This research will begin with the statement that change is a continuous process that occurs in every human being. It is an inevitable life event that initiated from the time of inception of life existence. There are several categories we can define each developmental stage however it can be generalized from a life developmental perspective as periods of childhood, adolescence, and adulthood. Each transition period is characterized by milestones that promote growth and maturity. The changing process doesn’t stop in the adulthood change though as development in other aspects such as psychological and social aspects can still progress. The adolescence period is vital among these changes as it is intermediary to childhood and adulthood. It poses great challenges to the metamorphosing individual as independence becomes interesting and the path towards it is resolutely sought. There is actually no standard definition of adolescence. Although it is often captured as an age range, usually from 10 to 18 years old, chronological age is but one way of defining adolescence. Physical, social and cognitive development can also form the basis of adolescence. The needs and capabilities of a child turning into an adolescent drastically change. And this transition process has been the basis of adolescence being known as the period of “storm and stress”, a perspective introduced by Hall and supported by the psychoanalytic tradition and Erikson’s description of adolescence as a period of identity crisis which popularised in the 20th century. The “storm and stress” perception of adolescence defines it as a turbulent process, accompanied by negative moods and a problematic relationship with parents, and risky behavior, including delinquency. However, it has to be noted that this viewpoint was minimized when more empirical data disproved it in the 1980s. Nevertheless, it can’t be denied that both adolescents and our society face challenges in this developmental stage and thus appropriate education and actions on developmental management must be addressed. This paper aims to discuss the various aspects of changes recognized during the adolescence period, define the posing challenges and, discuss and propose positive approaches that can manage and direct the “storm and stress” stage into a pleasant life stage experience. The Developmental Changes Biological and Emotional Changes A growth spurt involving radical changes occur in the physical anatomy of an adolescent as it matures in size and form. The cause of this is the high secretion of gonadal steroid hormones such as the testosterone and estrogens, in the reproductive organ. The developing body experiences anatomical changes contributory to the reproductive process, of which the emergence of secondary sexual characteristics, such as breast development and growth of facial hairs, is mostly observed. The pace of development, however, is very varied across individuals. And this impacts the psychological state of the adolescent in his sense of self and relations to others thereby making adolescence a delicate stage. The behavioral changes in adolescents that affect their emotional state are explained by the late maturation of the prefrontal cortex (PFC) – the brain part responsible for the regulation of emotions, planning, reasoning, and self-control. And so drastic changes occur in the neurotransmitters dopamine and serotonin, hormones responsible for stimulating emotions in the limbic system of the brain. These changes cause the adolescents to have the tendency to be more stressful and less susceptible to rewards. These are the internal changes occurring among adolescents, where we can only observe the results which are common emotional outbursts and shifts. ...Show more
The development of the prefrontal cortex is believed to play an important role in the maturation of higher cognitive abilities and goal oriented behavior (Casey, Tottenham, & Fossella 2002b; Casey et al., 1997a). Many paradigms have been used, together with fMRI, to assess the neurobiological basis of these abilities, including go/nogo, flanker, stop signal, and anti saccade tasks (Bunge et al 2002; Casey et al., 1997b; Casey, Giedd, & Thomas, 2000a; Durston et al., 2003; Luna et al., 2001). Collectively, these studies show that children recruit distinct but often larger, more diffuse prefrontal regions when performing these tasks than do adults. The pattern of activity within brain regions central to task performance (i.e., that correlate with cognitive performance) become more focal or fine-tuned with age, while regions not correlated with task performance diminish in activity with age. This pattern has been observed across both cross-sectional (Brown et al., 2005) and longitudinal studies (Durston et al., 2006) and across a variety of paradigms.
Although neuroimaging studies cannot definitively characterize the mechanism of such developmental changes (e.g. dendritic arborization, synaptic pruning) the findings reflect development within, and refinement of, projections to and from, activated brain regions with maturation and suggest that these changes occur over a protracted period of time (Brown et al., 2005; Bunge, Dudukovic, Thomason, Vaidya, Gabrieli, 2002; Casey et al., 1997a; Casey, Thomas, et al., 2002a; Crone, Donohue, Honomichl, Wendelken & Bunge, 2006; Luna, et al., 2001; Moses et al., 2002; Schlaggar et al., 2002; Tamm et al., 2002; Thomas, Hunt, Vizueta, Sommer, Durston, Yang, 2004; Turkletaub, Gareau, Flowers, Zeffiro & Eden, 2003).
Differential recruitment of prefrontal and subcortical regions has been reported across a number of developmental fMRI studies (Casey et al., 2002b; Luna et al 2001; Monk et al., 2003; Thomas et al., 2004). Outside of the functional neuroimaging literature, there is evidence to suggest a differential relative maturity of subcortical limbic brain structures as compared to prefrontal regions, which may be most pronounced during adolescence. Evidence for the continued pruning of prefrontal cortical synapses well into development has been established in both nonhuman primates and humans (Huttenlocher, 1997; Rakic, Bourgeois, Eckenhoff, Zecevic, & Goldman-Rakic, 1986), with greater regional differentiation suggested in the human brain (Huttenlocher, 1997) such that cortical sensory and subcortical areas undergo dynamic synaptic pruning earlier than higher-order association areas. This conceptualization of cortical development is consistent with anatomical MRI work demonstrating protracted pruning of gray matter in higher-order prefrontal areas that continue through adolescence (e.g., Giedd et al., 1999) relative to subcortical regions. Volumetric analyses of the human amygdala shows a substantially reduced slope of change magnitude relative to cortical areas in 4–18 year olds (Giedd et al., 1996). Taken together, these findings suggest a protracted developmental time course of the prefrontal cortex relative to subcortical regions.
Intense and frequent negative affect common during the early adolescent years, (Pine et al., 2001; Silveri et al., 2004; Steinberg, 2005) has led to a number of imaging studies of affect in adolescents (Baird et al., 1999; Killgore et al., 2005; Thomas et al., 2001; Yang et al., 2002). These show that the amygdala is engaged by affective cues, with exaggerated response magnitudes in adolescents relative to children or adults (Ernst et al., 2005; Guyer et al., 2008; 2009; Monk et al., 2003; Rich et al., 2006; Williams et al., 2006). In concert with these findings is the established role of the prefrontal cortex in the regulation of emotive behavior and its protracted maturation throughout adolescence (Galvan et al., 2006; Monk et al., 2003).
These findings suggest that exaggerated emotional reactivity during adolescence might increase the need for top-down control and put individuals with less control at greater risk for poor outcomes. To test this hypothesis, we examined the association between emotion regulation and frontoamygdala circuitry in 60 children, adolescents, and adults with an emotional go-nogo paradigm (Hare et al. 2005) and functional magnetic resonance imaging (fMRI). We went beyond examining the magnitude of neural activity and focused on neural adaptation within this circuitry across time with functional magnetic resonance imaging (Hare et al., 2008). Because individual differences in emotional reactivity might put some teens at greater risk during this sensitive transition in development, we also assessed everyday anxiety using the Speilberger Trait Anxiety Inventory.
Our results showed that adolescents have an initial, exaggerated amygdala response to cues that signal threat (fearful faces) relative to children and adults (see Figure 2 above). This age-related difference decreased with repeated exposures to the stimuli. Anonymous self report anxiety ratings predicted the extent of adaptation or habituation in the amygdala to empty threat. Individuals with higher trait anxiety showed less habituation over repeated exposures. This failure to habituate was associated with less functional connectivity between ventral prefrontal cortex (vPFC) and amygdala.
Exaggerated Amydala Response in Adolescents
This observed amygdala-vPFC network, showing imbalanced activity in adolescents, is consistent with a wide variety of work in animal (Baxter et al., 2000; Milad & Quirk, 2002) and human samples (Delgado et al., 2006; Etkin et al., 2006; Haas et al., 2007; Johnstone et al., 2007; Urry et al., 2006), implicating an inverse relationship between these structures that govern affective output. In particular, increased response in the vPFC is inversely correlated with responding in the amygdala, and predicts behavioral outcomes such as fear extinction (Gottfried & Dolan, 2004; Phelps et al., 2004), downregulation of autonomic responses (Phelps et al., 2004) and more positive interpretations of emotionally ambiguous information (Kim, Somerville et al., 2003; 2004). Therefore, it is not surprising that the particular circuitry observed to show an ‘imbalance’ in adolescents and giving rise to heightened emotional behavior is that of the amygdala and vPFC.
A number of studies have shown the significance of environmental factors such as stress and early adversity on brain and behavior (Liston et al., 2006; 2009; Tottenham et al., in press) and risk for psychopathology (Breslau et al., 1998; Kessler, Sonnega, Bromet, Hughes, & Nelson, 1995). Trauma exposure is a particularly potent environmental risk factor for anxiety and depression (Brown, 1993; Kendler, Hettema, Butera, Gardner, & Prescott, 2003; McCauley, Kern, Kolodner, Dill, & Schroeder, 1997). A recent study by our group examined the effects of a naturally occurring disaster on affective processing of cues of threat. Specifically, we used functional magnetic resonance imaging to assess the impact of proximity to the disaster of September 11, 2001, on amygdala function in 22 healthy young adults.
Our findings suggest that more than three years after the terrorist attacks, bilateral amygdale activity in response to viewing fearful faces compared to calm ones was higher in individuals who were within 1.5 miles of the World Trade Center on 9/11, relative to those who were living more than 200 miles away (all were living in the New York metropolitan area at time of scan). This effect was statistically driven by time since worst trauma in lifetime and intensity of worst trauma, as indicated by reported symptoms at time of the trauma (see Figure 4). These data are consistent with a model of heightened amygdala reactivity following high-intensity trauma exposure, with relatively slow recovery.
Amygdala activity and proximity to the WTC on September 11th, 2001
In the context of our model of adolescence, individuals who experience trauma during this period or have experienced multiple traumas may be especially vulnerable for developing symptoms of anxiety and depression as teens. In other words, while heightened emotional reactivity is typical during the period of adolescence, failure to suppress that emotional reactivity is associated with symptoms of anxiety. The large variability observed in our developmental studies of emotion regulation may in part be due to variation in individuals’ experiences. An imbalance in amygdala-PFC coupling has been implicated in the pathophysiology of psychiatric illnesses (mood and anxiety disorders) in adult (Blair et al., 2008; Drevets, 2003; Johnstone et al., 2007); and developing populations (Guyer et al., 2009; McClure et al., 2007; Monk et al., 2008; Rich et al., 2006; Pine, 2007) showing greater amygdala relative to prefrontal activity. As such, improving our understanding of the development of these circuits and the source of biased responding in some adolescents over others will facilitate our understanding of the most commonly experienced psychiatric illnesses of this developmental period (i.e., anxiety and depression).
A number of human genetic studies have begun to identify candidate genes that may play a role in increased risk for anxiety and depression. The main avenues for understanding gene function in these disorders have been in behavioral genetics on one end and on the other end, molecular mouse model. Attempts to bridge these approaches have used brain imaging to conveniently link anatomical abnormalities seen in knockout/transgenic mouse models and abnormal patterns of brain activity seen in humans. Recently we completed a study using human and mouse behavioral genetic together with imaging genetics. Each of these approaches alone, provide limited information on gene function in complex human behavior such as emotion regulation and its dysregulation in psychopathology, but together, they are forming bridges between animal models and human psychiatric disorders.
In this study, we utilized a common single nucleotide polymorphism (SNP) in the brain-derived neurotrophic factor (BDNF) gene that leads to a valine (Val) to methionine (Met) substitution at codon 66 (Val66Met). In an inbred genetic knock-in mouse strain that expresses the variant BDNF allele to recapitulate the specific phenotypic properties of the human polymorphism in vivo, we found the BDNF Val66Met genotype was associated with treatment resistant forms of anxiety-like behavior (Chen et al. 2006). A key feature of anxiety is impaired learning of cues that signal safety versus threat and unlearning of cues that signal threat when the association no longer exists (i.e., extinction). Thus, the objective of our study was to test if the Val66Met genotype could impact extinction learning in our mouse model, and if such findings could be generalized to human populations.
We examined the impact of the variant BDNF on fear conditioning and extinction paradigms (Soliman et al 2010). Approximately 70 mice and 70 humans were tested. The mice include 17 BDNFVal/Val, 33 BDNFVal/Met and 18 BDNFMet/Met. The human sample included 36 Met allele carriers (31 BDNFVal/Met and 5 BDNFMet/Met) and 36 nonMet allele carriers group-matched on age, gender and ethnic background. Fear conditioning consisted of pairing a neutral cue with an unconditioned aversive stimulus until the cue itself took on properties of the unconditioned stimulus (US) of an impending aversive event. The extinction procedure consisted of repeated presentations of the cue (i.e., conditioned stimulus or CS) alone. Behavioral responses of percentage of time freezing in the mouse and amplitude of the galvanic skin response in the human were the dependent measures. In addition, we collected brain imaging data using fMRI with the human sample.
Our findings showed no effects of BDNF genotype on fear conditioning in the mice or humans as measured by freezing behavior to the conditioned stimulus in the mice (F(2,65) = 1.58, p < 0.22) and by skin conductance response in humans to the cue predicting the aversive stimulus relative to a neutral cue (F(1,70) = 0.67, p < 0.42). However, both the mice and humans showed slower extinction in Met allele carriers than in nonMet allele carriers as shown in Figure 5A and B below. Moreover, human functional magnetic resonance imaging data provide neuroanatomical validation of the cross-species translation. Specifically, we show alterations in frontoamygdala circuitry, shown to support fear conditioning and extinction in previous rodent (Myers & Davis, 2002; Quirk et al., 2003;Milad & Quirk, 2002;LeDoux, 2000) and human (LaBar et al., 1998; Schiller et al., 2008; Delgado et al., 2008; Kalischet al., 2006; Gottfried & Dolan, 2004; Phelps et al., 2004) studies, as a function of BDNF genotype. Met allele carriers show less ventromedial prefrontal cortical (vmPFC) activity during extinction relative to nonMet allele carriers (Figure 5C), but greater amygdala activity relative to nonMet allele carriers (Figure 5D). These findings suggest that cortical regions essential for extinction in animals and humans (Quirk et al., 2003; Gottfried & Dolan, 2004; Lebron et al., 2004) are less responsive in Met allele carriers during extinction. Moreover, amygdala recruitment, that should show diminished activity during the extinction (Phelps et al 2004) remains elevated in Met allele carriers.
Altered behavior and neural circuitry underlying extinction in mice and humans with BDNF Val66Met
These findings are provocative as they provide an example of bridging human behavioral and imaging genetics with a molecular mouse model to suggest a role for BDNF in anxiety disorders. Moreover, these data suggest impaired learning of cues that signal safety versus threat, and in the efficacy of treatments that rely on extinction mechanisms such as exposure therapy. In the context of our model of adolescence, individuals with the BDNF Met allele may be more vulnerable for developing symptoms of anxiety and depression as teens, in that they show less vPFC activity and greater amygdala activity to repeated exposure to empty threat. These genetic data provide an example then of how an imbalance in amygdala-PFC coupling during typical development could be exacerbated and lead to clinical symptoms of anxiety.