experiment an excitation of 

 the skin of the non-poisoned region readily produced spasms and general tetanus, 

 thereby proving that a direct action on the afferent nerves is not required for the 

 production of these symptoms. 



We are now obliged to look for the cause of these effects to a direct action of 

 atropia on the central nerve-organs. The predominance of cerebral symptoms 

 during atropia-poisoning in animals of a higher development, suggested the 

 possibility of the tetanic symptoms being caused in frogs by an influence origi- 

 nating in the cerebral lobes, or, more probably, in the ganglia at the summit of 

 the medulla. Accordingly, on several occasions, the spinal cord of a frog in the 

 stage of tetanus was divided immediately below the brachial enlargement, with 

 results such as are described in the following experiment. 



Experiment XLIX. — A solution of fifteen -hundredths of a grain of sulphate 

 of atropia, in four minims of distilled water, was injected under the skin at the 

 left flank of a frog, weighing 152 grains. The stage of paralysis continued until 



* The experiments in this series were all performed in winter, when the low temperature of the 

 laboratory was favourable to a long-continued retention of nerve-irritability in parts cut off from the 

 circulation. 



