The death of Socrates in 399 BCE, as reported by Plato in the Phaedo, is usually attributed to poisoning with common hemlock. His progressive centripetal paralysis is characteristic of that poison. Socrates is said to have had a prominent loss of sensation extending centrally from his legs, which is not a feature of hemlock poisoning, and he seems not to have had the unpleasant taste or common gastrointestinal effects of that poison. It is suggested that Plato gave a modified account of the death of Socrates for political and other reasons by describing a more “noble” death.
- hemlock poisoning
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The execution of Socrates by the Athenian state in 399BCE is a dramatic event in the history of political philosophy. It has often been discussed from philosophical and historical viewpoints1–6 and almost as often by physicians trying to decide what poison was used to kill him.7–9
The common suggestion has been that he died after drinking an extract of hemlock (common hemlock; Conium maculatum L; sometimes mistakenly called Fools’ Parsley, Æthusa cynapium L—see, for example Ober8 and Bloch1), but just as the reasons for his trial and execution are disputed, doubt still remains about the true nature of the poison employed. The matter still deserves consideration because the accuracy of the account of his death bears directly on the greater controversy about the nature and quality of the reasons given for putting him to death.
It is proposed here that the fatal draught included more than hemlock based on evaluation of the pharmacology and toxicology of hemlock alkaloids and reassessment of the clinical feature of his terminal condition, including a somewhat neglected physical sign.
DEATH OF SOCRATES
The fullest near contemporary account is in Plato’s dialogue “Phaedo”, probably written a few months after the execution. Plato, a close pupil and the academic successor of Socrates, was not present at his death, but he recounts details given by another pupil Phaedo, who was present, to a mutual friend Crito.10
Xenophon, who was not present at the execution, also discusses the trial and death of Socrates but gives no additional information.11 His account was written several years after the event and its sources are not given.
The closing paragraphs in the Phaedo, where the effects of the poison on Socrates are described, have often been translated into English, with similar wording being used on every occasion. There are some problems in translating the Greek text,12 but they do not affect the more important features of the key paragraphs. A modern standard version, as used here, was published by Grube13 and is close in important details to a classical version by Jowett.14
The important text is:
… the man (gaoler) who was to administer the poison carrying it ready made in a cup. …. (Socrates asked) “…what must one do?” – “Just drink it and walk around until your legs feel heavy, and then lie down and it will act of itself.” …. [Stephanus 117a–b]
His words (Socrates) made us ashamed and we checked our tears.
He walked around, and when he said his legs were heavy he lay on his back as he had been told to do, and the man who had given him the poison touched his body, and after a while tested his feet and legs, pressed hard upon his foot, and asked him if he felt this, and Socrates said no. Then he pressed his calves, and made his way up his body and showed us that it was cold and stiff. He felt it himself and said that when the cold reached his heart he would be gone. As his belly was getting cold Socrates uncovered his head – he had covered it – and said – these were his last words – “Crito, we owe a cock to Asclepius; make this offering and do not forget.” – “It shall be done,” said Crito, “tell us if there is anything else.” But there was no answer. Shortly afterwards Socrates made a movement; the man uncovered him and his eyes were fixed. …” [Stephanus 117e–118]
CLINICAL FEATURES OF SOCRATES’ DEATH
That is all the information we have about the death. The subsequent analysis has been based solely on the symptoms and signs reported by Plato from Crito’s account.
The cardinal clinical features are:
A. Positive findings
Centripetal paralysis spreading from the feet to the abdomen and chest. Death appears to have been caused by respiratory failure, presumably as the diaphragm and chest muscles became affected.
A feeling of “cold” in the calves and “stiffness” there. Both feelings also spread upwards to the belly and it is implied to the chest before death as suggested by “.. the cold reached his heart..”.
Centripetal loss of peripheral sensation in the legs as Socrates became unable to feel pressure on his feet and calves.
The period between swallowing the poison and death is not certain. It must have been quite brief because the dialogue suggests that all the events, including the lengthy philosophical excursions, happened in less than a day and probably took only a few hours.
B. Negative findings
Pertinent general effects not reported are abdominal pain, nausea, vomiting or diarrhoea.
Other actions that can be excluded by Socrates’ behaviour and actions at the time are confusion or clouding of consciousness, unawareness of friends nearby or of current events, loss of speech, seizures, headache, abnormal movements and sweating.
The strength of the exclusion of these symptoms and signs depends on the quality and accuracy of Plato’s report of Crito’s account. As the description of positive effects by the gaoler and by Crito are so definite it seems reasonable also to accept the absence of these major clinical findings because they are not described.
WHAT POISON MIGHT HAVE BEEN USED
Analysis of the toxic actions must be based on what is stated in the Phaedo or can reasonably be deduced from it and on knowledge of the poison used for state executions in Athens at that time.
A striking clinical effect, which has dominated all previous discussions, is that of flaccid, centripetal paralysis of the legs, eventually extending to the abdomen and chest and not associated with any twitching or spasticity. There is no indication of any central disorder as Socrates was able to relate to and tell Crito to do something rational until what must have been only a short while before his death. The restriction of paralysis to the lower part of the body is noteworthy; his legs and eventually trunk were affected but Socrates was able to use his arms to uncover his face only a short while before his death.
Associated with that is a clear account of centripetal loss of pressure and pain sensation in the legs, which has been little considered except briefly by Ober,8 and in a superficial and misleading analogy with the Guillain–Barré syndrome by Bloch.1
The Greek text refers to the poison only by the general term “Pharmakon”, which is usually translated as “drug” and does not further identify the agent used.
The idea that “hemlock” (Greek “koneion”), more specifically the common hemlock (C maculatum L), was the poison is of considerable antiquity.1 Although attacked on linguistic as well as on medical grounds it has remained the favourite of all writers, at least since the 18th century, albeit sometimes with the important suggestion that other pharmacologically active substances might also have been present.
There are powerful linguistic and exegetic arguments for common hemlock.1 2 5 Their analyses and clinical considerations7–9 have been used to rule out extracts of other poisonous plants, such as water hemlock (Cicuta maculatum L) and water dropwort (Oenantha crocata L) on the basis that they would have produced an entirely different clinical syndrome, dominated by seizures, vomiting, abdominal cramps and diarrhoea.
They and others, especially Bonner,15 have rehearsed the evidence that common hemlock was known to grow in classical Greece, there was awareness of its poisonous properties, and that it was used in official executions in Athens.
It has been generally accepted that the symptoms and signs of Socrates, as reported in the Phaedo, could all be attributed to the known effects of “hemlock poisoning” (meaning common hemlock). It is concluded here that review of the experimental and clinical toxicology of common hemlock and its alkaloids does not bear out this simple notion because of the striking clinical feature of loss of sensation in the legs.
TOXICOLOGY OF COMMON HEMLOCK
Common hemlock contains eight identified alkaloids, all piperidine derivatives, five of which predominate in amount and toxicity. Their relative concentrations in different parts of the plant and at various times of the year may differ.16 17
The alkaloids of greater importance are coniine, γ-coniceine, conhydrine, psuedoconhydrine and N-methylconiine. The experimental pharmacology of the three most toxic compounds, coniine, γ-coniceine and N-methylconiine, has been extensively investigated.18–20
The studies show that all three alkaloids cause initial stimulation followed by dose dependent blockade of spinal reflexes due to actions within the spinal cord. The site of the inhibitory action is not certain and it probably involves actions on both central inhibitory and excitatory neurons. Direct neuromuscular blockade may also be found, due mainly to a reduction in the release of acetylcholine from motor nerve endings, and also to a complex “mixed” postjunctional action.18 Autonomic ganglia and reflexes can be stimulated and then depressed. Intravenous injection in the mouse resulted in convulsions, clonic and tonic contractions of the limbs, and frequently in micturition followed by paralysis before death. Only a very weak local anaesthetic action in the skin and cornea was found even after high intravenous doses in animals. Nociceptive responses were not affected. Autonomic and sensory reflexes were preserved until there was evidence of pronounced inhibition of spinal reflexes, when there was inhibition of peripheral ganglia and blockade of adrenal medullary secretions. No signs of effects at higher levels in the brain were found.
The relative potency of the three principal alkaloids in the mouse, as shown by their oral LD50s, was coniine 100 mg/kg, N-methylconiine 204.5 mg/kg and γ-coniceine 12 mg/kg; death occurred after 8–12 min.
A similar sequence of paralysis after convulsions in rats and mice injected intravenously with an extract of hemlock and with pure coniine has been independently described.19
The toxicity of hemlock in man and domestic animals has been described in detail over many years as the plant has often been eaten in mistake for parsley and carrots, and it has been grazed by foraging farm animals.
The clinical literature about human poisoning has been broadly reviewed8 9 19 and is more briefly covered by classicists.1 2 5 There are particularly clear accounts by Christison,7 based on his own studies of patients in Scotland and elsewhere who had mistakenly eaten hemlock, and by Sigmond21 and Thomson2 22 drawing on several sources. More recent series and case reports23–25 as well as overviews in monographs on poisonous plants and on toxicology have reported broadly similar findings.26–28 The older literature does sometimes show uncertainty about the species of hemlock involved in cases of poisoning,21 22 but their reports, and especially that by Christison,7 are still worth consulting because they are primary accounts of the pattern of the clinical disorders and not repetitions of previous descriptions.
A dominant finding in all cases has been of paralysis of the legs extending centripetally before death caused by respiratory failure once the diaphragm and chest muscles were affected. The rate of progress has depended on the dose (and doubtless on the concentration of alkaloid in the plant and the extracts). Many reports have mentioned a bad taste in the mouth, salivation, nausea and occasionally vomiting, and sometimes abdominal pain and diarrhoea; convulsions have been rare. Higher neurological functions, such as consciousness, speech and cognition have always been preserved until the end. The upper limbs appear not to have been clinically affected.
No account has mentioned abnormal feelings or loss of pain or pressure sensation in the legs or elsewhere in the body, apart from a few old anecdotes7 21 not repeated in more recent reports. Painful muscles were mentioned in a series of 11 cases of severe hemlock poisoning,29 suggesting that the loss of peripheral sensation might be surprisingly selective.
Farm animals and some species of birds, large numbers of whom may be poisoned by grazing on hemlock, show weakness and its consequences, paralysis, mydriasis, salivation, cold limbs and respiratory failure resulting in death. Non-lethal doses have sometimes been associated with central depression and sedation or coma. A prominent effect has been teratogenicity in pregnant animals. There has been no report of loss of peripheral sensation.
Thus, allowing for differences in dose and variable attention paid to different symptoms and signs by observers over several centuries, the principal reported effects of hemlock poisoning in several species, including humans, have been of centrally extending paralysis of the legs and a variable range of gastrointestinal disorders. There have been no reliable reports of loss of sensation in the legs or arms.
THE CAUSE OF SOCRATES’ DEATH
The paralysis of his legs extending up to the chest can readily be accounted for by the known effects of hemlock. The comments on their “coldness” and “heaviness” can reasonably be explained by the medical and physiological beliefs of the Greeks.1 The clinical features of hemlock poisoning would also account for the preservation of consciousness and rational thought and speech until the end, as shown by his request to Crito, and for retention of his ability to use his hands and arms to displace the face covering.
The apparent absence of nausea, vomiting, salivation and bad taste might be due to an understandable reluctance by Crito or Plato to record relatively minor but unpleasant complaints that could detract from the simple account of a noble death. An alternative proposal,19 that the fatal drink included sufficient opium extract to prevent gastrointestinal actions, seems less likely. Opiates would not suppress all the effects described and Socrates retained awareness and consciousness to the end unlike someone exposed to a high dose of an opium extract.
The major clinical finding emphasised in the Phaedo that cannot be explained by hemlock poisoning is centripetal loss of pain and pressure sensation in the legs. It has not been regularly associated with clinical reports of hemlock poisoning and it is not consistent with the experimental pharmacology of its principal alkaloids. This point was first made by Christison,7 who commented that it was not a feature of his cases of hemlock poisoning. The sensory loss is so clearly described in the dialogue that, unlike the vaguer “coldness” and “heaviness”, it cannot reasonably be attributed to the way in which the Greeks described their beliefs about vital functions. The possibility that the fatal drink also contained some opium extract cannot explain the peripheral anaesthesia.
An extensive search of the literature has not revealed any plant extract or other substance likely to have been available in the 4th century BCE or nowadays that could have produced this effect in a very short while after drinking it, nor is there any drug or chemical nowadays that would have had the same action acutely after oral administration without many other unmistakeable symptoms and signs.
It appears, therefore, that although the death of Socrates can reasonably be ascribed to poisoning with an extract of hemlock, the account in the Phaedo is not accurate because it describes a major clinical disorder that is not caused by hemlock poisoning. There is likely also to have been suppression of information about the effects of hemlock on the gastrointestinal system.
Why is the account inaccurate? The simplest explanation—that Plato was only recording second hand what Crito told him and that a mistake was made—is improbable because of the extended and detailed nature of the description of centripetal anaesthesia.
It seems more likely, as others have suggested,2 that the account of the death of Socrates was modified to present a more appealing and wholesome case for his greatness as shown by the nobility of his death. A further speculation, consistent with Greek ideas about vital functions of the body, is that as the great philosopher died the perception of onlookers was that his “vitality” withdrew from his body, resulting in concurrent centripetal paralysis and loss of sensation—lifelessness of the legs and trunk terminating in complete lifelessness—death.
I am very grateful for the friendly critique and generous advice of Professor C Gill, University of Exeter, and for the help of Dr J Green, Birkbeck College, London, and Ms Debbie Lancaster, Alpha Omega Alpha.
Competing interests: None declared.
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