UNIVERSITÀ DI PISA
Dipartimento di Medicina Clinica e Sperimentale
Scuola di Specializzazione in Psichiatria
Direttore: Prof.ssa Liliana Dell’Osso
TESI DI SPECIALIZZAZIONE
Emotional Dysregulation in Adult Patients with
Attention Deficit/Hyperactivity Disorder: A Neurodevelopmental Perspective
Relatore Candidato
Prof. Giulio Perugi Dott. Amedeo Lombardi
INDEX
ABSTRACT………..I
1. Introduction………..1
1.1 ADHD in Adulthood……….………...5
1.2 Emotional Dysregulation in ADHD patients………..15
2. Aim of the study………..26
3. Materials and Method………..…………..27
3.1 Sample………27
3.2 Data Collection………...27
3.3 Assessing Instruments………28
3.4 Statistical Analysis……….31
4. Results………..32
5. Discussion and Conclusions………...40
6. Limits………...46
7. Tables………...47
I
ABSTRACT
Background: Attention Deficit/Hyperactivity Disorder (ADHD) in adulthood have an heterogeneous and atypical presentation, notably with less externalizing and hyperactive symptoms and with a higher rate of psychiatric comorbidities. A symptomatological dimension that is also frequently associated in adult ADHD patients is the Emotional Dysregulation (ED), often with low frustration tolerance, impulsivity, irritability and affect and mood lability. Although it has long been recognized that many individuals with ADHD also have difficulties with emotion regulation, no consensus has been reached on how to conceptualize this clinically challenging domain. There are yet limited investigation into this aspect on the clinical picture of the disorder and it is discussed whether symptoms of ED could add a better description of the psychopathology of ADHD and an additional core symptom. The aim of this study is to explore the correlates of the presence of low and high level of ED in a sample of adult ADHD patients and its relationship with clinical, temperamental characteristics and other psychiatric comorbidities.
Method: Forty adult ADHD patients were enrolled in this study and all patients were assessed using the Diagnostic Interview for ADHD in Adults (DIVA 2.0), the Structured Clinical Interview for DSM-IV Axis I and II Disorders (SCID I/II), the brief Temperament Evaluation of Memphis, Pisa, Paris and San Diego–M (brief TEMPS-M), the Reactivity Intensity Polarity Stability Questionnaire (RIPoSt), the Semi-structured Interview for Mood Disorders (SIMD-R), the Barratt Impulsiveness Scale (BIS-11), the Adult Self-Report Scale (ASRS-v 1.1), the Global Assessment of Functioning (GAF) and the Functioning Assessment Short Test (FAST). We divided the sample into two groups using the RIPoSt mean score: one group with Low-Emotional Dysregulation (L-ED) and the second group with High-Emotional Dysregulation (H-ED).
II
Results: The multivariate linear regression analysis, showed that the variables mostly associated with the RIPoSt Total score (R-Tot) (higher ED) were Cyclothymic Temperament (p<0.000), Borderline Personality Disorder (p<0.003), FAST total score (p<0.001), Irritable Temperament (p<0.003), Anxious Temperament (p<0.011) and FAST Leisure subscale (p<0.040). Considering the RIPoSt subscale, the linear regression analysis showed that the variables mostly associated were the affective temperaments and some FAST subscales. Comparing the two groups we found that the mean score of ASRS (p<0.006), the mean score of the Dysthymic (p<0.010), Cyclothymic (p<0.000), Irritable (p<0.000) and Anxious temperamental subscale (p<0.000) of the briefTEMPS-M, the total score of the BIS scale (p<0.013) and of the BIS Attentional subscale (p<0.000) were statistically significant higher in patients with H-ED. Among other psychiatric disorders, The Bipolar Disorder-II (BD-II) (p<0.01), Cyclothymia (p<0.03) and Borderline Personality Disorder (BPD) (p<0.03) were significantly most associated in ADHD patient with H-ED.
Conclusions: The group of ADHD patients with H-ED showed a significant higher impulsiveness, a closer relationships with bipolar and personality disorder (Cyclothymia, BD-II, BPD) and a higher prevalence of Cyclothymic, Irritable, Anxious and Dysthymic Temperaments, compared to the patients of the L-ED group. Our results suggested that adult ADHD with high ED could represent a specific subgroup of patients with a higher severity of ADHD symptoms and a higher prevalence of affective disorders, configuring a new subtype of neurodevelopmental disorder. As reported in literature, we may hypothesize that the strong association and co-occurrence between BD, BPD and ADHD, it could depends on a shared common neurobiological basis between these supposedly distinct disorders and that the ED may represent the shared core dimension, with a key role in etiopathogenesis of disorders with affective instability.
1
1. Introduction
Neurodevelopmental Disorders typically debut very early in childhood and are characterized by a number of symptoms that negatively affect the global functioning and lead to a series of relevant consequences at social and relational level (APA 2013).
The Attention Deficit/Hyperactivity Disorder (ADHD) is characterized by inattention, hyperactivity and impulsiveness, going to negatively impact on the various aspects of life of these patients: especially they show more relational, educational and employment problems, compared to the general population (Asherson et al. 2012, Cox et al. 2011, Klassen et al. 2010, Kooij et al. 2012, Kooij et al. 2010). Other features of the disorder are mood instability (APA 2000, Di Nicola et al. 2014) and emotional dysregulation (ED) (Barkley and Murphy 2010, Corbisiero et al. 2013, Martel 2009, Retz et al. 2012, Surman et al. 2011).
Epidemiological and clinical studies have shown that individuals with ADHD show an increased risk for substance use disorders and other psychiatric conditions, such as mood and anxiety disorders (Bernardi et al. 2012, Biederman et al. 1991, Biederman et al. 2006b, Elkins et al. 2007, Kessler et al. 2006).
ADHD is particularly relevant in today’s society as it is one of the most common diagnoses in educational and children’s mental health setting, resulting in high individual and societal costs to the population (Matthies and Philipsen 2014, Pelham et al. 2007). Like all the neurodevelopmental disorders, ADHD starts in childhood but can persist into adulthood. Indeed, ADHD symptoms have been shown to persist into adulthood in 10-60 % of cases (depending on the reporting source and on definition criteria) (Barkley et al. 2002). The National Comorbidity Survey study found that 36% of adults who met criteria for ADHD as children continued to fulfill them as adults (Di Nicola et al. 2014, Kessler et al. 2006).
2 So, there is an increasing evidence that ADHD can persist into adolescence and early adult life (Bramham et al. 2012, Mannuzza et al. 2003). Moreover, the persistence of ADHD suggests that the impact of the disorder goes often beyond childhood and adolescence, and that most health care professionals, not only pediatricians and child psychiatrists, are likely to encounter individuals with ADHD in their clinical practice (Bernardi et al. 2012).
Clinical presentations of ADHD are heterogeneous, and the phenotypes are extremely variables in terms of severity and symtomatology. In other terms ADHD should be conceptualized as a disorder that rides along a continuum (Matthews et al. 2014). The trajectories of the the disorder and their clinical impact in adults depends on several factors, including the severity of the disorder itself, the presence of comorbidity (physical, neurological and psychiatric) and the potential interference with the social and family context of the subject as well as the possible complications. In fact, depending on these variables subjects with ADHD may develop compensatory strategies and can be able to achieve a normal functioning and also a discrete adaptation; more frequently, if not treated, the disorder shows a negative outcome and it is associated with increased rates of family conflict, poor peer relationships (Able et al. 2007, Barkley et al. 2006), unintentional injuries or trauma (Barkley et al. 1993, Swensen et al. 2004), impaired driving, substance use disorders, low educational achievement, decreased work performance (Kessler et al. 2009, Mannuzza et al. 1993), and high health-care costs (Leibson et al. 2001, Meyers et al. 2010, Bernardi et al. 2012)
Sometimes the diagnosis is not clear and delayed, especially when the disorder occurs with psychiatric symptoms (restlessness, emotional instability, low self-esteem, and sleep problems). Adult ADHD is highly comorbid with other mental disorders, most commonly mood, anxiety and substance use disorders (Murphy and Barkley 1996, McGough et al. 2005, Biederman et al. 2006, Kessler et al. 2006, Fayyad et al. 2007,
3 Cumyn et al. 2009). Personality disorders also often co-occur with adult ADHD. Particularly the risk of developing cluster B personality disorders in late adolescence is increased in children with ADHD (Miller et al 2008, Distel et al. 2011). Among the psychiatric disorders, Bipolar Disorder (BD) and Borderline Personality Disorder (BPD) are the most commonly associated in adulthood (Atmaca et al. 2009, Kent and Craddock 2003, Klassen et al. 2010, Scheffer 2007, Skirrow et al. 2012, , Philipsen 2006, Philipsen et al. 2009). The presence of such comorbidities may also have a patoplastic effect on the disorder (earlier onset of bipolar disorder, increased risk of substance abuse, greater number of manic episodes) (Wingo and Ghaemi 2007), and determining a delay in diagnosis. The comorbidity is also responsible of greater resistance to common psychiatric treatments and, in most cases, is the reason of the request for help to the doctor.
In adult with BD, the prevalence of comorbid ADHD has been reported to vary significantly (Bond et al. 2012). The National Comorbidity Survey study found that 21 % BD patients also suffer from ADHD (Kessler et al. 2006, Di Nicola et al. 2014).
Several studies report that bipolar adults with a history of ADHD present an earlier disease onset, more affective episodes, more suicide attempts, more violence and substance abuse, and a greater likelihood of suffering from anxiety disorders (Nieremberg et al. 2005, Sachs et al. 2000, Di Nicola et al. 2014). However, it remains still controversial the simultaneous diagnosis of adult ADHD and bipolar spectrum disorders, not knowing whether it is a diagnostic artifact or a specific clinical dimension (Wingo et Ghaemi 2007). To noted, moreover, that often in these patients the affective dimension shows a large impairment. These subjects are characterized by a marked difficulty in the management of emotions and emotional responses to stimuli, as well as negative feelings such as anger and frustration, in response to impulsive and sometimes aggressive behavior. So, there is a sort of affective disturbance or more specifically an ED (Able et al. 2007, Barkley and Fischer 2010, Reimherr et al. 2005, Reimherr et al. 2007, Surman et al. 2013, Corbisiero et al.
4 2012). Symptoms of ED in adult ADHD seem to compromise the severity of the ADHD symptomatology as well as its comorbid disorders (e.g. sleeping problems, somatic complaints, anxiety-tension, oppositional-defiant symptoms) and impairments in important domains of major life activities including social and occupational functioning, educational history, driving risk, criminal history, marital satisfaction, parenting stress, and severity of offspring disruptive behavior disorders (Reimherr et al. 2005, Reimherr et al. 2007, Reimherr et al. 2010, (Barkley and Murphy 2010, Robison et al. 2008, Corbisiero et al. 2012, Wehmeier et al. 2010).
The ED is also frequently observed in other psychiatric disorders, especially BD and BPD (Dadomo et al. 2016), which are also among the most frequent comorbid disorders with ADHD and with whom they share many symptomological aspects; thus, for this reason, it is hypothesized a common patogenetic substrate between these disorders (Philipsen et al. 2008, Perroud et al. 2014, Wingo et Ghaemi 2007, Baud et al. 2011, Lepouriel et al. 2016, Stone 2013). Although it has long been recognized that many individuals with ADHD also have difficulties with emotion regulation, no consensus has been reached on how to conceptualize this clinically challenging domain. (Shaw et al. 2014).
5
1.1 ADHD In Adulthood
ADHD is defined in DSM-5 as a neurodevelopmental disorder characterized by impairing levels of inattention, disorganization, and/or hyperactivity-impulsivity. In childhood, ADHD frequently overlaps with other "externalizing disorders," such as oppositional defiant disorder and conduct disorder, and often persists into adulthood, with resultant impairments of social, academic and occupational functioning (APA 2013).
DSM-5 describes three presentations, on the basis of the most prevalent current symptoms (e.g., primarily inattentive, primarily impulsive/hyperactive and a combination of both). The three presentations are explicitly not expected to be stable, as children diagnosed with the disorder can change presentation over time from year to year (Lahey et al. 2005).
Despite numerous potential improvements to the criteria, few substantive changes were made to DSM-5. The same two behavioral domains (inattention and hyperactivity- impulsivity) are still in force. Indeed, the literature of the last 20 years provides powerful evidence for the clinical utility and validity of distinguishing these two symptom domains that, despite being highly correlated predict different impairments and may have different neurophysiological correlates (Willcutt et al. 2012, Fair et al. 2013). In particular, symptoms of inattention-disorganization tend to predict academic problems, certain driving difficulties, and peer neglect. Symptoms of hyperactivity-impulsivity seems to predict aggression, peer rejection, and speeding citations (Matthews et al. 2014).
It is becoming increasingly clear that the DSM criteria are not sufficient to accurately describe ADHD in adults, mainly because they were designed to make the diagnosis in childhood, regardless of the evolutionary potential that often the disorder presents, as well, the changes involving nuclear symptoms. Indeed studies of symptoms trajectories in children with ADHD followed up during adolescence or early adulthood suggest that inattention symptoms remit at a slower rate than hyperactive or impulsive
6 symptoms (Hart et al. 1995, Biederman et al. 2000) and prevalence studies show that the inattentive subtype is more common than hyperactive subtype in adulthood (Wilens et al. 2009, Braham et al. 2012). Furthermore, the DSM-5 diagnostic criteria do not include those symptoms that best characterize most of the adults with ADHD such as affective lability, hot temper, explosive short-lived outbursts and emotional over reactivity that are only mentioned in section “Associated Features”.
Wender and colleagues (Wender et al. 1981, Wender et al. 2001, Ward et al. 1993) have formulated the more appropriate criteria for the diagnosis of ADHD in adults, the so-called Criteria of Utah, in which must be present history of childhood ADHD and a series of associated symptoms that are most refer to the sensations and subjective perceptions of patients rather than to their behavior for the diagnosis (e.g. hyperactivity, inattention, mood lability, short-fuse temper, disorganization, stress sensitivity and impulsivity) (Evenden et al. 1999, Davids and Gastpar 2005).
Specifically, Utah criteria are the following (Wender et al. 2001): A. Motor hyperactivity
Manifested by restlessness, inability to relax; “nervousness” (meaning inability to settle down, not anticipatory anxiety); inability to persist in sedentary activities (e.g., watching movies or TV, reading the newspaper); always on the go, dysphoric when inactive.
B. Attention deficits
Manifested by an inability to keep one’s mind on conversations; by distractibility (incapacity to filter extraneous stimuli); difficulty keeping one’s mind on reading materials or tasks (“mind frequently somewhere else”); frequent “forgetfulness”; by often losing or misplacing things; forgetting appointments, plans, car keys, purse, etc.
C. Affective lability
Usually described as antedating adolescence and in some instances as far back as the patient can remember. Manifested by definite shifts from a normal mood to depression or
7 mild euphoria or excitement; depression described as being “down,” “bored,” or “discontented”; anhedonia not present; mood shifts usually last hours to at most a few days and are present without significant physiological concomitants; mood shifts may occur spontaneously or be reactive.
D. Hot temper, explosive short-lived outbursts
A hot temper, “short fuse,” “low boiling point”; outburst usually followed by quickly calming down. Subjects report they may have transient loss of control and be frightened by their own behavior; easily provoked or constant irritability; temper problems interfere with personal relationships.
E. Emotional over reactivity
Subjects cannot take ordinary stresses in stride and react excessively or inappropriately with depression, confusion, uncertainty, anxiety, or anger; emotional responses interfere with appropriate problem solving—they experience repeated crises in dealing with routine life stresses; describe themselves as easily “hassled” or “stressed out.”
F. Disorganization, inability to complete tasks
A lack of organization in performing on the job, running a household, or performing school work; tasks are frequently not completed; the subject goes from one task to another in haphazard fashion; disorganization in activities, problem solving, organizing time; lack of “stick-to-it-iveness.”
G. Impulsivity
Minor manifestations include talking before thinking things through; interrupting others’ conversations; impatience (e.g., while driving); impulse buying. Major manifestations may be similar to those seen in mania and Antisocial Personality Disorder and include poor occupational performance; abrupt initiation or termination of relationships (e.g., multiple marriages, separations, divorces); excessive involvement in pleasurable activities without recognizing risks of painful consequences (e.g., buying sprees, foolish business
8 investments, reckless driving); inability to delay acting without experiencing discomfort. Subjects make decisions quickly and easily without reflection, often on the basis of insufficient information, to his/her own disadvantage.
H. Associated features
Marital instability; academic and vocational success less than expected on the basis of intelligence and education; alcohol or drug abuse; atypical responses to psychoactive medications; family histories of ADHD in childhood; Antisocial Personality Disorder and Briquet’s syndrome.
Despite only the dimension of attention/inattention and hyperactivity/impulsivity being among the most common symptoms described in individuals with ADHD, we can deduce from the above criteria that would seem to emerge two other important symptomatological areas: emotional instability and irritability/oppositivity (Jensen et al. 2001, Reimherr et al. 2007). All together, these four broad areas would be responsible for the different degrees of the disorder upgradeability over time (Reimherr et al. 2010).
Compared to the general population, adults with ADHD are twice as likely to be arrested, have a two-fold increased risk of being divorced, and a 78% greater risk of being unemployed (Faraone and Biederman, 2004). Moreover, ADHD in adult is associated with driving impairments, receiving more speeding tickets and license suspensions compared to controls (Barkley et al. 2002). At least one study suggests that adults with ADHD have a significantly lower household income compared to their peers (Biederman and Faraone, 2006). Finally, teens with ADHD also exhibit riskier sexual behaviors, are less likely to use contraception and are more at risk of unwanted pregnancies and sexually transmitted diseases (Barkley et al. 2002). Thus, ADHD clearly affects the patient's life at an educational, professional, and personal level (Klassen et al. 2010).
From a neurocognitive point of view several studies in adults ADHD have mainly investigated frontal lobe-related functions (executive functions); these have reported
9 impairments involving sustained attention, signal detection, working memory, time estimation, verbal fluency, speed of motor movement, mental processing speed, shifting/maintaining cognitive set, latency to respond to a stop signal and impulse control (Epstein et al. 1998, Dinn et al. 2001, Gallagher and Blader, 2001, Davids and Gastpar 2005).
Over the past two decades, neurobiological theories of ADHD have focused on two common, but not mutually exclusive, models. One model emphasizes top-down, controlled processing problems, such as those associated with cognitive control or executive functioning (Barkley 1997). Another model emphasizes bottom-up, motivational, and incentive or reward response (Sagvolden et al. 2005). There exist several lines of evidence that support both of these models and suggest both types of psychobiological systems are involved in ADHD.
The Top-Down Control or the Executive Control Theory has long been considered the leading theory to explain ADHD nuclear symptoms. Barkley et al. 1997 tried to explain by this theory as some of the characteristic behaviors of the subjects with ADHD derived substantially from an alteration in the inhibition mechanisms of response, that subsequent studies have confirmed (Doyle 2006, Nigg 1999, Nigg 2001, Seidman et al. 1997).
The response inhibition is the ability to inhibit or suppress an inappropriate, prepotent response in a certain context in favor of a more appropriate alternative and is believed to involve fronto-striatal and fronto-subthalamic circuits (Aron 2011). It is regarded as a prerequisite for self control (Muraven and Baumeister 2000), emotional regulation (Eisenberg and Morris 2002), and cognitive flexibility (Arbuthnott and Frank 2000).
In support of this theory it is also availables neuroanatomical and neurofunctional data that demonstrate how some of the brain areas and circuits responsible for executive
10 functioning are atypical in children with ADHD (Bush et al 1999, Rubia et al 1999, Fair et al 2012b, Mennes et al 2011).
Neurocognitive deficits involving vigilance, sustained attention, planning and working memory have been reported in association with childhood ADHD (Shue and Douglas 1992, Karatekin and Asarnow 1998, Pineda et al. 1998, Nigg et al. 2002). As many of these are similar to deficits in patients with frontal lobe lesions, it has been suggested that ADHD may, in part, reflect a neurodevelopmental disorder, mainly affecting functioning of regions of the frontal cortex or those regions projecting to the frontal cortex (Shue and Douglas 1992). There are, in fact, numerous neurocognitive studies in individuals with ADHD, which shows that these function are atypical. (Epstein et al. 1998, Dinn et al. 2001, Gallagher and Blader 2001). However, response inhibition is not the only executive process atypical in children with ADHD (Matthews et al. 2014).
In recent years, another neurocognitive theory of ADHD is receiving increasing attention. The theory is substantially based on the reward, motivation and emotional regulation, the so-called Bottom-Up theory (Barkley 2009, Luman et al. 2005, Nigg and Casey 2005, Sonuga-Barke 2005). Although not included among the diagnostic criteria, problems with emotions, such as difficulty with anger, mood, and affect regulation are commonly observed in ADHD.
In fact, the contribution of ED and consequently the lack of emotional control and self-regulation seems to be of primary importance in contributing, with the other neurocognitive alterations, to development ADHD symptoms (Barkley 2009, Nigg and Casey 2005). More precisely, it is likely that emotional self-regulation is closely connected to working memory systems and its dysfunction might be more related to inattentive symptoms (Barkley 2009). Emotional inhibition is associated with a skill of suppressing the prepotent emotional reaction to express a more socially accepted emotion or behavior; a deficit in emotional inhibition might be related to hyperactive and impulsive symptoms
11 (Barkley 2009). It is also important to note that is typical of ADHD subjects having an hedonic behavioral approach, they prefer the immediate gratification and rewards and they are unable to postpone in time the moment of gratification, why show excessive and immediate looking for experience with this type of characteristics, although this often means to persevere in risky behaviors and to encounter unfavorable and negative consequences (Casey and Nigg 2005).
The rule seems to be, from an early age, to seek and prefer small but immediate gratification rather than major and distributed in time (Luman et al. 2005). As a result of a negative emotions experienced when in a delay-rich environment, ADHD children manifest impulsive and overactive behaviors (Sonuga-Barke 2005). It’s important to note that core behaviors of ADHD are also common characteristics of other psychiatric disorders (Murphy and Adler 2004); some examples of common disorders with symptom-overlap are mood and anxiety disorder, other neuropsychiatric and personality disorders of borderline and antisocial character (Biederman et al. 1993, Wilens et al. 2009, Ebedol et al. 2012). Furthermore, adults ADHD are highly comorbid with other axis-I disorders. Most commonly associated with adults ADHD are mood disorders, anxiety disorders, and substance use disorders (Murphy and Barkley 1996, McGough et al. 2005, Biederman et al. 2006, Kessler et al. 2006, Fayyad et al. 2007, Cumyn et al. 2009, Distell et al. 2011). In particular, among Axis I disorder, comorbidity with BD is very frequent (Nieremberg et al. 2005, Tamam et al. 2008, Kessler et al. 2006, Bond et al. 2012, Ekinci et al. 2013).
The prevalence among adults ADHD ranges from 5 to 20% (Faraone et al. 2006c, Kessler et al. 2006, McGough et al. 2005, Skirrow et al. 2012, Tamam et al. 2006), and two studies reporting even a higher rates (respectively 32% (Halmoy et al. 2010) and 47% (Wilens et al. 2003)). On the other hand 10–21% of BD adult patients may have comorbid ADHD (Bernardi et al. 2010, Karaahmet et al. 2013, Kessler et al. 2006, Nierenberg et al. 2005, Perugi et al. 2013c, Tamam et al. 2006).
12 It is also true that ADHD and BD share many symptoms (Milberger et al. 1995, Ekinci et al. 2013) that often include the attention symptom domain such as low attention span, forgetfulness and distractibility as well as the activity symptom domain with increased psychomotor activity, impulsive and intrusive behaviors as well as affective symptoms of irritability and emotional lability which may be found in ADHD as well (Giedd 2000, Kent and Craddock 2003, Ebedol et al. 2012).
This has raised the question of whether these two disorders are clinically similar or biologically overlapping or share a common neurobiological basis (Kent and Craddock 2003). However, if we consider not only the BD, but the bipolar spectrum disorders (BSD), it is still true that the chronic course of ADHD, shows an high comorbidity with the bipolar spectrum disorder, and the significant positive impact of treatment on the course of both disorders increase the importance of screening for ADHD even during the adulthood period. The possible relationship between BSD and ADHD with highly overlapping symptoms such as excessive talking, attention deficit, and increased motor activity, has been gradually drawing more attention in all age groups (Sachs and Baldassano 2000, West et al. 1995, Winokur et al. 1993).
Therefore the number of studies investigating the relationship between these two disorders has increased. Some studies reported that the patients diagnosed with BSD in the childhood and adolescent periods had ADHD comorbidity ranging from 38% to 98% (Geller et al. 1998, Wozniak et al. 1995, Masi et al. 2006). The BSD patients with ADHD showed differences from BSD patients without ADHD in their core symptomatology, phenomenology, and disease course. In BSD patients with ADHD compared to the ones without ADHD, BSD has earlier onset, depressive and mixed episodes are more frequent, all episodes occur more often, the euthymic periods between episodes are shorter, and alcohol-drug addiction is more prevalent (Tamam et al. 2006, Nieremberg et al. 2005, Sachs et al. 2000, Karaahmet et al. 2013).
13 Also personality disorders, to date defined as Axis II disorders, often co-occur with ADHD in adult. Particularly the risk of developing cluster B personality disorders in late adolescence is increased in children with ADHD (Miller et al. 2008).
The relationship between ADHD and BPD has received most attention because of the similar clinical features of the two disorders. BPD is characterized by identity disturbances, interpersonal difficulties, impulsivity, and emotional lability (A.P.A 2000, Distel et al. 2011).
The significant association between ADHD and BPD, contrasts with the reported lack of continuity between childhood and adult borderline disorders (Lofgren et al. 1991). This finding needs not to be a surprise for several reasons: First, there are reports showing comorbidity of ADHD and BPD (Andrulonis and Vogel 1984, Biederman et al. 1991). Second, the criteria for diagnosis of BPD and ADHD have similarities. Third, ADHD is not an episodic disorder but a chronic condition in which symptoms might persist into adulthood in a variety of ways (Klein and Mannuzza 1991, Shaffer 1994). Fourth, an association between antisocial personality disorder and BPD is well demonstrated, and antisocial personality disorder is also a well-known adult outcome of ADHD (Eppright et al. 1993, Goldman et al. 1993, Klein and Mannuzza 1991). Finally, there are higher rates of antisocial personality disorder in the families of both children with BPD and children with ADHD (Biederman et al. 1993, Goldman et al. 1993, Davids et al. 2005).
Substance abuse constitutes another common comorbid disorder seen in ADHD adult patients, who may use alcohol, drugs and nicotine (Ohlmeier et al. 2007). There is emerging evidence that treatment of ADHD in childhood or adolescence might reduce the virulence and trajectory of substance use disorders in adulthood. For example, a recent study by Wilens et al. 2008 showed that treating children with ADHD with stimulants had a highly significant protective effect on later development of substance use disorders and cigarette smoking. Based on this information, we could hypothesize that treatment of
14 ADHD with stimulants in adults with concomitant ADHD and substance abuse could help manage the comorbid substance abuse disorder (Klassen et al. 2010).
In general we can say that there seems to be a strong link between mood disorders, particularly bipolar disorder and personality disorders (Borderline and Antisocial), substance use disorders and ADHD, and that all these conditions have a large area of overlap: the emotional dysregulation.
It’s important to note that the diagnosis and treatment of adult ADHD can be a challenge, because hyperactive symptoms tend to decrease with age, thus making it more difficult to diagnose adult ADHD (Nierenberg et al. 2005). Furthermore, adults with ADHD tend to present less with externalizing and hyperactive symptoms, compared to ADHD when initially diagnosed in childhood, which further complicates referral and diagnosis (Karam et al. 2008, Klassen et al. 2010). Therefore, overlapping features between ADHD and other syndromes, may adversely affect the reliability of diagnostic assessments of adult ADHD and the evaluation of treatment effects (Spencer et al. 1998) and contributes to increased use and costs of mental health services (Fischer et al. 2007).
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1.2 Emotional Dysregulation in ADHD patients
The emotions are multi-faceted processes which include subjective experience, behavior, and physiology (Mauss et al. 2005). Core features of emotion include situational antecedents, attention, appraisal, and multifaceted response tendencies (Werner and Gross 2010, Jazaieri et al. 2013).
The term “Emotional Regulation” refers to a series of strategies aimed at modulating and adjusting unpleasant emotional experiences (John and Gross 2004, Gross 2011). Emotional regulation is a multidimensional construct composed of the following traits: (1) awareness and acceptance of emotions; (2) skills to engage in behaviors aimed at a target; (3) flexible use of appropriate strategies to modulate the context’s intensity and the duration of the emotional response (Pedersen et al. 2014, Dadomo et al. 2016).
Emotion regulation can be defined also as an individual’s ability to modify an emotional state so as to promote adaptive, goal-oriented behaviors (Thompson 1994). It encompasses the processes that allow the individual to select, attend to, and appraise emotionally arousing stimuli, and to do so flexibly. These processes trigger behavioral and physiological responses that can be modulated in line with goals (Shaw et al. 2014).
Defined in this way, emotions are one type of affective response. We conceive of affect as an overarching term that includes emotions, moods, and stress responses (Gross & Thompson 2007, Wessa et al. 2014).
According to Gross & Thompson (2007) regulation of emotions refers to the process of increasing or decreasing current affect. Such a process may occur consciously or unconsciously on a continuum from effortless and automatic (unconscious) to effortful and controlled regulation (conscious).Within their model of emotion regulation, Gross & Thompson (2007), differentiate five types of emotion regulation strategies which can be broadly divided into (1) antecedent-focused strategies, occurring before full-blown emotional responses are elicited (situation selection, situation modification, attentional
16 deployment, and cognitive change), and (2) response-focused strategies, occurring after emotional responses are generated (response modulation).
When the emotional regulation system works properly, individuals are able to modulate their emotional states and functionally direct their behavior. Indeed adopting effective strategies of emotional regulation is considered one of the fundamental aspects of individual adaptation (Dadomo et al. 2016).
On the contrary, ED is that condition in which despite an individual’s best efforts, regulatory attempts are not achieving the individual’s emotion related goal(s) and the individual is unable to make necessary corrections to achieve the emotion related goal(s). ED practically is an impaired ability to regulate unwanted emotional states (Dadomo et al. 2016).
ED arises when these adaptive processes are impaired, leading to behavior that defeats the individual’s interests. It encompasses 1) emotional expressions and experiences that are excessive in relation to social norms and are context inappropriate; 2) rapid, poorly controlled shifts in emotion (lability); and 3) the anomalous allocation of attention to emotional stimuli (Shaw et al. 2014).
Some authors argue that even irritability is part of ED dimension, since it is frequently found in many psychiatric disorders and diagnostic criteria (Stringaris 2011, Mikita and Stringaris 2013) and that is often linked with reactive aggression and temper outbursts (Leibenluft 2011, Stringaris 2011, Dodge et al. 1991). The prevalence of irritability in childhood appears to be variable among 3% (severe) and 20 % (mild) (Brotman et al. 2006, Pickles et al. 2010). Other authors argue that when chronic, irritability could be a separately construct, defined as “Severe Mood Dysregulation”, characterized by chronic and severe irritability with frequent and developmentally inappropriate temper outbursts, along with negatively valenced mood in between outbursts. (Leibenluft et al. 2003).
17 It speaks more globally of “Affective Disturbance” as a disruption in the multi-system response (subjective experience, expressive behavior, physiology) of emotions, moods, and stress responses. Affective disturbance can refer to either negative affective states (e.g., anxiety or depression) or positive affective states (e.g., euphoria or mania). One prominent cause of affective disturbance may be difficulties with emotion regulation. From this perspective, then, emotion regulation and potential subsequent ED are subordinate to the broader construct of affective disturbance. Further, emotion regulation is neither good or bad, while ED and affective disturbance are by definition considered to be dysfunctional states.
ED (Reimherr et al. 2003), emotional impulsiveness (Barkley and Fischer 2010), mood instability (Gudjonsson et al. 2013) and emotional lability (Sobanski et al. 2010) have been used to refer to similar conceptualizations (Martel 2009, Corbisiero et al. 2013, Skirrow et al. 2009).
It has been for several years that has been recognized, not only in psychiatry, but also and especially in the field of childhood neuropsychiatric, a strong association between ED and neurodevelopmental disorders, particularly with ADHD. (Robinson et al. 2008, Surman et al. 2013, Richard-Lepouriel et al. 2016).
While symptoms of deficient emotional self-regulation (DESR) have been long associated with ADHD, there has been limited investigation into this aspect of the clinical picture of the disorder (Shaw et al. 2014). In fact, there is still a debate about whether the classical tripartite division of core ADHD symptoms of inattention, hyperactivity and impulsivity is sufficient to describe the syndrome adequately, especially in adults (Gibbins and Weiss 2007). In this regard there are studies that have shown the instability over time of the three classic dimensions of psychopathology (Biederman et al. 2000, Faraone et al. 2006) and others in which in addition to the classic symptoms are also included other
18 dimensions as the nuclear symptoms, to characterize the most of the ADHD in adults (Barkley and Murphy 2006, Corbisiero et al. 2012).
The problem of the ED, to date, is still more evident and the most recent studies have shows that would seem to be a third nuclear dimension of the disorder, of comparable importance to the two most well-known (Shaw et al. 2014, Richard-Lepouriel et al. 2016). In this regard it is interesting to note that historically, in the early conceptualization of ADHD as reflecting “minimal brain damage” ED was placed along with inattention among the cardinal symptoms (Clements 1966, Shaw et al. 2014).
Since the 1968 version of DSM, deficits in emotional regulation were included as associated symptoms of ADHD but not as core features (only with the publication of DSM-III did emotional symptoms became an “associated feature” rather than a diagnostic criterion of ADHD) (APA 1968, APA 1987, APA 2000, Barkley 2006, Surman et al. 2013). The DSM-5 doesn’t provides yet the inclusion of the emotional dimension in the basic symptoms of ADHD and it is only mentioned in the section of disruptive disorders that takes into account the evaluation of the emotional symptoms for possible diagnosis (Corbisiero et al. 2013).
Dr. Paul Wender highlighted the association between ADHD and affective lability as well as stress intolerance, and the Utah Criteria for ADHD include temper, mood instability, and emotional over-reactivity as core features of ADHD (Wender 1995). Based on these criteria, Wender and colleagues have developed a diagnostic tool used for the diagnosis of adults ADHD, the WRAADDS scale, which uses three subscales: affective lability, temper control, emotional over-reactivity (Ward et al. 1993, , Wender 1995, Rösler et al. 2008a, Rösler et al. 2008b, Corbisiero et al. 2013, Van Stgralen 2016). Conceptions of ADHD represented by the Brown Adult ADHD rating scale (Brown 1996) and Conners’ Adult ADHD rating scale (Conners et al. 1999) also include emotional symptoms. The proposals suggested by these three authors for conceptualizing the ED in ADHD are partly
19 different but partly overlap and share many emotional symptoms that are considered in this case, nuclear, along with the other most well-known aspects of the disorder.
Barkley (1997a) proposed that ED traits should be considered a core feature of ADHD rather than associated symptoms. This would be consistent with conceptualizations of ADHD as a disorder of self-regulation of affect, as well as of attention, motivation, and arousal (Nigg 2005, Surman et al. 2013).
The significance of the conceptualization of ED as a part of the symptomatology of ADHD is justified from different perspectives: clinical, theoretical, and empirical: clinical because patients’ statements time and again suggest that the classic triad of ADHD symptoms, inattention, hyperactivity, and impulsivity, is not sufficient to adequately describe the psychopathological facets and functional impairment of patients suffering from adult ADHD combined type. These patients consistently report on mood swings, which significantly change more rapidly than in affective disorders; that is, they may be saddened for the day, or there may be several mood swings a day, from elated to death. Patients have many problems to deal with in stressful situations and are frequently and quickly irritated by little things in everyday life (e.g. to get angry fast). This is consistent with the theoretical findings: it could be shown that there is an association of the classical ADHD symptoms not only with cognitive deficits and neuroanatomical substrates, but also with mood variability (Skirrow et al. 2009). Of particular importance is, moreover, the mounting empirical evidence for the significance of symptoms of ED (Corbisiero et al. 2013). Furthermore, the premorbid temperamental characteristics, such as being fussy, angry, irritable, uncooperative or difficult to control, when present in childhood have shown a certain degree of correlation with the subsequent appearance of ADHD with ED.
It has already been suggested by some authors as individuals with ADHD are often characterized by particular symptoms of affective and emotional sphere, especially a negative one (Martel and Nigg 2006, Nigg et al. 2002a, Nigg et al. 2002b) and as such
20 disorder is often associated with the presence of aggressiveness, symptom that, as mentioned above, reflects the size of ED (Dodge et al. 1991, Becker et al. 2006, Sobanski et al. 2010, Shaw et al. 2014).
Most epidemiological research has focused on children and has found a strong association between ADHD and ED, with varying percentages (Sjöwall et al. 2013, Stringaris and Goodman 2009, Sobanski et al. 2010, Anastopoulos et al. 2011, Spencer et al. 2011, Strine et al. 2006, Becker et al. 2006). A population study in 5326 children with ADHD reported a prevalence rate of ED of 38% (Stringaris and Goodman 2009a). Another clinical study in young people with ADHD reported a prevalence of ED between 24 and 50% (Stringaris and Goodman 2009b, Goldsmith et al. 2004, Bates et al. 1998, Carlson et al. 1995, Olson et al. 2002).
Also in adults with ADHD prevalence rates of ED is high, varying from 34 to 70% (Able et al. 1997, Barkley and Fischer 2010, Reimherr et al. 2005, Reimherr et al. 2007, Surman et al. 2013). In several number of empirical studies it has been shown a definite link between ADHD and ED (Surman et al. 2011, Surman et al. 2013, Vidal et al. 2014).
Barkley et al. (2008) reported on the prevalence of such traits (ED) in adults with ADHD presenting to an ADHD clinic. They found that impatience, being quick to anger, being easily frustrated, overreacting emotionally, and being easily excited by nearby activities were each endorsed by over 60 % of adults with ADHD and less than 15 % of control subjects.
It was also seen as the presence of ED is more common in those with persistent ADHD than in those in which there was a remission of symptoms, such as to show a developmental coherence: the improvement of ADHD symptoms is parallel to the improvement of ED (Barkley and Fischer 2010). This information was indirectly confirmed also by two other clinical trial study (Reimherr et al. 2005, Reimherr et al. 2007) in which we observed an improvement in ED after specific therapy for ADHD adding a
21 further step: treatment with specific drugs for ADHD, reducing the symptoms of ADHD and of ED at the same time, in adults (Rösler et al. 2010, Marchant et al. 2011, Reimherr et al. 2005, Reimherr et al. 2007, Kooij et al. 2010) and children (Childress et al. 2013, Lopez et al. 2013), confirming the hypothesis that the ED is a constitutive symptom of ADHD.
To note also that among the mental disorders described in the DSM about half are characterized by ED (APA 1994, Barlow 2000, Kring and Sloan 2010, Kring and Werner 2004, Werner and Gross 2010). Particularly associated are mood and anxiety disorders (Cole et al. 1994) and especially BD and cluster B personality disorders (Dadomo et al. 2016). Indeed, affective disturbances are thought to be important features of psychopathology some diagnostic disorders are defined primarily in terms of disturbed emotions (Mineka and Sutton 1992), and a failure “to regulate intense, negative, and shifting emotional states” (Bradley et al. 2011). ED has been closely tied to psychopathology and it is often an indicator of that. (John and Gross 2004). It is clear, thus, that the regulation of emotions is an essential component to mental health (Gross & Muñoz 1995). Given that, ADHD shows a high comorbidity with other psychiatric disorders, some authors argue that the ED would not be a direct consequence of ADHD but would result from the presence of comorbid disorders (Surman et al. 2013).
For these reasons, some of them believe that the ED, showing low specificity, can not be considered as a specific symptom of ADHD, but instead represent a cross feature found in different psychiatric disorders (Sonuga-Barke 2003, Skirrow et al. 2009). In fact some studies have shown that the presence of ED in those with ADHD is independent of comorbidity with other mental disorders (Vidal et al. 2014, Reimherr et al. 2005), while instead it is seeming that the presence of comorbidity correlates with a higher severity of the ED both in adults and in children (Sobanski et al. 2010). In any case, ED, showing high sensitivity to discriminate among subjects with ADHD, suggests that in a patient in which
22 this dimension is detected, is always advisable to carry out a diagnostic screening for ADHD (Skirrow et al. 2009, Philipsen 2006).
Alterations in multiple brain networks and neuropsychological impairments have been implicated in the aetiology of ADHD. While these neuropsychological alterations and the related brain dysfunctions are not specific to ADHD (Banaschewski et al. 2005), they might nevertheless explain the frequent co-occurrence of ADHD and ED symptoms.
Among the most important and studied cerebral networks we find those involved in the process "Bottom-Up" and "Top-Down" (Ochsner and Gross 2005, Philips et al. 2008). For example, it was seen as in subjects with ADHD there is a deficit of early attribution of salience to emotional stimuli with excessive perception of negative emotional stimuli (Du et al. 2006, Williams et al. 2008) and the tendency to prefer immediate smaller rewards, as the distinctive trait of impulsivity and that reflects a refusal to refer these patients for the reward (Sonuga-Barke et al. 2003, Sagvolden et al. 2005). Another important aspect is the top adjustment ability on the modifications induced by emotional stimuli on the autonomic nervous system (considered as a detector of the valence of emotional stimuli) (Musser et al. 2013) and the capacity, always mediated by the superior control (top-down) to maintain or divert attention to one emotional stimulation so as to control the emotion aroused or achieve a goal (Gross 1998).
In studies on the amygdala of subjects with ADHD it was found a tendency of hiperattivation in the processing of visual emotional stimuli (facial expression) (Marsh et al. 2008, Brotman et al. 2010, Posner et al. 2011, Schlochtermeier et al. 2011) and in the processing of delayed rewards (Scheres et al. 2007, Ströhle et al. 2008, Stoy et al. 2011). Other studies of ADHD patients have found abnormalities in the morphology of the orbitofrontal cortex and during the attivation mechanisms of the rewards control, as well as a reduction of connectivity between the orbitofrontal cortex and amygdala. Finally functional neuroimaging studies find reduced ventral striatum responsiveness in ADHD
23 during the anticipation (and receipt) of rewards, thus contributing to aversion to delay (Shaw et al. 2014).
So, in view of these neuropsychological acquisitions we can assume that ED in ADHD patients can result from increased bottom-up emotional reactivity and/or reduced top-down emotional regulation skills, implicating possible dysfunctions of various subcortical (e.g. amygdala, hippocampus, and ventral striatum) and/or cortical brain regions or an altered connectivity between those regions (Meyer-Lindenberg et al. 2006, Banaschewski et al. 2012). Evidence suggests dysfunction in a network encompassing the amygdala, ventral striatum, and orbitofrontal cortex that processes emotional stimuli and is implicated in emotion regulation (Shaw et al. 2014).
According to the model proposed by Barkley (1997a,1997b) the primary deficit in inhibition control presented in ADHD patients when faced with emotionally charged situations, as well as being responsible for the deficits in executive functions (Barkley 2010) may also be responsible for a greater ED, than in general population (Van Stralen 2016). A large study with children ADHD saw that, despite many neuropsychological functions were related to ED (Banaschewski et al. 2012), this relationship was mediated mainly by the degree of severity of ADHD symptoms. Thus, is true that the ED in individuals with ADHD is linked to the typical neuropsychological alterations, even if it’s not enough to explain the association with ADHD. Recently, it shows that ED symptoms are not a mere epiphenomenon of ADHD symptoms severity and can only partially be explained by the level of psychiatric comorbidity (Sobanski, et al. 2010). However, the frequent occurrence of ED in patients with ADHD might arise from risk factors or pathophysiological components that influence both ADHD and ED symptoms.
Recent work suggests that the prefrontal cortex, particularly the anterior cingulate (with dopaminergic and serotoninergic neurotransmission involvement), likely functions to integrate emotion and cognitive control processes (Holroyd & Coles 2002). In this way,
24 emotion and regulation (or cognitive control) appear to have some ‘crosstalk’ and may be able to work together to achieve some goals, such as evaluation of information and execution of action (Bell and Wolfe 2004, Martel 2009).
The exact balance of symptoms between ADHD and ED in an individual may depend on the degree to which each neural network or level is compromised. It seems that individuals with ADHD characterized by a functional deficit of cortical regions, predominantly in the lateral prefrontal/parietal cortical regions, have more inattentive than emotional symptoms. While indeed, subjects in which the deficit is greater in paralimbic areas, it seems to predominate the emotional dysregulation symptoms and with an ADHD symptomatology closer to the hyperactive-impulsive subtype (Shaw et al. 2014). Indeed, the symptoms of hyperactivity-impulsivity are considered the greatest predictors of ED (Van Stralen 2016). It has also been suggested that the association between ADHD and ED constitutes a specific subgroup of patients marked by particular genetic features. Robinson et al (2010) found a high frequency of association of a single nucleotide polymorphism (SNP) with the presence of ED in ADHD patients. In another study it was seen that siblings of probands with both ADHD and ED also had significantly elevated rates of this combination (Surman et al. 2011). These results suggest that ED could be present in a familial subtype of ADHD.
Additionally, symptoms of ED in adults ADHD seem to compromise the severity of the ADHD symptomatology as well as its comorbid disorders (e.g. sleeping problems, somatic complaints, anxiety-tension, oppositional-defiant symptoms) and impairments in important domains of major life activities (Reimherr et al. 2005, Reimherr et al. 2007, Reimherr et al. 2010, Robison et al. 2008). Gender differences were examined: Women with ADHD seem furthermore to have a higher level of emotional symptoms. These symptoms would complicate the ADHD symptomatology and may, particularly in women, obscure the diagnosis of ADHD (Robison et al. 2008). Barkley and Murphy argue that ED
25 makes significant contributions to impairment in numerous forms of major life activities including social and occupational functioning, educational history, driving risk, criminal history, marital satisfaction, parenting stress, and severity of offspring disruptive behaviour disorders. Even more, symptoms of emotional dysregulation contribute to impairments in major life activities beyond those associated with the traditional dimensions (inattention, hyperactivity, and impulsivity) of ADHD symptoms (Barkley and Fischer 2010, Barkley and Murphy 2010).
In summary, it is possible to identify three hypothetical models that might be useful to explain the association between ADHD and ED, even though, with the current evidence, it’s impossible definitively choose:
The first model, which harks back to earlier conceptualizations of ADHD, posits that ED is a core defining feature of ADHD that is as central to the disorder as hyperactivity, impulsivity, and inattention (Barkley and Murphy 2010). This is the model in which is sustained the association between emotional and cognitive regulation systems. But, it also true that there are many studies in which ADHD subjects show no impairment of emotional regulation.
The second model holds that the combination of ADHD and ED defines a distinct entity (Surman et al. 2011, Biederman et al. 2012) and it is based on the evidence of a shared genetical basis (Sobanski et al. 2010, Surman et al. 2011).
The third model holds that symptoms of ADHD and ED are distinct but correlated dimensions, each underpinned by partly overlapping but dissociable neurocognitive deficits.
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2. Aim of the study
The main purpose of the present investigation is to explore the possible relationships between emotional dysregulation and mood episodes, illness course, and associated clinical and temperamental features in an adult ADHD sample grouped on the basis of the low/high emotional dysregulation (L/H-ED). We evaluated the severity and the characteristics of ED by means of the RIPoSt scale, a specific questionnaire exploring different dimension of emotional regulation such as intensity, reactivity, polarity and stability. To our knowledge, this is the first study on a sample of adult ADHD patients that evaluate the presence of emotional dysregulation using the RIPoSt questionnaire.
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3. Materials and Method
3.1 Sample
This study involved 40 patients recruited in the outpatient settings of the Psychiatry Unit, Department of Clinical and Experimental Medicine, University of Pisa, over a period of about 1 year. The sample included 13 female (32.5%) and 27 male subjects (67.5%) meeting DIVA 2.0 criteria for Attention Deficit/Hyperactivity Disorder (ADHD). Patients were divided into two groups: the first group including patients with high emotional dysregulation (High-ED) and the second group including patients with low emotional dysregulation (Low-ED), using the RIPoSt questionnaire. Inclusion criteria were age 18-65 years and ADHD diagnosed in adulthood. All the subjects participating to the study signed the informed consent format.
3.2 Data Collection
All the patients included in the study have undergone an assessment session performed by residents of the Specialization School of Psychiatry, supervised by expert psychiatrists of the research group which provided the first diagnostic overview of the patients and the subsequent evaluation for specific comorbidities. The diagnoses of ADHD were confirmed using a specific diagnostic instruments, the DIVA 2.0. The SCID-I was used for the assessment of all other psychiatric diagnosis, according to DSM-IV, and with the SCID II module for BPD. The RIPoSt questionnaire (Hantouche, CTAH, 2010) was utilized for the emotional features, to distinguish the patients into two groups: low emotional dysregulation (low score) and high emotional dysregulation (high score). The SIMD-R was used to collect the participants' demographic and retrospective clinical data of patients with mood disorders. Further assessing instruments included the brief TEMPS-M, for the evaluation of affective temperaments, the BIS-11 used to measure the degree of impulsivity of patients, the ASRS-v 1.1 for a self-evaluation of presence and severity of
28 ADHD, the GAF and FAST scales for the evaluation of current severity of the illness and impact of symptoms on functioning.
3.3 Assessing Instruments
Diagnostic Interview for ADHD in adults (DIVA 2.0) (Kooij and Francken 2010): The DIVA, developed by an European group, has been translated into multiple languages by members of the European Network Adult ADHD. DIVA 2.0 is available free of charge at www.divacenter.eu (Kooij and Francken 2010). DIVA 2.0 is a semi-structured interview based on DSM criteria for ADHD. The first part of the DIVA is dedicated to explore ADHD symptoms and is divided in two sets of questions: the first for the inattentive domain, the second for the hyperactivity/impulsivity domain. Each set provides nine questions (one for each DSM criterion) and for each question two sections, one for the symptom during the adulthood and one for the childhood. Each section is enriched by several examples which can help investigating the presence or absence of the symptom. The second part of the evaluation provides the investigation of the age at onset and the areas of impairment. DIVA is largely based on the judgment of the clinician: it should be performed by a trained evaluator.
Structured Clinical Interview for DSM-IV Axis I and II Disorders (SCID-I and II) (First et al. 1995, First and Gibbon 1997): The SCID is a semi-structured interview projected for the evaluation of psychiatric patients according to DSM-IV criteria. SCID I can be used for the diagnosis of the majority of Axis I psychiatric disorders (First et al., 1995) and SCID II is used for the diagnosis of Personality Disorders (First and Gibbon, 1997). The SCID is constituted by different modules, each of them including specific questions addressed to the detection of diagnostic categories criteria. Each module is independent and it could be used separately in specific researches. The majority of the interview is under the clinical judgment of researcher who has the assignment of
29 extrapolate the evaluation from both the patient’s answers and other sources: this implies that SCID should be better performed by trained interviewers (Cassano, 2006).
Reactivity Intensity Polarity Stability Questionnaire (RIPoSt) (Hantouche Elie, 2010): the RIPoSt is a 60-items self-administered questionnaire exploring the emotional dimension in its various components. The scale is composed of 4 subscales: reactivity, intensity (the usual force), polarity and stability of emotions, each of whom characterized by 15 items. It can be a useful tool for measuring the emotional features and providing an assessment of the degree of emotional dysregulation.
Semi-structured Interview for Mood Disorders (SIMD-R) (Cassano et al. 1989): the SIMD-R is a semi-structured diagnostic interview for assessment of mood disorders. It systematically collects information on different familiar, demographics, medical history and clinical aspects. This interview has been developed to gather systematic information on family history, previous episode number and polarity, suicide attempts (current and lifetime), and psychotic symptoms of any polarity. Thanks to this tool it was also possible checking the main affective diagnosis and the type of mood episode currently in progress. Whenever possible, collateral clinical data, including information obtained from other informants as well as any available past medical records, were used to support patient information, and in particular, to corroborate the onset age and polarity of the participants' first illness episode.
Temperament Evaluation of Menphis, Pisa, Paris and San Diego-M (Munster translation by Erfurth) (briefTEMPS-M) (Erfurth et al. 2005): it is a 35-items self-administered questionnaire exploring affective and anxious temperaments. Each question provides for a 5-point Likert scale (from absent to very much). The patient is asked to specify for each question the value better describing his/her feelings during the majority of the life. Five temperaments are explored: depressive, cyclothymic, hyperthymic, irritable and anxious.
30 Barratt Impulsiveness Scale (BIS-11) (Patton et al. 1995): the BIS-11 is self-report questionnaire designed to assess the personality/behavioral construct of impulsiveness. It is the most widely cited instrument for the assessment of impulsiveness. The current version of the scale is composed of 30 items describing common impulsive or non-impulsive (for reverse scored items) behaviors and preferences. The items are scored to yield six first-order factors (attention, motor, self-control, cognitive complexity, perseverance, and cognitive instability impulsiveness) and three second-order factors (attentional, motor, and non-planning impulsiveness).
Adult Self-Report Scale (ASRS-v 1.1) (Kessler et al. 2005): it is a self-reported questionnaire used to assist in the diagnosis of adult ADHD and a valid and useful tool for the screening of adult ADHD. The ASRS has eighteen questions, which are consistent with the DSM-IVcriteria and address ADHD symptoms in adults. The first six of the eighteen questions were found to be the most predictive of symptoms consistent with ADHD. These six questions are the basis for the ASRS v1.1 Screener and are also Part A of the Symptom Checklist. Part B of the Symptom Checklist contains the remaining twelve questions.
Global Assessment of Functioning (GAF) (Hall 1995): it is a Likert scale, presented in DSM-IV as the Axis V beyond the multi-axial system. It allows the evaluation of the global functioning (psychological, social and occupational) of the person. It provides a score ranging from 0 to 100, proportional to the adjustment of the patient.
Functioning Assessment Short Test (FAST) (Rosa et al. 2007): it is an interviewer-administered instrument which is designed to be used by a trained clinician, developed for the clinical evaluation of functional impairment presented by patients suffering from mental disorders including bipolar disorder. It is a simple instrument, easy to apply and that requires a very short time to be administered. There are 24 divided among 6 specific areas of functioning: autonomy, occupational functioning, cognitive functioning, financial issues, interpersonal relationships and leisure time. All of items are rated using a
31 4-point scale, 0 = no difficulty, 1 = mild difficulty, 2 = moderate difficulty and 3 = severe difficulty. The global score is obtained when the scores of each item are added up. The higher the score, the more serious the difficulties are, so FAST is actually measuring disability.
3.4 Statistical Analysis
Multivariate linear regression models were used to identify the predictive value of the diagnostic, temperamental and functional variables. For comparison between the two groups, we used chi-square test for categorical variables and Student’s t-test for continuous variables. The analysis involved many tests of statistical significance, raising the potential of type I and type II errors. Given the sample size and the number of comparisons, we commented as significant differences with a p < .05. We used the statistical routines of SPSS 20 for Windows.
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4. Results
The study population included 40 patients suffering for ADHD; 13 were female (32.5%) and 27 males (67.5%), with a mean age of 32.4 years (sd 12.6); 27 (67.5%) patients have never been married, 11 (27.5%) patients were married or lived with a partner; 2 patients (5%) were divorced. Regarding the educational level, the majority of patients had a tertiary (50%) school degree. The educational level distribution of the rest of the sample was the following: 16 (40%) patients had a secondary school degree and 4 (10%) were graduated. Regarding the occupational status, 12 patients were students (30%), 8 patients were unemployed (20%) and 20 patients were employed (50%).
We compared two subgroups of patients with ADHD: the first group with low emotional dysregulation (L-ED) and the second group with high emotional dysregulation (H-ED), evaluated on the basis of the RIPoSt questionnaire mean score.
Results are showed in Table 1, Table 2, Table 3, Table 4, Table 5, Table 6, Table 7, Table 8, Table 9 and Table 10.
Multivariate linear regression analysis forward procedure of diagnostic, temperamental and functional variables on RIPoSt Total scale (R-Tot) in 40 adult ADHD patients. A multivariate linear regression analysis was run including the R-Tot scale as the dependent variable and the diagnostic, temperamental and functional features as the independent variables (bipolar I disorder, bipolar II disorder, cyclothymic disorder, borderline personality disorder, dysthymic temperament, cyclothymic temperament, hyperthymic temperament, irritable temperament anxious temperament, age of the patients, GAF scale, FAST total, FAST Autonomy subscale, FAST Occupational Subscale, FAST Cognitive subscale, FAST Financial subscale, FAST Interpersonal subscale, FAST Leisure subscale, ASRS total, BIS total, BIS Attentional subscale, BIS Motor subscale, BIS NonPlanning subscale). The analysis revealed that the variables mostly associated with the R-Tot scale, in order of statistical significance, were Chyclothymic Temperament
