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Intoxicated automatism: legal concept vs. scientific evidence.

The concept of automatism as a consequence of severe alcoholic intoxication received much public and media attention as a result of the decision of the Supreme Court of Canada in the case of Daviault v. R. and decisions in several other courts subsequently. As a result of public indignation over the decision in Daviault v. R., the Minister of Justice introduced legislation to the House of Commons to eliminate intoxicated automatism as a possible defense in such crimes as assault and sexual assault. This legislation eventually came before the Standing Committee on Justice and Legal Affairs, which was required to decide whether or not to recommend this proposed change in the Criminal Code. In its deliberations, the committee was required to make a number of explicit or implicit decisions about whether or not such automatism really exists, whether it should or should not be available as a defense, and, if so, under what circumstances it should be available. The present paper was originally prepared with the hope of facilitating the committee's decisions by setting out as clearly as possible the scientific evidence concerning automatism and how this evidence impinges upon the legal and social issues.

For this purpose, the paper reviews briefly the concept of automatism as it appeared to be understood in the courts at that time, how the term is used in medicine and in psychiatry, and the evidence concerning the possible or actual occurrence of automatism as a phenomenon associated with intoxication by alcohol and other drugs.

"Automatism" as understood by the courts

It is beyond the scope of this paper to review in detail the use of the term automatism throughout the legal and judicial system and the legal literature. However, to point out the problems for which scientific evidence is needed, it may be informative to examine the apparent meaning of the term as used in four recent and much-publicized judgments.

1. In Daviault v. R. (Supreme Court of Canada), the majority decision referred to "extreme intoxication akin to automatism or insanity." The testimony of an expert witness used the French term "amnesie-automatisme," which the Court interpreted as "blackout." The accused was presumed to have a blood alcohol level (BAL) of 400-600 mg per 100 ml.

2. In R. v. Sullivan (Court of Appeal for British Columbia), the accused's BAL was estimated as 160-200 mg per 100 ml. One expert testified that the accused was probably in a state of automatism due to both organic and psychological causes, and thus was unable to form criminal intent. A second expert witness was of the view that the accused was in a "dissociated state" at the time of the offense and therefore unlikely to have had any intent to commit the crime.

3. In R. v. Blair (Alberta Court of Queen's Bench), the expert witnesses stated that automatism was directly related to the height of the BAL, being virtually 100% certain at a BAL of 400 mg per 100 ml and 75% probable at a BAL of 200 mg per 100 ml. In this case, one expert estimated the accused's BAL as 550-750 mg per 100 ml.

4. In R. v. Dinh-tri Nguyen (Ontario Court [Provincial Division]), testimony was presented in the trial concerning the fact that the accused was a known "crack" addict and that he was in a highly abnormal and mentally deranged state at the time of the offense. However, no expert evidence was brought before the court with respect to the actions of cocaine and its mental effects on the user. The judge concluded that he could not admit the defense of automatism because he had no evidence on this phenomenon and no understanding of its precise nature.

These four cases raise a number of questions that should be resolvable by the consensus of scientific evidence. The fourth case makes clear that the courts are in fact dependent upon the expert testimony offered during trials, and that there is no clear legal concept of automatism that is distinct from, or independent of, the scientific (or allegedly scientific) concepts advanced by the expert witnesses. In the four cases cited above, the courts in question appear to have understood automatism to be a direct consequence of intoxication, increasing in likelihood as the BAL increases and equivalent to blackout or a dissociative state. Among the questions that it is important to answer, therefore, are the following: Exactly what is automatism, and what is its relationship to blackout, dissociative disorders, brain damage, or insanity? Is the likelihood of automatism directly related to the height of the BAL? How common is the phenomenon? How can one be certain whether a person was or was not in a condition of automatism at the time of an offense? The following sections present a brief summary of scientific evidence on these and related issues, as prepared for consideration by the parliamentary Standing Committee.

Meaning of "automatism" in medicine and psychiatry

The term automatism does not appear in either the ICD-10 (International Classification of Diseases, 10th edition, World Health Organization) or the DSM-IV (Diagnostic and Statistical Manual, 4th edition, American Psychiatric Association), but it is encountered with some frequency in medical journals and textbooks. For example, a search of a computerized database of the medical literature ("Medline") turned up over 60 papers in the past five years in which the term was used. In the great majority of those papers, however, it was used to refer to physiological properties of tissues or organs, such as the automatic rhythmic contraction of heart muscle or the spontaneous, involuntary twitching of limb muscles in patients with spinal cord injury.

In relation to behavior, the term has been defined in various ways, but a fairly typical definition is the following composite based on articles by Blair,(1) Fenwick(2) and Beran:(3) "Automatism is a behavior of which the person is unaware and over which that person has no conscious control. It is usually inappropriate to the circumstances, and may be out of character for the individual. It can be complex, coordinated and apparently purposeful and directed, though lacking in judgment. There is usually full or partial amnesia afterwards, for the period in which this behavior occurred."

The word automatism appears to have been used first by the British neurologist John Hughlings Jackson, to designate the episodes of bizarre behavior shown by patients with temporal lobe epilepsy. These attacks, sometimes referred to as psychomotor epilepsy and now known as complex partial seizures, are characterized by a sudden onset, stereotyped repetitive behavior, clouded consciousness, short duration (a few minutes) followed by deep sleep, and amnesia for the attack on awakening.(4) The bizarre behavior may consist of endless repetition of whatever the person was doing just before the start of the attack, or it may be new behavior that commenced with the attack, but it is usually inappropriate to the surrounding circumstances and rather simple in character. Such automatism tends to follow the same pattern each time the patient has an attack, and it is accompanied by characteristic changes in the pattern of the electroencephalogram (EEG, or "brain waves") during the attack, so the diagnosis can be proven objectively. Attacks of rage and violence during such seizures are very rare but do occasionally occur.(4) In one series of seven cases described by Delgado-Escueta et al.,(5) six were found to have pre-existing brain damage or mental deficiency; moreover, the aggressive acts were "simple, stereotyped, unsustained, and never supported by a consecutive series of purposeful movements." A large body of literature demonstrates general agreement about these features of epileptic automatism.

There have been other instances of similar automatism described in association with organic or metabolic disease of the brain, such as head injury, deficiency of oxygen, or very low blood sugar level.(6)

Another example of automatism that appears to be accepted without any major disagreement is that of sleepwalking, which is listed in both the DSM-IV and the ICD-10. The automatism in question shares most of the features of epileptic automatism, though there is no recognizable organic brain damage. The attacks usually occur during the first third of the night, during the phase in which the EEG shows a characteristic pattern known as Slow Wave Sleep. The person sits or stands up, does not appear conscious, has a blank stare, and is relatively unresponsive to others speaking to him. If the sleepwalker speaks, the speech is usually poorly articulated and sometimes unintelligible, and there is rarely any true dialogue. The person engages mostly in routine repetitive behaviors of low complexity (though occasionally they can be complex, e.g., operating machinery). It is also frequently inappropriate behavior, such as that of a sleepwalking child who urinates in a bedroom closet instead of the bathroom,(7) or the adult who goes out of the house naked during a sleepwalking episode.(8) The person is very difficult to awaken, and there is usually a brief period of confusion after the episode, difficulty of orientation, and then a gradual recovery of full consciousness, but amnesia for the episode itself.

Another instance of automatism that is not associated with brain damage is hypnosis. A person who has been hypnotized is clearly not conscious and in possession of critical faculties, because that person's perception of reality is under the external control of the hypnotist. Yet a hypnotized subject is capable of carrying out quite complex and apparently purposeful acts that obey to an inner logic insofar as they correspond to the "inner reality" induced by the hypnotist, even though they may not be appropriate to the external reality. Hypnotic automatism can be regarded as a prototypic psychogenic automatism (i.e., produced by purely psychological mechanisms), epileptic automatism as a prototypic organic form, and sleepwalking as possibly something in between, with some features of both of the other two types.

Dissociative disorders are also not associated with organic brain damage in most cases, but are regarded as psychiatric illnesses and are listed in both the ICD-10 and the DSM-IV. Dissociation is defined as a disruption in the usually integrated functions of consciousness, memory, identity, and perception of the environment. Such disruptions may be sudden or gradual in onset and transient or chronic in duration. Various patterns of dissociation are recognized, including dissociative amnesia, dissociative fugue (in which the person inexplicably flees from the normal home and work environment and travels long distances to an unknown location), multiple personality disorder,(9) depersonalization, etc. Many of these disorders were formerly referred to in psychiatry as forms of "hysteria"--hysterical fugue, hysterical paralysis, and so forth. Since consciousness and perception of reality are, by definition, altered and divorced from emotions and behavior in these conditions, the person is not capable of exercising conscious control over behavior. Thus the behavior can properly be viewed as automatism, analogous to that seen in hypnosis. The difference, however, is that dissociative states are regarded clinically as functional mental disorders or diseases, whereas the hypnotic state is not.

In summary, automatism as a symptom of temporal lobe epilepsy, sleepwalking, and a variety of organic or metabolic brain disorders is characterized by a sudden onset of a brief period of absence of consciousness, inappropriate behavior that is usually repetitive and of low complexity, absence of real communication with other people during the attack, confusion and disorientation during the recovery phase, and subsequent amnesia for the period of the attack. There is rarely violent behavior, and even more rarely a sufficiently organized pattern of violence to sustain an attack on another person. There is frequently or usually evidence (EEG, radiological, biochemical or other) of some organic injury or malfunction of the brain. The automatism seen in hypnosis or in dissociative states may be considerably more complex and apparently purposeful in character, but by definition it is also associated with absence of normal consciousness and judgment.

Does automatism occur in association with alcohol intoxication?

There is no scientific evidence whatsoever that automatism is directly caused by alcohol intoxication alone, no matter how severe the intoxication. The concept of automatism set out above is that consciousness is lost, while the ability to perform physical activities of varying degrees of complexity is retained, so that such activities are carried out in an unconscious state--i.e., not under the voluntary control or with the conscious intent of the person who is acting. The typical action of alcohol on the brain, however, is to progressively decrease all types of nerve cell activity, including those involved in coordinated movements and those involved in consciousness and memory, more or less in parallel.(10,11) Thus, when consciousness is lost, complex coordinated movement is also lost and the person has "passed out." Conversely, as long as the person is able to carry out reasonably complex coordinated movements, some consciousness is also present. Therefore automatism is not a characteristic of uncomplicated intoxication, no matter how severe.

However, one must consider other possible ways in which alcohol intoxication might give rise to automatism. The most frequently proposed of these possible ways are summarized below:

Pathological intoxication (or "alcohol idiosyncratic intoxication," as it is called in the DSM-IV) is defined as a marked behavioral change, usually including inappropriate belligerence or assaultiveness, following ingestion of a small quantity of alcohol (sometimes as little as one drink) that is not enough to produce the usual signs of intoxication. It is characterized by marked confusion and disorganization of thought, incoherent or deluded speech, and an explosive outburst of fury in which homicide or suicide is possible; it is followed by deep sleep and partial or total amnesia for the events in question.(12) Some authorities, such as the internationally renowned British expert Professor Griffith Edwards, doubt whether such an entity really exists; Edwards says that in most cases the amount drunk was really very much more than the small amount claimed by the drinker, and that there is seldom proof that the person really was in a trance state or displaying automatism.(13) Others, however, argue that the amount of alcohol consumed does not have to be small, and that the essential features are the sudden outburst of rage and senseless violence, automatic behavior, absence of the motor incoordination and slurred speech that characterize ordinary intoxication, brief duration, deep sleep, and subsequent amnesia.(14) All experts agree that if this condition does occur, it is merely triggered by alcohol in an individual with a predisposing abnormality, such as a mental disease or defect, or an organic injury or metabolic anomaly of the brain.

Temporal lobe epilepsy (psychomotor epilepsy), as noted above, is one of the brain malfunctions that is capable of producing automatism by itself. There has been a considerable amount of clinical study of the possibility that alcohol may trigger such seizures and, in that way, give rise to automatism. Among the best of the studies are those in which patients with histories of "pathological intoxication" with violence, or of epileptic attacks while under the influence of alcohol, were given alcohol experimentally in order to study the effects on behavior and on the EEG. Bach-y-Rita et al.(15) gave alcohol intravenously to 10 patients with a history of "pathological intoxication," in a dose of 35-70 grams (equivalent to two and a half to five bottles of beer) over a 30-minute period, while continuously monitoring the EEG. No seizures or abnormal behavior occurred. However, these patients had been given a sedative beforehand and were instructed to try to sleep during the procedure. In contrast, Marinacci(16) carried out a much larger study in 402 patients with a history of temporal lobe epilepsy, giving them one to four bottles of beer or one to four ounces of spirits over a 90-minute period, and found characteristic temporal lobe seizures in 18 of them. Similarly, Maletzky(17) studied 22 patients with a history of alcohol-induced attacks of violence, giving them intravenous alcohol at a rate of 50 grams of alcohol per hour. After total doses of 100-300 grams (equivalent to seven to twenty-one beers), producing BALs of 95-275 mg per 100 ml, nine of the 22 became suddenly violent, four became psychotic, and two showed both violent and psychotic behavior; five of these 15 showed temporal lobe abnormalities in the EEG during these attacks. Thus the strongest evidence supports the idea that alcohol can trigger temporal lobe epileptic seizures, with violence and subsequent amnesia, in patients with a demonstrated predisposition to such seizures. The observed behavior could be compatible with automatism, but no systematic observations appear to have been made of these patients' state of consciousness or their ability to exercise conscious control over their behavior.

Blackout, as noted at the outset of this paper, is frequently equated with automatism. This is a serious error of concept. Blackout means nothing more than the failure of subsequent recall of events that occurred during a limited time in which the person was intoxicated. This occurrence says nothing about the state of that individual's consciousness during the period of intoxication itself. Edwards(13) states that "the person who subsequently claims amnesia . . . may during that [blacked-out period] be engaging in any type of activity, and to the observer he will not obviously be in an abnormal state of mind (other than his being intoxicated)."

It is essential to remember that all true automatisms are characterized by amnesia afterwards (i.e., a blackout), but not all amnesia is associated with automatism. As we learn in elementary logic from the study of true and false syllogisms, every horse has four legs, but not everything with four legs is a horse.

There are two possible mechanisms of production of alcoholic blackouts. Both involve intoxication with high BALs; blackouts generally occur after periods in which the BAL reached 250 mg per 100 ml or more. One mechanism, operating at very high BALs, involves temporary inhibition of the biochemical reactions in the brain that are necessary for the formation of new memory traces,(18) so no memory is formed, and it is therefore impossible for the person to remember later what happened during that period, even with prompting. The other mechanism involves purely psychological processes, and the person can remember the blacked-out events either when prompted or when intoxicated again. This fact was well known clinically more than 150 years ago(19,20) and was proved experimentally more than 25 years ago.(18,21,22) In the case of the second mechanism especially, it is clear that the person must have been conscious during the blacked-out period, or it would have been impossible to form the memory that was subsequently recalled.

Intoxication may also cause automatism in those rare cases in which it is merely the precipitating factor in an individual with mental or organic brain disease, in whom the automatism can occur in the absence of alcohol.

Can alcoholic intoxication impair consciousness without producing automatism?

The answer to whether alcoholic intoxication can impair consciousness without producing automatism must clearly be a qualified "yes," depending on the magnitude of the BAL and the degree of tolerance of the individual. A severely intoxicated person who is not yet unconscious is nevertheless impaired in many ways. As Cohen(12) puts it, "Drunkenness produces impaired judgment, reduction of controls over behavior, and paranoid misrepresentation of the environment. The result can be an alcohol-provoked rage." In such a state, the person is still capable of physical activity that is probably clumsy and poorly coordinated but still effective enough to permit aggressive violent behavior. However, two points directly relevant to the present discussion must be recalled: (1) the person is not unconscious and therefore is not behaving in a state of automatism; and (2) the intoxicated state is, obviously, a temporary chemically induced malfunction of the brain, but it is a self-provoked malfunction that the individual has consciously produced.

This latter point does not mean that consumption of alcohol is always wholly voluntary and deliberate; by definition, someone who suffers from clinically diagnosed alcoholism has impaired ability to abstain from drinking, despite knowing that he or she should abstain and in many cases despite wishing to do so. Nevertheless, that person's consumption of alcohol is conscious, and with knowledge of the probable or possible consequences.

It is also very important to bear in mind the magnitude of tolerance to alcohol that can develop in regular heavy drinkers. A number of reports(23-26) have described heavy drinkers who appeared sober in the judgment of experienced clinical observers, despite having BALs as high as 400 mg per 100 ml or more. These observations were made under special circumstances that do not generally apply. Nevertheless, it is important to remember that many heavy drinkers and alcoholics acquire such a degree of tolerance that although obviously intoxicated, they can continue to walk, talk, know who and where they are, drive vehicles (even though with impaired control), and engage in a variety of activities despite BALs that would cause unconsciousness in light social drinkers. For the purposes of the courts, therefore, knowledge or estimates of the BAL do not necessarily provide, by themselves, a clear assessment of the state of mental function of the individual in question; it is also necessary to have eyewitness descriptions of the person's behavior and responses.

Can other drugs produce true automatism?

A small number of drugs can indeed produce automatism as a direct consequence of their pharmacological action in the brain. These are the so-called dissociative anesthetics, a group that includes ketamine, phencyclidine (PCP) and related substances that are or were used as veterinary anesthetics and have had some vogue among illicit-drug users. As the name of the group implies, they produce a dissociative state resembling that described above, and in that state there may be true automatism.(27) However, such cases are relatively rare, because experience has taught the street drug users to avoid high doses of these substances. Therefore in a given case it will still be necessary to provide evidence to prove whether that individual, using a stated amount of the drug, on that occasion, was or was not in a state of automatism.

A number of other drugs, including amphetamines, cocaine and cannabis, can in high doses cause a paranoid state, characterized by delusions, fear and anger, that may cause serious misperception of the external reality.(28-30) As a result, the user may react with violence against an imagined threat or danger. Consciousness is still present, but understanding and judgment are so impaired by the drug's effects as to constitute, again, a chemically induced temporary insanity. Indeed, such drug-induced states have been used as experimental models of schizophrenia and other mental diseases.

A brief review of the evidence in the court cases cited

In light of the preceding discussion, it may be informative to re-examine briefly the expert testimony in three of the four court cases cited at the beginning of this paper.

In Daviault v. R., the majority decision was based on testimony that linked automatism to a blackout. As noted earlier, this is an incorrect linkage, because blackout does not by itself constitute evidence of automatism. Further, the decision emphasized the role of very high BAC as a causal factor in such automatism, and, as also noted earlier, there is no basis for this in scientific fact.

Similarly, in R. v. Sullivan, great importance was attributed to the BAL of 160-200 mg per 100 ml, but, as noted above, in a regular heavy drinker such a BAL can by no means be accepted as evidence of a loss of consciousness sufficient to characterize the behavior as automatism. Moreover, the testimony of the other witnesses in that case suggests strongly that the accused was in fact quite conscious and able to know the difference between right and wrong. Thus he engaged in true dialogue with his wife and their friend throughout the events in question, during his own testimony he recalled clearly the conversation with his wife, and after shooting his wife he acknowledged to their friend that he had "fucked up," indicating that he knew at the time that he had done something wrong. Therefore it is difficult to see what evidence justified the conclusion that he was in a "dissociated state" and acting automatically.

Finally, in R. v. Blair, the conclusion that the accused, Blair, was acting automatically was apparently based entirely on the estimated BAC of 550-750 mg per 100 ml and the expert testimony that such levels would invariably produce automatism. As noted above, this is a completely unfounded statement; such levels, if true, would be far more likely to produce coma and even death. There is, moreover, reason to doubt the estimated BAC. Using the testimony of the witness Whiting, who had been Blair's drinking partner on that occasion, concerning the amount of alcohol Blair drank on the two days in question, and assuming that Blair was about 6'2" in height and 225 pounds in weight, standard methods of calculation suggest that his BAC at the time of the events in question would have been in the range of 960-1200 mg per 100 ml--a level that, if it had really occurred, would very likely have been fatal.(31,32) It is therefore necessary to question the accuracy of the testimony concerning the amount that Blair drank. In addition, two witnesses, Whiting and Mrs. Blair, who were present during the events in question, described Blair as being very drunk but did not refer to any strange appearance or behavior that might have been suggestive of automatism.

Thus in these three cases there is substantial reason to doubt the scientific validity of the evidence on which the courts' decisions about automatism were based. In addition, pathological intoxication would not be relevant to any of these cases, because in all three the BAL was high, and ordinary signs of intoxication were clearly present.

Conclusions

From the foregoing review of clinical and scientific evidence, it is clear that no basis exists for the concept of automatism due to alcohol intoxication per se. Rather, the following conclusions are scientifically permissible:

1. Automatism can occur as a consequence of various physical and psychiatric disorders affecting brain function, and in a few cases alcohol may act to trigger automatism caused by these disorders, but it should be possible in such cases to provide medical evidence proving the existence of those disorders.

2. Alcohol-induced blackout or amnesia does not constitute evidence that the person so affected was unconscious or in a state of automatism at the time of the events that have been "blacked out" from memory.

3. A few drugs known as dissociative anesthetics can in high doses produce true automatism by their direct chemical actions in the brain, but it would be necessary to prove in any given case that this had in fact happened.

4. Severe alcohol intoxication impairs the ability to respond rationally to external events by interfering with judgment, perception of external reality, and self-control over one's behavior, but this is more accurately regarded as a self-provoked temporary, chemically induced brain malfunction than as automatism.

Notes

(1.) Blair D: The medicolegal aspects of automatism. Medicine, Science & the Law 17: 167-182 (1977).

(2.) Fenwick P: Automatism, medicine and the law. Psychological Medicine--Monograph Supplement 17: 1-27 (1990).

(3.) Beran RG: Automatisms--the current legal position related to clinical practice and medicolegal interpretation. Clinical & Experimental Neurology 29: 81-91 (1992).

(4.) Trimble MR, Bolwig TG (eds.): Aspects of Epilepsy and Psychiatry. Chichester: Wiley Medical Books (1986). See especially Chapter 4 (Fenwick P: Aggression and Epilepsy).

(5.) Delgado-Escueta AV, Mattson RH, King L, Goldensohn ES, Spiegel H, Madsen J. Crandall P, Dreifuss F, Porter RJ: The nature of aggression during epileptic seizures. New England Journal of Medicine 305: 711-716 (1981).

(6.) Hales RE, Yudofsky SC, Talbott JA: Textbook of Psychiatry, 2nd Edition. Washington, DC: American Psychiatric Press (1994). See especially in Chapter 38 (Simon RI: The Law and Psychiatry) the section on automatisms and intoxication, pp. 1324-1325.

(7.) Buchanan A: Sleepwalking and indecent exposure. Medicine, Science & the Law 31: 38-40 (1991).

(8.) Hamer BA, Payne A: Sleep automatism: Clinical study in forensic nursing. Perspectives in Psychiatric Care 29: 7-11 (1993).

(9.) Slovenko R: The multiple personality and the law. Medicine & Law 12: 329-340 (1993).

(10.) Wallgren H, Barry H, III: Actions of Alcohol. Amsterdam: Elsevier Publishing (1970). See especially Chapter 6 (Integrative Functions of the CNS) and Chapter 7 (Complex Behavioral Effects).

(11.) Kalant H, Woo N: Electrophysiological effects of ethanol on the nervous system. Pharmacology & Therapeutics 14: 431-457 (1981).

(12.) Cohen S: The Substance Abuse Problems: Vol. 2, Issues for the 1980s. New York: Haworth Press (1985). See especially Chapter 18, Pathological Intoxication, pp. 105-110.

(13.) Edwards G: The Treatment of Drinking Problems. London: Grant McIntyre (1982). See especially pp. 75-76.

(14.) Tiffany LP, Tiffany M: The Legal Defense of Pathological Intoxication. New York: Quorum Books (1990). See especially pp. 1-2, 260, 266.

(15.) Bach-y-Rita G, Lion JR, Ervin FR: Pathological intoxication: clinical and electroencephalographic studies. American Journal of Psychiatry 127: 698-703 (1970).

(16.) Marinacci AA: A special type of temporal lobe (psychomotor) seizures following ingestion of alcohol. Bulletin of the Los Angeles Neurological Society 28: 241-250 (1963).

(17.) Maletzky BM: The diagnosis of pathological intoxication. Journal of Studies on Alcohol 37: 1215-1228 (1976).

(18.) Kissin B, Begleiter H (eds.): The Biology of Alcoholism: Vol. 2, Physiology and Behavior. New York: Plenum Press (1972). See especially Chapter 8 (Overtop DA: State-Dependent Learning Produced by Alcohol and Its Relevance to Alcoholism) and Chapter 9 (Mello NK: Behavioral Studies of Alcoholism).

(19.) Wilson GR: Drunkenness. London: Swan Sonnenschein & Co. (1893), pp. 36-37.

(20.) MacNish R: The Anatomy of Drunkenness, 4th edition. Glasgow: W. R. McPhun (1832), p. 46.

(21.) Goodwin DW, Powell B, Bremer D, Hoine H, Stern J: Alcohol and recall: State-dependent effects in man. Science 161: 1358-1360 (1969).

(22.) Goodwin DW, Othmer E, Halikas JA, Freemon F: Loss of short-term memory as a predictor of the alcoholic "blackout." Nature 227: 201202 (1970).

(23.) Urso T, Gavaler JS, Van Thiel DH: Blood ethanol levels in sober alcohol users seen in an emergency room. Life Sciences 28: 10531056 (1981).

(24.) Davis AR, Lipson AH: Central nervous system tolerance to high blood alcohol levels. Medical Journal of Australia 144: 9-12 (1986).

(25.) Perper JA, Twerski A, Wienand JW: Tolerance at high blood alcohol concentrations: A study of 110 cases and review of the literature. Journal of Forensic Sciences 31: 212-221 (1986).

(26.) Sullivan JB Jr, Hauptman M, Bronstein AC: Lack of observable intoxication in humans with high plasma alcohol concentrations. Journal of l;orensic Sciences 32: 1660-1665 (1987).

(27.) Jaffe JH: Phencyclidine and related compounds. In Gilman AG, Goodman LS, Rall TW, Murad F (eds.): Goodman and Gilman's The Pharmacological Basis of Therapeutics, 7th edition. New York: Macmillan (1985), pp. 565-567.

(28.) Kalant OJ: The Amphetamines--Toxicity and Addiction, 2nd edition. Toronto: University of Toronto Press (1973). See especially Chapter 4, Amphetamine Psychosis.

(29.) Kalant OJ (ed.): Maier's "Cocaine Addiction" (Der Kokainismus). Toronto: ARF Books (1987).

(30.) Fehr KO, Kalant H (eds.): Cannabis and Health Hazards: Proceedings of an ARF/WHO Scientific Meeting. Toronto: ARF Books (1983).

(31.) Heatley MK, Crane J: The blood alcohol concentration at postmortem in 175 fatal cases of alcohol intoxication. Medicine, Science & the Law 30: 101-105 (1990).

(32.) Leopold D: Zur Todesursache bei sehr starker akuter Ethanolin-toxikation [On the causes of death in very severe acute alcohol intoxication]. Beitrage zur gerichtlichen Medizin 48: 163-167 (1990).

Harold Kalant is professor emeritus in pharmacology at the University of Toronto and director emeritus of the Clinical Research and Treatment Institute at the Addiction Research Foundation (33 Russell St., Toronto, Ont. M55 2S1, Canada). Dr. Kalant has also served as an expert witness in numerous criminal and civil cases involving evidence of intoxication.

AUTHOR'S NOTE: This paper was originally prepared as a submission to the House of Commons Standing Committee on Justice and Legal Affairs, and was presented before the Committee in Ottawa on June 13, 1995. The views expressed in this document are those of the author and do not necessarily reflect the policies or official views of the Addiction Research Foundation of Ontario.
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Title Annotation:Intoxication as a Legal Defense: Recent Canadian Experience with Changes in Criminal Law
Author:Kalant, Harold
Publication:Contemporary Drug Problems
Date:Dec 22, 1996
Words:5341
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