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ABSTRACT
Deliberate physical harm to one’s own body without the intention of dying is a frequent and difficult to treat psychiatric phenomenon. Self-injurious behavior (SIB) is a self-destructive behavior causing obvious tissue damage. In different psychiatric conditions such as psychotic states, mentally retardation, and personality disorders, SIB is a paradoxical sign since it would seem that the mechanisms related to pain, whose purpose is the detection of an actual or potential damage to individual integrity, would cause the opposite effect: direct tissue damage.
In this work we argue that SIB is due to a dysfunction of the cerebral limbic structures involved in the cognitive and emotional processing of pain. Such dysfunction constitutes an anomaly in the integration of pain as a conscious experience whereby it is conceived as an unpleasant sensation. We suppose that such disturbed pain perception can be considered as a consequence, manifestation, or symptom of a problem in self-consciousness, resulting from the interaction between biological and environmental factors.
Studies in animals
SIB has been shown to develop in rhesus monkeys reared in socially deprived environments. The severity of SIB correlates with the extent of isolation in terms of total duration and age at which it began. In socially deprived juvenile rhesus monkeys, Damphetamine elicits SIB, and a dose-dependent increase of norepinephrine in cerebro-spinal fluid (CSF).
Rodents with a neonatal chemical denervation of dopamine terminals, bite themselves when administered apomorphine or L-dopa. This response seems to be mediated through a D1-receptor supersensitivity.
Adult rats, when administered high doses of caffeine, pemoline or amphetamine, display SIB. The effects of dopamine, NMDA, opiate, and serotonin related agents on acute metamphetamine induced SIB in mice, while D1 antagonists and 5HT precursors reduced the incidence of SIB, and NMDA antagonist completely removed it; neither D2 antagonists nor naloxone affected SIB. It is possible to generate SIB in rats after inducing peripheral nerve lesions and inflammation process in a limb. This behavior is enhanced by electric stimulation of the cingulum or by the destruction of the ventral tegmental area (VTA), while the electric stimulation of VTA diminishes it.
In conclusion, dopaminergic system plays an important role on the genesis of SIB, particularly on some brain structures related to the affective-motivational components of pain processing such as VTA, anterior cingulate cortex (ACC), and anterior thalamus.
SIB in mentally retarded patients
About 15 to 20% of the patients with learning disabilities or mentally retardation who attend health or social services show SIB. One hypothesis suggests that severe SIB is associated with a release of endorphins resulting in relative analgesia and a rewarding mood state. Thus, a cycle of escalating tissue damage may follow since SIB is necessary to maintain a chronic release of endogenous opiods. This hypothesis is supported by the observation that opiate antagonists attenuate severe SIB in a subgroup of autistic patients.
The dopaminergic system is believed to be responsible for SIB on Lesch-Nyhan syndrome through a receptor supersensitivity. It can be proposed that these patients have a dopaminergic supersensitivity of D1 receptors in the cingulate bundle of the prefrontal cortex that causes a dysfunction in the cognitive processes related to pain.
SIB in personality disorders
Self-injurious behavior occurs in 70 to 80% of patients who meet DSM-IV criteria for borderline personality disorder (BPD). In 1990, Gardner found in BPD patients that lower levels of CSF 5-HIAA were significantly associated with a history of suicide attempts and SIB. Moreover, the degree of SIB was significantly correlated with impulsivity, chronic anger and somatic anxiety. A significant negative correlation was found with the number of platelet imipramine receptor sites. BPD patients with SIB showed a blunted prolactin response to meta-clorophenylpiperazine that appears to be in inverse relation with the frequency of physical and sexual abuse in infancy.
About 30 to 40% of BPD patients report that they do not feel pain during SIB and show lower experimental pain ratings than BPD patients who do experience pain during SIB. They also exhibit higher ratings of depression, anxiety, impulsiveness, and dissociation, as well as suicide attempts and childhood sexual abuse. The abnormal perception of pain in this group of patients may be related to a tendency to show dissociative symptoms. Thus, EEG theta activity in patients that do not feel pain during SIB, is significantly correlated with the Dissociative Experience Scale score.
Pain perception and dissociation
Theta rhythm is recorded in hypnotic states as well as during anticipation and control of painful stimulation in healthy individuals. This activity seems to be generated in medial prefrontal cortex and cingulate cortex, the same structures involved in the affective component of pain. Possitron emission tomography revealed significant changes in pain evoked activity within ACC, consistent with the perceived unpleasantness in normal subjects under pain stimulus. The three main dimensions of pain (intensity sensation, unpleasantness and secondary affect) are processed in brain structures that receive serial and parallel information. Spinal pathways to limbic structures and medial thalamic nuclei provide direct input to brain areas involved in affect. Another pathway is through somato-sensorial thalamic and cortical areas and then by a corticolimbic pathway. Both arrive to the same cortical and subcortical structures of the cingulum. This structure integrates nociceptive stimuli with contextual information and memory to provide the adequate cognitive mediation of pain.
In 1998, Sierra and Berrios proposed that the state of increased alertness in despersonalization results from an activation of prefrontal attentional systems (right dorsolateral prefrontal cortex) and a reciprocal inhibition of the ACC, leading to experiences of “mind emptiness” and “indifference to pain”. On the other hand, left prefrontal mechanisms would inhibit the amygdala resulting in a dampened autonomic output.
Dissociative symptoms and SIB in BPD patients are common clinical signs. Besides, BPD patients show hypometabolism in prefrontal cortical areas and ACC. It is proposed that the same structures that lead to dissociative states may change the perception of pain by cognitive processes.
Conclusions
The authors hypothesize that the structures involved in processing the cognitive component of pain (anterior cingulate and medial prefrontal cortex) are altered in those patients who exhibit selfinjurious behavior.
The adequate physiological response to a noxious stimulus, requires that the individual perceives himself in order to maintain his integrity. Therefore, the alteration of pain perception could be the consequence of problem in self-consciousness.
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