Journal of Law, Information and Science
Case Comment: The Trial of William Palmer, a Mid-Nineteenth Century English Scientific Evidence Case
In 1856 William Palmer, dubbed the ‘Rugeley Poisoner’ was tried and convicted at the Old Bailey for poisoning a fellow gambler. The charges levelled against him were astounding: not only was he charged with the death of his betting partner, he was also indicted for the deaths by poison of his mother and brother to obtain the sums for which their lives were insured. This was of course sensational, with voluminous press coverage, including the publication of several trial transcripts and sensational Fleet Street accounts of his life. Perhaps as many as 20-30,000 people attended Palmer’s public hanging in Stafford and the public impact of his crimes is illustrated by a sermon given by the Rev John Scott of St Mary’s, Hull who used the case of William Palmer as an example of the evils of gambling and the dangers of insurance. Public interest in the case spanned the Atlantic, with multiple references to the case in the New York Times, including a scandalous account of the public reaction to the case and to Palmer’s execution. In short, the trial of William Palmer was notorious.
This case was also remarkable for a variety of reasons apart from the public notoriety it generated, not least among them its astonishing length (12 days), its location (special legislation was required to move the trial to London), and the considerable number of medical and scientific experts who testified during the course of the trial. The Palmer case turned on medical expertise since it was their testimony alone that could prove whether the victim had been poisoned or had died of natural causes. To this end, the prosecution and the defence called over a dozen witnesses, including well-known members of the English and Scottish scientific community as well as medical practitioners.
With multiple medical experts testifying, it should not be surprising that there was significant question after the trial as to whether Palmer had been justly convicted. This fear was remarkably persistent and as late as 1957, Robert Graves, best known for his novel I, Claudius published a book arguing that Palmer had been unjustly convicted. One possible reason for this persistent belief in Palmer’s innocence was that there was significant scientific controversy centered around the testimony of the leading prosecution witness, Alfred Taylor, who felt the need to respond to his critics in subsequent editions of his treatise On Poisons, a response heated enough to attract the negative comments of an American reviewer.
Not only was this case important in its day, it has also attracted the interest of a number of writers. For example, the courtroom controversy over Taylor’s evidence also led to a public scientific controversy that has been studied by Ian Burney. Burney used the debate over Taylor’s evidence as a lens through which to focus a larger discussion about the place of scientific evidence in the nineteenth century courtroom. Noel Coley’s biographical sketch of, Alfred Taylor, describes how his reputation was harmed by the controversy over Palmer. The Palmer case has also been discussed in the context of cases of poisoning, notably by Katherine Watson in her larger study of English poisoners. It was also referred to in Tal Golan’s history of scientific expert testimony as well as in Stephen Landsman’s historical survey of the use of expert testimony. Christopher Hamelin has used Palmer in comparing Victorian concerns over conflicting expert testimony with those of the 1980s. Thomas Forbes discussed the case in his history of medical testimony at the Old Bailey.
The focus of many of these writers is on how the Palmer case fits into larger Victorian concerns about the role of scientific expert evidence and the controversy that developed over the evidence presented at Palmer’s trial. This paper will discuss this question as well, but the focus will be slightly different than that of these writers. Instead of focusing on the role of the experts, this paper will focus on the role of the jury and in particular on the logic their decision had to follow in order to convict Palmer. This paper will argue that the Victorian jury in this case had to do a very modern thing: reach a verdict that required them to evaluate conflicting scientific evidence; in short, to make a scientific decision itself. To do so, this paper will analyse Palmer as if it were a scientific evidence case from today. When analysed from this perspective, Palmer’s case seems strikingly contemporary. As with many contemporary cases that turn on scientific evidence, the key issue in Palmer was how to interpret uncertainty in the scientific evidence presented to the jury. Leading chemists of the day were unable to detect the presence of poison in the victim’s stomach contents, perhaps in part because of interference by Palmer during the autopsy (he was able to participate as the victim’s friend and doctor). In order to resolve this quandary, both the prosecution and the defence called numerous medical experts to discuss the meaning of the lack of detection of poison; for if the poison ought to have been detectable then the lack of its detection represented powerful exculpatory evidence. If, on the other hand, the circumstances of the autopsy and the limits of the analytical chemistry of the day made the detection of poison unlikely, then no conclusion could be drawn one way or the other.
While there was substantial circumstantial evidence to suggest that Palmer had acquired poison and that he had ample motive to carry out such a plot, the diagnosis of the symptoms presented by the alleged victim, John Parsons Cook, were also subject to considerable debate. The poison that was alleged to have been used was strychnine, a poison that yields symptoms that are in many respects similar to those presented by tetanus, and the defence argued this alternative explanation for the symptoms exhibited by Cook, an explanation supported by the existence of a rarely-seen form of tetanus that was not preceded by an infected wound of one sort or another. Here as with the evidence of the stomach contents the jury needed to decide whether to accept that tetanus was a possible explanation or whether, as the prosecution argued, that this form of tetanus was so rare as to be an extremely unlikely explanation for Cook’s symptoms.
These decisions, made by the jury but doubtless strongly influenced by the long and detailed instruction given by Lord Chief-Justice Campbell, occur at the crossroads of scientific and legal dispute. The disputes as presented above are purely scientific yet they are without anything but purely academic meaning outside the courtroom setting. In the courtroom however, a man stood to be hanged on their resolution. Indeed it is hard to imagine the jury considering these issues individually outside of the context of the significant non-scientific circumstantial evidence that was presented in this case.
The case of William Palmer can be looked at as a scientific evidence case. Although there are many differences between this mid-nineteenth century British trial and a contemporary criminal case, many of the basic issues that needed to be addressed are strikingly contemporary and the ‘dueling experts’ who drew contradictory conclusions from the available data seem to present many of the difficulties contemporary writers concerned with ‘junk science’ tend to fret about.
However, in one key aspect, the way science is handled in the Palmer trial is very different than that of contemporary trials. Today, when scientific evidence seems unreliable its admissibility is usually questioned. The admissibility inquiry serves to do much of the ‘work’ of evaluating scientific evidence. In this nineteenth century case, on the other hand, there is little hint of significant dispute over the admissibility of any of the evidence presented, leaving most questions as to the relative importance of one or another expert’s opinion to be decided by the jury as a matter of weight, and in doing so they were therefore quite dependent on the judge’s summation. It is in that summation that the remarkable role of the jury in the Palmer trial comes into focus. In Palmer the jury was not only asked to choose between scientific experts, it was also asked to make its own scientific determination of sorts, blurring the roles of the courtroom and the laboratory.
The primary allegation against William Palmer was that he poisoned his gambling friend John Parsons Cook with strychnine (also called strychnia during this period). Along with this charge, Palmer was also indicted for the murder of his wife and of his brother, also by poison. These indictments were not proceeded with as Palmer was convicted of Cook’s murder and sentenced to death. There were also allegations in the yellow press that he had murdered his mother. All these poisonings were alleged to have been done for the purpose of obtaining money to pay gambling debts. The Palmer case also involved life-insurance, which was relatively new at the time, and it was alleged that Palmer had killed his brother in order to obtain the £13,000 for which Palmer had insured his life and that Palmer’s wife had died for a similar reason.
This was without a doubt a ‘trial of the century’ sort of case. The allegations against Palmer played on many fears and moral fixations of the era, primarily moral reprobation for gamblers and the fear that life insurance, now readily available to the middle class, created a substantial motive for the commission of the perhaps undetectable crime of poisoning. The sums of money involved were also quite large, totaling £13,000. Lurid descriptions of the case were published by the Fleet Street press along with sermons suggesting that Palmer’s fate was to be seen as a warning against the gambler’s life.
Against this lurid backdrop, the case itself focused on narrower issues: why did Cook die? Was he poisoned? What was the poison, was it strychnia? If so, could it have been administered by Palmer? These technical questions are also wrapped up in the non-technical evidence: the time frame of the events and the evidence supporting the contention of Palmer’s motive for committing the crime, for example. In his introduction to his 1912 book on the case, G H Knott remarks that: ‘We can hardly imagine a reader not being satisfied morally as to the guilt of Palmer, but were he to take the medical and chemical evidence alone ... we could at least imagine him holding his judgment in suspense.’ It was the jury that had to interpret all this evidence.
The trial itself was held on 14 May 1856 at the Old Bailey courts in London because of the intense public sentiment in Rugeley. Pre-eminent counsel represented all parties. The Attorney-General Sir Alexander Cockburn was lead counsel for the Crown with Edward James QC, Bodkin, Welsby, and Huddleston as juniors. Mr Serjeant Shee led the defence case, with Grove QC, Gray, and Kenealey. The case was presided over by a three-judge panel: Lord Chief Justice Campbell, Mr Justice Cresswell, and Mr Baron Alderson. The trial was also extraordinarily long, lasting 12 days, sitting eight hours a day. The prosecution’s case lasted until the sixth day of the trial on the 20th of May. The defence case went through to the tenth day, Saturday the 24th. The Court did not sit Sundays, and Lord Campbell reported in his diary that it took fourteen hours of preparation that Sunday to prepare for his summation. Lord Campbell’s summation to the jury itself went over two days with the trial finally concluding on Tuesday May 27th when the jury, after an hour and eighteen minutes deliberation returned a guilty verdict and Lord Campbell sentenced Palmer to death.
As often happens with controversial trials, many books were published after the fact. Multiple transcripts of the trial were published, and one grew so long that the original single volume publication grew into two. The scientific evidence presented led to a scientific controversy that continued after the trial was over. Egos had been bruised.
Much of the evidence presented was what we would today term forensic medical evidence. The prosecution led evidence that tended to show that Cook had died of strychnia poisoning. This scientific evidence was supported by circumstantial evidence that suggested that Palmer had both motive and opportunity to commit such a murder. The defence evidence focused on questioning whether Cook had been poisoned at all.
The analysis that follows is based on a close reading of the case as though it were a contemporary scientific evidence case. Of primary interest is to understand just how much of the scientific controversy found its way into the courtroom and how courtroom actors chose to handle this evidence, with particular reference to the role of the jury. Accordingly, this paper will focus on the scientific evidence and provide only a brief sketch of the other evidence presented and significant time will be devoted to the analyses provided in the closing addresses of both counsel and finally on Lord Campbell’s address to the jury.
The events leading to William Palmer being indicted for the murder of John Cook occurred in November of 1855, yet the prosecution argued that events preceding the murder by several months created sufficient motive to explain Palmer’s murder of Cook. The prosecution’s theory of the crime was that Palmer had abandoned his medical practice for horseracing and had over the last three years become indebted to various moneylenders. Palmer had forged a series of bills using his mother’s name and had discounted these bills with several moneylenders. He had been able to pay off debts of £13,000 to one moneylender as a result of the death of his wife whose life had been insured for that sum and Palmer had taken out a similar policy on the life of his brother, Walter, that was used to secure bills to the amount of £11,500 with a moneylender, Pratt. On Walter Palmer’s death the insurer refused to pay on the grounds that Walter’s death remained suspicious.
By November of 1855, Palmer was thus in very serious money trouble. Since these bills were secured using Palmer’s mother’s name, should Pratt decide that Palmer was in default he would sue Palmer’s mother, exposing William’s forgery as well as ruining him. This had become particularly urgent because on the 6th of November Pratt had issued writs against Palmer and his mother but had withheld service providing that Palmer continued to pay portions of the bills. The Attorney-General argued that it was this immediate need for money that caused William Palmer to kill his friend Cook.
Cook and Palmer had gone together from Rugeley to Shrewsbury, and it was at Shrewsbury where Cook’s mare ‘Polestar’ had won the Shrewsbury handicaps on the 13th of November, which gave Cook winnings of £2050 from which he had drawn about half and of which £1020 remained to be collected on Monday the 19th. Cook first became ill on the night of the 14th of November after drinking a glass of brandy that Palmer had adulterated, as the prosecution alleged. Palmer must have reassured Cook, for despite his concern over the brandy, the two men returned together to Rugeley and Cook stayed at the Talbot Arms, across the street from Palmer’s house, from the 15th of November. It was there that he died on the night of the 20th.
Palmer made several attempts to collect Cook’s additional winnings and make payments to the moneylenders he was indebted to; Palmer first traveled to London for this purpose on the 19th of November while Cook lay ill and again after Cook’s death on the 21st. It appeared that Mr Fisher, Cook’s betting agent, advanced Palmer £200 on the strength of Cook’s winnings and a letter to him from Cook written on the 16th. Another £450 was drawn from Cook’s winnings. This money and the previous £200 were applied toward Palmer’s debts to Pratt.
Cook, who had appeared healthy on the 16th, began to show signs of illness after drinking a cup of coffee given him by Palmer, showing similar symptoms as he had in Shrewsbury. The prosecution alleged that this was because on both occasions Palmer had adulterated Cook’s drink with antimony. Broth, also supplied by Palmer, appeared to have made Cook sick. Cook was not the only victim of the poisoned broth: the chambermaid who had warmed it tasted a spoonful, became sick thereafter, and was obliged to go early to bed. Cook remained ill throughout Saturday and Sunday (the 17th and 18th). Dr Bamford, eighty years old, attended Cook and prepared opiate pills containing morphia, among other ingredients. Cook revived on Monday while Palmer was in London. Palmer returned Monday evening and purchased strychnia from Mr Newton, a pharmacist’s assistant, according to Newton’s testimony. Another pharmacist, Hawkins, testified that Palmer purchased further strychnia on the morning of the 20th. Palmer remained with Cook until his death, and the prosecution alleged that Palmer had tampered with the pills prescribed by Bamford, substituting pills containing strychnia and that these pills killed Cook.
This sketch only presents the barest outline of the case the prosecution developed, but it does demonstrate how important medical evidence supporting a diagnosis of death by strychnia was to the prosecution’s case. If the prosecution could prove that Cook had in fact been murdered and that the murder was by strychnine, there was sufficient circumstantial evidence to point to Palmer as the likely culprit. Finding Palmer guilty would therefore require the jury to be convinced that he had been poisoned and the prosecution’s case was strengthened if they accepted that strychnine was the poison used. Crucial to that case were the circumstances of the post-mortem conducted on Cook and especially the behavior of Palmer who was present. However, before turning to the scientific evidence we shall first examine how the defence set about undermining the prosecution’s case.
The defence case followed two paths. The first was to cast doubt on the unflattering picture presented of Palmer by the prosecution witnesses. While acknowledging that Palmer had substantial debts, the defence questioned all key elements of the prosecution’s circumstantial case. Most importantly, they questioned the prosecution’s assumption that Cook was unwilling to help Palmer with his debts and suggested that Cook was helping Palmer, thereby removing Palmer’s primary motive as suggested by the prosecution. To this end, the defence used the letter of 16th November to support the contention that the bills being paid were part of a joint transaction taken by Palmer and Cook, and that Palmer had Cook’s authority to use Cook’s winnings to pay down Palmer’s debts. This was important as it suggested that Palmer had little motive to want Cook dead. The defence also attacked the testimony of Newton, the pharmacist’s assistant, arguing that he should have come forward earlier as to his testimony that Palmer had purchased strychnia from him which was given only during the trial.
However, despite these and other attacks on the credibility of prosecution witnesses, the defence’s case centered on refuting or casting doubt on the prosecution’s contention that Cook had been poisoned by strychnia. To this end the defence adduced expert evidence that Cook had been in poor health, that disease not poisoning might have led to his demise, and that his death had therefore likely been from natural causes. The key to the defence case was to establish that some agent other then strychnine might have caused Cook’s death and if possible that strychnine had not been the cause. The defence, like the prosecution, used substantial numbers of expert witnesses and the key to the defence case lay in their testimony.
This approach is similar to one that might be used today, in that it sought to make the jury doubt not only the connection of the death to Palmer but also make them doubt the very fact that a homicide had been committed.
The prosecution case depended on proving, first, that Cook had not died from natural causes and, second, that the cause of his death had been poison. No matter what the poison Palmer seemed the likely culprit based on the circumstantial case, but the case was enormously strengthened if the poison used was strychnia as Palmer had been observed purchasing that poison. All elements of this case could only be proved through expert testimony for poisoning, unlike physical violence, left no cause of death obvious to the layman. The defence attempted to counter these three elements of the prosecution case at every opportunity, with varying degrees of success. Many witnesses gave testimony on all three points, but it is useful to bear in mind this logical structure as the medical evidence is reviewed.
The medical testimony began on the second day of the trial. During the second and third days the prosecution sought to establish that Cook had been in good health and that his death occurred because of tetanus. Two types of tetanus were discussed at Palmer’s trial: the first was what would commonly be called tetanus today and is always associated with a cut or wound of some sort, which is now understood to allow entry of the tetanus bacterium into the body. The second type, called ‘idiopathic tetanus’ in the transcript, refers to tetanus symptoms without the presence of a cut. What caused these symptoms was not well known, but one possible cause was strychnine poisoning. The prosecution relied on the testimony of Cook’s doctor and the chambermaid who both supported the description of Cook’s symptoms as tetanus. In particular, the testimony of Mr William Henry Jones, the medical practitioner who had attended Cook at his death, was used to provide a graphic and detailed picture of his death as well as a preliminary diagnosis. While there was some effort by lead counsel for the defence, Serjeant Shee, to impeach Jones’ testimony based on the transcript of the Coroner’s report, this approach was not particularly successful. Testimony from Jones, Mr Henry Savage, who was Cook’s physician, as well as testimony from Dr John Thomas Harland who conducted two post-mortem examinations of the deceased was used to support the contention that not only had Cook been in good if not robust health, but that there was also nothing found during the autopsy to suggest a natural cause for his death.
Having established that Cook died of tetanus symptoms, the prosecution needed to establish that it was not an incidence of one of the usual forms of tetanus. To this end five experts on tetanus presented evidence. Since no wound had been found on Cook’s body a diagnosis of traumatic tetanus was not possible. Idiopathic tetanus had similar symptoms, but without the presence of a wound. It was extremely rare in England.
The witnesses for the prosecution gave their opinions that the progress of the disease observed in Cook could not have been idiopathic tetanus. Both idiopathic and traumatic tetanus had clear and well-defined patterns of progression with the tightening of the jaw muscles invariably being one of the earlier symptoms. Cooks’ ability to take drink shortly before his death would have been impossible for one suffering from either usual form of tetanus. Also telling was the break in Cook’s symptoms on the 19th as pauses in the progression of tetanus symptoms were not observed. The defence also suggested that epilepsy or apoplexy (a stroke) might have led to Cook’s symptoms, but these possibilities were dispensed with on symptomatic grounds and based on the autopsy findings. All prosecution witnesses concluded the strychnia could have caused the observed symptoms but lacked clinical experience with strychnia poisoning.
Up to this point the main focus of the prosecution’s case was to weed out other possible causes for the symptoms experienced by Cook. The first part of the prosecution’s case was to prove to the jury that the symptoms observed could not be the result of idiopathic tetanus and therefore could not be from some source other than poison. The next step was to prove that they could only have been caused by the administration of strychnia. To this end the prosecution presented three cases of poisoning by strychnia described by eight witnesses both medical and lay. They described symptoms similar to those experienced by Cook leading to the inference that his death could likely have been brought about through the administration of strychnia. Crucial to this testimony was the personal and clinical nature of the experience of the observers.
If strychnia had been found during the post-mortem then the prosecution case would have been complete. With today’s analytical techniques it could hardly have been missed, but the analytical techniques of the mid-nineteenth century were considerably limited and the ability of the chemists to detect the poison had been additionally hindered by the circumstances of the autopsy including the alleged interference of the accused in the collection of the stomach contents. The stomach contents and the stomach itself had been sent to the preeminent analyst, Dr Alfred Taylor, best known for a treatise on poisons and their detection. Taylor had failed to detect the presence of strychnia, a failure he attributed to the use of the minimum lethal dose as well as the circumstances under which the samples were collected. Taylor’s conclusions were supported by his inability to detect strychnia, Taylor declared that there was no other possible cause of the symptoms Cook experienced.
This was very damning testimony, for it linked Palmer directly to the death by virtue of his purchase of strychnia. It also provided a point of attack for the defence: if Taylor should have been capable of detecting strychnia not only would that impeach his professional credibility it would also cast significant doubt as to whether Palmer caused Cook’s death since the only direct, as opposed to circumstantial, link to Palmer was through his purchase of the poison. Serjeant Shee vigorously cross-examined Taylor but was unable to shake his testimony. However, Taylor was sufficiently perturbed by this examination and the subsequent controversy that attended his role in Palmer’s trial that he felt the need to defend himself. He published a pamphlet describing the evidence in the case in 1856, and in the Second Edition of On Poisons, in 1859, Taylor attacked the character of the defence witnesses in the Palmer trial:
It argues but little for the knowledge or moral feelings of medical witnesses, and must shake the confidence of the public, as it has already done to a great extent in the trustworthiness of medical opinions. Such must be the result when scientific witnesses accept briefs for a defence; when they go into a witness-box, believing one thing, and endeavor to lead a jury by their testimony to believe another,—when they make themselves advocates and deal in scientific subtleties, instead of keeping to the plain truth. Such men should be marked by the public, and their efforts at endeavoring to confer impunity on the foulest crimes, and to procure the acquittal of the most atrocious criminals should be duly noted.
In his 1875 edition of On Poisons Taylor continued to respond to the criticism leveled at him in the Palmer trial. Nineteen years later, the experience still smarted.
The defence case focused on casting doubt in the minds of the jury about the diagnosis of strychnia poisoning that the prosecution’s case rested upon. Their first witness, Thomas Nunneley first attempted to re-characterise Cook as being in generally poor health and to suggest that his symptoms did not coincide with those for strychnia poisoning. This witness was very effectively cross-examined. He proved unable under cross-examination and the questioning of Lord Campbell to distinguish the symptoms of the known strychnine poisoning cases from the symptoms experienced by Cook, and in a strikingly modern moment this witness was asked how much of his research on strychnia occurred in preparation for the trial, thus casting aspersion on the validity of his results.
The defence also presented testimony of four witnesses who gave evidence that strychnia should have been detected in the body despite the condition of the sample available to the prosecution’s witness, Dr Taylor. In particular Dr Henry Letheby suggested that strychnia could have been detected by means of the ‘color test’, a test Taylor discounted because of the possibility of giving false positives. This testimony was much more effective than that of Thomas Nunneley in that it raised serious questions as to the technical competence of Dr Taylor (perhaps explaining his heated reply). However, while the defence might have convinced the jury that it may have been possible to detect strychnia in the stomach contents as presented to Dr Taylor they were not able to state that Dr Taylor’s methods should have detected it. This is a crucial distinction and a fundamental weakness in the defence case, and one noted by Lord Campbell in his charge to the jury.
The final element of the defence case rested on supplying alternate diagnoses for Cook’s symptoms. There were suggestions that it could have been idiopathic tetanus, that it could have been caused by arachnitis (a swelling of tissues in the spine), or that it could have been caused by some sort of convulsive fit. Epilepsy was considered to have possibly been brought on by hysteria or ‘a passion’ as one witness termed it and this therefore related well to the earlier concern over the state of Cook’s health.
The defence thus attempted to cast doubt on the prosecution’s explanation of Cook’s symptoms and provided an alternate explanation for them. Up to this point in the trial, what is remarkable is how contemporary the logic of the prosecution and defence cases is. If one were to defend Palmer today, while the specifics of trial procedure and scientific evidence have changed, one would likely construct a reasonable doubt defence in precisely the same manner. In this sense, the way the defence confronted damning scientific evidence by casting doubt on its viability and suggesting an alternate interpretation seems comparable to what might be done today.
Much of Lord Campbell’s charge to the jury consisted of reading back large portions of the transcript and in particular of medical evidence provided by prosecution witnesses. Lord Campbell also summarised elements of the medical evidence or provided commentary after the transcript was read. The following will concentrate on those instances where Lord Campbell chose to provide analysis of the medical evidence to the jury.
Lord Campbell first explained to the jury that they could convict on circumstantial evidence and warned them not to place much weight on the potential motive of the accused. Lord Campbell then made the following address:
It seems to me, gentlemen, you will have to consider well whether the symptoms of Cook’s death are consistent with poisoning by strychnia. If they are not, if you believe that death arose from natural causes, the prisoner is at once entitled to a verdict of not guilty at your hands; but if the symptoms are consistent with poisoning by strychnia, then you will have another and important question to consider, whether the evidence which has been presented is sufficient to convince you that it was a death by strychnia, which the prisoner administered.
Thus the jury is asked to consider all three key elements of the prosecution’s case that must be proven to reach the conclusion that Palmer had poisoned Cook. Further, Lord Campbell instructed them that the ultimate verdict should not be based on ‘medical’ or ‘moral’ evidence alone but rather was based on the both taken together.
Lord Campbell also provided a few helpful indicators for determining credibility: he stressed the danger of witnesses not becoming advocates and to take notice of the manner with which certain testimony was given (eg, Mr Nunneley). He also stressed that regard should be had for the professional status and personal experience of witnesses when evaluating their testimony.
Much of the testimony for the prosecution was simply read to the jury without comment, including the evidence given by Dr Taylor. However, there was substantial discussion of the defence witnesses. In this discussion, Lord Campbell suggested that the weight of the evidence led to the conclusion that the lack of a wound made it likely that the cause of death was not traumatic tetanus and that the ‘symptoms vary most materially in their appearance’ when compared with idiopathic tetanus. He also strongly impugned the testimony of Dr M’Donald, and more or less suggested that he had devised a new form of epilepsy to support the defence, but suggested to the jury that: ‘from the symptoms you will say whether you can come to that conclusion.’ While this approach to jury instruction is unimaginable today, their verdict was necessarily predicated on reaching a decision on a scientific fact: the cause of Cook’s death.
After a short wrangle with the lead defence counsel over the wording of the final charge, the case was sent to the jury and they returned in 1 hour and 18 minutes with a guilty verdict after which Palmer was sentenced to death. Later one of the jurors said that they consulted for 20 minutes, voted on a guilty verdict, and spoke of other matters for an hour before returning their verdict. This suggests little doubt in their minds of the validity of the evidence against Palmer.
The first observation one might make is that though over 150 years old this case seems very modern. This is so in several ways. First, the prosecution’s case is predicated on a determination of wrongful death that depends on a scientific finding: death by poison. Second, the way that death occurred, allegedly by strychnia, implicated the defendant circumstantially. Third, the defence’s response to the prosecution’s case was to cast doubt on their scientific evidence by using their own scientific expert testimony. Fourth, the jury’s finding, because they needed to find that there had been a wrongful death, necessarily required that they accept at least the first part of the prosecution’s theory of poisoning. This presentation of a prosecution theory of the case complete with an interpretation of forensic medical evidence has changed little, nor would the defence tactic of casting doubt on individual elements of the analysis and providing alternative theories seem out of place in a courtroom today.
The overall feel, as one reads the case, is that but for the Victorian language and trial procedure, this case could occur today. This feeling extends to minor elements of the trial like, for example, the method by which the stomach contents were collected, leading to questions that are in a way similar to contemporary chain of custody issues. However, what is most strikingly contemporary is the role the jury assumed in the Palmer trial.
The imperatives of legal decision-making obliged the legal actors, the judges and the jury, to become scientific actors in the sense that deciding whose testimony to believe involved making a scientific judgment. This can be seen clearly in Lord Campbell’s summation where he invites the jury to make their own diagnosis, and proceeds to do so himself in summarising the evidence presented. In the Palmer case, members of the jury were therefore required to act as diagnosticians presented with a description of symptoms, and a series of possible diagnoses. In such a case it is the jury in its role as fact-finder that becomes burdened with the task of developing an appropriate diagnosis of the victim’s illness as a necessary part of reaching a verdict. We cannot know what was said in the jury room or what went on in the jurors’ minds. However, if they followed the rationale for convicting Palmer set out in Lord Campbell’s charge, they must have come to some conclusion regarding the likely cause of Cook’s symptoms and death, a conclusion that was, at its heart, a scientific one.
This role of the jury as scientific fact-finder is a controversial one, to the extent that Justice Blackmun mentioned it in his decision in Daubert but Palmer demonstrates that it is not a novel one. Christopher Hamlin looked at a number of mid-nineteenth century English cases, including Palmer, and was struck by the similarity between the disagreements that occurred between experts then and now. A similar observation could perhaps be made about the role of the jury. If so, we need to think of the jury’s role as a scientific fact-finder as one that emerged with the development of the modern jury trial, and emphasise the historical continuity of this role as opposed to seeing it as novel.
If there is much that seems contemporary about this case there is also much that is clearly different from a contemporary criminal case involving controversial scientific evidence. Even before the decisions in Mohan in Canada and the earlier Daubert decision in the United States and subsequently, there has been a tendency to tighten up the admissibility requirements for scientific evidence. Following those decisions, there has been a tendency for courts to specify the kind of science they would like. With DNA evidence as the model, courts tend to prefer empirically and statistically validated evidence, while the Palmer case suggests a nineteenth century preference for individual clinical experience coupled with professional position as the primary evaluative criteria.
However, despite differences in courtroom procedure and drastic changes in scientific practice, the fundamental problem faced by the court when addressing scientifically controversial evidence was precisely the same as that faced by modern courts: how do courts make valid scientific decisions about controversial scientific evidence? Ultimately, a court must make a decision, and when the scientific community is in disagreement it seems impossible for the end result to be anything but controversial. As Ian Burney has noted, there was no firm line delineating the legal, scientific, and public controversy that erupted from the case, something also readily apparent in the ‘science wars’ of the 1980s and 1990s in the United States.
What Palmer shows is that many of the elements that are associated with today’s scientific testimony were present in this Victorian case. In light of this, when thinking about scientific evidence, perhaps the most appropriate approach is not to consider today’s scientific evidence issues as exceptional and new but instead to see them as part of an historical, longstanding relationship between science and the law.
[*] Assistant Professor, School of Public Policy and Administration, York University, Toronto, Ontario, Canada.
 See A Bennett, Verbatim Report of the Trial of William Palmer at the Central Criminal Court, Old Bailey, London (J Allen, 1856); and G H Knott (ed), Trial of William Palmer: Notable English Trials (Canada Law Book Company, 1912). The 1912 version is an edited version of Bennett’s shorthand notes. All page references will refer to this later edition unless otherwise noted. See also, G Lathome Browne and C G Stewart, Reports of Trials for Murder by Poisoning (Stevens and Sons, 1883).
 Eg see Ward and Lock, Illustrated Life and Career of William Palmer, Rugeley: Containing details of his conduct as a school-boy, medical student, racing-man, and poisoner; with original letters of William and Anne Palmer, and other authentic documents; together with the whole of his private diary up to the hour of his arrest, and the fullest particulars respecting his execution at Stafford (Ward and Lock, 1856).
 Ibid 111.
 Rev John Scott M A, The Fatal Consequences of Gambling (J Pulleyn, 1856), see pages 9-10 for his thoughts on the dangers of insuring lives for ‘princely sums.’
 ‘The Great Poisoning Case’, New York Daily Times (New York) 9 February 1856, 4; ‘One Week Later From Europe’, New York Daily Times (New York) 11 February 1856, 1; ‘The English Poisonings’, New York Daily Times (New York) 11 February 1856, 4; ‘The Palmer Poisonings’ New York Daily Times (New York) 16 June 1856, 1.
 ‘A National Taste in Great Britain’ New York Daily Times (New York) 28 June 1856, 4.
 Katherine Watson, Poisoned Lives: English Poisoners and their Victims (Hambledon and London, 2004) 102; Central Criminal Court Act 1856, 19 & 20 Vict, c 16.
 G H Knott, above n 1, Introduction.
 Eg see T Wakley, The Cries of the Condemned: Proofs of the Unfair Trial of William Palmer (C Elliot, 1856).
 R Graves, They Hanged my Saintly Billy: The Life and Death of Dr. William Palmer (Doubleday, 1957).
 A S Taylor, On Poisons in Relation to Medical Jurisprudence and Medicine (2nd American ed, Blanchard and Lea, 1859).
 Anonymous, ‘Notices of New Books: On Poisons, by Alfred Swaine Taylor’ (1858-1859) 7 American Law Register 573.
 I A Burney, ‘A Poisoning of No Substance: The Trials of Medico-Legal Proof in Mid-Victorian England’ (1999) 38(1) Journal of British Studies 59; and I A Burney, Poison, Detection, and the Victorian Imagination (Manchester University Press, 2006).
 Noel G Coley, ‘Alfred Swaine Taylor, MD, FRS (1806-1880): forensic toxicologist’ (1991) 35 Medical History 409.
 Watson, above n 7.
 Tal Golan, ‘The history of scientific expert testimony in the English courtroom’ (1999) 12 Science in Context 7; and Tal Golan, Laws of Men and Laws of Nature: The History of Scientific Expert Testimony in England and America (Harvard University Press, 2004).
 Stephan Landsman, ‘Of Witches, Madmen, and Product Liability: An Historical Survey of the Use of Expert Testimony’ (1995) 13 Behavioral Sciences and the Law 131, DOI: 10.1037//1076-89188.8.131.52.
 Christopher Hamelin, ‘Scientific Method and Expert Witnessing: Victorian Perspectives on a Modern Problem’ (1986) 16 Social Studies of Science 485.
 Thomas Rogers Forbes, Surgeons at the Bailey: English Forensic Medicine to 1878 (Yale University Press, 1985).
 Although Forbes does cite the charge to the jury. See ibid 148.
 See P W Huber, Galileo's Revenge: Junk Science in the Courtroom (Basic Books, 1991). The junk science framework has been extensively criticised: see, for example, G Edmond and D Mercer, ‘Trashing “Junk Science”’ (1998) Stanford Technology Law Review 3.
 The wife was probably poisoned with antimony and the brother with prussic acid. See Watson, above n 7, 103.
 Ibid 101-102.
 Knott, above n 1, 1.
 Ibid, Lord Campbell’s diary at 289.
 Palmer was subsequently indicted for both deaths, see ibid at 4. Knott provides an excellent summary of the events leading to the trial, ibid at 1-17.
 Tetanus in this case does not refer to the bacterial disease for which we commonly use the word today but rather to the symptoms associated with that disease.
 Knott, above n 1, 44-48.
 Ibid 49.
 Ibid 63-69.
 Ibid 70-74.
 Ibid 55-58.
 Ibid 75-83.
 Alfred S Taylor, On Poisoning by Strychnia; with Comments on the Medical Evidence at the Trial of W. Palmer for the Murder of J. Cook (London, 1856).
 Taylor, above n 11, 703.
 Alfred S Taylor, On Poisons in Relation to Medical Jurisprudence and Medicine (J & A Churchill, 1875) at 725-726 not only defends himself but feels moved to chastise the defence witnesses:
If strychnia has been administered in pills and, after death, the stomach has been cut open and the contents lost, there will be little hope of discovering the poison, although in Reg. v. Palmer (C.C.C. May 1856) some experts affirmed that this state of things would not materially interfere with the chemical process for its detection! ...
It is satisfactory to find that a correct view of this remarkable case, and its true bearing on science, has been shown by continental jurists. In an analysis of this case, by the late Professor Casper (Horn’s ‘Vierteljahrsschrift,’ Juli 1864. p. 26), not only are the chemical results justly regarded as negative, by reason of the gross mismanagement of those who inspected the body, but the post-mortem appearances themselves, for a similar reason, are considered as throwing no light upon the effects of strychnia on the body. The active co-operation of a professional poisoner, at the examination of the body of his victim, is an exceptional circumstance, even for the liberal customs of this country! It was only in the natural course of things that attempts should be made to defeat a chemical analysis, but when such attempts have proved successful, it is not usual to find scientific witnesses actively struggling for the honour of defending a prisoner, not because the deceased did not die from poison, but because it was not chemically detected in his body. The failure of this branch of evidence furnished a favourable opportunity for introducing a variety of ingenious speculations on the cause of death.
 Knott, above n 1, 161-174.
 Ibid 174-180.
 Ibid 269.
 Ibid 269-270.
 Ibid 271-272.
 Ibid 278-279.
 Ibid 281.
 Ward and Lock, above n 2.
 William Daubert et al v Merrell Dow Pharmaceuticals Inc USSC 99; , 509 US 579 (1993).
 Christopher Hamlin, ‘Scientific Method and Expert Witnessing: Victorian Perspectives on a Modern Problem’ (1986) 16 Social Studies of Science 485.
 R v Mohan,  2 SCR 9.
 Hamlin, above n 46.
 See, eg, US National Research Council, Committee on identifying the needs of the forensic science community, Strengthening Forensic Science in the United States (National Academies Press, 2009).
 For an understanding of the ‘science wars’ see, Segerstråk, Ullica ‘Science and Science Studies: Enemies of Allies?’ in Ullica Segerstrak (ed), Science Wars: The Missing Discourse about Science and Society (SUNY Press, 2000) 1; and S J Gould ‘Deconstruction the “Science Wars” by Reconstructing an Old Mold’ (2000) 5451(287) Science 253.