14.

It was interrupted in C. 10, 11.

Consciousness was entire in C. 1, 2, 12, 13, 14, 16, 18.

Unconsciousness occurred in 3, 4, 9.

Dyspnoea was present in C. 4, 8, 9, 10, 14, 16, 18.

The faculty of swallowing remained in C. 14.

Inability to swallow in 3, 10, 14.

Increased heat of body in 8, 12, 18.

No increased heat of body is noted to have been observed in

Coldness of the extremities in C. 13.

The skin assumed a dark colour in 4, 14.

The complexion was dark in 14, 18.
The face pale in 14, 18.

The face red in 1, 4, 6, 10, 13, 16.
The features distorted in 1, 10, 12.
The eyes projected in C. 4, 6, 14.
The eyes distorted in 3, 10, 14.

The pupils dilated in 1, 4, 8, 14, 16, 17.
The pupils contracted in 10.

The duration of the fatal fit was in C. 15 minutes; in 1, half an hour; in 2, one hour; in 3, three hours; in 12, sixty hours; in 14, one hour and a half.

Resumé of the appearances noted in the cases examined post mortem.

The following cases only were examined: C., 1, 2, 3, 12, 13, 14, 15, 17.

Stiffness in the body in C. 3, 12, 14, 15, 17.

No stiffness present two days after death in 2.
The jaws stiffly clenched in C. 13, 15.

The hands clenched in C. 13, 15.

The hands not clenched in 1.

The arms stiff in C. 15.

The feet distorted, C. 2, 14.

The abdomen distended, 13, 14, 17.

The body dark coloured in 12, 13, 14, 15, 17.

The muscles dark coloured in 13, 14.

The blood fluid in C. 2, 14, 15.

The blood dark coloured in C. 14, 15, 17.

The brain congested in 14, 15.

No congestion of the brain in C. 1, 17.

Effusion in the brain in 3, 12, 15.
No effusion in the brain in C. 1, 17.
Congestion of the spinal cord in 3, 14, 15.
No congestion of spinal cord in C. 1, 17.
Effusion on the spinal cord in 3, 12, 14, 15.
No effusion on the spinal cord in C. 1, 17.

Softening of spinal cord in 14, 15.

Granules or tubercles on membranes of cord in C. 12.

Congestion of lungs in C. 3, 12, 15, 17.

Heart contracted in C. 1, 2.

Heart flaccid in 14, 15.

Heart full in 15, 17.

Heart empty in C. 1, 2, 3, 14.

Effusion into pericardium and pleura in 3.
Inflammation of the stomach 12, 13, 14, 15 (?).

Inflammation of bowels in 12, 13, 14.

Congestion of the liver in 12, 14.

Congestion of the kidneys in C.

From the above cases of Strychnine poisoning, and the resumé we have given of the symptoms they presented, and the morbid changes observed after death, the reader will perceive that the symptoms and morbid alterations produced by Strychnine are not so fixed and uniform as some would have us believe them to be. He will perceive that though the history of Mr. Cook's case may well give rise to suspicion of the administration of Strychnine, the symptoms he presented do not exactly correspond to those of any of the cases we have detailed. Almost all the symptoms Cook presented occurred in one or other of the poisoning cases, but none of the latter offered the whole of those observed in his case. It is curious to observe that the case (14) which, in the symptoms observed during life, most closely resembles that of Cook, is precisely the one which differs most completely from him in the post mortem appearances. How to account for this discrepancy on the supposition that both are cases of Strychnine poisoning, we know not.

On the whole we cannot share the unmingled satisfaction of some of our medical contemporaries with the medical evidence in this remarkable trial.

The symptoms in Cook's case were not so exactly those of Strychnine poisoning as to justify a positive conclusion that they

were, in the absence of any finding of Strychnine by chemists of experience. Several medical witnesses of respectability and experience, said they might be owing to natural disease. On this point we would be loath to put forward any opinion of our own, but when we consider the diversity of natural diseases,* the difficulty of judging from report of the exact character of symptoms, the liability of men to misrepresent and misinterpret where they have a foregone conclusion, we cannot forbear to express our regret that a verdict of guilty should have been returned in the absence of the chemical proof of Strychnine poisoning. If what was stated by the great chemical authorities, the witnesses for the defence, be true, respecting the absolute certainty of the discovery of Strychnine in the body of any animal poisoned by it, than the failure to discover Strychnine by experienced chemists, is more than mere negative evidence, it must be positive evidence that Strychnine was not the cause of death. If we believe the testimony of those distinguished chemists, we must adopt one or other of these two alternatives—either those eminent analytical chemists, Drs. Taylor and Rees, are bunglers at their own vocation, or Cook was not poisoned by Strychnine: neither of which alternatives is very satisfactory.

Not for Palmer's sake-for being hanged and probably deservedly so, if not on Cook's account, yet for other crimes—but for the sake of removing the uneasiness that the failure to discover Strychnine has occasioned in many minds, we would earnestly desire that Cook's body should be exhumed, and made over for analysis to Messrs. Herapath, Nunneley and Letheby.

As the case at present stands, we know not but what we may be poisoned by Strychnine so adroitly that no one shall even suspect the murder. For supposing our poisoner had the wit to procure his Strychnine more cunningly than Palmer, supposing also that the symptoms presented, in place of resembling Cook's case, more nearly resembled some of the fatal cases we have related above, then if he have but the skill to give his doses in the proper manner, he may kill without risk of detection by all the resources of chemistry. Surely it would be worth while settling this question by the exhumation of Cook at the risk of proving Drs. Taylor and Rees unskilful chemists, or that Palmer did not murder Cook by Strychnine, if at all.

*Want of space alone prevents us detailing a number of cases that have occurred in our own and others' practice, of sudden death from convulsions, and of unaccountable tetaniform fits, where no suspicion of poison was possible.

Discussion on the Adulteration of Drugs at the Med. Soc. of London, April 12, 1856. DR. CHOWNE, President.

Dr. Lankester said there could be no question that drugs were adulterated to an enormous extent, and it was a serious question how the evil could best be remedied. With regard to liquorice, he was a little comforted to think that it was not adulterated with anything that was likely to produce serious effects upon the system.

Mr. Rogers Harrison expressed an opinion that the Medical Society was not a fit arena for the discussion of the composition and adulteration of liquorice. As to other drugs, their adulteration by such substances as starch, potatoes, and the like, was perhaps, rather a matter of rejoicing than otherwise, as it might serve to diminish the strength of the doses prescribed. (A laugh.) ·

Dr. Rogers adverted to the difficulty connected with the prescribing of drugs whose strength was uncertain.

Mr. Jabez Hogg said, he had seen sulphate of lime and rice starch mixed with powdered liquorice. Some drugs, he said, were so extensively adulterated, that persons who ought to be competent judges were ignorant as to the composition of the real article. In one instance a quantity of calamine ointment was returned to this country from India, as not genuine, the fact being that it was a perfectly genuine article, but differing so much from what had been previously supplied, (the drug being nearly always adulterated,) it was supposed to be impure.

The President stated, that he had known ipecacuanha to be sold with one part in three of sago dust; and said that the person who was considered the best druggist was he who could adulterate the best without detection, and could best detect the adulteration of others. Dr. Snow wished that the author had included some other drugs in his paper. He mentioned that the censors of the College of Physicians once found in their visitations a barrel of antimonial wine so adulterated, that they had it turned out into the street. The excuse of the druggist was, that it was "only intended for exportation."

66

Mr. I. B. Brown said, until a better system was introduced medical men would necessarily go on prescribing with uncertain results.

Glycogenic Function of the Liver.

Nouvelle Fonction du Foie, 1853; et Leçons de Physiologie Expérimentale, 1855. Par M. CLAUDE BERNARD, Membre de

l'Institut de France, &c. &c.

Physiology and medicine are indebted to M. Claude Bernard for one of the most important discoveries of the present century—that of the glycogenic function of the liver.

If, in a carnivorous animal, the blood of the vena portæ, or veins passing from the stomach and intestines into the liver, be carefully examined, not a trace of sugar is to be detected. If the blood of the hepatic vein of the same animal, or the veins proceeding from the liver, be tested in its turn, sugar is found to exist in it in considerable quantity. During the circulation of this blood through the liver, then, sugar is formed! A new phenomenon, a new function, a new object of physiological and medical study has been discovered. This discovery has placed the name of Bernard in the first rank of discoverers in physiological science.

We proceed to lay before our readers the special points involved in this discovery in detail. We shall, then, briefly notice several objections which have been made to it, for this discovery has undergone the usual lot of discoveries in physiology especially, and M. Bernard has had to wage war with many disputants. But we believe that the glycogenic function of the liver still remains as a part of physiology, and, in its excess, as in diabetes, which it explains for the first time, of pathology.

Extraordinary as the fact may be, this last discovery in material physiology coalesces with the latest discovery in the physiology of the nervous system, for the glycogenic function of the liver appears, from M. Bernard's investigations, to be an example of internal diastaltic function, in which the pneumogastric is the ascending or incident nerve, and the ganglionic the descending nerve, the medulla oblongata being the centre.

The following are the principal facts in regard to the glycogenic function:

Sugar exists in the liver of man and of all animals in health.

This sugar exists in the liver of carnivorous as well as herbivorous animals, during the state of digestion, or of fasting. It is therefore independent of the food.

In the carnivorous animal, there is no sugar in the vena portæ ;