2002, Number 5
Salud Mental 2002; 25 (5)
Palacios L, Heinze G
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ABSTRACTFrom the first descriptions of the effects of the traumatic events of war reported by Abraham Kardiner’s in 1941; a series of studies have been carried out to describe in an exact way the chronical psychobiologic alteration that produces stress (6). With the introduction and definition of the diagnosis approaches of the posttraumatic stress disorder (PTSD) in 1980 in the DSM III (1), a series of studies that provide support to the validity of the etiology and typical phenomenology of this dysfunction have been made (3, 44, 66, 104). In the 4th. meeting of the Group of International Consent on depression and anxiety, carried out in Montecatini, Italy, in April of 1999, PTSD was considered as the most important subject due to its high prevalence, social impact, and financial burden on society. In the last 3 decades the biological guidelines of the dysfunction have begun to be established; new and effective treatments are being developed (4, 51).
PTSD is a chronic dysfunction and inability, for which so far, only partially effective treatments exist (65). A better and deeper knowledge of the psychobiological core of this dysfunction can constitute a tool of great help to liberate patients of feelings or behaviors belonging to the past (67).
The biological essence of this illness represents the long term consequences of a failure of the organism to recover from a traumatic situation, or the biological consequences that take place in answer to memories of events that are not happening in real time (111). Due to its nature, the biology of this dysfunction is different from the biology of stress, because it is a process that takes place after the stress situation is no longer physically present (81). Therefore two fundamental questions are to be made: why a failure of the organism takes place when returning to the pretraumatical state and, why some individuals recover and others don’t (111).
In the PTSD abnormal psychophysiological reactions take place at two different levels: 1). - in answer to specific memories of the traumatic event and 2). - In answer to intense but neutral stimuli, as strong noises. This indicates that people with PTSD suffer a loss in the discrimination of stimuli (6, 53).
High concentrations of suprarenal steroids have a potentially suppressive effect on the immunity system, and those stressfull events that activate the hypotalamo-hypofiso-adrenal system, can suppress certain immunitary activities (81. Many patients with chronic TPEP have physical problems and a high rate of use of the medical services (104).
It has been demonstrated that the age at which an initial traumatic event is experienced, is a significant factor for the development of PTSD, because traumatic experiences during childhood are associated to bigger risks and more severe symptoms (12). Therefore, sexual abuse in childhood, physical abuse, or both, are linked to more victimization indexes in adults (90). Neuroimage has promoted a new focus on the neuronal filters that are involved in the interpretation of sensorial information: the interactions among the parts of the CNS that process and interpret the meaning of incoming information, just as tonsil, hippocampus, the callous body, fore cingulum and prefrontal cortex (6).
At the present time there is evidence that indicates that the disregulation of the glutamatergic, noradrenergic, and serotoninergic systems and of certain neuroendocrinal systems plays a fundamental part in this illness (65).
Threre are three aspects to handle PTSD: education, treatment and/or psychosocial support and psychopharmacological treatment (5). Health professionals in general, assume an immediate educational rol when entering in contact with patients with this dysfunction, by explaining to the victim which is the normal stress reaction to the traumatic event. Two different procedures of Behaviour Cognitive Therapy (BCT) have been commonly employed with this dysfunction: exposure and handling of anxiety (5, 42, 105). The objectives of pharmacotherapy are to reduce the symptomatology of PTSD, to reduce inability, to improve the quality of life, to improve the resistance to stress, and to reduce comorbidity (5, 18, 26, 30, 68). Well controlled data show the clinical effectiveness of SSIR in TPEP (26, 16, 18, 58, 68, 102). The FDA approved, in February 2000, sertraline’s commercialization in the treatment of the PTSD. Studies that support the effectiveness of BZD in PTSD don’t exist. On the contrary, some evidence suggests that the clinical condition of patients with PTSD deteriorates, when they are treated with BZD, there is deterioration in learning in a clinical situation; besides BZD produce annoying symptoms when supressed (18, 26, 33).