Sociopathy & Neural Substrates

Teresa Binstock binstoct at essex.hsc.colorado.edu
Sat Jul 29 21:16:04 EST 1995


Newsgroups: sci.med.psychobiology, bionet.neuroscience
Subject: Sociopathy & Neural Substrates
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Organization: University of Colorado, Health Sciences Center
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Herewith are some references that point toward learning about neural 
substrates that are at least associated with sociopathic behavior and 
that may well be, in some individuals, causally related to those 
behaviors. 

Frontal, prefrontal, and anterior cingulate are themes in these 
references. Therefore I'd like to speculate that at least some persons 
with persistent sociopathic behavior may have experienced some relatively 
"innocent" injury to the frontal portion of their brain, perhaps during 
childhood. Surely, most of us fall or in other ways injure ourselves, 
bump our heads strongly, and do not develop Antisocial Personality 
Disorder. Nonetheless, for every 10,000 seemingly innocent head-bumps 
during childhood (or later) perhaps some are so severe and so precisely 
located as to induce reduced inhibition and sociopathic-type behavior. 
No doubt this kind of "syndrome" has numerous causes, making statistical 
studies difficult... (Many soft correlations, nothing clear as "the 
cause"). 

I'll close by saying, neither sociopathy nor head-bumps are my primary 
area, tho' I do lots of other "stuff" in neuro research. No doubt, 
"substrates of sociopathy" is a very important focus...


                 SOME SOCIOPATH/NEURO REFERENCES

1. Devinsky, O., Morrell, M.J. and Vogt, B.A. Contributions of
anterior cingulate cortex to behaviour.  
## Brain 118:279-306, 1995. 
**  - Assessments of anterior cingulate cortex in experimental
animals and humans have led to unifying theories of its
structural organization and contributions to mammalian behaviour.
The anterior cingulate cortex forms a large region around the
rostrum of the corpus callosum that is termed the anterior
executive region. This region has numerous projections into motor
systems, however, since these projections originate from
different parts of anterior cingulate cortex and because
functional studies have shown that it does not have a uniform
contribution to brain functions, the anterior executive region is
further subdivided into 'affect' and 'cognition' components. The
affect division includes areas 25, 33 and rostral area 24, and
has extensive connections with the amygdala and periaqueductal
grey, and parts of it project to autonomic brainstem motor
nuclei. In addition to regulating autonomic and endocrine
functions, it is involved in conditioned emotional learning,
vocalizations associated with expressing internal states,
assessments of motivational content and assigning emotional
valence to internal and external stimuli, and maternal-infant
interactions. The cognition division includes caudal areas 24'
and 32', the cingulate motor areas in the cingulate sulcus and
nociceptive cortex. The cingulate motor areas project to the
spinal cord and red nucleus and have premotor functions, while
the nociceptive area is engaged in both response selection and
cognitively demanding information processing. The cingulate
epilepsy syndrome provides important support of experimental
animal and human functional imaging studies for the role of
anterior cingulate cortex in movement, affect and social
behaviours. Excessive cingulate activity in cases with seizures
confirmed in anterior cingulate cortex with subdural electrode
recordings, can impair consciousness, alter affective state and
expression, and influence skeletomotor and autonomic activity.
Interictally, patients with anterior cingulate cortex epilepsy
often display psychopathic or sociopathic behaviours. In other
clinical examples of elevated anterior cingulate cortex activity
it may contribute to tics, obsessive-compulsive behaviours, and
aberrent social behaviour. Conversely, reduced cingulate activity
following infarcts or surgery can contribute to behavioural
disorders including akinetic mutism, diminished self-awareness
and depression, motor neglect and impaired motor initiation,
reduced responses to pain, and aberrent social behaviour. The
role of anterior cingulate cortex in pain responsiveness is
suggested by cingulumotomy results and functional imaging studies
during noxious somatic stimulation. The affect division of
anterior cingulate cortex modulates autonomic activity and
internal emotional responses, while the cognition division is
engaged in response selection associated with skeletomotor
activity and responses to noxious stimuli. Overall, anterior
cingulate cortex appears to play a crucial role in initiation,
motivation, and goal-directed behaviours.(ABSTRACT TRUNCATED AT
400 WORDS) 
 
2. Gabel, S., Stadler, J., Bjorn, J., Shindledecker, R. and
Bowden, C.L. Monoamine oxidase and homovanillic acid in boys with
predispositions to substance abuse. 
## Alcoholism,.Clinical.&.Experimental.Research. 18:1137-1142,
1994. 
**  - Both dopaminergic dysregulation and abnormalities in
monoamine oxidase (MAO) have been postulated as etiological
factors in substance abuse. This study assessed whether MAO
activity differed in sons of substance-abusing fathers compared
with sons of nonsubstance-abusing fathers. It also assessed the
levels of homovanillic acid (HVA), the metabolite of dopamine,
and MAO in a group of substance-using/-abusing boys compared with
peers without this history in the same setting. Sixty-five boys
admitted to a residential center were evaluated on blood tests
for HVA and MAO, and on a series of diagnostic instruments and
questionnaires designed to elicit information about parental
substance abuse and about the subject's own substance use/abuse.
The results indicated tentatively that younger (< 12.0 years)
sons of substance-abusing fathers had higher levels of MAO than
younger sons of nonsubstance-abusing fathers. Levels of MAO in
older (> or = 12.0 years) sons of substance-abusing and
nonsubstance-abusing fathers did not differ. Boys with histories
of significant use/abuse of substances themselves had
significantly higher MAO levels and significantly lower HVA
levels than peers of the same age without substance use/abuse
histories   
 
3. Goyer, P.F., Andreason, P.J., Semple, W.E., Clayton, A.H.,
King, A.C., Compton-Toth, B.A., Schulz, S.C. and Cohen, R.M.
Positron-emission tomography and personality disorders. 
## Neuropsychopharmacology. 10:21-28, 1994. 
**  - This study used positron-emission tomography to examine
cerebral metabolic rates of glucose (CMRG) in 17 patients with
DSM III-R diagnoses of personality disorder. Within the group of
17 personality disorder patients, there was a significant inverse
correlation between a life history of aggressive impulse
difficulties and regional CMRG in the frontal cortex of the
transaxial plane approximately 40 mm above the canthomeatal line
(CML) (r = -.56, p = 0.17). Diagnostic groups included antisocial
(n = 6), borderline (n = 6), dependent (n = 2), and narcissistic
(n = 3). Regional CMRG in the six antisocial patients and in the
six borderline patients was compared to a control group of 43
subjects using an analysis of covariance with age and sex as
covariates. In the borderline personality disorder group, there
was a significant decrease in frontal cortex metabolism in the
transaxial plane approximately 81 mm above the CML and a
significant increase in the transaxial plane approximately 53 mm
above the CML (F[1,45] = 8.65, p = .005; and F[1,45] = 7.68, p =
.008, respectively   
 
4. Raine, A., Buchsbaum, M.S., Stanley, J., Lottenberg, S., Abel,
L. and Stoddard, J. Selective reductions in prefrontal glucose
metabolism in murderers. 
## Biological.Psychiatry 36:365-373, 1994. 
**  - This study tests the hypothesis that seriously violent
offenders pleading not guilty by reason of insanity or
incompetent to stand trial are characterized by prefrontal
dysfunction. This hypothesis was tested in a group of 22 subjects
accused of murder and 22 age-matched and gender-matched controls
by measuring local cerebral uptake of glucose using positron
emission tomography during the continuous performance task.
Murderers had significantly lower glucose metabolism in both
lateral and medial prefrontal cortex relative to controls. No
group differences were observed for posterior frontal, temporal,
and parietal glucose metabolism, indicating regional specificity
for the prefrontal deficit. Group differences were not found to
be a function of raised levels of left-handedness, schizophrenia,
ethnic minority status, head injury, or motivation deficits in
the murder group. These preliminary results suggest that deficits
localized to the prefrontal cortex may be related to violence in
a selected group of offenders, although further studies are
needed to establish the generalizability of these findings to
violent offenders in the community   
 
5. Stein, D.J., Hollander, E., Cohen, L., Frenkel, M., Saoud,
J.B., DeCaria, C., Aronowitz, B., Levin, A. and Liebowitz, M.R.
Neuropsychiatric impairment in impulsive personality disorders. 
## Psychiatry Research. 48:257-266, 1993. 
**  - It has been suggested that impulsivity and aggression are
associated with neuropsychiatric impairment. Neurological soft
signs may be a useful marker of nonspecific brain damage, and may
therefore be increased in impulsive and aggressive patients
compared with normal control subjects. A structured examination
was used to evaluate neurological soft signs in 28 patients with
personality disorders characterized by impulsivity and 28 healthy
control subjects. All of the patients met DSM-III-R criteria for
borderline personality disorder, and 10 also met criteria for
antisocial personality disorder. All patients were questioned
about past history of physical aggression, and a subset of 18
patients underwent neuropsychological testing with a select
battery. Left-sided neurological soft signs were significantly
increased in patients compared with normal control subjects.
Patients with a history of aggression, however, had significantly
more right-sided neurological soft signs than those without a
history of aggression. Increased neurological soft signs were
associated with impairment on the Wisconsin Card Sort, a test of
frontal lobe executive function. Specific neuropsychiatric
abnormalities, such as lateralized neurological soft signs and
associated impairment on select neuropsychological tests, may be
present in patients with personality disorders characterized by
impulsivity   
 
6. Elliott, F.A. Violence. The neurologic contribution: an
overview.  
## Archives.of.Neurology 49:595-603, 1992. 
**  - The role of cultural forces in either promoting or
discouraging interpersonal violence is so obvious that it has
been allowed to obscure the part played by biologic disorders in
determining responses to endogenous and environmental challenges.
Neuroscientists and clinicians have demonstrated, however, that
aggression has a neuroanatomic and chemical basis, that
developmental and acquired brain disorders contribute to
recurrent interpersonal violence, that both biologic and
sociologic factors are involved, and that to ignore either is to
invite error. 
 
7. Tonkonogy, J.M. Violence and temporal lobe lesion: head CT and
MRI data. 
## Journal.of.Neuropsychiatry.&.Clinical.Neurosciences.
3:189-196, 1991. 
**  - Head computed tomography and magnetic resonance imaging
scanning were done in 23 patients with organic mental syndromes.
Violent behavior was observed in 14 patients. A nonviolent group
consisted of nine patients. Five cases of local lesion in the
anterior-inferior temporal lobe were revealed in the violent
group. It is suggested that the release of programs for violent
behavior may result from the unilateral destruction of amygdaloid
nuclei or adjacent structures coupled with the paroxysmal
stimulation of preserved limbic structures by the mechanisms of
kindling   
 
8. Lueger, R.J. and Gill, K.J. Frontal-lobe cognitive dysfunction
in conduct disorder adolescents. 
## Journal.of.Clinical.Psychology. 46:696-706, 1990. 
**  - Behavioral similarities between antisocial behavior
disorders and frontal-lobe cerebral impairment have led to
suggestions that conduct disorders are attributable to
disinhibition deficit associated with frontal-lobe cerebral
functions. This study compared the performance of 21 conduct
disorder adolescents on measures of cognitive processes
associated with frontal-lobe functions with that of a matched
comparison sample. Conduct disorder adolescents performed more
poorly on measures sensitive to frontal-lobe dysfunction
(conceptual perseveration, poorly sustained attention, impaired
sequencing on memory and motor tasks), but not on non-frontal-
lobe specific cognitive measures. Although the findings support a
neurobehavioral explanation of antisocial behavior as a product
of cerebral disinhibition, caution is urged in overinterpreting
causal relationships through neurobehavioral data   
 
9. Weiger, W.A. and Bear, D.M. An approach to the neurology of
aggression.  
## Journal.of.Psychiatric.Research. 22:85-98, 1988. 
**  - Aggressive behavior is controlled at multiple anatomical
levels within the human brain. To illustrate hierarchical neural
controls over aggression, we compare and contrast the roles of
the hypothalamus, amygdaloid complex, and orbital prefrontal
cortex in terms of their distinctive sensory inputs, effector
channels, and principles of integration as deduced from
observations in animals and man. We illustrate characteristic
syndromes of human aggression resulting from hypothalamic,
temporolimbic, or frontal cortical lesions. The application of
this perspective to research on criminal violence is discussed.  


EOF.


Teresa, Researcher
Developmental and Behavioral Neuroanatomy
Denver 




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