FUNCTIONAL IMPAIRMENTS IN PATIENTS WITH BORDERLINE PERSONALITY DISORDERS DEMONSTRATED BY NEUROSPECT HMPAO Tc 99 m IN BASAL CONDITIONS AND UNDER FRONTAL ACTIVATION

Psychiatric semiology began to consider borderline personality disorders as early as 1801 (Pinel), however it was Kraepelin in 1905 and Kurt Schneider in 1923 that defined the concept of psychopathic personalities and abnormal personalities, formally considering the diagnosis of what would later on be viewed as personality disorders.

There is a semi-consensus among many investigators that these clinical entities have not been investigated in depth in Neuroscience (1) (2) because they are part of axis II of DSM-IV. It is for this reason that in this paper we are attempting to contribute to the biological aspects of these pathological entities.

There are valuable consensus documents (3, 4) that allow in many occasions to deepen the understanding of the personality disorders such as DSM-IV (Diagnostic and Statistical Manual of Mental Disorders). The terminology of borderline personality disorders in DSM-IV is a phenomenological-descriptive criteria based on investigations by Gunderson et al. It has the advantage of being a list of descriptive symptoms, easily diagnosable and useful for operational definitions and empirical research.

The prevalence of borderline personality disorders according to the DSM-IV is as high as 2% of the general population, it increases to 10% in out-patient psychiatric consultations and 20% of in-patient psychiatric consultations. This fact justifies the need of progress from different approaches in the assessment of this type of pathology that produces severe suffering of these patients and their families.

Apparently, there is an important genetic trait; as this type of diagnosis is 5 times as prevalent among relatives of first biological degree than in the general population. In these families there is also a frequent diagnosis of antisocial personality, mood disorders, symptomatology secondary to the use of psychoactive substances. Table I describes the diagnostic features for Borderline Personality.

A more biologically mediated Physiopathology of this clinical entity leads us to consider the neurotransmission system of the brain and there we have outlined the behavioral features that are shared by different pathologies such as personality disorders described in class B of DSM-IV and Major Depression. Both entities show a high correlation between suicidal attempts and a low response to phenfluramine (There is a significant diminution of the prolactine secretion after phenfluramine administration). These observations correlate with CSF levels of 5HIAA (metabolite of serotonine) where low levels are associated with suicidal attempts, more than depression. However, both features suggest a low serotoninergic activity associated with a behavioral pattern (5). Other studies concerned with a poor response of prolactine demonstrate the presence of antisocial aggressive behavior (auto and heteroaggression such as inflicting cuts and knifing, etc.) and irritability but not anxiety, or other pathological symptoms.

These facts explain why patients with dysfunctional serotoninergical systems have a higher frequency of auto and heteroaggression, this is frequently observed in patients with borderline personality disorders. Also noradrenaline participates in aggressiveness, it mediates the reactivity of a person with his/her environment, and noradrenaline make our environment more sharp in its perception, increasing contrasts. There are animal studies that demonstrate that it is necessary for the noraderenergic system to be intact in order to observe an increase in aggressiveness due to a low serotoninergic level (6).

When an individual is disconnected from the environment and turns into himself such as in sleep, feeding or grooming, the noradrenergic system is shut down, demonstrating that this system is a regulator of rhythms.

The studies of the noraderenergic system were defined by means of growth hormone released after an administration of clonidine (patients with depression produce less growth hormone versus normal controls after administration of clonidine).

Considering these facts one could define a relationship described in Table II that analyses the interrelation of two neurotransmission system, noradrenergic and seretoninergic with hyporeactive to both in-patients with severe depression and high risk of suicide. Both noradrenergic and serotoninergic functions are diminished and loss of control of aggressive behavior that cannot be addressed to the environment (due to low NA) and self-punishment can emerge (Upper left quadrant).

Another clinical condition can be related to the presence of high Norepinephrine levels and low Serotonine levels determining that patients will interact intensively with the environment, (the borderline patient will respond with idealization-devalorization or manipulation), and all the responses are coupled with loss of control of aggressiveness.

TABLE II

The right superior quadrant could correspond to the presence of excessive autoprotection (obsessive-compulsive actions of body protection). The right inferior quadrant is associated with high intensity reactivity to the environment with anxiety symptoms and personality traits (Otto Kernberg describes this as "borderline panneurosis") (8).

One has to consider also the participation of dopamine, particularly before the D4 receptor that is linked to behavioral feature of "Searcher of Novelty", described by Cloninger (9), that is frequently observed in borderline disorder patients.

Finally it is important to consider the participation of the cholinergic system, this influences the animal behavior inhibiting exploratory behavior that present with intense and sudden changes of mood, these are normalized with Physostigmine injections simulating the cholinergic system by enzymatic inhibition (5).

In the present paper we will analyze three of the five frontal subcortical circuits that correspond to the prefrontal dorsolateral circuit associated to higher intelligence function, the anterior cyngulate circuit associated to cognitive and motor motivation and the orbital frontal subcortical that is associated to mood changes.

The description of the different circuits and their physiological meanings has been described in ^*http://www.alasbimnjournal.cl/revistas/3/pradoia.htm "Cerebral functional changes in major depression demonstrated by Neurospect under basal and frontal stimulation conditions".

The purpose of this paper is to correlate functional changes observed in the basal state and during frontal activation by means of the Wisconsin test demonstrated by Neurospect of cerebral perfusion.

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