Attention Deficit Disorder

[lauren18808]

On the constant badgering of my friend, I compromised going to some kind of doctor by going to the college councellor person. He told me to list all the weird stuff in my personality, everything from suicide attempt(s) to bad habits to pet peeves to eating habits. After I'd done this he sat quiet for a minute before he said 'Do you ever find concentration dificult?, do you dislike situations were your behaviour has to be restricted?.' I told him i didn't (who does?), he then went to comment on one of my bad habits (Having to get up and run around the house when I am either in a daydream or when I've been sat down too long, which is wierd yes, but It can't be that uncommon can it?) he then went on asking questions like 'Are you or have you ever been diruptive either at school and at home? Do you dislike people giving you instructions' To which I gave fairly balanced answers (sometimes depending on the context of the situation etc etc)

He sat for an other minute looking at me (In a 'Then why are you here?' way I must add) he said 'I think you might have <<Insert something technical sounding I won't attempt to try and spell>>...(on my blank look) ADD you might know it as"

Me: Oh, how do you know that?

Councellor: You just gave me a fairly good discription.

Me: Are you that good that you can diagnose me with it within ten minutes?

Councellor:...You might find you will grow out of it pretty soon enough.

And I left.

Whether it's true or not, I find it a bit wooly what he came to this conclusion within 10 minutes, I didnt go to him asking to be diagnosed, I went asking to talk it out.. I mean does anyone know what it is? All I know is that its what we were told(excuse the generalising) the bad kids at school had. And I had my parents in once or twice with certain teachers, but I was never that bad.

I don't know if it can be linked with suicidal tendencies and Insomnia and general depressiveness and the like, but then again i dont really know anything about it. Does it even fit the criteria? Because ten minutes is a very short time to tell someone theyve got ADD and noone else has ever noticed. If I'm supposed to be growing out of it, how come I've been getting worse as I've gotten older? Anyone else find this a little hard to believe, and if it's true, am I pathetic for bellyaching about it?

I dont understand this at all, all he did was say 'You have this' and sent me on my way.

I know I should probably stop coming here expecting answers from everywhere but theres no harm in asking right? Or wrong I dunno, I dont know who to ask about all this at all. I'm very confused.

I'm just wondering if anyone else here has it or knows anything about it and could shed a little bit of light, it's very likely that the councellor is a bag of wank but I thought I'd ask anyway.

Help and advice very much appreciated.

Lauren.

[LadyMacbeth]

A school counselor cannot diagnose you. I remember my friend's therapist mentioned he may have ADD and referred him to see a psychiatrist to get tested and it turned out he didn't. If you have some concerns talk to your psychiatrist.

[calyps]

Yeah, I've heard or read somewhere that BPD can co-exist with ADD- is it called ADHD now? i have the impossible to concentrate and restlessness thing going on, but i was a good little swot at school. I don't think it's possible to be diagnosed in 10 minutes. isn't what he gavce you the same thing as those tests on the web about your personality, I think they can lead you in the right direction but don't have real integrity. To be honest, the only way I finally got to the bottom of what anyone thought I may or not have was to find a really nice Doctor and thrash it out with him.

Take care

Anwen

[LadyMacbeth]

It was ADHD...my friend was tested for not ADD.

[Lauren]

I was given a dx of adhd as a teenager. Bsed on the fact that my younger brother had it badly and the way I walked lol. wtf?

I still have really bad concentration and am easily distracted a lot.

[lauren18808]

Yeah, like I said. I went for some kind of assurance that I wasn't an idiot for thinking the way I do. What he said shocked me, no councellor is in any position to diagnose you are they? It's absurd.

This is were I'm confused I only lack concentration when I dont like the person in authority or when I'm not interested in what I'm doing. But isnt that the case with lots of people?

Thats the last time I got to him.

[Doctor Dysphoria]

Yeah, I've heard or read somewhere that BPD can co-exist with ADD- is it called ADHD now?  i have the impossible to concentrate and restlessness thing going on, but i was a good little swot at school.  I don't think it's possible to be diagnosed in 10 minutes.  isn't what he gavce you the same thing as those tests on the web about your personality, I think they can lead you in the right direction but don't have real integrity.  To be honest, the only way I finally got to the bottom of what anyone thought I may or not have was to find a really nice Doctor and thrash it out with him. 

Take care

Anwen

<{POST_SNAPBACK}>

Abstract of research by Fossati A, Novella L, Donati D, Donini M, Maffei C., Sept. 2002

"BPD subjects showed a significantly higher mean WURS total score compared to all control groups (minimum t = 7.93, maximim t = 11.63, all Ps <.001). These contrasts remained significant even controlling for potential confounders such as antisocial personality disorder (ASPD) diagnosis, gender, inpatient status, and axis I diagnoses. The results of this study seem to support the hypothesis of an association between history of childhood ADHD symptoms and adult BPD diagnosis."

Numerous conflicts have arisen within analytical, biological, and social learning schools of thought regarding the name, definition, etiology, and treatment of borderline personality disorder (BPD). The present study (N = 140) attempted to merge the examination of neuropsychological factors and diagnosis in childhood of BPD. It was hypothesized that children with BPD features would have greater executive dysfunction (EF), attention deficit/hyperactivity disorder (ADHD), and comorbid personality disorders than children with other personality disorder features (not BPD) and a control group (with no personality disorder features). The Coolidge Personality and Neuropsychological Inventory for Children (CPNI; Coolidge, 1998), a standardized, 200-item, DSM-IV aligned, parent-as-respondent inventory, assessed psychopathology. Results indicated the BPD children had more EF, ADHD, and comorbid personality disorders. Thus, the findings argue for a neuropsychological etiology of BPD that may be diagnosed in children.

Neuropsychological Dysfunction in Children with

Borderline Personality Disorder Features

The origin of borderline personality disorder (BPD) has been varied and contentious. Numerous conflicts have arisen within analytical, biological, and social learning schools of thought regarding its name, definition, etiology, and treatment. The following sections will review these four issues.

History

The word ‘borderline’ was originally conceived to refer to patients who were on the border between a neurosis and psychosis. In 1938 Stern first used the term ‘borderline’ in conjunction with patients who were suffering from a milder or atypical form of schizophrenia. Zilboorg labeled borderline patients as ‘ambulatory schizophrenics’ in 1941, while Deutsh called them ‘as if’ schizophrenic patients in 1942. Hoch and Polatin referred to BPD patients as ‘pseudo-neurotic schizophrenics’ in 1949, and Knight labeled them as ‘patients with borderline states’ in 1950 (Silk, 1994). Notably, before the succinct term ‘borderline personality disorder’ was coined, different conceptualizations of BPD existed. As Coolidge and Segal (1998) discussed, there appears to have been an evolution of this personality disorder. As evidenced by the early labels applied to this disorder, an affiliation with schizophrenia was believed to exist. This affiliation may have provided the original impetus for BPD patients to appear as if on the border between neurosis and psychosis (Kaplan & Sadock, 1998). The term ‘borderline’ did not become popular until the mid-seventies when a series of empirical studies, primarily conducted by Gunderson and Singer (1975) and Perry and Klerman (1978), defined and operationalized a set of criteria that led to a formalized and accepted diagnosis of BPD.

Grinker, Werble, and Drye (1968) were the first to define borderline subgroups that did not have a relationship to schizophrenia. In this initial empirical study of borderline patients, four subgroups were noted: (a) bordered on neuroses, ( bordered on psychoses, © ‘as if’ patients, and (d) core borderline group. This last group represented those individuals now diagnosed with BPD. Studies distinguishing BPD from schizophrenia are still taking place, and new subcategories are still being determined (Andrulonis, Glueck, Stroebel, & Vogel, 1982)

In the first edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM, 1952) the category for what is now known as BPD was termed emotionally unstable. In the second edition of the DSM (1968), the category for BPD was entirely eliminated, and the latent type of schizophrenia was said to include those who were diagnosed as having borderline schizophrenia. Individuals falling into this category were later differentiated into having BPD or schizotypal personality disorder in the DSM-III (1980). In addition to its own categorization, in this subsequent version of the manual BPD was thought to be associated with identity disorder. Identity disorder was said to be diagnosed in childhood and was proposed to later meet the criteria for BPD.

While the borderline diagnosis of the past seemed to be related to schizophrenia, the classification of BPD in the DSM-III (1980) was reserved for more interpersonally unstable and affectively labile patients. In this DSM-III categorization, those patients connected with schizophrenia were classified under schizotypal personality disorder (Silk, 1994). It was thought that schizophrenia may have developed as a complication of schizotypal personality disorder and that this disorder was in actuality a prodromal phase of schizophrenia. Individuals who met the criteria for both BPD and schizotypal personalitiy disorder, which was said to occur frequently, were then diagnosed with both of the disorders.

The revised edition of the third edition, DSM-III-R (1987), continued to associate identity disorder in children with BPD, however the manual asserted that BPD "…should be diagnosed in children and adolescents rather than the corresponding childhood categories if the personality disorder criteria are met, the disturbance is pervasive and persistent, and it is unlikely that it will be limited to a developmental stage" (American Psychological Association, 1987, p. 336).

Currently, the DSM-IV (1994) maintains a distinct BPD category, which is characterized by "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…" (American Psychological Association, 1994, p. 654; see diagnostic criteria). There are several key features in the literature that are considered to be both salient and common in BPD. Instability and ambivalence are two features that have been proposed to intrude pervasively on the borderline patient’s consciousness. (Millon, 1992; van Reekum, 1993). These characteristics result in unpredictable and erratic emotions (affective instability), manipulative and volatile dispositions, and a general impulsivity, which is a characteristic that has been recognized by clinicians as being central to the pathogenesis of BPD (van Reekum, Links, & Fedorov, 1994; Judd, & Ruff, 1994). By displaying such attributes, it seems that borderline patients would elicit rejection rather than the support they seem to fervently seek.

Depression and self-destructive acts, including self-mutilation and suicide, have also been associated with this disorder (Silk, 1994; Silk, Goodson, Benjamin, & Lohr, 1994; van Reekum, 1993). The BPD patients’ manipulation of their despair is often seen as a means of expressing their frustration, hostility, and anger. Also, by focusing on their difficulties, responsibilities are often shifted to be the burden of others (Millon, 1992). These dual impositions function as punitive and attention-getting behaviors, which serve to passively express explosive emotions while securing the nurturance they implore. This demeanor makes for very unstable and intense interpersonal relationships.

Cognitively, among other complications, there appears to be a true identity disturbance in BPD patients. Their self-image wavers in the medium of being both dependent and hostile. Kaplan and Sadock (1998) outlined a picture of the borderline patient as one who cannot tolerate being alone and prefers the frantic search for companionship, no matter how unsatisfactory. Their rapidly changing thoughts and feelings leave many to experience extreme emptiness. Millon (1992) states that their own unworthiness, their own failures, and their own bad temper are the true causes of their misery and the pain they bring to others, reinforcing the notion of their ambivalence. BPD patients do not have an integrated sense of wholeness, rather they are more likely to present with a segmented sense of being that is subject to the influx of their own paradoxical attitudes and actions.

When considering differential diagnoses, the concept of deficient social competence seems to set BPD patients apart. As opposed to individuals with other personality disorders, borderline patients seem to create incessant complications for themselves and continually re-experience the same setbacks. While those with other disorders appear to proportionately achieve social achievement consistent with their natural aptitudes and talents, borderline patient’s repeated disruptions characterize their struggles with the educational, vocational, and marital aspects of their lives (Millon, 1992).

The BPD patient’s experience of psychotic episodes as rather brief and transitory is also another feature that sets them apart from other disorders. Although psychotic thought processes may occur frequently, they are not prolonged and prominent, as in those with severely decompensated personalities (Millon, 1992).

With respect to the diagnosis of personality disorders in childhood or adolescence, the DSM-III noted that personality disorders "…by definition begin in childhood or adolescence and are characteristic of most adult life" (American Psychological Association, 1980, p. 306). This version of the manual also asserted that personality disorders may be applied to children in those cases where the maladaptive traits appear to be stable. In the DSM-III-R (1987) emergence of personality disorders were said to be recognizable by adolescence or earlier. Additionally, according to the DSM-IV (1994) personality disorders may be diagnosed in children and adolescents who have shown stable maladaptive features that have been present for at least 1 year.

Etiology

One major issue of contention has been the etiology of BPD. Two major camps have emerged: organic - biological causes and psychogenic causes. Organic schools of thought have postulated that BPD is caused by genetics, temperamental bases, and/or traumatic brain injuries. Psychogenic schools of thought have primarily promoted early sexual abuse as a causative agent for BPD.

Organic

Neurological. The neurological dysfunction of borderline patients was initially considered because patients frequently report problems in concentration, memory, learning, confusion, and perceptual distortions, which are symptoms of a biologically dysfunctional nature (O’Leary & Cowdry, 1994; Swirsky-Sacchetti et al., 1993). Early biological approaches to etiology centered on the relationship of BPD to the mood disorders, as biological probes already existed for these affective disturbances. (Silk et al., 1994; Yehuda, Southwick, Perry, & Giller, 1994). Although the queries into the neurological functioning in relation to BPD have been limited, many studies are now trying to pinpoint the exact part of the brain involved in the etiology of this disorder.

Computerized tomography scans have been utilized to examine the Ventricular/Brain Ratio in BPD patients. Several studies found evidence that patients with BPD have smaller ventricles (when compared to schizophrenic populations), which is hypothesized to be associated with the pathophysiology of the disorder (Lucas, Garnder, & Cowdry, 1989; Schulz, Kohler, & Kishore, 1983).

Electroencephelogram (EEG) findings measure electrophysiological dysfunction (dysfunction in brain wave patterns), and have also been employed in neurological research of BPD patients. These types of tests were initially utilized because symptoms common in BPD are also common in temporal lobe dysfunction, such as depersonalization, derealization, impulsivity, transient psychosis, and affective lability (Fenwick, 1981).

Synder and Pitts (1984) used EEGs in their study of BPD and dysthymic (patients with chronic, mild depression) controls (N = 74). They found that 19% of BPD patients had marginally abnormal EEGs and another 19% had definitely abnormal EEGs. Both of these findings were significantly higher than controls. They also noted that slow-wave activity was significantly more common in BPD patients than the dysthymic controls. Cowdry, Pickar, and Davies (1986) corroborated these findings, in a study (N = 59) showing that definite abnormalities were significantly more common in the EEGs of BPD patients than the depressed controls (46% versus 10%, respectively).

Streeter, van Reekum, Shorr, and Bachman (1995), also suggested that EEG irregularities as well as soft neurological signs contributed to the diagnosis of BPD. In their study centering on traumatic brain injuries (TBI) of male veterans (N = 43), they found that patients with BPD had significantly higher occurrences of TBI, learning disorders, attention deficit hyperactivity disorder (ADHD), and seizures than the control group. Also of interest was their discussion about the similarities between individuals with varying regional lesions and BPD patients. Individuals with orbitofrontal lesions were similar to BPD patients in that they shared the characteristics of disinhibition and predisposition to emotional lability and antisocial actions. Those with temporal lesions displayed aggression, depression, anxiety, and impulsiveness, also similar to patients with BPD. This concurrence between lesioned areas of the brain and BPD offers evidence that neurological dysfunction may be involved in the etiology of BPD. Some of the major limitations of this study, however, are that it was conducted with only male veterans whose mean age was 34 years-old (while the DSM-IV says that BPD is more likely to occur in females), all data collection was conducted in a retrospective manner, and the reviewers were not blind to whether the participants were in the quasi-experimental or control groups.

Evidence supporting the relationship between head trauma and BPD was provided by Andrulonis et al. (1982). This research centered on an organic hypothesis of BPD and its role in the development of psychopathology. Researchers found that 14% of nonschizotypal borderline patients had a history of head trauma, encephalitis, or epilepsy, and 26% had a history of ADHD or learning disorders. BPD patients were significantly more likely than control participants to have a history of organic disturbance as well as a history of head trauma, encephalitis, or epilepsy. Additionally, they found that male BPD patients had a significantly higher percentage of organic disturbance (52% versus 29%) than female BPD patients, as well as a significantly higher percentage of histories with ADHD or learning disorders (40% versus 14%).

van Reekum (1993), in a study of 48 male veterans with BPD, found that 81% of the patients had a history of neuropsychological disorder. Of those, several had a definite history of developmental delay (44%) or an acquired central nervous system (CNS) injury (58%). In this study acquired CNS injuries included TBI, seizures, and other CNS lesions (e.g., tumors, encephalitis). Developmental delays included ADHD and learning disorders. van Reekum also found a higher prevalence of EEG abnormalities in BPD patients than in controls. BPD patients were also found to be more impulsive, engage in more self-mutilative behavior, and have more affective disinhibition, all of which were correlated with dysfunction in the limbic and frontal sites of the brain. Again, these findings offer support to the hypothesis of neuropsychological dysfunction as a causal agent of BPD.

These studies indicate that the characteristics found in BPD sufficiently resemble the characteristics of brain-injured patients to suggest that these phenomena are neurologically associated. The area of the brain most often pinpointed in these studies was the frontal lobe. With the technology of brain imaging, it seems that research more precisely examining the differential structure of the BPD patient’s brain should be performed. Brain imaging may be able to detect structural differences (or anomalies) in specific areas in BPD patients, similar to the precise regions that have been noted with respect to the brains of schizophrenics. Generally, this topic seems to be controversial, particularly regarding whether neurological dysfunction predisposes patients to acquire BPD, or whether BPD precipitates injurious behavior (e.g., head injury) that leads to neuropsychological dysfunction. This controversy promises to be an interesting topic for future research.

In addition to neurological dysfunction, many studies have found heightened rates of BPD in first-degree relatives, suggesting implications of a genetic component (Zanarini, 1993). Also notable are proposed intrauterine effects on fetal development and their relation to BPD. These effects may include malnutrition, drug and alcohol abuse, and environmental stress. Wagner and Linehan (1997) noted that children of mothers who had these experiences demonstrated difficulties with emotion regulation similar to those of borderline individuals. As an example, fetal alcohol syndrome includes hyperactivity, impulsiveness, distractibility, irritability, and sleep difficulties, all of which are characteristics that are present in BPD.

Neuropsychological. Murray (1979) tied the proposition of neuropsychological dysfunction in BPD with the idea that childhood minimal brain dysfunction (MBD) leads to BPD in adults. MBD is considered to be deviations of functions of the nervous system manifested in neuropsychologically based impairments of perception, conceptualization, language, memory, control of intention, and impulse or motor function. He demonstrated that children with MBD and adults with BPD, showed immature ego processes involved in planning, organization, judgment, and reasoning, functions that are thought to be associated with the frontal lobe.

Another neuropsychological area that has been explored in BPD is executive functions (EF). EF, in the literature, refer to cognitive abilities that include self-regulation, selective inhibition of responding, response preparation, cognitive flexibility, and organizing time and space (Reader, Harris, Schuerholz, & Denckla, 1994). It has also been defined as the ability to maintain an appropriate problem solving set for attainment of a future goal (Welsh and Pennington, 1988). Although the regions of the brain responsible for these tasks have not been specifically identified, the area of origin is usually referred to as having frontal localization. Pennington and Ozonoff (1996) suggest that a "frontal metaphor" (p. 52) has guided research on EF in childhood and adulthood. This metaphor involves the patients ‘looking frontal,’ meaning that their behavior or test profile resembles those of patients with frontal lesions. Features of lesions in children have been shown to include behavioral problems with attention, poor peer relationships, and a lack of empathy, and have also been suggested to produce social, cognitive, and behavioral effects similar to those observed in adults. Coolidge, Thede, and Young (in press) in a study of 224 twin children, have recently found that EF appear to be strongly heritable (approximately 79%).

EF has been put forth as being associated with ADHD based on observations that frontal lesions in experimental animals and human patients sometimes produce hyperactivity, distractibility, or impulsivity (Fuster, 1989; Stuss & Benson, 1986). The fundamental symptoms of ADHD include hyperactivity, impulsivity, and distractibility, as reported by parents, teachers, and health care professionals (Pennington & Ozonoff, 1996). The age of onset for ADHD is typically during early childhood between 3 and 4 years of age, with a lifetime prevalence rate of 1-7 percent (Hinshaw, 1994; Palfrey, Levine, Walker, Sullivan, 1985). Reader, et al. (1994) found that bright ADHD children performed below average on tests of EF. Similarly, Harris, et al. (1995) found in their study of EF in children with tourette syndrome and/or ADHD that EF was found to be greater in the ADHD only group than in any other group.

Neurologically, Pennington and Ozonoff (1996) assert that a plausible theory of the connection between ADHD and EF includes the EF of ADHD children being caused by structural and biochemical changes in the prefrontal lobes. These changes are detectable by a reduced blood flow. Distinct EF patterns have been found for ADHD children when compared with children who had other disorders, such as autism, conduct disorder, and tourette’s syndrome (Pennington & Ozonoff, 1986).

In terms of ADHD and its comorbidity with other disorders, Jensen, Martin, and Cantwell (1997) note that ADHD commonly occurs with other conditions. Several studies have supported this assertion, showing that among children diagnosed with ADHD (N = 222), 93.0% had comorbid conduct/oppositional disorders, 50.8% had anxiety disorders and 26.8% had depressive disorders (Bird, Canino, & Rubio-Stipec, 1988). Similarly, Cohen, Velez, Brook, and Smith (1989) reported that among those children diagnosed with ADHD (N = 93), 56.0% had comorbid conduct disorder, 54.0% had oppositional defiant disorder, and 13.0% had major depressive disorder. Also, Coolidge, Thede, and Young (in press), in a study of 224 twins, found ADHD to be comorbidly heritable with EF (82%). Often times, ADHD children with comorbid disorders have been excluded from studies, therefore past results of research may not be generalizable to the majority of children who usually have comorbid disorders. Preliminary findings have indicated an association between ADHD and other psychiatric disorders (West, McElroy, Strakowski, Keck, & McConville, 1995; Wozniak, Biederman, & Kiely, 1995). Jensen, et al. (1997) suggest that comorbidity be more fully considered in the design of future studies rather than ADHD being regarded as ‘noise’ that is to be controlled for or eliminated.

According to Elia, Stoff, and Coccaro (1992) there is a growing body of research supports the conclusion that there is an underlying neurobiological basis for ADHD and BPD in children and adolescents. Research in twins by Coolidge, Thede, and Jang (in press) has found that BPD is 60% heritable in children and Coolidge, Thede, and Young (in press) found ADHD to be strongly heritable (82%).

Another contentious issue in BPD is its diagnosis in childhood. The DSM-IV (1994) notes that the diagnosis of borderline personality disorder can be made by early adulthood with the supplemental addition that if the maladaptive patterns of pathology are present for more than 1 year the diagnosis of any personality disorder may be made in childhood. Bernstein, Cohn, Skodol, Bezirganian, and Brook (1996) report that there exist a few well controlled studies that support the continuity of borderline symptoms from childhood through adolescence and early adulthood. They found that there are childhood antecedents that are associated with higher rates of personality disorders. Specifically, they reported that conduct problems, depressive symptoms, and immaturity were all features associated with the personality disorder cluster that BPD fell into. Additionally, they found that childhood problems were intercorrelated with one another and tended to occur comorbidly. Interestingly, they conceptualized that in adolescence the behavioral difficulties begin to manifest themselves into more differentiated forms of these personality disorders.

Vela, Gottlieb, E., and Gottlieb H. (1983) identified six behavioral symptoms regarding the diagnosis of BPD in children. They are as follows: (1) disturbed interpersonal relationships, (2) disturbances in the sense of reality, (3) excessive anxiety, (4) impulsive behavior, (5) ‘neurotic like’ symptoms, and (6) uneven or distorted development.

Kernberg (1983) emphatically suggested that BPD in children can be considered to be a definable entity, and it may be significantly associated with MBD and depression. She noted that the differential features of the disorder in children are: a sudden shift in functioning, lack of a sense of identity, inability to accept responsibility for their own actions, and inability to experience pleasure in play. These manifestations are similar to the descriptions of BPD in adults. Also similar to adult BPD studies is the extraordinarily high incidence of neuropsychological dysfunction in BPD children. These findings seem to substantiate the findings in an earlier study by Lewis (1976) focusing on the same issue. Additionally, Lewis suggested that MBD may actually mask a borderline condition, as once the label of MBD is applied, significant personality difficulties may be inadequately treated or overlooked altogether in the child.

Psychogenic. Wolff (1993) noted that an appreciation of childhood causal factors is essential if one is to make sense of repetitive maladaptive behavior in adult life. When examining organicity in BPD, alternative explanations must be considered as potential precursors to this disorder. The primary competing perspective to neuropsychological dysfunction is the impact of childhood sexual abuse. Four models addressing this issue have been put forth, including: (a) the interaction of trauma and neurological factors, ( trauma leading to neurobiological consequences, © neurological vulnerability predisposing children to abuse, and (d) two existing subpopulations of BPD – those stemming from abuse and those stemming from neuropsychological dysfunction (Kimble, Oepen, Weinberg, Williams, & Zanarini, 1997; Teicher, Ito, Glod, Schiffer, & Gelbard, 1994). However, Zanarini, Kimble, and Williams (1994) suggested that a childhood history of physical or sexual abuse seems to be significantly associated only with physicians’ decision to order neurological tests on BPD patients. All in all, the hypotheses of abuse leading to BPD seem to be closely tied to the presence, and even predominance of neuropsychological factors. Sexual abuse alone cannot account for factors such as genetic components and the success of drug interventions with BPD patients. Another limitation of the sexual abuse viewpoint includes the fact that many are retrospective studies that look back at childhood after BPD has been diagnosed (Friedman, 1993). These studies cannot verify the truth or falsity of retrospective patient self-reports. Even independent confirmations may yield reliability but not necessarily validity. Also, many of these studies have relatively small sample sizes, which may not give sufficient power to find significant between-group differences.

Sexual abuse has been implicated as being connected with BPD because of analogous components between BPD and posttraumatic stress disorder (Fossati, Madeddu, & Maffei, 1999). However, Paris and Zweig-Frank (1992) noted that studies examining childhood sexual abuse as a component of BPD were often limited by the evidence of a multifactorial etiology of BPD, as well as by a general oversimplification of the childhood sexual abuse model. Fossati et al. in their meta-analytic study of childhood sexual abuse and BPD found that there was a moderate pooled effect size for the association between these two variables (pooled r = .28, p < .001). Additionally, they found that larger effect sizes were strongly linked to smaller, less representative samples and concluded, based on this evidence, that childhood sexual abuse does not seem to be a major psychological risk factor for BPD, or a causal antecedent of BPD. Millon (1981) offers the idea that "…although it is often necessary to separate biogenic from psychogenic factors as influences in personality disorder, this bifurcation does not exist in reality." Millon’s statement supports the current notion that there may be a diathesis -–an inherited genetic predisposition for the development of BPD, that can be triggered by the stress of sexual abuse.

Treatment

The literature is replete with examples of the difficulties of treating BPD patients. It is generally well-accepted that BPD patients do not respond well to treatment and tend to have a poor prognosis (e.g., Docherty, 1993; Waldinger, 1993). In all models of treatment for BPD, it has been noted that a certain level of skill and flexibility is required on the part of the therapist, with essential features including establishment of trust, caring, warmth, and patience (Shea, 1993). There are several treatment strategies that have been postulated for BPD, considering both the biogenic and psychogenic etiologies that may be at work. Psychoanalysis has been recommended for BPD patients, employing special parameters dealing with both transference and countertransference (Murray, 1979). Drug therapy has also been suggested to be effective in many borderline personalities, specifically tri-cyclic antidepressants. The benefits of drug treatments have included a more even general mood, greater frustration tolerance, and improved attentional processes (Murray, 1979). A multisensory approach to treatment has also been proffered, as many BPD patients appear to have disruptions of basic internal language functioning, which suggests adjunct methods must be employed (Murray, 1979). The main technique in this model includes combining auditory, visual, and kinesthetic modalities. Additionally, role-playing may serve as an effective therapeutic treatment as well. By acting out conflicts in a secure environment, the BPD patient may use concrete means of expression without embarrassment and hesitation. Family therapy is another mode that may be suitable for the BPD patient. The active nature of this therapy and its emphasis on both intrapsychic and interpersonal systems seem to make it especially fitting. Cognitive therapy may also be useful, as the disruption of affective processes and language functions as a result of a lack of neuropsychological integrity can result in problems with thinking and cognition (Murray, 1979). Behavioral therapy may allow impulsive behavior to be brought under control through structure, support, and direction (Hurt, Clarkin, Munroe-Blum, & Marziali, 1993). Group therapy has been suggested to be effecting in diluting the transference relationship, providing multiple targets of emotional investment, and an opportunity for identification with other patients and therapists. However, including BPD patients in group treatment may be counterproductive to the cohesiveness and growth of the group (Munroe-Blum, 1993). Finally, multi-modal treatment has been suggested to be the key treatment for BPD patients, as it draws on techniques from many different modalities (Waldinger, 1993). In summary, various treatments have demonstrated the potential to be effective with BPD patients. Each perspective of treatment acknowledges that the BPD patient is notoriously difficult to treat and may require special implications within the modality. It is likely that determining the integral treatment, or combination of treatments, would be essential in considering the best care for the BPD patient.

Hypotheses

As the whole of this research suggests, it appears that neuropsychological dysfunction is a concomitant symptom picture of the BPD. Two of the most likely syndromes of neuropsychological dysfunction in BPD appear to be ADHD and EF deficits. Furthermore, a review of the literature and the DSM-IV suggests that BPD is one of the most severe and chronic of all personality disorders, and is often accompanied by a poor prognosis. Thus, since research has shown and the DSM-IV suggests that personality disorders are more likely to appear comorbidly with each other than alone, it might be expected that BPD would be one of the most likely personality disorders to have other comorbid disorders.

Hypothesis 1. It is specifically hypothesized that a sample of children whose parents rate them greater than one standard deviation above the mean (compared to normative groups) on the Borderline scale of the Coolidge Personality and Neuropsychological Inventory for Children (Coolidge, 1999; CPNI), a standardized measure of BPD based on the criteria in the DSM-IV, will have greater comorbidity on personality disorder scales than another sample of children whose parents rate them greater than one standard deviation above the mean on another personality disorder scale of the CPNI, but not BPD (OPD group).

Hypothesis 2A. Additionally, it is hypothesized that the same sample of BPD children will demonstrate greater neuropsychological dysfunction, as measured by EF (a neuropsychological scale on the CPNI), than either the OPD group or a sample of children whose parents rate them as not having any personality disorders (control group).

Hypothesis 2B. It is also hypothesized that the same sample of BPD children will demonstrate greater neuropsychological dysfunction than either the OPD group or the control group in ADHD (a neuropsychological scale on the CPNI).

The current research was designed primarily to determine the extent to which neuropsychological dysfunction plays a part in the development and diagnostic picture of children with BPD features. This correlational research design does not lend itself to conclusions of causation. In clinical studies, psychopathology cannot be randomly assigned to participants; however, correlational designs may still yield clues as to causation. By using children, instead of adults, the present design maximizes the possibility that the participants will not, as of yet, have experienced a major head injury (as is true of many adult BPD studies in which prior head injuries confound conclusions of causation). By eliminating the latter as a factor in the production of BPD, the present design, although correlational, makes it more likely to identify other factors in the causation of BPD, or at the very least, the determination of comorbid neuropsychological features in BPD.

Method

Participants

The study was approved by the University of Colorado Institutional Review Board as well as by a research committee, indicating that it met the standards of research outlined by the American Psychological Association. The participants included the parents of 140 children (aged 8 to 15 years old) recruited by university students. The students were asked to approach parents of troublesome or difficult children.

The ethnic makeup of the children was as follows: 72% Caucasian, 10% Hispanic, 9% African American, 3% Asian, and 6% other. The participants were divided into three groups that included 35 parents of BPD children (26 males and 19 females; M age = 14.2, SD = 3.6), 45 parents of children (26 males and 19 females; M age = 13.6, SD = 3.4) who were elevated on another personality disorder scale (not borderline personality disorder), and 60 parents of children (31 males and 29 females; M age = 12.3, SD = 5.5) who scored within normal ranges on the 12 personality disorder scales of the CPNI. The BPD children were identified as those scoring one standard deviation above the mean on the CPNI Borderline Personality Disorder Scale. The OPD children were identified as those scoring one standard deviation above the mean on any of the CPNI Personality Disorder Scales, excluding the Borderline Personality Disorder Scale. The students received extra credit in a psychology class for their recruitment efforts. Informed consent was obtained from all of the parents.

Materials

The demographic information was obtained for the parents about themselves and their children. The information included age, gender, education, race, marital status, as well as other specifics regarding the medical history, legal guardian, and diagnosis of the child. Copies of the demographic surveys are included in Appendices A and B.

The CPNI previously known as the Kidi-CATI, was used to test the hypotheses of the study (see Appendix C). The CPNI was designed to assess children and adolescents, with a three-fold purpose: (a) to measure the 10 personality disorders on Axis II of the DSM-IV (1994) and the two personality disorders in its appendix (depressive and passive-aggressive), ( to measure neuropsychological dysfunction, and © to assess DSM-IV Axis I disorders of separation anxiety disorder, oppositional defiant disorder, ADHD, and other clinical scales. The 200-item CPNI uses a 4-point Likert scale (1 = strongly false, 2 = more false than true, 3 = more true than false, and 4 = strongly true) and is designed to be filled out by a primary caregiver, teacher, or individual who is intimately acquainted with the child’s behavior (Coolidge, 1998).

The current normative sample of the CPNI consists of 329 children, ages 5 to 17 years old. The 12 personality disorder scales of the CPNI possess a median scale reliability of .67. For all scales, preliminary validity studies support the use of the CPNI in a variety of clinical settings (Coolidge, 1998).

The BPD scale of the CPNI contains nine items and has an internal scale reliability (Cronbach’s alpha) of .62. While this could indicate weak internal scale reliability, Cronbach (1951) has noted that it may alternatively suggest a lack of high first factor concentration. The latter appears to be the case in the BPD scale of the CPNI (F. L. Coolidge, personal communication, April 8, 2000). The items on the scale measure all of the criteria for BPD in the DSM-IV: interpersonal and affective instability, recurrent suicidal behaviors or threats, real or imagined abandonment, impulsivity, identity disturbance, stress-related paranoid ideation, inappropriate anger, and feelings of emptiness.

The EF scale was empirically derived from the neuropsychological literature to assess dysfunction of the frontal lobes of the cortex. This scale contains eight items and has an internal scale reliability of .86. The EF assessed by the CPNI scale include decision-making difficulties, organizational impairment, and trouble with planning, perseveration, and sequentialing difficulties. The ADHD scale consists of 18 items and has an internal scale reliability of .91. This scale is also based on the DSM-IV criteria. The items cover two major categories: inattention and hyperactivity-impulsivity. The questions focus on subjects such as trouble paying attention, fidgeting, interrupting, distractability, impulsivity, and hyperactivity.

The BPD, EF, and ADHD scales do not have any overlapping items. Pencil and paper scales of neuropsychological dysfunction are measures of behavior associated with neuropsychological disorder and neuropsychological tests have been shown to be more sensitive measures of behavior than static measures like CAT scans or autopsies. Furthermore, neuropsychological assessment measures have empirically been shown to be better predictors of the behaviors in question (e.g., how good is a child’s memory, how well can they attend, etc.) than static neuropsychological measures (Lezak, 1995).

Procedure

The parents were given a packet by the students that included an informed consent to participate (see Appendix D), two demographic surveys, the CPNI, and a debriefing statement (see Appendix E). They completed the packet in a single session, either at home or at the university.

Results

Hypothesis 1

To test hypothesis 1 (the BPD group will have greater comorbidity on personality disorder scales than OPD) two independent t-tests were performed upon the mean number of other personality disorders that the two groups endorsed. As the possible number of personality disorders in the BPD group could be greater than the OPD group, because the OPD group could not include an elevation on the BPD scale of the CPNI, a t-test was performed on the mean percentage of T scores that were greater than 60. The results indicated that the BPD group endorsed a significantly greater mean percentage of personality disorders than the OPD group, t (78) = 6.78, p < .001, r = .609. The second t-test was performed on the mean percentage of T scores that were greater than 70. The results indicated the same pattern of group comparison as was found in T scores greater than 60, t (78) = 7.62, p < .001, r = .653. See Table 1 for the mean percentages of these groups.

The relationship of the BPD (according to the T score elevation) to the comorbidity of other personality disorders (according to the number of other personality disorders greater than 60) was also examined. The Pearson product-moment correlation was r = .82, p < .001.

Hypothesis 2A

Hypothesis 2A (the BPD group will demonstrate greater EF deficits than either the OPD or the control group) was tested using a one-way analysis of variance (ANOVA). The results indicated that there were significant differences between the groups, F (2, 137) = 38.29, p < .001, ?2 = .35. Tukey’s HSD tests (at p < .05) revealed that consistent with the hypothesis, the BPD group had a significantly greater mean T score on the EF scale than both the OPD and the control group. Additionally, the OPD group’s mean was significantly greater than the control group’s mean (see Table 2).

Hypothesis 2B

Hypothesis 2B (the BPD group will have a greater T score on the ADHD scale than either the OPD or the control group) was tested using a one-way ANOVA. The results indicated that there were significant differences between the groups, F (2, 137) = 36.35, p < .001, ?2 = .34. Tukey’s HSD tests (p < .05) revealed, consistent with this hypothesis, that the BPD group reported a significantly greater ADHD T score than the OPD or the control group. Additionally, comparisons revealed that the OPD group had a significantly greater mean than the control group (See Table 2).

Discussion

The diagnosis of personality disorders in children is an innovative and contentious issue in psychology with an increasing focus. Recent editions of the DSM have asserted that personality disorders may begin in childhood or adolescence and according to the most recent edition, DSM-IV (1994), personality disorders may now be diagnosed in children and adolescents who have shown stable maladaptive features that have been present for at least 1 year. BPD has been a major controversial topic in this area, particularly with respect to its etiology. Recent meta-analytic studies have demonstrated that early sexual abuse is no longer considered to be a major psychological risk factor or a causal antecedent of BPD. It appears that neuropsychological dysfunction (perhaps of genetic origin, Coolidge, Thede, & Jang, in press) now appears to account for a majority of the variance associated with the behavior of BPD children. The present study attempted to demonstrate the connection between neuropsychological dysfunction and BPD in children, as well as the possibility that as BPD increases in severity so does the number of comorbid personality disorders.

The first hypothesis tested the assumption that BPD, as one of the most severe and chronic of all personality disorders, is more likely to appear comorbidly with other personality disorders. The results of this study confirmed the hypothesis, as it was demonstrated that the BPD group (as defined by a T score > 60 or > 70) was associated with significantly more comorbid personality disorders than the OPD group. The DSM-IV (1994) notes that it is often the case that a patient meets criteria for more than one personality disorder, and when considering the results of this study, the findings appear to support this contention, particularly with respect to BPD. A correlation coefficient was calculated as a measure of effect size and a large effect (as defined by Cohen, 1992) was found. This suggests that 37% of the variance in comorbidity can be accounted for by being in either the BPD or OPD group when looking at T scores above 60, and 43% of the variance in comorbidity can be accounted for by being in the BPD or OPD group when looking at T scores above 70. This pervasive comorbidity is likely to contribute to the poor prognosis that individuals with BPD often receive (Docherty, 1993; Waldinger, 1993). As previously stated, researchers and clinicians recommend a multi-modal treatment approach to BPD, as no one therapeutic strategy has been identified for successful treatment with these patients. Given that features of many personality disorders are likely to play a part in the comprehensive picture of individuals with BPD, more so than in other personality disorders, the use of a multitude of treatments with BPD patients seems appropriate.

In addition to examining comorbidity, the second hypothesis of this study suggested that individuals with BPD would demonstrate greater neuropsychological dysfunction. This premise centered on only soft neurological signs, such as EF deficits and ADHD. The neurological dysfunction of BPD patients was originally considered because those patients frequently reported problems in concentration, memory, learning, confusion, and perceptual distortions, which are symptoms of a biologically dysfunctional nature (O’Leary & Cowdry, 1994; Swirsky-Sacchetti et al., 1993). These studies indicated that the characteristics found in BPD sufficiently resemble the characteristics of brain-injured patients to suggest that these phenomena are neurologically associated. However, as the brains of BPD patients show no overt neurological damage (i.e., there are no hard neurological signs), these individuals are said to have soft neurological signs. This study demonstrated that the BPD group reported significantly greater EF deficits than both the control group and the OPD group. Omega-squared was calculated as a measure of effect size and a large effect was found (Coolidge, 1998). This suggests that 35% of the variation in the scores on EF can be accounted for by being in the BPD, OPD, or control group. Overall, the BPD children seem to have more problems associated with behavioral problems with attention, poor peer relationships, and a lack of empathy, all symptoms associated with EF deficits in children (Pennington & Ozonoff, 1996).

Previous studies have also suggested that this neurological dysfunction may be indicative of a frontal lobe disorder (Murray, 1979; Streeter, et al., 1995). Utilizing the technique of brain imaging may aid in detecting any structural differences in specific areas in BPD patients. When considering these implications of the neuropsychologically associated etiology, it would seem essential to begin diagnosing BPD in children, leading to earlier detection and treatment. This assertion is further supported by the findings that EF appear to be strongly heritable and that there are heightened rates of BPD in first-degree relatives, suggesting implications of a genetic component (Coolidge, Thede, & Young, in press; Zanarini, 1993).

The present study also hypothesized that BPD children would have more ADHD symptoms than the OPD group, and this hypothesis was supported. Omega-squared was calculated as a measure of effect size and revealed a large effect. This suggests that 34% of the variance in the ADHD scores can be accounted for by being in the BPD, OPD, or the control group. Some prior research has suggested that ADHD symptoms should be considered to be a confound or "noise" in BPD studies, and children comorbid for both should be eliminated from analyses. Past results of studies may therefore not be generalizable to the majority of comorbid children seen in clinical settings. Jensen, et al. (1997), on the other hand, have argued future studies should take in account ADHD symptoms, as did the present study. Previous research that has demonstrated BPD patients display a higher percentage of histories of ADHD (Andruolonis et al., 1982; van Reekum, 1993) supports this finding. Another advantage of the present study over prior research is that the ADHD symptoms were current, unlike most prior retrospective methods of examination of ADHD in adult BPD patients. These findings suggest that those individuals in the BPD group demonstrate greater hyperactivity, impulsivity, and distractibility than individuals in the OPD group. The controversial juncture that arises at this point is whether neuropsychological dysfunction predisposes patients to acquire BPD, or whether BPD leads to the development of ADHD and EF deficits, or do they occur concurrently because of a common biological factor. This controversy promises to be an interesting topic for future research.

The present study was limited by a small sample size. Although psychometricians often note that a sample of 30 is sufficient, when trying to make inferences to millions of BPD children, a larger compilation of individuals is obviously needed. In addition to increased sample size, future studies should include better sampling methods that consider gender, ethnicity, region, and parental income. Another limitation of this study is that no measures other than the CPNI were used. As with any singular test, using clinical interview as well as other corroborating data would be beneficial in identifying clinical diagnoses. Direct measures of ADHD and EF (e.g., the Tower of Hanoi) should also complement CPNI diagnoses in future studies.

Furthermore, although no parents of BPD children said that their child had a major head injury, a few indicated they had a concussion. These cases could also be eliminated from further analysis to further the possibility of clues to causation. Additionally, parental bias was not considered in the present study. To control for this potential effect, further studies should collect both parents’ evaluation of the child, and perhaps include only those who overlapped. A teacher’s confirmation would also be beneficial, to account for the child’s behavior in the school setting. This amalgamation of evaluation would provide a more complete picture of the child, and would lead to increased confidence in the clinical diagnosis.

Many researchers have debated the etiology of BPD, and recent studies have placed support for neuropsychological factors at the forefront of that dispute. The diagnosis of BPD in children has also been a controversial issue. Wolff (1993) noted that to make sense of repetitive maladaptive behavior in adult life it is essential to have an appreciation of childhood factors. Similarly, Lewis (1976) suggested that significant personality difficulties may be inadequately treated or overlooked altogether in the child. Few studies have looked at the combination of both neuropsychological factors and childhood diagnosis. The results of this study support the identification of BPD features in children and associate those with neuropsychological factors, although causation between these variables has yet to be determined. Previous studies have identified the heritability of BPD as well as characteristics of how BPD is manifested in children. These findings paired with those from the present study certainly warrant researchers’ and clinicians’ attempts to study and diagnose BPD as early as possible. With empirical demonstration and the increasing support of the DSM this connection between neuropsychological factors and the emergence of BPD in children may be more fully realized. BPD patients are notorious for their difficulty in treatment; early diagnosis as well as consideration of the neuropsychological factors that may contribute to BPD may facilitate greater knowledge and aid in treating this severe and chronic personality disorder.

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Vela, R., Gottlieb, E. H., &am

[pinklady66]

I have ADHD. I didn't get a dx until I was in my late twenties. I have the hyper spells where I can't sit down for too long. I have trouble paying attention and I certainly don't grasp the finer details of things. When I was in school, the dx of ADHD orADD,wasn't in the medical dictionary. Kids who were hyper in class were just called disruptive, or slow learners. In fact many kids who have the disorder are very bright.

To be dx with the disorder, you have to be tested for it first.

I hope that answers your question.