Threat management systems.

Arbaizar B. Psiquiatria.com. 2013; 17:8.
http://hdl.handle.net/10401/6170

Artículo especial
Threat management systems
Sistemas de manejo de amenazas

Beatriz Arbaizar1*, Paula Suarez-Pinilla2, Javier Llorca3

Resumen
Varios mecanismos de gestión de riesgos están involucrados en la respuesta hacia diferentes
peligros o amenazas potenciales: el sistema de detección de amenazas, dirigido a enfrentarse a
peligros-visicitudes-amenazas reales, y el sistema de respuestas de precaución, dirigido a hacer
frente a amenazas hipotéticas. En este artículo, nos centramos en las relaciones entre estos
sistemas y los trastornos de ansiedad. Nuestro objetivo es sistematizar varios subsistemas, sus
mecanismos de acción y las enfermedades relacionadas con la respuesta alterada de estos
subsistemas.
Palabras claves: Sistema de manejo de amenazas, subsistema de autoprotección, subsistema
de evitación de la enfermedad, sistema de manejo de riesgos.
Abstract
We try to systematize the risk assessment mechanism in two general threat management
systems 1) the threat detection: intended to face current threats, 2) and the precautionary
responses: intended to face hypothetical threats. These mechanisms could act via several
specific subsystems, including the self-protection subsystem, the disease avoidance subsystem,
one that we hypostatize and have called the security sense subsystem, and very probably others.
Keywords: Threat management systems self-protection subsystem, disease avoidance
subsystem, risk management system.

Recibido: 09/11/2012 ­ Aceptado: 03/01/2013 ­ Publicado: 22/02/2013

* Correspondencia: llorcaj@unican.es
1y2 University Hospital Marques de Valdecilla, Santander, Spain.
3 University of Cantabria, Santander, Spain; CIBER Epidemiologia y Salud Publica (CIBERESP), Spain;
IFIMAV, Santander, Spain.

Psiquiatria.com ­ ISSN: 1137-3148
© 2013 Arbaizar B, Suarez-Pinilla P, Llorca J.

Arbaizar B. Psiquiatria.com. 2013; 17:8 - http://hdl.handle.net/10401/6170

Introduction
In this paper we are going to follow an evolutionary perspective, as a result of that we have
assumed that there are several risk assessment mechanisms that have evolved in response
towards different potential dangers or threats, these adaptive patterns would have the task to
enhance the fitness and survival rates of the own specie.
Several risk assessment mechanism in mammals that will increase the opportunities to achieve
reproductive success have been described basing in the evolutionary theory. As result of this
certain mental disorders as the anxiety disorders can be understood as deregulations of these
adaptive mechanisms.
Some confusion could exist in the usual terminology for describing this threat management
system. For instance, security motivation system (Woody and Szechtman.2011), threat detection
and precautionary responses (Stein and Nesse.2011), etc. From here on, we are going to use the
terms contributed by Stein and Nesse; therefore, we use "threat detection" and "precautionary
responses" as the names for the two principal categories of the risk management system; then,
we use the terms "self protection" and "disease avoidance subsystem" (Neuberg et al.2011) for
some subcategories of our attempt to schematizing this risk management system; moreover, we
are going to take advantage of the criterion "inferred-manifested threat" use by Boyer and
Lienard (2006).
We also are going to use the concept of dimensions that have been described in OCD; these
dimensions could have differential neural correlates and treatment responses (Pinto et al.2007;
Pine.2011).
The five described factor-dimensions in OCD we are going to work with are:
·

Symmetry / ordering

·

Hoarding

·

Taboo thoughts: sexual, aggressive, and religious obsessions

·

Doubt / checking

·

Contamination / cleaning

Although several authors integrate the taboo thoughts (violent, sexual, and religious thematic)
with the checking compulsions (Cavallini et al.2002;Katerberg et al.2010; Abramowitz et al.
2010), we follow the classification that other authors obtain after consider separately the
aggression factor of the taboo thoughts (violent, sexual, and religious thematic) of the
unintencional fear of harm in checking compulsions
(Pinto et al.2007;Williams et
al.2011;Wheaton et al.2012).
In this review we are going to center our interest in the "self protection subsystem", the "disease
avoidance subsystem" and in one new theoretical system that we have called "sense control
subsystem" (table 1).

Threat management systems
Adaptive evolutionary patterns increase enduring reproductive success. Threat management
systems have evolved since ancient times to face physical integrity and health protection risks.

2

Arbaizar B. Psiquiatria.com. 2013; 17:8 - http://hdl.handle.net/10401/6170

Fear circuitry-Self protection subsystem
The field of action of the self protection system is to detect potential threats to the individual
and to others (Woody and Szechtman.2011). When the fear becomes specific in an immediate
future, a number of possible evolutionarily adaptive behaviors can be adopted depending on the
qualitative evaluation of the danger, such as flight, fight, tonic immobility, etc. The amygdala
constitutes the backbone of the circuit of the fear­self protection subsystem (Flannelly et
al.2007).
The amygdala plays a key role in fear circuitry, but the circuit implicated in detection and
response to potential external threats embraces not only the amygdala but also the anterior
cingulated cortex and regions of the prefrontal cortex; they are connected to the hypothalamus,
pituitary and adrenal (HPA) axis where the autonomic (e.g. heart rate, blood pressure) and
endocrine (hormone release) responses take place (Craig and Halton.2009).
In fact, humans with amygdala damage have deficits in emotional perception of danger (Calder
et al.96), and damage to the amygdala (Bechara et al.1995) also produces deficits in fear
conditioning in humans. Fear conditioning leads to increases in amygdala activity, which can be
measured by functional magnetic resonance imaging (Buchel et al.1998) More specifically, the
fear circuitry is located in the lateral amygdala (LA) - an important site of plasticity in auditory
fear conditioning- and the thalamic afferents towards LA synapses use glutamate as a
neurotransmissor (Radly et al.2007; Sah et al.2003;Tsvetkov et al.2004). It has also been
proved that drugs such as glutamate N-methyl-D-aspartate (NMDA) antagonists may block the
conditioned fear (Garakani et al.2008).
Summarising, the fear circuitry-self protection subsystem is activated by fear emotion and is
centralized in the amygdala.
Disease Avoidance Subsystem
The fear of contamination is the most common object of obsessions, and at least 50% of the
OCD patients suffered it (Rachman.2004;Brady et al.2010).
In the disease avoidance subsystem (Lienard.2011), the goal is to avoid health risks, this
adaptive response ­fear of contamination- could be mediated by disgust sensitivity and its
response could be avoidance behaviors. Disgust sensitivity could be a mediator of contamination
fear and could have an adaptive function in preventing disease acquisition through avoidance of
contact with possibly contaminated stimuli (Deacon and Olatunji.2007;Olatunji et al.2004;
Olatunji et al 2005, Neuberg et al.2011;Brady et al.2010).
Disgust sensitivity is greater in females as possible result of differential investment in offspring
development; increased contamination avoidance is also seen in pregnancy, probably due to the
higher reproductive investment cost (Lienard.2011;Björkland and Hursti 2004). Disgust
sensitivity is also increased during the first trimester of pregnancy, when the immunological
defenses are momentarily diminished (Lienard.2011;Forray et al.2010). Postpartum has also
been associated with the onset of OCD (Forray et al.2010; Labad et al.2005), although
obsessions in this period are usually characterized by the fear of harming the baby, so they are
probably unrelated with disgust sensitivity.
The pattern of activation during a disgust-inducing task in OCD subjects is different to that of
healthy subjects, including greater activation in the right insula, parahippocampal region, and
inferior frontal sites ( Olatunji et al.2004; Olatunji et al 2005;Shapira et al.2003).

3

Arbaizar B. Psiquiatria.com. 2013; 17:8 - http://hdl.handle.net/10401/6170

It has recently been noticed that the cingulated cortex and insula are particularly implicated in
less immediate threats ­ such as risk of contamination (Woody and Szechtman.2011;
Fiddick.2011) . According to suggestions of Vogt (Vogt et al.1992), the anterior cingulated cortex
is devoted to scanning ego-generated or internal signals of threat and the posterior cingulated
cortex evaluates environmental threats.
Summarising, the disease avoiding subsystem implicated in fear contamination could be
activated by disgust emotions -mainly involving the cingulated cortex and insula. The
orbitofrontal cortex is implicated in generating the closure signals that end the defensive
responses (Pritchard et al.2008; Szechtman and Woody. 2004). We adopt the Woody and
Szechtman hypothesis (Szechtman and Woody. 2004; Woody and Szechtman. 2011): the lack of
a clear and objective signal that the threat has been removed due the impossibility of
verification that this threat has been neutralized could be the cause of the precaution behavior
becoming a compulsion, and these repetitive behaviors ­ compulsions observed in the
deregulation of disease avoidance subsystem could be the result of the absence of frontal
inhibition.

Security-control sense subsystem
In this text, we use the term ritualized as a repetitive response: mental compulsions or repetitive
external behaviors that are logically unconnected with intrusive thought; compulsion will be
used as a repetitive behavior with an apparently logical connection with the initial thought, such
as washing or doubting compulsions.
The taboo thoughts, mainly religious, sexual, and aggressive, tend to appear together (Grant et
al.2006) and as several authors described OCD patients with taboo thought concerns especially
engage in mental rituals [Williams et al.2011], which usually neutralize these obsessions in an
illogic manner.
It should be remarked that humans have the capacity of anticipation; they can represent
different scenes of their past and of their future through cognitive mechanisms, and this quality
allows humans to anticipate the possible dangerous consequences of some actions.
Rituals are widely present in our daily activity; they appear in numerous social activities
(Turbott.1997; Boyer and Lienard.2006). They are repeated actions that must be executed
according to certain procedures and serve to confer a sense of controllability of dangerous
situations that are beyond our rational capacity of control; they usually serve to ensure good
luck or avoid misfortune (Turbott.1997; Eilam et al.2011), repeating the same acts following a
few very precise procedures enables the reduction of danger from an abstract or internal source.
Using a stereotyped series of actions, carried out according to a strict procedure, the most
unpredictable dangers are avoided or good luck is invoked. Ritualistic responses are usually
unconnected in a realistic way to the specific fear and behavior is unrelated to the original
context, incorporating a change in its function. Our suggestion is that the security-control sense
subsystem could be associated to taboo thoughts ­ sexual, religious and aggressive obsessions;
in this case, the origin of the threat is preferentially internal, and it could be neutralized by an
illogical way through the so-called "magic thinking".

4

Arbaizar B. Psiquiatria.com. 2013; 17:8 - http://hdl.handle.net/10401/6170

Summarizing neurobiology of OCD

Now we briefly review some relevant aspects of the neurobiology of OCD
The cortico-striato-thalamo-cortical circuitry ­that include orbitofrontal cortex(OFC), anterior
cingulate cortex(ACC),dorsolateral prefrontal cortex(DLPFC), thalamus and amygdala- has been
repeatedly implicated in OCD symptomatology (Woody and Szechtman.2011;Fineberg et
al.2011;Wu et al.2012;Pittenger et al.2001;Albelda and Joel.2012; Goddard et
al.2008;Andersenet al.2010). The two major neurotransmitters of cerebrum are glutamate as
excitatory transmitter and GABA as inhibitory transmitter. Both of them are modulated by
dopamine and serotonin; there is an increasing number of data ­neurobiological, genetic,
pharmacological, animal modelspointing at alterations involving the glutaminergic,
dopaminergic and serotoninergic transmission, although we cannot forgot that serotonin and
dopamine have also complex interactions with each other.
The serotoninergic hypothesis comes from the clinical observation that OCD patients improve
with SSRIs. Although the SSRIs have been the most recognized pharmacological treatment for
OCD, the response rates are poor, and 30 to 50% of patients remain refractory to this treatment;
even the responders are usually only partially responders (Piggot and Seay.1998; Goddard et
al.2008;Andersenet al.2010). These data have favoured the emergency of the
hyperdopaminergic hypothesis.
Behavioral models of OCD/compulsive behaviors would seem to be compatible with
hyperdopaminergic hypothesis. Psychostimulant drug administration is known to induce
stereotypic behaviors in animals, while dopamine agonist and psychostimulant drugs can induce
OCD symptoms in humans (Guegant and Crochette.2000;Yang et al 2003).
Thus, it is not surprising that atypical antipsychotics combining D2 receptor blockade and 5HT2A antagonism show a favourable profile of effects in resistant forms of OCD ( Goddard et
al.2008). We also know that the dopamine D1 and D2 receptor antagonists decrease the
repetitive and compulsive behavior in rabbits [Hoffman and Rueda Morales.2012]. In fact
Tourette's syndrome is characterized by the presence of brief, stereotyped motor or vocal
behaviors that respond preferentially to DA antagonists, and usually the SSRIs do not have
beneficial effects in them.
The motor manifestation of compulsive behaviors in OCD is controlled from the striatum, more
specifically by the dorsal striatum, also called the motor striatum; cingulotomy is effective in
reducing obsessive symptoms, but is totally ineffective in reducing tics associated with
Tourette's syndrome (Baer et al.1994).
The more recent contributions link the difficulty to initiate new actions to glutamate
hyperactivity in frontal and cingulated areas, while the motor aspect of compulsions-rituals
could be executed in the striatum area, where we might find that dopaminergic hyperactivity
holds the inhibitory frontal control and, itself, is controlled by the brainstem serotonergic
inhibition (Woody and Szechtman. 2011; Pritchard et al.2008;March and Maia .2009;Finenberg
et al.2010).
Some normal childhood behaviors resemble some OCD symptoms, it has been supposed that
these behaviors will disappear when the maturation of the prefrontal cortex takes place, in fact it
is supposed that some compulsions could be the result of a failure in the orbitofrontal inhibitory

5

Arbaizar B. Psiquiatria.com. 2013; 17:8 - http://hdl.handle.net/10401/6170

control mainly due a hiperglutaminergic activation in this cortex.(Fineberg et al.2011;Wu et
al.2012; Pittenger et al.2001;Rosenberg et al.2004;Whiteside et al.2006).
OCD has also been associated with the so-called cognitive flexibility alteration, this could be
related with the inability of these patients to stop the already initiated action and change it for a
new response; this function could be preferentially located in the frontal lobe (Boulougouris et
al.2009); as a result, some authors think that this difficulty to initiate new actions could be
linked to glutamate hyperactivity in frontal and cingulated areas (Pritchard et al.2008).

Discussion
In our opinion there are several entities, such as compulsive cleaning, reassuring, phobic fear of
certain animals, hypochondria and possibly other disorders that could be included in disorders
related to deregulations of threat management systems. We propose differentiating several
subsystems for facing threats: the self protection subsystem, when the threat is external and
expected in an immediate o proximal future; the security ­control sense subsystem, when the
threat is internal ­inacceptable thoughts- that could be neutralized through magic thinking and
ritualised behaviors, and disease avoidance subsystem, when the threat is inferred but his
resolution is not totally verifiable, then the message of stop action to the frontal inhibition
centre would not occur and the precaution response would become a compulsion.
In our scheme, the doubt-checking compulsions, hoarding and symmetry/ordering would also
be integrated in the precautionary responses; in the doubt-checking compulsion cases,
symmetry/ordering compulsions and hoarding we would have to hypothesize a primary
deregulation in the frontal inhibition center, this could corresponded with the characteristic
cognitive process described in OCD patients and denominated cognitive inflexibility; it has
been interpreted as a possible OCD cognitive endophenotype [Chamberlain et al 2007].
Our suggestion is that rituals ­mental compulsions as repetitive unrelated behaviors- observed
in taboo obsessions could be an instrumentation of a security control sense subsystem towards
the aggressive, sexual and religious thoughts; this subsystem could neutralize this unacceptable
thoughts trough the magic thinking process that would serve to provide the individual with a
sensation of control over his/her existence and future.
We are conscious that our try to schematizing is very simple and need further contributions and
exhausted revisions. It's only an attempt to introduce some order in an important and recent
appeared concepts.In spite the immaturity of our initial scheme we think it could be an step for
other authors later development structuration in this area of the correspondence between
anxiety disorders and the threat management systems.

6

Arbaizar B. Psiquiatria.com. 2013; 17:8 - http://hdl.handle.net/10401/6170

References
1.

Andersen SL, Greene-Colozzi EA, Sonntag KC. A novel, multiple symptom model of obsessive-compulsive-like
behaviors in animals. Biol Psychiatry. 2010; 15;68 (8):741-7.

2.

Turbott J. The meaning and function of ritual in psychiatric disorder, religion and everyday behavior. Aust N Z J
Psychiatry 1997; 31 (6):835-43.

3.

Goddard AW, Shekhar A, Whiteman AF, McDougle CJ. Serotoninergic mechanisms in the treatment of
obsessive-compulsive disorder. Drug Discov Today 2008; 13 (7-8):325-32.

4.

Pigott TA, Seay S. Biological treatments for obsessive-compulsive disorder. Literature review. In ObsessiveCompulsive Disorder: Theory, Research, and Treatment (Swinson RP, Antony MM, Rachman S, Richter MA,
eds.) pp. 298-326. 1998. Guilford Press, New York.

5.

Guegant G, Crochette A. Methylphenidate, tics and compulsions Encephale 2000; 26 (2):45-7.

6.

Yang PB, Amini B, Swann AC, Dafny N. Strain differences in the behavioral responses of male rats to chronically
administered methylphenidate. Brain Res 2003; 971 (2):139-52.

7.

Rosenberg DR, Mirza Y, Russell A, Tang J, Smith JM, Banerjee SP, Bhandari R, Rose M, Ivey J, Boyd C, Moore
GJ. Reduced anterior cingulate glutamatergic concentrations in childhood OCD and major depression versus
healthy controls. J Am Acad Child Adolesc Psychiatry 2004; 43:1146­1153.

8.

Whiteside SP, Port JD, Deacon BJ, Abramowitz JS. A magnetic resonance spectroscopy investigation of
obsessive­compulsive disorder and anxiety. Psychiatry Res Neuroimaging 2006; 146:137­147.

9.

Pinto A,Eisen JL, Mancedo MC, Greenberg BD,Stout RL,Ramussen SA. Taboo thoughts and doubt/checking: a
refinement of the factor structure for obsessive-compulsive disorder symptoms. Psychiatry Res 2007; 151:255258.

10. Woody EZ, Szechtman H. Adaptation to potential threat: the evolution, neurobiology and psychopathology of
security motivation system. Neurosci Biobehav 2011; 35(4):1019-33.
11.

Flannelly, KJ, Koening HG, Galek K, Ellison GC. Beliefs, mental health, and evolutionary threat assessment
systems in the brain. J Nervous Mental Dis 2007; 195:996-1003.

12. Craig IW, Halton KE. Genetics of human aggressive behavior. Hum Genet 2009; 126:101­113.
13. Calder AJ, Young AW, Rowland D, Perrett D, Hodges JR, Etcoff NL. Facial emotion recognition after bilateral
amygdale damage: differentially severe impairment of fear. Cogn Neuropsychol 1996; 13:699­745.
14. Bechara A, Tranel D, Damasio H, Adolphs R, Rockland C, Damasio AR. Double dissociation of conditioning and
declarative knowledge relative to the amygdala and hippocampus in humans. Science 1995; 269:1115­18.
15.

Buchel C, Morris J, Dolan RJ, Friston KJ. Brain systems mediating aversive conditioning: an event-related fMRI
study. Neuron 1998; 20:947­57.

16. Radley JJ, Farb CR, He Y, Janssen WG, Rodrigues SM, Johnson LR, Hof PR, LeDoux JE, Morrison JH
Distribution of NMDA and AMPA receptor subunits at thalamo-amygdaloid dendritic spines. Brain Res 2007;
1134(1):87-94.
17.

Sah P, Faber ES, Lopez De Armentia M, Power J. The amygdaloid complex: anatomy and physiology. Physiol Rev
2003; 83:803­834.

18. Tsvetkov E, Shin RM, Bolshakov VY. Glutamate uptake determines pathway specificity of long-term potentiation
in the neural circuitry of fear conditioning. Neuron 2004; 41:139­151.
19. Garakani A, Mathew SJ, Charney DS. Neurobiology of anxiety disorders and implications for treatment. Mt Sinai
J Med 2006; 73 (7):941-9.
20. Rachman S. Fear of contamination. Behav Res Ther 2004; 42 (11):1227-55.
21. Lienard.P. Life stages and risk-avoidance:
Neurosci.Biobehav Rev 2011; 35(4):1067-74.

Status-and

context-sensitivity

in

precaution

systems.

7

Arbaizar B. Psiquiatria.com. 2013; 17:8 - http://hdl.handle.net/10401/6170

22. Deacon B, Olatunji BO. Specificity of disgust sensitivity in the prediction of behavioral avoidance in
contamination fear. Behav Res Ther 2007; 45:2110­2120.
23. Olatunji BO, Sawchuk CN, Lohr JM, de Jong PJ. Disgust domains in the prediction of contamination fear. Behav
Res Ther 2004; 42:93­104.
24. Olatunji BO, Williams NL, Lohr JM, Sawchuk CN. The structure of disgust: Domain specificity in relation to
contamination ideation and excessive washing. Behav Res Ther 2005; 43:1069­1086.
25. Neuberg SL, Kenrick DT, Schaller M. Human threat management systems: Self-protection, and disease
avoidance. Neurosci Biobehav Rev 2011; 35(4):1042-51.
26. Björklund F, Hursti TJ. A Swedish translation and validation of the Disgust Scale: a measure of disgust sensitivity
Scand J Psychol 2004; 45 (4):279-84.
27. Forray A, Focseneanu M, Pittman B, McDougle CJ, Epperson CN. Onset and exacerbation of obsessivecompulsive disorder in pregnancy and the postpartum period. . J Clin Psychiatry 2010; 71 (8):1061-8.
28. Labad J, Menchón JM, Alonso P, Segalàs C, Jiménez S, Vallejo J. 2005. Female reproductive cycle and obsessivecompulsive disorder. J Clin Psychiatry 2005; 66 (4):428-35; quiz 546.
29. Shapira NA, Liu Y, He AG, Bradley MM, Lessig MC, James GA, Stein DJ, Lang PJ, Goodman WK. Brain
activation by disgust-inducing pictures in obsessive­compulsive disorder. Biological Psychiatry 2003; 54:751­
756.
30. Fiddick L. There is more than the amygdala: Potential threat assessment in the cingulate cortex. Neurosci
Biobehav Rev 2011; 35(4):1007-18.
31. Vogt BA, Finch DM, Olson CR Functional heterogeneity in cingulate cortex: the anterior executive and posterior
evaluative regions. Cerebral Cortex 1992; 2:435­443.
32. Boulougouris V, Chamberlain SR, Robbins TW. Cross-species models of OCD spectrum disorders. Psychiatry
Res. 2009; 170(1):15-21.
33. Pritchard T, Nedderman E, Edwards E, Petticoffer A, Schwarz G, Scott T. Satiety-responsive neurons in the
medial orbitofrontal cortex of the macaque. Behav Neurosci 2008; 122:174­182.
34. Szechtman H, Woody E. Obsessive-compulsive disorder as a disturbance of security motivation. Psychological
Review 2004; 111:111­127
35. Grant JE,Pinto A,Gunnip M,Mancebo MC,Eisen JJL,Rasmussen SA. Sexual obsessions and clinical correlates in
adults with obsessive-compulsive disorder. Compr Psychiatry 2006; 47(5):325-9.
36. Eilam D, Izhar R, Mort J. Threat detection: Behavioral practices in animals and humans. Neurosci Biobehav Rev
2011; 35(4):999-1006.
37. Boyer, P, Lienard P. Why Ritualized behavior? Precaution systems and action parsing in developmental,
Pathological and cultural rituals. Behav Brain Sci 2006; 29:595-650.
38. Baer L, Rauch SL, Jenike MA, Cassem NH. Cingulotomy in a case of concomitant obsessive-compulsive disorder
and Tourette's syndrome. Arch Gen Psychiatry 1994; 51:73­74.
39. March R,MaiaTV, Peterson BS. Funtional disturbances within frontostriatal circuits across multiple childhood
psychopathologies. Am J Psychiatry 2009; 166(6):64-74.
40. Finenberg NA,Potenza MN, Chamberlain SR,Berlin HA,Menzies L, Bechara A,Sahakian BJ,Robbins
TW,Bullmore ET,Holander E. Probing compulsive and impulsive behaviors, from animal models to
endophenotypes: a narrative review. Neuropsychopharmacology 2010; 35:591-604.
41. Camberlain SR,Fineberg NA,Blackwell AD, Bullmore ET, Robbins TW, Sahakian BJ. Impaired cognitive
flexibility and motor inhibition in unaffected first-degree relatives of patients with obsessive-compulsive
disorder.Am J Psychiatry.2007,164:335-8.

8

Arbaizar B. Psiquiatria.com. 2013; 17:8 - http://hdl.handle.net/10401/6170

42. Hoffman KL,Rueda Morales RI.D1 and D2 dopamine receptor antagonists decrease behavioral bout duration,
witjout altering the boug's repeated behavioral components, in a naturalictic model of repetitive and compulsive
behavior.Behav Brain Res.2012.230(1):1-10.
43. Albelda N, Joel D.Current animal models of obsessive-compulsive disorder:an update.Neuroscience.2012;211:83106.
44. Stein DJ,Nesse RM.Threat detection, precaurionary responses and anxiety disorders.Neurocience and
Biobehavioral Reviews.2011;35:1075-1079.
45. Fineberg NA,Chamberlain SR,Hollander E,Boulougouris V,Robbins TW.Translational approaches to obsessivecompulsive disorder:from animal models to clinical treatment.British Journal of Pharmacology.2011;164:10441061.
46. Williams MT,Farris SG,Turkheimer E,Pinto A,Ozanick K, Franklin MA,Liebowitz M, Simpson HB,Foa ED.The
myth of the pure obsessional type of obsessive-compulsive disorder.Depress Anxiety.2011;28(6):495-500.
47. CavaliniMC,Di Bella D,Siliprandi F,Malchiodi F,Bellodi L.Exploratory factor analysis of obsessivecompulsivepatients and association with 5-httlpr polymorphism.Am J Med Genet .2002;114:347-353.
48. Katerberg H,Delucchi KL,Stewart SE,Lochner C,Denys DAJP,Stack DE,Andresen JM,Grant JE, Kim SW,Williams
K A,den Boer JA, van Balkom AJLM, Smit JH, Van Oppen P,Polman A, Jenike MA, Stein DJ,Mathews CA, Cath
DC.Symptom dimensions in OCD.Item ­level factor analysis and heritability estimates.Behav
Genet.201o;40:505-517.
49. Brady RE,Adams TG,Lohr JM.Disgust in contamination based obsessive disorder:a review and model.Expert
Rev. Neurother.2010;10(8):1295-1305.
50. Pittenger C,Bloch MH,Williams K.Glutamate abnormalities in obsessive-compulsive disorder:Neurobiology,
pathophysiology, and treatment,Pharmacology& Therapeutics.2011;132:314-332.
51.

Wu K,Hanna GL, Rosenberg DR, Arnold PD.The role of glutamate signalling in the pathogenesis and treatment
of obsessive-compulsive disorder.2012;100:726-735.

52. Wheaton MG,Mahaffey B,Timpano KR,Berman NC,Abramowitz JS.The relationship between anxiety sensivity
and obsessive-compulsive symptom dimensions.J Behav.Ther&Exp Psychiat.2012;434:891-895.
53. Pine DS.Editorial:categories and dimensions:reflections on obsessive-compulsive disorder(OCD).Journal of
Child Psychology and Psychiatry.2011;52(12):1221-1222.
54. Abramowitz JS, Deacon BJ, Olatunji BO, Wheaton MG, Berman NC, Losardo D, Timpano KR, McGrath PB,
Riemann BC, Adams T, Björgvinsson T, Storch EA, Hale LR. Assessment of obsessive-compulsive symptoms:
development
and
evaluation
of
the
dimensional
obsessive-compulsive
scale.Psychological
Assessment.2010;22:180-198.

9

Arbaizar B. Psiquiatria.com. 2013; 17:8.
http://hdl.handle.net/10401/6170

Table 1. Suggested threat management systems

Threat detection

Threat

Mediator

System

Pathological/ normal response

Future Immediate extern danger

Fear circuitry

Self
subsystem

protection

Panic attack./flight-flee

Future immediate extern danger

Avoidance

Self
subsystem

protection

Animal phobias, thunder phobia.../flee

Future proximate extern potential
danger

Rumination

Self
subsystem

protection

General Anxiety Disorder /Anticipation-Precaution

Internal

Magic thinking

Security sense subsystem

Mental compulsions-repetitive unrelated behaviors / sense
of control

Disgust

Disease
subsystem

avoidance

Cleaning compulsions/ Cleaning

Vigilance/check

Disease
subsystem

avoidance

Hypochondria/ Self-care

Avoidance

Social
subsystem.

protection

Social anxiety disorder/ Caution

Doubt

Verification subsystem?

Aggression-ethical concerns
Precautionary
responses

Inferred
Risk for health
Inferred
Threat for health
Inferred
Conspecific threat
Inferred

Psiquiatria.com ­ ISSN: 1137-3148
© 2013 Arbaizar B, Suarez-Pinilla P, Llorca J.

Checking compulsions/Security

Arbaizar B. Psiquiatria.com. 2013; 17:8 - http://hdl.handle.net/10401/6170

Unintentional harm
Inferred
Future preservation ?

Verification?

Inferred

Accumulation?

Verification system?

Symmetry / ordering compulsions.

Prevention system?

Hoarding

Future availability ?

2

Arbaizar B. Psiquiatria.com. 2013; 17:8.
http://hdl.handle.net/10401/6170

Correspondencia
Javier Llorca
Facultad de Medicina
Avda. Herrera Oria s/n
39011 Santander (Cantabria)
Spain
Tel. 34-942 201 993
Fax. 34-942 201 903
Email. llorcaj@unican.es

Cite este artículo de la siguiente forma (estilo de Vancouver):
Arbaizar B, Suarez-Pinilla P, Llorca J. Threat management systems. Psiquiatria.com [Internet].
2013 [citado 22 Feb 2013];17:8. Disponible en: http://hdl.handle.net/10401/6170

Psiquiatria.com ­ ISSN: 1137-3148
© 2013 Arbaizar B, Suarez-Pinilla P, Llorca J.