Studies have repeatedly demonstrated that the metabolites of serotonin are altered amongst those who have attempted suicide (Asberg et al. 1976) or manifest externally-directed aggression (Coccaro 1998). Those who display impulsive aggression consistently show blunted neuro-endocrinal responses to agents that enhance serotonergic activities (Coccaro et al. 1996). It seems that impulsiveness, autoaggression, and outwardly-directed aggression are all associated with dysfunctions of the serotonergic system indicated by low 5-hydroxyindoleaceticacid levels in lumbar cerebro-spinal fluid (CSF) (Linnoila and Virkkunen 1992) and blunted neuroendocrine responses to fenfluramine (O’Keane et al. 1992; Herpertz et al. 1995; Cleare et al. 1996).
There is some degree of cortical localization of these abnormalities to areas involved in inhibiting limbic aggression in the orbital-frontal cortex, ventralmedial
cortex and cingulate cortex which show decreased activation in response to serotonergic probes (Siever et al. 1999; New et al. 2002). Reduced serotonergic modulation of these inhibitory areas may result in the disinhibition of aggression. It is consistent with this assumption that selective serotonin re-uptake inhibitors (SSRIs) appear effective in reducing impulsive aggression independent of depression when used in higher doses and/or for longer durations ( Markovitz et al. 1991; Coccaro et al. 1997). The study of 5HT synthesis capacity using PET in medication-free BPD subjects (Leyton et al. 2001) provided evidence of reduced 5HT synthesis capacity in cortico-striatal sites, including the medio-frontal gyrus, anterior cingulated gyrus, superior temporal gyrus, and corpus striatum. Notably, the indication of 5HT synthesis capacity correlated with impulsivity scores.
There is some evidence of enhanced dopaminergic activity in association with psychotic-like thinking in PD, particularly schizotypal PD. Increased dopamine concentrations have been found in the CSF of schizotypal patients (Siever et al. 1999) including BPD patients with co-morbid schizotypal presentations. Psychotic symptoms are induced by amphetamines (a dopamine agonist) in BPD patients (Schulz et al. 1988). These findings are consistent with clinical reports that amphetamines benefit BPD patients with psychotic symptoms. Noradrenergic abnormalities have been noted in BPD associated with risk taking and sensation seeking.
Neurotransmitter abnormality
The course of BPD
There is surprisingly little information about the childhood precursors of adult PD. The Collaborative Longitudinal Personality Disorder Study suggests that a history of MDD with insidious onset in adolescence and recurrence, chronicity and progressive severity is particularly likely to be associated with adult PD (Skodol et al. 1999). A study of a random sample of 551 youths (Kasen et al. 2001) reported that the presence of MDD in adolescence increased the likelihood of the diagnosis of dependent PD, ASPD, passive-aggressive and histrionic PD, but not BPD. However, the odds ratios in this report were adjusted for childhood maltreatment and if MDD in BPD was principally a reaction to childhood abuse then MDD would not be observed to be associated with BPD in this analysis. A longitudinal study of 407 adolescents (208 boys and 199 girls) recruited from a community sample looked at the predictive significance of internalizing and externalizing symptoms for the development of Cluster B characteristics (Crawford et al. 2001b). The pattern for girls indicates that externalizing symptoms in adolescence (12–17) predict Cluster B symptoms
at 17–24, even when earlier Cluster B symptoms are controlled for. However,
early (10–14) internalizing symptoms (anxiety and depression) also predicted
Cluster B symptoms in adolescence. The pattern for girls at least appears from
this study to be that early internalizing symptoms predict adolescent Cluster B
symptoms but adolescent externalizing symptoms predict adult Cluster B
symptoms. The findings are intriguing because for boys there appears to be no
forward prediction of Cluster B symptoms from either internalizing or externalizing
symptoms.
This finding complements the retrospective observation that antisocial behaviour in female adolescents is associated with BPD symptoms in early adulthood (Goodman et al. 1999). There are those who recommend the establishment of the diagnosis of BPD in childhood. A review of the literature (e.g. Ad-Dab’bagh and Greenfield, 2001) supports the creation of a new diagnostic label to describe a population of children whose symptoms are currently subsumed under the labels ‘borderline’ or ‘multiple complex developmental disorder.’ A full characterization of the syndrome, including its evolution, would require prospective studies and may differ from the known
evolution for PD and/or pervasive developmental disorders.
There are a number of studies of the course of BPD although most have methodological problems. The studies tend to show reasonable stability for BPD, although less than one might expect for a PD (Paris 1998a; Grilo et al. 2000). The clinical course is somewhat heterogeneous even within samples. Borderline patients improve symptomatically over time. One exceptionally long (27-year) follow-up (Paris and Zweig-Frank 2001) showed that borderline patients continued to improve in late middle-age with only 8% of the BPD sample meriting diagnosis of BPD. Long-term outcome in this study was associated with severity of the disorder and the quality of adaptation (functioning) at the start of the study but not with parenting quality or child abuse or trauma (Zweig-Frank and Paris, 2002).
A definitive study (Zanarini et al. 2003) followed the syndromal and sub-syndromal phenomenology of 362 adult in-patients with PD over 6 years of prospective follow-up. The cohort was assessed with the Revised Diagnostic Interview for Borderlines (DIB-R) and BPD module of the Revised Diagnostic Interview for DSM-III-R Personality Disorders. Of these patients, 290 met DIB-R and DSM-III-R criteria for BPD and 72 met DSM-III-R criteria for other axis II disorders (and neither criteria set for BPD). Over 94% of the total surviving subjects were reassessed at 2, 4, and 6 years by interviewers blind to previously collected information. Of the subjects with BPD over one-third met the criteria for remission at 2 years, half at 4 years, and over two-thirds at 6 years. When the entire follow-up period was considered almost three quarters could be considered to have recovered at some stage and only 6% of those with remissions experienced recurrences. Importantly, the comparison subjects with other axis II disorders did not develop BPD over the course of the follow-up. The patients with BPD had declining rates of symptoms but remained symptomatically distinct from the comparison subjects. Comparing the rate at which categories of symptoms decline, the study found impulsive symptoms to resolve most quickly and affective symptoms to be the most chronic. Cognitive and interpersonal symptoms were intermediate in the rate of decline. The results suggest that symptomatic improvement is both common and stable, even among the most disturbed borderline patients, and that the symptomatic prognosis for most, but not all, severely ill borderline patients is better than previously recognized.
This contrasts with the relative stability of the disorder in late adolescence and young adulthood. In a study of the stability of Cluster B symptoms between the ages of 12 and 20, Crawford and colleagues reported higher stability for PD symptoms than for Axis I symptoms (internalizing and externalizing) (Crawford et al. 2001a). The stability for Cluster B symptoms was 0.63 for boys and 0.69 for girls whereas the stability for internalizing symptoms was 0.24 and 0.39 and externalizing symptoms 0.32 and 0.38 for girls and boys respectively. These findings underscore the persistence of normal and abnormal personality constellations. The lower stability of Axis I symptoms may be disguised by some developmental heterotypy (i.e. different manifestations of the same underlying disorder at different developmental stages). Nevertheless, the stability of Cluster B disturbance is striking and many might interpret this as supporting the link of Cluster B with biologically predetermined personality dispositions such as novelty seeking where genetic loadings are high
(Livesley et al. 1998).
Borderline personality disorder patients who have been sexually abused in childhood (Paris et al. 1993; 1994a,b) or have been victims of incest (Stone, 1990) have a poor prognosis. If the patient’s first psychiatric contact takes place at an early age (Links et al. 1993) and his/her symptoms are chronic, spontaneous recovery is less likely (McGlashan 1992). Phenomenological factors that predict poor outcome include higher levels of affective instability, magical thinking, and aggression in relationships (McGlashan 1992), impulsivity and substance abuse (Links et al. 1993), and greater severity of disorder (Links et al. 1998). Further, if the patients have co-morbid schizotypal (McGlashan 1986), antisocial (Stone 1993), or paranoid features, then the prognosis is likely to be poor (Links et al. 1998). The evidence consistently suggests that even if the diagnosis of BPD ceases to be applicable, patients tend to remain functionally seriously impaired (Skodol et al. 2002c).
Dimensional models of BPD
Alternative to categorical descriptions of BPD are approaches that assume that PD is an amplification of normal personality traits (Paris 1998b). The best established is Cloninger et al.’s eight-factor model incorporated in the Temperament and Character Inventory (Cloninger et al. 1993). The dimensions suggested are: (1) novelty seeking, (2) harm avoidance, (3) reward dependence, (4) persistence, (5) self-directedness (autonomy), (6) co-operativeness, (7) compassion, and (8) self-transcendence (identity). More recently, Shedler and Westen proposed a clinician-oriented dimensional assessment procedure that asks the clinician to sort 200 personality characteristics into stacks of increasing applicability to an individual patient (Westen 1998; Westen and Shedler 1999a,b; Shedler 2002). The sort yields similarity scores to prototypes (profiles of characteristics) well-recognized by clinicians: (1) psychological health, (2) psychopathy, (3) hostility, (4) narcissism, (5) emotional dysregulation, (6) dysphoria, (7) schizoid orientation, (8) obsessionality, (9) thought disorder, (10) oedipal conflict, (11) dissociated, and (12) sexual conflict.
A range of studies reported BPD to be associated with temperament characterized by a high degree of neuroticism (i.e. emotional pain) and a low degree of agreeableness (i.e. strong individuality) (Clarkin et al. 1993a; Soldz et al. 1993; Trull 1993; Zweig-Frank and Paris 1995). BPD has also been shown to be associated with a high degree of harm avoidance (i.e. compulsivity) and novelty-seeking (i.e. impulsivity) (Svrakic et al. 1993). For BPD the key dimensions are likely to involve impulsive aggression and affective instability.
In a factor analysis of 18 personality traits assessed in the general population (n = 939), in patients with PD (n = 656), and in twins (n = 686 pairs) a four-factor solution was found (Livesley et al. 1992). The four factors were emotional dysregulation, dissocial behaviour, inhibitedness, and compulsivity.
There seems to be a general consensus that impulsivity and negative affectivity/ emotional dysregulation characterize BPD and possibly mediate the influence of psychosocial factors on BPD (Gurvits et al. 2000; Paris 2000; Silk 2000; Trull et al. 2000). It is the combination of impulsivity and negative affectivity that appears uniquely characteristic of BPD. Negative affectivity can be found in
Narcissistic personality disorder (NPD) while impulsivity is evidently marked in
ASPD.
Naturally, personality traits like affective instability or impulsive aggression are not unrelated to the putative intrapsychic disturbances such as identity disturbance or defense mechanisms such as passive aggression. In one study of 140 PD patients, degree of affective instability was found to be correlated with identity disturbance, chronic emptiness and boredom, defensive splitting, projection, acting out, and somatization (Koenigsberg et al. 2001). This kind of association is to be expected given that the phenomena upon which these apparently alternative modes of observation are made are the same.
However, the question of causality is moot. While dimensions such as affective instability and impulsiveness are known to be in part biologically-determined, the association with intrapsychic defenses may not be accounted for by the biological components of these traits. Nevertheless, the associations of trait and psychodynamic descriptions of BPD indicate the desirability of a multimodal approach to the aetiology of BPD.
Personality disorder :What Families Need to Know about the symtpoms
• Borderline personality disorder (BPD) is a serious and complex disorder affecting an estimated 1%–2% of the general population.
• The name borderline refers to the original notion that the disorder lies in between or on the border with the psychotic and neurotic mental disorders.
• The core symptoms common to most people with BPD are disturbed, unstable relationships with other people; emotional dysregulation (the inability to control mood or feelings); and impulsive behavior.
• Although BPD has some features in common with other personality disorders and with mood disorders (such as anxiety and depression), it is distinct from them.
• Women receive a diagnosis of BPD more frequently than men do, and this may be the result of biological and sociocultural factors. A partial explanation of this difference may be that women seek help more often than men for psychological problems.
• Although early reports suggested that those with BPD had a history of physical or sexual abuse, large-scale studies of child abuse in the general population show that 80% of adults with abuse histories do not develop any psychological problems.
• The current hypothesis (theory) suggests that individuals may be genetically prone to developing BPD and that certain stressful events may trigger the onset of BPD.
DSM-IV-TR diagnostic criteria for borderline personality disorder
A pervasive pattern of instability of interpersonal relationships, self-image, and
affects, and marked impulsivity beginning by early adulthood and present in a
variety of contexts, as indicated by five (or more) of the following:
(1) Frantic efforts to avoid real or imagined abandonment. Note: Do not
include suicidal or self-mutilating behavior covered in Criterion 5.
(2) A pattern of unstable and intense interpersonal relationships characterized
by alternating between extremes of idealization and devaluation
(3) Identity disturbance: markedly and persistently unstable self-image or sense
of self
(4) Impulsivity in at least two areas that are potentially self-damaging (e.g.,
spending, sex, substance abuse, reckless driving, binge eating). Note: Do not
include suicidal or self-mutilating behavior covered in Criterion 5.
(5) Recurrent suicidal behavior, gestures, or threats, or self-mutilating behavior
(6) Affective instability due to a marked reactivity of mood (e.g., intense
episodic dysphoria, irritability, or anxiety usually lasting a few hours and
only rarely more than a few days)
(7) Chronic feelings of emptiness
(8) Inappropriate, intense anger or difficulty controlling anger (e.g., frequent
displays of temper, constant anger, recurrent physical fights)
(9) Transient, stress-related paranoid ideation or severe dissociative symptoms
Source : Reprinted from American Psychiatric Association: Diagnostic and Statistical Manual
of Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric
Association, 2000. Copyright 2000, American Psychiatric Association. Used with permission.
