Alcohol Medical Scholars Lecture

Antisocial Personality Disorder

Karin Neufeld MD MPH





Who was Gary Gilmore?

Example of severe ASPD (see appended biography)

A.     History and importance:



Long history of identification.

a)      “Moral insanity” by Pritchard1: repeated immoral behaviors from psychological deficits.

b)      Psychopathic character:

(i)      Late 1800’s: socially unacceptable personality characteristics. 

(ii)    Cleckley2 influenced DSM I and II3.

c)      Sociopathy4:

(i)      Coined in 1930;

(ii)    “Anything deviated or pathological in social relations”.

d)      Antisocial Personality Disorder (ASPD):

(i)      Robins5 studied adults 40 yrs after involvement in juvenile court system.

(ii)    Antisocial Personality Disorder (ASPD) adopted in 1980 (DSM III):           largely based on Robins’ work6.



Most valid and reliable of the personality diagnoses.

a)      Only personality diagnosis derived from empirical data5.

b)      Includes the childhood precursor of Conduct Disorder (CD) in         diagnosis6.

c)      Inter-rater reliability of diagnosis is average to good (.75)7,8.. 



Great public impact.

a)      6 X hrisk of death in adolescence and young adults with antisocial behavior9.

b)      High psychiatric comorbidity: 80% of ASPD have substance use disorder (SUD)10.

c)      High cost of incarceration and law enforcement:

(i)      50% male prisoners with ASPD11.


(ii)    41 billion $/yr (US) for prison system.



Purpose of this lecture:

1.      Review diagnosis.

2.      Describe epidemiology.

3.      Review possible etiologic mechanisms (risk factors).

4.       Describe the course.



Review treatment of the disorder.

C.     Key points about ASPD:

1.      Very common among those with SUD.

2.      Caused by interplay between genetic and environmental factors.

3.      Associated with great morbidity and mortality.

4.      Difficult to cure but possible to help.



II.    Diagnosis according to DSM IV12



Pervasive pattern of behavior:

1.      Persistent disregard and violation of the rights of others since age 15.

2.      Presence of 3 + of:

a)      Repeatedly failing to obey the law.

b)      Repeated lying, aliases, conning for profit or pleasure.

c)      Impulsivity or failure to plan ahead.

d)      Irritability, aggressiveness, repeated physical fights or assaults.

e)      Reckless disregard for safety of self or others.

f)        Enduring irresponsibility: no sustained work or meeting $ obligations.

g)      Lack of remorse for hurting/mistreating others.



Age criterion: At least 18 years of age.

C.     Childhood precursors:

1.      Meets criteria for conduct disorder (CD): onset < 15 years.

2.      Conduct problems cause impairment.

3.      Behaviors repeated over 12 + mo period.

4.      3 + behaviors from:

a)      Aggression to people or animals,

b)      Destruction of property,

c)      Deceitfulness or theft, or

d)      Serious violation of rules.

D.    Diagnostic exclusions: Behaviors not only in course of schizophrenia or a manic episode.





 Descriptive epidemiology

A.     Prevalence in general population:

1.      3% of general population = ASPD10,13-15.

2.      6% of males, 1% of females in community16.


B.     Prevalence in special populations:

1.      Health care settings.

a)      Primary health care settings: ASPD is h (8%) but study designs are not strong13.

b)      Mental health care settings: Admissions to psychiatric facilities ~ 10%13.
c)      Substance use disorder (SUD) population:
(i)      Very strong association of ASPD with all SUD17-19.
(ii)    ASPD most commonly co-occurring disorder with SUD10,20.
(iii)   80% of ASPD had SUD in the lifetime10

2.      Prison populations. ASPD found in 50% male prisoners and in 20% females11,13.



Associated characteristics:   

1.      Sex distribution.: males: h6 X’s13.

2.      Age:

a)      Young (25-44 yrs) had highest prevalence14.

b)      May be due in part to

(i)      Increased death rate.


(ii)    Remission of the disorder over the lifespan.


(iii)   h frequency of the disorder in the population (cohort effect).

c)      Evidence for all three: but remission important = 30% remit by age 4014,21.


3.      Race: no difference in prevalence between white and non-whites14.

4.      Leaving school early: 5 X’s h ASPD in those dropping out by 11 yrs10. 

5.      Abuse/neglect in childhood: 50% h risk of adult criminal behavior22,23.



Risk factors




1.      Family studies.


a)      ASPD h in male relatives of males with ASPD at least 5X’s > population prevalence24,25.


b)      Increased prevalence doesn’t help separate genetic vs environmental.


2.      Twin studies.


a)      Genetic impact is great: heritability of ASPD ~ 70%26-29.


b)      Genetic impact is less for juvenile antisocial behaviors: heritability ~30%30


c)      Genes may code for several disorders including CD, ASPD and SUD31.

3.      Adoption Studies.

a)      Male adoptees with biological ASPD parent32=

(i)      4X’s h aggressivity in childhood (e.g. CD behaviors).

(ii)    3X’s h of ASPD.

(iii)   Compared to adoptees without ASPD parent.




Male adoptees with h childhood aggressivity32 =

(i)      9X’s h of ASPD.

(ii)    7X’s h SUD.

(iii)    Compared to adoptees without h aggressivity.


c)      ASPD genetic vulnerability pathway: g childhood aggressivity g ASPD g SUD.

d)      Adverse environments increase expression of vulnerability33,34:

(i)      Adverse adoptive home = marital problems and discord, anxiety, depression, SUD, or legal problems in adoptive parents.


(ii)    Adoptees with biological ASPD parent + adverse environment 8X   aggressivity as those without ASPD bio parent.




Laboratory findings:

1.      EEG.

a)      “Event related potentials” = brain responses to visual or auditory stimuli.

b)      P300 amplitude: relates to ability to recognize a rare or “target” stimulus.

c)      P300 amplitude:  i in ASPD and their sons27. 

d)      Not specific to ASPD:

(i)      Decreased amplitudes in alcoholics and their sons35.

(ii)    Decreased in schizophrenia, depression and Alzheimer’s.

(iii)   While nonspecific, may be marker for CD, ASPD, and SUD27. 



Neuroimaging studies.

a)      MRI findings:  i brain volume in prefrontal region36.

b)      PET and SPECT studies: suggest lower prefrontal subcortical activity37.

c)      Decreased executive function and increased impulsivity.

3.      Biologic Markers.



Central serotonin (5HT)  dysfunction:


(i)      i 5HT metabolites in CSF of normal subjects: predicts h aggression38.


(ii)    i 5HT metabolites in CSF of ASPD compared other personality     disorder39


b)      Serotonin transporter protein:

(i)      Regulates presynaptic reuptake of 5HT; regulates production40.


(ii)    h STP activity ~ h aggression in male adoptees with ASPD parent 41.


(iii)   i STP activity ~ h CD, aggression and ADHD in males and females in        other settings 40-42 .


(iv)  Contrary findings due to small effects, multiple genes acting together.




Monoamine Oxidase (MAOA ):

(i)      Another candidate for serotonin regulation.


(ii)    MAO breaks down monoamines (e.g. serotonin) intracellularly.


(iii)   i MAO ~ i  serotonin production





(iv)  Gene on X chromosome coding for MAOA enzyme.


(v)     400 + children genotyped;  ffed over 20 years43.


(vi)  Antisocial index: criminal records, ASPD, CD sx, informant report.


(vii) i MAOA + Abuse: h ASPD






A.     Continuity from childhood:

1.      Temperament44: irritability and impulsivity at 3 yrs: 3 X’s h ASPD.

2.      Conduct Disorder (CD).

a)      Integral to diagnosis of ASPD12.

b)      Only 25% of CD develop ASPD as adults5.

c)      5 yr olds with CD > 3 symptoms had 2 X’s the educational difficulties at age 745.

d)      Earlier/more CD symptoms: 61% of ASPD: CD onset before 8 yrs5,46.

3.      Attention Deficit Hyperactivity Disorder (ADHD)


a)      h in childhood in ASPD18,23.


b)      ADHD + CD g h severity of ASPD 23.



B.     Longitudinal course over lifespan:


1.      Only follow-up of hospitalized ASPD or criminal system involvement.


2.      29 year follow-up: 26 of  71 hospitalized ASPD patients21,47:


a)      24% dead at follow-up.


b)      Of those alive and followed:


(i)       28% were in remission.


(ii)    30% improved with some symptoms.


(iii)   50% no change: many psychiatric, medical, and social complaints.




1.      Psychiatric: SUD most common co-occurring disorders in ASPD:

a)      70% lifetime prev: alcohol use disorder14.


b)      50 % lifetime prev: drug use disorder other than alcohol14.


c)      At least 25% of in treatment alcohol dependent male patients48-50.


d)      At least 25% of in treatment opioid dependent13,51-53.


e)      80% ASPD seeking treatment have multiple drug dependence17,54


f)        SUD + ASPD: h severity of SUD with earlier onset, heavier use, more family/social/legal problems48,55,56.


g)      # of SUD treatment episodes h 4-fold if ASPD55.


h)      SUD + ASPDg hsuicide especially in males57.





a)      ASPD at h risk of HIV and other STD’s52,59:


(i)      ASPD/opioid dependent: 2.5X’s h HIV+ than non-ASPD opioid 60.


(ii)    Shared needles 2X’s as often as non-ASPD61.


(iii)   Shared with 4X’s as many different people61.


b)      ASPD: h SUD morbidity +h medical complications62,63.

c)      ASPD: hinjuries; 112 non-intentional injuries with surgical admission:           ~10%=ASPD64. 

3.      Mortality.

a)      ASPD associated with h risk of death:

(i)      18 year follow-up of 1000 Swedish youths in probation: risk of death          h6X’s9.

(ii)    80% of deaths were by violent means.

b)      Includes suicide, homicide and non-intentional injuries: 

(i)      ASPD psychiatric inpatients followed up to 12 yrs: unnatural deaths h 15    X’s compared to ref. pop.65.

(ii)    ASPD associated with 4X h odds of committing suicide66.

4.      Other:


a)      Parental child abuse: 40% self-admitted child abusers: ASPD, +/or alcohol   problems67.


b)      Spousal abuse: 2 X’s as likely to have ASPD68.






Treatment options:

1.      Effectiveness difficult to evaluate:

a)      Clinicians often believe: “it can’t help”.


b)      Patients rarely request treatment specific to ASPD69.


(i)      Little insight.


(ii)    Longstanding disturbances.


(iii)   Person less concerned than the relatives.


(iv)  Usually ask help for: SUD, depressive or anxiety sx.



B.     Treatment elements:


1.      Take careful history.


2.      Establish a therapeutic relationship69.


a)      Set firm behavioral limits.


b)      Maintain clear professional boundaries.


c)      Maintain professional attitude: develop empathy.


d)      Set clear behavioral treatment goals in advance69.


(i)      Negotiate agreement.


(ii)    Focus on measurable behavioral goals (i.e. i drug use).


C.     Treatment expectations:



No cure for the personality disorder. 

2.      Teach patient how to decrease problems.

a)      i impulsive actions.

b)      Anticipate problems with novelty seeking.

c)      h empathy of the patient: help to see from others point of view.




Treatment outcomes:


1.      SUD literature has best evidence of treatment impacts:


a)      ASPD + opioid dependence in methadone clinics71:


(i)      Retained equal to non-ASPD in 6/8 studies71.


(ii)    Drug use i among ASPD with treatment: standard methadone = 50%         positive urines over 6 months (vs 35% for non-ASPD)72.


(iii)   HIV high risk behaviors i with 6 mo. treatment: needle sharing = to non-     ASPD71.


(iv)  Continued benzodiazepine / cocaine use result in poor outcomes: 2X’s risk   of early discharge71,72.


(v)    h criminal activity among ASPD groups in 2 studies71.


b)      Psychotherapeutic modalities:


(i)      ASPD/opioid response to psychotherapy is mixed19,71,73.


(ii)    Depressed ASPD patients: respond to therapy similar to non-ASPD       depressed19,73.


c)      Behavioral treatments:


(i)      Contingency management = use of pleasant or unpleasant consequences to   h or i behaviors. 


(ii)    Structured routine aspects of treatment (e.g. methadone take-homes doses, dosing times) = “consequences” to i drug-use in ASPD74.


(iii)   Increases treatment attendance: 83% vs. 53% control 70, 74.


(iv)  Drug use reduced over 6 months: 30% drug positive urines vs. 46% control             – no contingency condition70.




Pharmacotherapy for ASPD.

a)      Data are poor.


b)      Mood stabilizers (divalproex sodium, lithium carbonate) i impulsive aggression        by 50% in prisoners75,76.


c)      SSRI’s anecdotal evidence for i impulsive aggression.


d)      Antipsychotics: few data; don’t seem to work.


e)      Avoid habituating drugs (i.e. benzodiazepines): dependence liability.



Summary: ASPD is:

1.      Very common among those with SUD.

2.      Caused by interplay between genetic and environmental factors.

3.      Associated with great morbidity and mortality.

4.      Difficult to cure; possible to help.

Addendum: Biography of Gary Gilmore

(from “” on 3/22/06)

Gary Mark Gilmore was born in a rural Texas town in December 1940, the second of four sons. His parents drifted around the country most of the time while he and his brothers were growing up, with his father peddling and scamming people with phony magazine and newspaper subscriptions.

The Gilmore family settled in Portland, Oregon in the early 1950s, where Gary Gilmore began getting into trouble with the law, with offences ranging from shoplifing to assault and battery charges. He dropped out of high school at age 15 and drifted across the Midwest making a living out of robbing houses and stores.

He was convicted of armed robbery in Indianapolis, Indiana in 1964, and received an 18-year prison sentence. He was conditionally paroled in March 1976 and sent to Provo, Utah to live with a distant cousin of his who tried to help him find work and make a living for himself. But Gilmore's self-destructive nature soon got the best of him, as he couldn't stay away from the quick and easy life of crime as he saw it. Gilmore began stealing money and items from stores and homes.

Gilmore was convicted of killing Ben Bushnell, a motel manager, in Provo, Utah on July 20, 1976. He had also been charged with murdering Max Jensen, a Sinclair gas station employee in Orem, Utah the previous day, but that case never went to trial apparently because there were no witnesses. Gilmore's trial was held from October 5 to October 7, 1976 – he was quickly convicted of the murder, mostly because there was no defense on his part. The jury also recommended the death penalty for Gilmore due to the special circumstances to the crime. Because Utah then had two methods of execution, firing squad or death by hanging, Gilmore was given a choice, in which he replied, "I'd prefer to be shot."

During the three months Gilmore was on death row awaiting his execution, he attempted suicide twice. The first was on November 16, 1976 and the second was a month later on December 16. The execution was stayed three times. While incarcerated, Gilmore developed a deep dislike for two of his fellow inmates, convicted murderers and rapists Dale Selby Pierre and William Andrews, the "Hi-Fi Murderers." Gilmore had to pass the men's cells on his way to the firing squad, and as he was led past he laughed at the men and called out, "I'll see you in Hell, Andrews and Pierre!"

Gilmore was shot by a firing squad on January 17, 1977 after angrily telling his lawyers to drop the appeals they had filed in defiance of his wishes. The night before, Gilmore had requested an all-night gathering of friends and family at the prison mess hall. On the morning of the 17th, he enjoyed a last meal consisting of a hamburger, hard-boiled eggs, a baked potato, a few cups of coffee, and three shots of whiskey. He was then taken to an abandoned cannery behind the prison which served as the prison's death house. He was strapped to a chair, with a wall of sandbags placed behind him to absorb the projectiles of the bullets. Five prison guards stood concealed behind a curtain with five small holes cut for them to place their rifles through which were aimed at him. Gilmore's last words were: "Let's do it."

Gilmore requested that, following his execution, his eyes be used for transplant purposes. Within hours of the execution, two people received his corneas, inspiring the British punk rock band The Adverts to write and release "Gary Gilmore's Eyes" later that year.

According to Mikal Gilmore's memoir, Utah's tradition dictated that five men comprise a firing squad - four of them with loaded rifles and one with a gun containing a blank, so as to not know who fired the fatal shot. Upon inspecting the clothes worn by Gary Gilmore at his execution, Mikal noticed five holes in the shirt - indicating, he wrote, that "[t]he state of Utah, apparently, had taken no chances on the morning that it put my brother to death" (p. 390).


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