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Several problems exist with historical research into the incidence of

serial murder. In addition to the hurdles encountered in attempts to locate
old data sources and the problem of less than rigorous practices in past
record keeping, many cases of serial killings probably went officially unde-
tected. Itinerant murderers would have travelled and killed more freely in
pre-telecommunication days. Early mass and serial murderers may have
been characterized as demons, witches, or werewolves rather than as crim-
inal offenders (Hickey, 1997). Violence and murder were much more com-
mon in Europe during the medieval period than today (Brantingham, 1987;
Brantingham & Brantingham, 1984; Wilson, 1984; see also Goodman &
Waddell, 1987; Gurr, 1989a; Johnson, 1988). Conversely, offenders were
likely apprehended much sooner in rural or village settings than large urban
areas. Many potential serial murderers would thus have been caught and
executed after their first victim.

Jenkins (1993b) also points out that a growth in the number of potential

offenders does not necessarily follow from an increase in reported cases of
serial murder. He argues that the construction of official records of serial
killing is influenced as much by victimological and bureaucratic factors as
by the population of actual murderers:

Rather, the vital elements [in the production of “crime waves” of serial
murder] may be the increasing opportunities to find vulnerable people to
victimize, and the chance to escape apprehension after committing a mur-
der. The opportunities might increase as a consequence of economic devel-
opments, or as a result of changes in mores, while bureaucratic and political
factors might well affect the likelihood of detection. In either case, though,
a murder “wave” could occur independently of the changing characteristics
of the offender population. (p. 471)

These definitional and measurement issues make assessments of serial

murder levels difficult, and it is not easy to predict the development of future
trends. The FBI has suggested the following factors may have had influences:
mobility, “easy” victims (in terms of target selection), urbanization, social
anonymity, violence in the mass media, pornography, and illicit drug use
(Mathers, 1989; Ressler & Shachtman, 1992).

It is important to understand the level and seriousness of this crime

without succumbing to unreasonable fear and unwarranted panics. Kiger
(1990) puts the problem in perspective when she refers to the dark figure of
serial homicide and warns that “the incidence of serial murder in the United
States is currently unknown, as is the prevalence of active offenders” (p. 47).
The magnitude and exact growth of serial homicide is not yet measurable
with any degree of accuracy, and inflated estimates and unfounded theories
may create more problems than they solve.

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2.1.3 Theories

A mind full of fire, and a fist full of steel.

— Graffiti, Vancouver, British Columbia, April 1995

Explanations for serial murder run the gamut from the biological to the
psychological to the sociological. While this crime is currently not fully
understood, there have been some efforts to explore its aetiology. Lunde
(1976) states that almost all multiple killers are clinically insane white males,
and their psychoses typically take the form of paranoid schizophrenia or
sexual sadism. He suggests childhood experiences may play a role in shaping
the distorted world views commonly held by such offenders. Bartol and
Bartol (1986) caution that it would be a mistake to “assume with Lunde that
almost all mass murderers are mentally disordered in the clinical sense of
that term .... they tend to be extremely introverted persons who perceive and
think about the world in ways much different from our own” (p. 185).
Criminal courts have demonstrated a pattern of decreeing most serial killers
legally sane (see also Ogle, Maier-Katkin, & Bernard, 1995), and some com-
mentators have cautioned that insanity is a label lacking demonstrable reli-
ability and validity (Boyd, 1988; Szasz, 1971).

Brittain (1970) observes that sexual sadists may repeatedly kill when

provoked by actions that cause a perceived loss of self-esteem. But by replac-
ing the term “serial murderer” with the labels “paranoid schizophrenic” and
“sexual sadist” in their explanations, neither Lunde nor Brittain make real
progress towards the understanding of the causes of this form of destructive
behaviour. They also ignore the fact that most people in these groups never
become murderers, let alone repetitive killers.

Adopting a biosocial approach, Norris (1988) suggests that serial mur-

derers suffer from a medical pathology and their violent actions are caused
by organic brain malfunctions that lead to episodic and uncontrollable acts
of violence. He views serial killers as having lost their free will, as victims of
a form of contagious disease.

Serial murderers share a significant number of common medical/psycho-
logical patterns that include evidence of possible genetic defect, soft and
hard signs of brain damage resulting from injuries or other physical trauma,
severe chemical imbalances brought about by chronic malnutrition and
substance abuse, an absence of a sense of self which is the result of consis-
tently negative parenting or nonparenting, and an almost hair-trigger vio-
lent response to external stimuli with no regard for the physical or social
consequences. (p. 40)

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The violent upbringing and negative parenting experienced by these

offenders as children may have led to the reversal of the traditional dichot-
omies of reward and punishment, love and hate, resulting in the development
of a “nonpersonality type,” incapable of controlling harmful impulses and
functioning within the context of a normal social framework. Norris (1988)
proposes that serial killers go through a ritual of murder comprising seven
key phases:

1. Aura phase — the killer withdraws from reality;
2. Trolling phase — the compulsive search and hunt for the next victim;
3. Wooing phase — the victim is conned into the killer’s trap;
4. Capture phase — the offender’s penultimate moment;
5. Murder phase — the killer’s fantasies are ritually enacted;
6. Totem phase — the reliving of the crime through souvenirs in order

to sustain the “high”; and

7. Depression phase — the killer loses the power he realized through the

murder, setting off the whole process once again.

Lange and DeWitt, Jr. (1990b) state there is evidence that many serial

killers suffer from head injuries or physical brain pathology. Their research
examined 165 motiveless murderers, from 1600 to the present, representing
all parts of the world. Neurological malfunctions, caused by head injuries,
epilepsy, or other forms of subtle deep temporal lobe spiking, generates inter-
ictal or post-ictal seizures that can lead to irresistibly compulsive autonomic
or “automatic” behaviour. Their hypothesis is that serial murderers become
victims of uncontrollable brain activity that leads to “fits” or “dazes” within
which the killings occur.

Biological and genetic theories of crime are not currently popular in

criminology and it is often difficult to obtain the data necessary to test
offender hypotheses at the biological level (Vold & Bernard, 1986). Still,
several new research initiatives have been developed in the biosocial area over
the last decade (see, for example, Fishbein, Lozovsky, & Jaffe, 1989). On one
hand, the temptation to explain complicated patterns of human behaviour
in a simple manner is strong, especially when that behaviour is violent,
frightening, and alien (Boyanowsky, 1990). Such theories are comforting as
they physically and congenitally separate the rest of us from the “monsters”
in our society. Our culture, and therefore we as individuals, can then avoid
all responsibility for these savage crimes. But on the other hand, serial murder
is a rare phenomenon and individual-level explanations undoubtedly play a
part.

Biological theories must be integrated with sociopsychological or socio-

logical theories to address the cultural dissimilarities found in crime, murder,

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and multiple murder (Ressler et al., 1988). On their own they lack the ability
to explain historical and geographic differences in criminal activity. In sum-
marizing the evidence connecting neurochemical dysfunctions with impul-
sivity, negative affect, sensation-seeking, and other cognitive correlates of
antisocial behaviour, Fishbein (1998) notes that any biological predisposition
will be influenced by triggering socio-environmental factors. “Put simply,
abnormalities in certain neurobiological mechanisms heighten sensitivity to
adverse environmental circumstances, increasing the risk for an antisocial
outcome” (p. 3).

Levin and Fox (1985) criticize the narrow theoretical focus on the

offender in studies of multiple murder, stressing that while the role of biology
and the effects of early experience cannot be ignored, “situational factors —
experiences and learning beyond the fifth year of life ... are at least as critical
in encouraging a murderous response from someone who may or may not
be predisposed to violence” (p. 39). Cater (1997) also argues that serial
murderers learn to become such, and therefore are products of society. He
suggests that social profiles may help in early identification of warning signs.

Holmes and De Burger (1988) employ a sociopsychological approach to

understanding serial murder, suggesting repetitive homicidal behaviour pat-
terns are generated from a mind-set with the following critical features:

1. An intrinsic and persistent motivation to kill;
2. An expressive orientation to murder reinforced by the ability to psy-

chologically “gain” from such violent acts (often linked to consistent
fantasies); and

3. Central sociopathic features (e.g., absence of guilt, warped notions of

love, capacity for extreme but casual and emotionless aggression,
impulsivity, uncontrolled desires, asocial perspectives).

Holmes and De Burger (1988) warn that serial killers are not a homo-

geneous group, either in their actions or biographies. They therefore eschew
a single causative theory, suggesting instead that if the dominant motives
develop in conjunction with a certain mind-set under the right conditions,
repetitive homicidal behaviour can result. Such a structure is seen to be
necessary, but not in itself sufficient. They do not explain what such condi-
tions and motives might be, or how such a mind-set comes about.

The sources of the repetitive homicide pattern are thus seen as psy-

chogenic — the killer’s psyche is characterized by values, norms, beliefs,
perceptions, and propensities that facilitate and legitimate multiple acts of
murder. But while the motivations are aberrant and their locus intrinsic, they
are not the result of psychopathology or organic brain disease. Sociogenic
factors, while not a direct cause, are important for understanding the context

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within which propensities for murder develop. Holmes and De Burger’s
comments should be seen as more of a set of descriptive propositions rather
than as a comprehensive theory.

Noting the frequency with which examples of dissociative processes can

be found in the literature on serial murderers, Vetter (1990) suggests that
systematically administering Bernstein and Putnam’s Dissociative Experi-
ences Scale (DES) to known serial killers might prove to be a fruitful avenue
for new research. In his view, the behaviour of many such killers shows
evidence of what he terms the Mephisto Syndrome, a combination of disso-
ciation and psychopathy (see also Carlisle, 1993).

Dissociative disorders feature “a disruption in the usually integrated

functions of consciousness, memory, identity, or perception of the environ-
ment” (American Psychiatric Association, 1994, p. 477). Dissociation ranges
from common daydreaming to the controversial multiple personality disor-
der. The disorders, as presently defined in the 

Diagnostic and Statistical Man-

ual of Mental Disorders

 (4

th

 Edition) (DSM-IV), include dissociative amnesia,

dissociative fugue (formerly psychogenic fugue), dissociative identity disor-
der (formerly multiple personality disorder), depersonalization disorder, and
dissociative disorder not otherwise specified.

Thrill-seeking, pathological glibness, antisocial pursuit of power, and

lack of guilt characterize the extreme “true” psychopath (Vetter, 1990). The
DSM-IV employs the term antisocial personality disorder (ASPD), rather
than sociopath or psychopath. The ASPD diagnostic criteria in the DSM-IV
have been significantly revised from those in the previous edition, DSM-III-R,
as they had come under attack for being too broad and behaviourally oriented
(Hare, Hart, & Harpur, 1991).

These critiques led to the development of the Psychopathy Checklist —

Revised (PCL-R) by Robert Hare of the University of British Columbia. Based
on the work of Cleckley (1982) and others, this instrument is a more accurate
measure of psychopathy as a personality disorder (Hare, 1993; Hare, Harpur,
Hakstian, Forth, Hart, & Newman, 1990; Hare, McPherson, & Forth, 1988;
Hart, Hare, & Harpur, 1991, 1992). Research on psychopathy with the PCL-R
helped inform the development of the modified ASPD diagnostic criteria now
used in the DSM-IV.

Hare (1993) developed key diagnostic symptoms to assess psychopathy

based on the traits outlined in Hervey Cleckley’s 

Mask of Sanity

. These can

be grouped into two factors, one describing personality, and the other behav-
ioural, characteristics:

•

Emotional/interpersonal: (1) glib and superficial; (2) egocentric and
grandiose; (3) lack of remorse or guilt; (4) lack of empathy; (5) deceit-
ful and manipulative; and (6) shallow emotions.