\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
Note: Edited in March 2021
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 191 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 261 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
Note: Edited in March 2021
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There are many publications on wound healing, but this book intends to give an overview of its current perspectives so as to be useful to practice care in wound healing and to improve the quality of life. It is considered that this book will be useful for clinicians who are interested in wound care.",isbn:"978-1-78985-538-8",printIsbn:"978-1-78985-537-1",pdfIsbn:"978-1-83880-645-3",doi:"10.5772/intechopen.73808",price:119,priceEur:129,priceUsd:155,slug:"wound-healing-current-perspectives",numberOfPages:260,isOpenForSubmission:!1,hash:"fa7b870ad29ce1dfcf6faeafdc060309",bookSignature:"Kamil Hakan Dogan",publishedDate:"May 10th 2019",coverURL:"https://cdn.intechopen.com/books/images_new/7046.jpg",keywords:null,numberOfDownloads:12662,numberOfWosCitations:6,numberOfCrossrefCitations:11,numberOfDimensionsCitations:28,numberOfTotalCitations:45,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"March 22nd 2018",dateEndSecondStepPublish:"May 16th 2018",dateEndThirdStepPublish:"July 15th 2018",dateEndFourthStepPublish:"October 3rd 2018",dateEndFifthStepPublish:"December 2nd 2018",remainingDaysToSecondStep:"3 years",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:"Edited by",kuFlag:!1,biosketch:null,coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"30612",title:"Prof.",name:"Kamil Hakan",middleName:null,surname:"Dogan",slug:"kamil-hakan-dogan",fullName:"Kamil Hakan Dogan",profilePictureURL:"https://mts.intechopen.com/storage/users/30612/images/system/30612.jpg",biography:"Kamil Hakan Dogan MD, PhD is a Full Professor and Chair in the Department of Forensic Medicine at Selcuk University, Faculty of Medicine in Turkey. Dr. Dogan received his MD from Gazi University, Faculty of Medicine in 2000. After his extensive research in the forensic medicine field, he received his PhD in Biochemistry in 2012. He gives lectures on Forensic Medicine and Medical Ethics to medical students as well as students of the dentistry and law faculties. He is a reviewer for several international journals and he has published over 200 articles in refereed journals, chapters in textbooks and abstracts in scientific meetings. 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A.",surname:"Barku",slug:"victor-y.-a.-barku",fullName:"Victor Y. A. 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Those with this movement disorder exhibit tremors, bradykinesia (hypokinesia), rigidity, balance and posture impairment, loss of automatic movements, and speech difficulties. PD affects millions across the world; the European Parkinson’s Disease Association states that 6.3 million people have the neurodegenerative disorder globally [2]. Those who suffer with PD are without a cure and must resort to methods of PD treatment for relief. Currently, the “gold standard” treatment for PD is the use of levodopa (l-DOPA). A precursor to dopamine, l-DOPA is a small enough molecule to pass the blood-brain barrier and enter the basal ganglia where it is acted upon by DOPA decarboxylase to create an increase in dopamine levels. As DA neurons degenerate, an influx of dopamine from exogenous l-DOPA reverses the negative effects of PD [3]. In conjunction with l-DOPA, monoamine oxidase inhibitors (MAOI) are used to also increase dopamine levels as a co-treatment by inhibiting the DA-degrading enzyme monoamine oxidase. Thus, inhibiting monoamine oxidase in conjunction with l-DOPA treatment creates higher levels of DA in PD patients to help alleviate their symptoms. However, patients who experience long-term l-DOPA and MAOI treatment may develop unwanted side effects such as hyperkinesia, an increase in muscular activity that may be excessive or abnormal [4].
\nPrevious studies have suggested that estrogen (E2) has neuroprotective effects in DA neurons and can regulate the synthesis of DA as a pro-dopaminergic agent [5]. In addition, studies show that DA neurons of the central nervous system have E2 receptors and the presence of the E2 synthesis enzyme aromatase [5]. It is clear that there is a connection between E2, the central nervous system, and movement disorders like PD. Indeed, premenopausal women are less likely to show PD symptoms with a majority of patients being male and over 60 [6]. Thus, there appears to be a sexual dimorphism between males and females when it comes to PD prevalence [6]. As a result of the hormonal differences, E2 is considered a neuroprotectant molecule, but there is no evidence for a similar role for testosterone [6]. Recently, this effect has been examined in female rats which have been treated with the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxin and have shown the ability to resist muscular activity loss compared to males [6]. In addition to being neuroprotective, there is also accumulating evidence that E2 may also cause detrimental effects such as hyperkinetic/chorea/dystonia symptoms in females on postmenopausal replacement therapy after hysterectomy [5]. There is also the recent case of a patient suffering from adult-onset Sydenham’s chorea who discontinued E2 replacement therapy and months later these hyperkinetic/chorea symptoms were significantly diminished [7].
\nPart of the mechanism by which E2 may exert its influence in the nigrostrital (BG) of PD patients is through its documented influence on nitric oxide (NO) levels through its regulation of the expression of nitric oxide synthase (NOS) [8]. NO, a gas released by the actions of the NOS enzyme on l-arginine, acts as a signaling molecule with direct actions on existing metabolic pathways, as well as through genomic mechanisms [9, 10]. As a gas, NO can diffuse across cellular membranes without the aid of membrane-bound transport proteins or receptors. NO can interact directly with its end targets either in the cell in which it was synthesized or in surrounding cells. In turn, its actions are precisely controlled due to its very short half-life and restricted diffusion distance [11, 12]. At higher concentrations NO can act as a free radical in some situations or binds to superoxide anion (O2−), causing pathophysiological oxidative stress effects [13]. It is under these conditions that NO is thought to play a role in the genesis of such neurological diseases as PD [4]. On the other hand, NO at lower concentrations can act as a cellular protectant through prevention of apoptosis, excitotoxicity, neuronal depolarization, and regulation of the redox state in the mitochondria [14, 15]. In particular, NO has been implicated in the neuromodulation/neuroprotection of DA neurons in the nigrostrital (BG) pathway associated with either animal models of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or 6-hydroxydopamine (6OHDA) neurotoxicity that create PD-like symptoms or from PD patient clinical data. NO acting at the cellular level interacts with either its soluble guanylyl cyclase (sGC) receptor molecule to produce cyclic GMP (cGMP) which activates a cascade of cellular enzymes or causes
Zebrafish (
It is the hypothesis of this study that when embryonic zebrafish are treated with either E2 or l-DOPA/MAOI that a de novo-induced hyperkinetic movement disorder phenotype will be generated. In conclusion, these results establish a rapid turnover zebrafish model for the study of the role of NO-E2-related DA actions in normal and hyperkinetic movement phenotypes.
\nThe compound
All E2-related reagents for treating zebrafish have been previously tested in a dose-response paradigm to insure optimal results and proper survival [26]. Based on previous studies, E2 (17β-estradiol, Sigma) used at 1 and 5 μM, and initially solubilized in a 100% ethanol stock solution diluted down to the base treatment solution with ERS, ensuring that the ethanol concentration in the final solution was equal to or lower than 0.5%. The control group consisted of ERS salt solution plus 0.5% ethanol. The reagent 4-androstene-3,17-dione (4-OH-A, MW-286.4, Sigma) was used as an aromatase inhibitor (AI) to block the production of E2 from androgens [24, 25, 28]. It was used at 50 μM and made from a 100% ethanol stock solution diluted down to the base treatment solution with ERS, ensuring that the ethanol concentration in the final solution was equal to or lower than 0.5%.
\nAll NO-related reagents for treating zebrafish have been previously tested in a dose-response paradigm to insure optimal results and proper survival. Based on literature review, baseline target concentrations were identified. Proadifen hydrochloride (Sigma) was used as a selective nNOS inhibitor (nNOSI). With ERS as the diluent, fish were tested at 10, 30, and 50 μM. The 50 μM concentration provided optimal results in its ability to create the hypokinetic (listless) condition, and this dose was used throughout the current study.
\nDiethylenetriamine/nitric oxide adduct (DETA-NO, Sigma) was used to provide a slow extended release of exogenous NO as a co-treatment with some of the inhibitors used in the experiments in an effort to show that NO inhibition-mediated symptoms exhibited by fish can be rescued. It was dissolved into ERS resulting in working concentrations of 400–50 μM with 50 μM providing the best results.
\n1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, Sigma) was used as a soluble guanylyl cyclase (sGC) inhibitor which compromises the NO-cGMP-dependent pathway by reducing cGMP production. It was dissolved into a 0.1% DMSO solution and then diluted with ERS to a working concentration of 30 μM for application. In addition, DTT (dithiothreitol, Sigma) was used as an inhibitor of the NO-cGMP-independent pathway which prevents S-nitrosylation events at a concentration of 100 μM.
\nThe l-DOPA DA precursor l-DOPA ethyl ester (l-3, 4-dihydroxyphenylalanine methyl ester, Sigma) are used at concentrations up to 10 mM, which is the limit of its solubility in the ERS control solution. l-DOPA is acted upon by DOPA decarboxylase to be converted into DA. It was used to elevate the neurotransmitter in deficient fish starting at ranges prescribed previously for zebrafish embryos [29, 30]. The optimal dose was 10 mM and used throughout the current study.
\nMonoamine oxidase inhibitor (MAOI) is an agent used to manipulate the zebrafish DA neurons by preventing DA degradation at the synapse. The MAOI, l-deprenyl (Sigma), was used at a concentration of 50 μM to elicit hyperdyskinetic behavior in a co-treatment paradigm with l-DOPA.
\nA DA receptor antagonist (haloperidol, Sigma) was used at a concentration of 1–50 μM as prescribed for zebrafish embryos [31] and 1 μM was found to be optimal.
\nFish at 5 dpf were co-treated with l-DOPA + MAOI for up to 48 h or E2 alone for 3–6 h to induce a hyperkinetic state. Using this protocol, additional experiments were also designed to determine whether either l-DOPA or MAOI alone could cause the hyperkinetic phenotype. Specifically, fish were treated with either l-DOPA, MAOI, or a l-DOPA + MAOI co-treatment along with the ERS controls. Next, studies were designed to determine if the hyperkinetic phenotype could be modified changing NO levels in the l-DOPA + MAOI-treated fish. Specifically, the co-treatment (l-DOPA + MAOI) was compared to the l-DOPA + MAOI + nNOSI tri-treatments along with their respective controls. Next, experiments were designed to test recovery of 5 dpf fish after a 40-h treatment with l-DOPA + MAOI which was followed by either ERS, nNOSI, or DETA-NO post-treatment washouts. The third set of experiments looked at the role of E2 in the generation of the hyperkinetic state. Specifically, fish were treated with either E2, at various concentrations, l-DOPA + MAOI, and l-DOPA + MAOI + AI. Similar co-treatment studies were carried out with E2 according to the following protocols: E2 + haloperidol and E2 + nNOSI.
\nFor visual analysis, fish were characterized using a dissecting microscope, as expressing the hyperkinetic dyskinesia phenotype when their swimming behaviors became significantly different from ERS controls. Specifically, the ‘hyperkinetic dyskinesia’ phenotype was identified as showing rapid, erratic, and brief spurts of swimming movements and was either calculated as a percent of the treated group or by video capture analysis using a Nikon SMZ1500 microscope to measure the number of spontaneously initiated swimming movements per minute. Also, fish were timed (seconds) as to the duration of their startle/escape response to being touched by a probe on the tail region. The percent survival under the various experimental conditions was also determined for both the hyperkinetic treatment conditions.
\nData were analyzed for significant differences either by a z-test for two-population proportions or for multiple proportions using chi-square contingency table test, followed by a Marascuilo’s post-hoc analysis. In addition, for timed video capture movements and startle/escape responses, statistical analysis by using either a two-tailed
Figure 1A shows the percentage of zebrafish that demonstrated a hyperkinetic phenotype when co-treated with l-DOPA + MAOI over 40 h of treatment compared with ERS controls. These data show that a significant portion of a population exhibited hyperkinesia after 24 h (55%) in the co-treatment and rises to 90% after 40 h (
The effects of an
Figure 1B demonstrates that co-treated fish remain stable for the duration of the treatment paradigm with no significant deaths when compared to ERS controls (
Figure 2 shows photomicrographs from video capture of zebrafish fin movements under various treatment conditions. Note that control fish exhibited synchronous and symmetrical adduction (Figure 2A) and abduction (Figure 2B) of fin positions during movement or at rest. In contrast, the l-DOPA + MAOI co-treated fish show asymmetric and asynchronous adduction and abduction in their pectoral movements (Figure 2C). Behaviorally, these fish exhibit a lack of control of swimming movements and chorea/catatonic excitement-like symptoms.
\nVideo capture photomicrographs of 5 dpf fish fin movements 40 h post-treatment. (A and B) Pictures represent ERS control zebrafish pectoral fin synchronous movements in the adduction (A) and abduction (B) states (arrows). (C) Asymmetric pectoral fin movements in response to
Figure 3 shows the frequency of initiated movements among ERS control, l-DOPA, MAOI, and co-treatment (l-DOPA + MAOI) fish. This experiment tested which of the two DA-related reagents in the co-treatment was more responsible for generating the hyperkinetic phenotype. These data show that MAOI is the primary facilitator of de novo hyperkinesia in the co-treatment when compared to l-DOPA (
The number of spontaneous movements that 5 dpf zebrafish initiated over a 1-min duration after 40 h under various treatment conditions. Note that ERS controls initiated movements at approximately 41 times/min,
Figure 4 shows the effect of nNOSI on the l-DOPA + MAOI-induced hyperkinetic phenotype. During the first 48 h of treatment, ERS controls showed no hyperkinesia; however, l-DOPA + MAOI co-treatment demonstrated 94% hyperkinesia. Note that Figure 4A shows that the l-DOPA + MAOI + nNOSI tri-treatment significantly reduced the co-treatment-induced hyperkinesia after 48 h of treatment (43% vs. 94%, respectively,
The effect of nNOSI on the
Figure 5 depicts experiments testing recovery of 5 dpf fish after a 40 hours treatment with l-DOPA + MAOI to induce the hyperkinetic phenotype. Data were collected after a 24 hours post-treatment washout with either ERS or nNOSI. Figure 5A shows that fish treated continually with ERS demonstrates normal (non-hyperkinetic) swimming behaviors and the fish that were not washed out with ERS (just kept in the co-treatment) had a 0% recovery rate. However, the fish that were washed out with ERS solution after the initial co-treatment had approximately an 80% recovery back to normal swimming patterns. Figure 5B shows that post-treatment washout with nNOSI post-treatment (less than 20%) washouts showed significantly less recovery (
Demonstration of the percentages of 5 dpf fish that recovered after 24 hours of post-treatment (washout) with various treatments from the hyperkinetic state initially induced by the co-treatment of
Figure 6 shows what happens to swimming durations when at 5 dpf, zebrafish were treated with different concentrations of E2. At 6 h post-treatment, fish were lightly touched with a probe and their escape response timed (s—seconds) until they stopped. When the ERS control fish were stimulated they swam for 0.5 ± 0.3 s. Fish treated with 1 μM E2, responded by swimming 1.2 ± 0.5 s, which was not significantly (
Zebrafish at 5 dpf are treated with different concentrations of E2 and at 6 h post-treatment, fish were lightly touched with a probe and their escape response timed (s—seconds) until they stopped swimming. Note that a 5 μM E2 concentration caused a significant increase in hyperkinetic swimming activity when compared to a 1 μM E2 dose (*
When exposed to various treatments with the reagents AI, and l-DOPA + MAOI or l-DOPA + MAOI + AI, 5 dpf fish exhibited several different swimming phenotypes (Figure 7). Specifically, fish treated with AI were 67% listlessness, a significantly higher proportion (
Effects of AI treatment on
Figure 8A shows the effect of HA on E2-induced hyperkinesia. Specifically, the addition of HA to E2 in a co-treatment paradigm (E2 + HA) significantly reduced (
The effect of HA and nNOSI on E2-induced hyperkinesia. (A) Note that the addition of HA to E2 as a co-treatment significantly reduced (*
The goal of this study was to explore the hypothesis that the co-treatment of l-DOPA + MAOI, and E2 by itself will produce a zebrafish model of de novo hyperkinesia which are both dependent on the NO pathway for its expression. Also, the current study explored the possibility of using nNOSI as a modulating agent to reduce the de novo hyperkinetic dyskinesia phenotype in the zebrafish.
\nData from the current study shows that 5 dpf zebrafish exhibited hyperkinesia as early as 24 h after treatment with an l-DOPA + MAOI co-treatment. Specifically, the hyperkinetic fish demonstrated spontaneous swift, erratic, and chorea/catatonic excitement-like movements, as well as, a significant increase in the number of spontaneous movements when compared to controls. This is the first report of de novo l-DOPA + MAOI-induced hyperkinesia in embryonic zebrafish. However, l-DOPA has been shown in older zebrafish larvae to facilitate recovery of swimming speed after treatment with the antipsychotic fluphenazine [29]. In addition, data from the current study also show that MAOI is the primary facilitator of hyperkinesia in the co-treatment when compared to l-DOPA. Specifically, both MAOI and the l-DOPA + MAOI co-treatment initiated by approximately twofold the number of spontaneous movements than that of either ERS or l-DOPA alone. In an interesting corollary to this finding, it was shown in an earlier study that l-DOPA administered to zebrafish reduced the number of neurons in its nigrostriatal-like pathway which was partially rescued by monoamine oxidase inhibition [32]. This study was focused on the possibility that l-DOPA contains a neurotoxic product that may cause oxidative stress to DA neurons. We saw none of these symptoms in our study perhaps due to the fact that our findings were collected over a matter of 1–2 days duration which was not long enough to see these potential side effects. On the other hand, the fact that monoamine oxidase inhibition increased fish motor activity by a post-treatment paradigm is in support of our findings [32].
\nThe current study also reported that the de novo l-DOPA + MAOI-induced hyperkinetic phenotype is dependent on NO for its initiation and recovery. Specifically, the l-DOPA + MAOI + nNOSI tri-treatment significantly reduced the l-DOPA + MAOI co-treatment-induced hyperkinesia. Similar results in earlier studies have shown that in hemiparkinsonian rats nNOSI improves l-DOPA-induced dyskinesia [4]. The findings are also in line with earlier suggestions of the possibility that nNOSI could be used as a therapeutic agent to reduce the dyskinetic side effects of long-term l-DOPA therapy [33]. In turn, current post-treatment studies demonstrated that NO accelerates recovery from the l-DOPA + MAOI-induced hyperkinetic phenotype when compared to ERS controls. In contrast, nNOSI post-treatment significantly reduced the rate of recovery from the hyperkinetic phenotype. These findings are most likely explained by the documented effects of NO on DA dynamics. Specifically, in the BG, NO has been shown to affect DA release, influence transporter function, and elicit neuroprotection of DA neurons [19].
\nIn the present study, it was also determined that E2 can cause a de novo hyperkinetic phenotype in zebrafish. Specifically, a 3–6 h treatment with E2 elicited a tenfold increase in fish swim duration when compared with that of ERS controls. E2 was also found to significantly affect the l-DOPA + MAOI co-treatment-induced de novo hyperkinetic phenotype. Specifically, the addition of AI to the l-DOPA + MAOI co-treatment significantly reduced the response time of fish exhibiting the hyperkinetic phenotype returning them back to control levels. These data suggest that E2 is linked to the DA system regulating motor activity in the embryonic zebrafish. This finding was further validated in this study by results showing that the DA receptor antagonist, haloperidol (HA), significantly diminished the E2-induced de novo hyperkinetic activity. Specifically, a co-treatment of E2 + HA significantly reduced by fourfold the hyperkinetic phenotype when compared to just an E2 treatment. This evidence leads to the conclusion that the E2-induced hyperkinetic phenotype acts through the DA D1/D2 receptor system. This conclusion is further substantiated by an earlier study that showed that HA significantly reduced the level of larval zebrafish locomotor activity along a similar time line [31]. Furthermore, the effects of E2 on stimulating/regulating DA levels and thus motor activity have been well documented in other animal models. Specifically, it has been shown that E2 influences DA dynamics in the nigrostrital pathway that is crucial for normal motor function and is the site of PD pathology [5]. In this system, similar to NO, E2 affects the synthesis, release and turnover of DA, as well as DA transporter and receptor expression [5]. E2 derivatives have also been shown to cause hyperactivity in animal models. Specifically, the addition of bisphenol A, a xenoestrogen exhibiting E2-mimicking hormone-like properties, was shown to cause hyperactivity in newborn mice, adult male rats, and larval zebrafish [34, 35, 36]. However, the present study reports for the first time a rapid de novo E2-induced hyperkinetic response over just a 3–6 h duration in the embryonic zebrafish. In addition, the current de novo E2-induced hyperkinetic zebrafish model appears to correlate with accumulating evidence that E2 may also cause detrimental effects such as hyperkinetic/chorea/dystonia symptoms in female patients either through postmenopausal replacement therapy or through E2 replacement therapy after hysterectomy [5]. There is also the recent case of a patient suffering from adult-onset Sydenham’s chorea who discontinued E2 replacement therapy and months later these hyperkinetic/chorea symptoms were significantly diminished [7].
\nThe current study was designed to determine whether embryonic zebrafish treated with either E2 or l-DOPA/MAOI would develop a de novo-induced hyperkinetic movement disorder and that they rely on the NO pathway to elicit this hyperkinetic phenotype. Results from this study indicate that 5 dpf fish treated with an l-DOPA + MAOI co-treatment or E2 elicited the development of a de novo hyperkinetic phenotype. In addition, the de novo l-DOPA + MAOI- and E2-induced hyperkinetic phenotypes are dependent on NO and E2 for its initiation and recovery. In conclusion, these findings point to the central role that both NO and E2 play in the facilitation of de novo hyperkinesia. In turn, the actions of both E2 and l-DOPA + MAOI in the induction of the hyperkinetic phenotype is dependent on the NO pathway and acts through the DA system. Most significantly, nNOSI has the capacity in this model to modulate the de novo hyperkinetic phenotype which suggests the possibility that it may be further tested for its therapeutic value in patients suffering from long-term l-DOPA-induced dyskinetic side effects.
\nThis research was supported from grant funding from the Reid ’41 Institute Professorship in the Arts and Sciences (awarded to JET), the VMI Department of Biology, and the VMI Center for Undergraduate Research.
\nThe authors have no conflicts of interest.
Each person has a set of personality traits that are unique and make up one’s personality.
Temperamental characteristics show high stability and are developmentally associated with personality traits during adulthood including extraversion or high energetic level, agreeableness, conscientiousness, neuroticism (emotional stability), and openness [2]. An important personality trait is
Personality disorder (PD) is defined as an enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individual’s culture, is pervasive and inflexible, and leads to distress or impairment [4]. People with PD have disrupted behavior, cognition, and emotions when in contact with other people and society, while the individuals and the people around them suffer [1]. The ICD-10 classifies the following PD: paranoid, schizoid, dissocial, emotionally unstable (impulsive and borderline type), histrionic, anankastic, anxious (avoidant), dependent, and other (e.g., narcissistic) [5]. The DSM-5 divides PD into three clusters. Cluster A personality disorders are characterized by unusual and odd-eccentric behavior and introverted individuals including paranoid, schizoid, and schizotypal PD. Cluster B personality disorders are associated with dramatic, emotional, and erratic behavior: antisocial, borderline, histrionic, and narcissistic PD. Cluster C includes avoidant, dependent, and obsessive-compulsive PD associated with anxious and fearful disorders. The division into three groups is useful for educational and research purposes; however, it also has its limitations. Clinically, there is a lot of overlapping between various PDs. The frequency of individual PD varies from study to study, and even greater differences are present when looking at the frequency of individual PD in a given population. Borderline PD is present in 0.9–3% of the general adolescent population, in 11% of outpatient adolescents, and 49% of admitted adolescents [4].
People diagnosed with PD from one group may also meet the diagnostic criteria of PD from the other, which occurs in about 9% [4]. Individuals from group C and A most commonly have an associated PD (6.0 and 5.7%, respectively), while this occurs only in 1.5% of individuals in the group B [4]. Due to PD overlapping and for other reasons as well, the PD criteria in ICD-11, which will come into effect in January 2022, have been modified [6]. ICD-11 follows a dimensional understanding of PD and largely abandons the categorical view. The new division of PD follows the psychodynamic tradition, the scientific model of the core PD characteristics, and thus provides guidance for clinical treatment [7]. It provides an assessment of the severity of the disorder, and enables to diagnose three levels of PD and code subthreshold personality difficulty. ICD-11 specifies five domain qualifiers of personality, which include negative affectivity, detachment, dissociality, disinhibition, and anankastia. In addition to these five markers, a borderline pattern qualifier can also be specified. The latter may be applied if at least five out of nine borderline PD criteria according to DSM-5 are present. An example of a diagnosis of borderline PD following the new features in ICD-11 is for example a moderate PD with borderline pattern, negative affectivity, disinhibition, and dissociality [7].
Borderline PD is one of the most common PDs and these individuals are also more likely to seek medical help and suffer from significantly more associated mental disorders (depression, anxiety disorders, psychoactive substances abuse, and hyperkinetic disorder) compared to the general population [8]. Vulnerability for borderline PD can be clearly recognized during the development period. The concept of borderline personality has evolved throughout history. Morel and Kraepelin used this term to describe the states between neurotic and psychotic conditions primarily based on phenomenological clinical descriptions and by ignoring the developmental and dynamic aspects of pathology [9].
Kernberg linked the classical psychoanalysis, the object relations theories, the psychology of self (immature integrative self-functions) with the psychobiological and neurobiological theories, and defined the concept of borderline personality disorder as a pathological personality organization that is intermediate between psychotic disorders and neuroses—symptomatically, structurally, and genetically-dynamically [10, 11]. This concept was further enhanced by the Linehan’s biosocial model [12].
According to DSM-5, at least five of the following nine criteria must be present to code borderline personality disorder [4].
Frantic efforts to avoid real or imagined abandonment
Unstable and intense relationships
Identity disturbance, seen in an unstable self-image or sense of self
Impulsivity
Suicidal behavior
Affective instability (episodic dysphoria, irritability, anxiety: lasting a few hours to days)
Chronic feelings of emptiness
Displays of inappropriate anger (verbal/physical fights)
Micropsychotic episodes, transient stress-related paranoid ideation/dissociative symptoms
In addition, these patterns are enduring, inflexible, and clinically relevant to diminish social, educational, or professional functioning. The onset of this pattern is traced back at least to adolescence or early adulthood and it is not a manifestation of another mental disorder and is not due to the consumption of psychoactive substances [4].
Quite a few features of borderline PD (impulsivity, emotional instability, dysfunctional interpersonal relationships, impaired self-image, and identity diffusion) may also—to some extent—be characteristics of adolescent period. In order to diagnose a borderline PD in an individual during adolescence, the features must have been present for at least 1 year and cause severe dysfunction [4]. If the adolescent reacts highly destructive, has transient psychotic reactions and behavioral problems, uses psychoactive substances, has emotional disorders associated with the loss of a relationship with the important other or negative emotions, one can suspect a borderline PD [13].
In the clinical picture of borderline PD in adolescents, one often sees anger towards parents, depression without any existential despair, tension, loss of empathy, impulsive behavior, and brief psychotic episodes including a paranoid thoughts and depersonalization without thought disorder [14].
It is a legitimate question whether to diagnose or not to diagnose PD before the age of 18. That is during adolescence – the time of major developmental changes, when the personality is not yet fully formed. However, relevant classifications and guidelines, based on a number of studies, allow us to diagnose a PD before 18 years of age. According to ICD-10, a PD can be diagnosed regardless the age of person if the diagnostic criteria are met; however, this is exceptionally rare before the age 16 or 17 years [5]. This is even more clearly defined in ICD-11, where the diagnosis of PD is made whenever the diagnostic criteria are met [6].
The DSM-5 allows for a diagnosis of PD in children and adolescents, when personality traits are particularly maladapted, permanent, and not related to a specific developmental period, mental disorder, or cultural background with the exception of antisocial PD, which cannot be diagnosed before the age of 18. For a diagnosis to be made, the characteristics of PD should have been present persistently for at least 1 year [4]. One should keep in mind that the characteristics of PD identified in childhood will change and that some types of PD will become less obvious or even disappear in later developmental periods (borderline, antisocial PD). The NICE recommendations do not define a chronological age at which a PD can be diagnosed. Instead, they focus on the individual level of developmental maturity and an understandable therapeutic plan to be provided to the person diagnosed with PD [15]. However, PD should not be diagnosed in individuals under the age of 13 and is not applicable until an individual finishes puberty. Because PDs have long been considered as therapy resistant, this diagnosis is misused even today as an excuse to refuse a patient. When diagnosing a person with PD, especially if it is an adolescent, an appropriate treatment must be provided along with the diagnosis. Prevention, early detection, and timely treatment are essential [15].
The purpose of diagnosing PD is to provide the adolescent with the appropriate treatment. It is the adolescent period that has a corrective potential and by introducing a therapy in time, we can significantly influence the course of PD. Adolescents with PD should be treated by a team of highly qualified professionals with a clearly structured intervention model and therapeutic plan [8, 13, 15]. Primarily, the patient must be provided with continuity and consistency. Adolescents with PD, especially borderline patients, have a tendency to form intense relationships; therefore, it is necessary to set clear time and space framework for treatments with different therapists. It is essential to organize treatments adequately—not too much and too little. Team members often have different views on the adolescent’s problems and symptoms, which often lead to conflicts within the team; therefore, supervision is necessary. Often, many services (social services, school, general physician, previous therapist) are involved in the treatment; therefore, roles and tasks need to be clearly identified and coordinated. One of the main treatment goals of all team members is to support the adolescent in his separation and individualization and to actively involve him in the decision-making process. Many adolescents with borderline PD have experienced traumatic events; however, trauma processing is often not the primary intervention. Primarily, it is necessary to reduce suicidality and increase emotional stability [15, 16].
There are many different psychotherapeutic approaches to treat PD. Mentalization-based therapy (MBT), dialectical-behavioral therapy (DBT), and adolescent identity treatment (AIT) are among the most common. It is not so important which specific psychotherapeutic approach is used in the therapy but that certain changes outside the therapeutic relationship are triggered [13, 16]. According to Lambert, these changes are to be accountable for 40% of success in psychotherapy [17]. It is important to include the rest of the family in the therapy, to generate changes in the school, and that all significant others receive appropriate psychoeducation. Psychotherapeutic factors such as therapeutic posture, curiosity, optimism, consistency, empathy, and warmth contribute 30% to the success of a therapy. The adolescent’s expectations of how successful the therapy will be contributing a further 15%. In addition, 15% is contributed by the specific psychotherapeutic techniques [17].
To achieve an optimal therapeutic process, regardless of the type of therapy, the therapist needs to be open, accepting, and optimistic and maintain a positive mental representation of the adolescent as well as curiosity and interest in getting to know the adolescent as a holistic personality, not only in the context of his or her disorder [16]. Since AIT is a younger and not so known therapy as MBT and DBT, it will be explained in more detail than the last two therapies below.
Adolescent identity treatment (AIT) is an integrative therapeutic approach based on the principles of Paulina Kernberg, which includes modified elements of transference- focused psychotherapy, psychoeducation, behavior-oriented home plans, therapeutic contract, and intensive family work with adolescents and parents (adapted from [16]). Identity diffusion and interpersonal misfunctioning are regarded as the core of the borderline PD in adolescents and, as such, forming a base for the essential principles of AIT. The AIT focuses on identity stabilizing and integration of the concepts of the self and significant others, which gradually affects interpersonal relationships and leads to resolving interpersonal conflicts. The AIT applies verbal and nonverbal communication as well as countertransference. The basic principle of the AIT is to work on the dominant affect. The therapist focuses on the dominant affect the adolescent is affected by—here and now. Clarification, confrontation, and interpretation are applied as therapeutic techniques.
I did not understand…
Did I get this right? You said…
What did you mean by saying…?
Please, could you explain that to me in detail?
Is it because you do not have words to describe it, or because you have not thought about it?
You are telling me about a rather excruciating pain, but you are laughing at the same time. This does not fit. Do you have any idea what could this mean?
You are saying that you are fine, but I see fresh cuts. How do these things fit?
You are telling me you are not disappointed, yet you are struggling with tears. Can you explain this?
This is how I see it, but correct me, if I am wrong.
On the one hand, you are telling me that you are fine, but I see many fresh wounds on your arm.
Then you tell me that no one would be sad if you killed yourself.
Could it be that all these contradictory images are within you and that you do not know exactly whether you are feeling well or maybe you are still sad?
Regardless of the psychotherapeutic approach, sincerity, empathy, and warmth are the key characteristics of a therapist. AIT, however, added playful flexibility to the list, with the therapist explaining his/her thoughts, offering possible explanations as a hypothesis (interpretation) and adjusting to the adolescent. The therapist maintains a sound and meaningful stance, knows right from wrong, and maintains his or her position. Optimism is a necessary condition for the therapist to develop an idea of the adolescent as a healthy and stable person, including therapist’s attitude that the adolescent is able to cooperate in sessions and that he or she can develop. The therapist maintains hope for change during therapy stagnation and when the risk of discontinuation of therapy occurs. The absolute presence of the therapist is crucial for the therapy. It can be manifested as curiosity and a genuine interest in the adolescent’s experiences. The therapist is absolutely present when his or her nonverbal/body language and tone of speech reflect the adolescent’s experience of the here and now. The therapist is a role model. For an adolescent, therapist may be the first person to ever really take a truly interest in him or her. By doing so, the therapist engages the adolescent to be curious, motivated, and interested in himself/herself.
Body language is an important factor in AIT. Therapists must be fully aware of their tone, facial expressions, thinking, and interest, paying attention to the adolescent in the treatment, and how all of this is being acknowledged by the adolescent. Nonverbal information is vital in therapy with PD adolescents, who are overly sensitive to possible rejection, split, and are not able to recognize contradictions in verbal and nonverbal communication or are prone to misjudging it. It does matter how the therapist dresses and whether he/she has a piercing or a tattoo. The latter, in particular, can be an important message of how a therapist treats his/her body or allows for various manipulations.
Intensive parental involvement in therapy is especially important in adolescents with PD and is therefore a crucial element of AIT. Working with parents can only be successful if there is no attribution of blame to the parents for the development of PD in their adolescent. If the parents are viewed as the “bad guys,” then the therapist may cause the adolescent to see him/her as a “better parent” and a “savior,” which brings many risks to the therapy. At the beginning of therapy, even very competent and functional parents can appear to be “pathological” due to psychological burden when living with an adolescent with PD.
It is important that the parents are not viewed as bad and invalidating by the therapist. If parents are not included in the therapy, the power of family dynamics and interactions significantly shaping the adolescent is being underestimated. It is essential to educate parents on the adolescent’s heightened sensitivity to emotional stressors, such as criticism, rejection, and separation, and how stressors can be avoided or reduced. Parents need an explanation that the therapy will not change the adolescent’s temperament; however, it will help him to control it more easily. Their job is to encourage the adolescent to go to therapy.
Therefore,
At the beginning of therapy, a
A home plan involves clearly agreed responsibilities of both the adolescent and parents. This includes clear measures for self-injurious behavior such as addressing the wound without any additional comments, threats, rewards, or conversation; the adolescent will discuss this with his/her therapist at the next regular session. If the wounds are deep, the adolescent should be taken to see a surgeon. Behaviors that violate the home plan resulting in the revocation of privileges are agreed upon and set out in the contract, including a reward system for behavior if the adolescent sticks to the home plan.
Mentalization-based therapy is a psychosocial therapy to treat borderline PD (adapted from [18]). It derives from psychoanalysis, attachment theory, and developmental psychopathology and is based on mentalization. It was first intended for the treatment of adults with borderline PD, later on a version for adolescents (MBT-A) was developed. Mentalization is the ability to understand our own mental states and the mental states of other people and represents the capacity that makes us human. We mentalize when we are aware of the mental states of others and ourselves. MBT is based on the assumption that instability in mentalization is a key problem of borderline PD. Similar to AIT, the therapist takes the position of a curious listener, who does not know what is going on and therefore encourages the adolescent to explain. The therapist observes the capacity for attachment and mentalization and applies various interventions to improve or at least maintain the adolescent’s capacity to mentalize.
Dialectical behavioral therapy was developed by the psychologist Marsha M. Linehan and colleagues in the late 1980s to treat borderline PD [19]. Later on, Rathus and Miller developed a version of DBT for adolescents (DBT-A) [20].
The DBT is based on cognitive-behavioral therapy, dialectical philosophy, and on the findings of M. Linehan that people with borderline PD are prone to more intense and dramatic responses when facing specific emotional situations (e.g., romantic, friendly, and family relationships) compared to people without PD. People with borderline PD have quick and strong emotional reactions in the situations described above, remain emotionally aroused, and require more time to calm down than people without borderline PD [19]. As a result, DBT does not focus on the core unconscious conflict, such as in MBT. Instead, it focuses on how to change problematic responses with a range of different behavioral strategies [21].
DBT-A is a 16-week treatment that includes individual adolescent therapy once a week, family therapy as required, and a skills training group for families of adolescents with borderline PD [22]. It is aimed at reducing life-threatening and undesirable behaviors in therapy and behaviors that impair the quality of life. It empowers the adolescents to regulate their emotions, to appropriately deal with interpersonal relationships and cope with stress, and encourages mindfulness [20].
The 2001 American Psychiatric Association recommendations [23], the 2009 NICE guidelines [15], which were reaffirmed in 2018 [24], and the Australian NHMRC guidelines for the treatment of borderline PD [25] do not recommend the use of pharmacotherapy as the first-line therapy. The World Federation of Societies of Biological Psychiatry recommendations mentions several studies reporting the efficacy of serotonin reuptake inhibitors (SSRIs), such as fluoxetine and fluvoxamine and second-generation antipsychotics in the treatment of PD [26].
The 2019 Timaus et al. study confirms clinical observations that most patients with PD are also treated pharmacotherapeutically [27]. Polypharmacy is high, which can also be attributed to the great comorbidity of PD with at least one additional mental disorder. For the most part, tricyclics, first-generation antipsychotics, and mood stabilizers are being omitted in the pharmacotherapy of PD. The mood stabilizer lamotrigine did not prove to be successful in the treatment of PD in a 2018 study [28]. The use of the atypical antipsychotic quetiapine and the opioid antagonist naltrexone has been increasing [27]. However, more studies are required to support the justification for using these medicines.
Prevention and early detection of PD are essential in order to prevent long-lasting effect of PD on adolescent’s overall functioning and interpersonal relationships. When diagnosing a PD in adolescence, we are obliged to provide an appropriate and a PD specialized treatment (AIT, DBT-A, MBT-A). By introducing a therapy in time and by a licensed therapist PD treatment is very effective especially in the adolescent period which has a strong corrective potential.
This work was part of a Slovenian Research Agency project J4-9434.
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