The Grieving Child in the Classroom

A Guide for School-Based Professionals

Sue Trace Lawrence

• Publisher: Routledge
• Year: 2019
• eBook ISBN: 9780429619250
• Topic: Education
• Subtopic: Behavioural Management

The Grieving Child in the Classroom integrates the latest research on children's bereavement and adapts it for use in the classroom.

Chapters tackle the neurological, cognitive, emotional, and social effects of childhood grief and demonstrate the ways in which those reactions can manifest in the classroom. By recognizing individual differences in coping styles and considering variables such as developmental stage, nature of the loss, and availability of support, teachers and staff can become better equipped to respond to the bereaved child's needs. The book incorporates theoretical explanations of grief responses as well as practical suggestions for supporting bereaved children in real-world settings.

Whether the loss affects one child or the entire student body, educators can turn to this comprehensive guidebook for ways to support grieving students in their classrooms.

Section 1
Defining Grief Within a Developmental Context

Chapter 1
Neuronal Pathways in the Brain

Neuropsychology, the field that is ostensibly a marriage between traditional psychology and neuroscience, has been growing in recent years. The focus of neuro-psychology is on explaining established psychological ideas in neurological terms. Concepts that had been abstract are now connected to the workings of the brain and nervous system. For instance, today’s behaviorist understands that while experience molds behaviors, it does so via neural pathways. Every time we learn something new, we change our brains. We use this mechanism in direct instruction and indirect learning. Researchers have studied how early experiences, especially negative ones, influence neural development (DeBellis, Hooper, & Sapia, 2005; Perry & Pollard, 1998). Today, educators take courses in brain-based learning, and with that instruction comes a basic understanding of how the immature nervous system works and matures. Although teachers and other staff may be familiar with the neuroscience of learning, technical jargon and nuances of this information are easily forgotten. While educators can apply these concepts to learning in a classroom, integrating anatomical and physiological knowledge with the grief response may be unexplored territory.

When a baby is born, most of the body’s systems are mature enough to operate as they will into adulthood. One major exception is the nervous system. An analogy is the comparison of the immature brain to a new computer. A buyer travels to the neighborhood electronics store and purchases the essential parts, including the hardware and software, but has yet to connect these components. Another perspective is to envision constructing a new town or housing development on open land. Although the blueprints and raw materials may be in place, nothing is yet built. At birth, a human baby has the raw materials he or she needs for a functional nervous system: brain, spinal cord, and neurons. Yet much is unconnected. Throughout life, primarily in the first seven years, an individual’s neurons form communication pathways. Nerve cells do not touch each other, but they align in such a way as to allow quick and efficient communication. This takes place when chemical messengers, or neurotransmitters, release from the end of one cell (the axon terminals) and flow into the space, or synapse, between this cell and the next. That cell then picks up the neurotransmitter’s message via receptors located in the dendrites. Dendrites are branch-like structures of the neuron, and receptors are designed to receive messages from specific neurotransmitters. This message then gets passed along the receiving cell and then moves ahead to subsequent cells. Through learning and maturation, neurons that perform specific physical and mental tasks connect in this way. Neurons necessary for desired actions become more intricately “wired,” while those synapses unnecessary for the tasks are pruned away. Pruning allows for more efficient workings of the remaining pathways, while the ability to accomplish unessential or underutilized tasks lessens (Schwartz & Begley, 2002). One excellent example of this process involves learning language skills. A newborn has the neurons it needs to produce sounds of any dialect, but its brain will become wired to make only the sounds for the language it routinely hears. This explains why a child raised to speak English has trouble trilling Rs when studying a foreign language as a teenager. The neuronal pathways that control moving the mouth and tongue to make that sound were pruned away, making this a difficult task. Although speaking French is awkward, this teen can produce English sounds with ease because of the powerful connections formed within the brain while learning English, the native language (Lawrence, 2015). Pruning of unneeded neuronal connections is an essential mechanism that allows those skills we need to become more ingrained in our brain, while unnecessary skills fade into the background.

Certainly, we can acquire new skills and ideas later in life. Normal human brains remain plastic throughout the lifetime, so they can always learn new information and actions. If this were not the case, there would be no reason for any of us to attend school or read this book. As we age, learning might just need more conscious effort. Teachers understand how young kids’ brains resemble sponges by soaking up the variety of information to which the environment supplies. For us adults, learning takes extra concentration and focus. If we draw once again on the computer analogy, it may require additional energy to reprogram an old computer. Erasing and overriding programs require more effort than installing them. Likewise, constructing a grid of roads and highways in an open desert is simpler than rerouting established streets within a city. While a blank slate may take time to fill with information, erasing and revising is a greater chore. We may tap into greater amounts of energy because the past must be purposefully ignored. If you are trying to trill the letter R but can only remember how to produce this sound in English, the task becomes a high hurdle to overcome (Lawrence, 2015).

The brain develops from the bottom upward, with lower-level areas maturing faster than the complex cerebral hemispheres. Physical maturation originates in the zygote stage when the rudimentary organ is forming (Kolb & Whislaw, 2003; Santrock, 2017). We often refer the brain to as the “triune brain” because we can observe and describe three primary levels. The first and lower most part is the brainstem which controls life-sustaining functions. This part maintains heart and lung physiology and plays roles in the control of arousal, sleep/wake cycles, and focused attention. We refer to this as the “reptilian” brain, a reference to our scaly, cold-blooded ancestors who possessed brains that are commonly believed to conduct similar primitive functions. We sometimes refer the higher-level middle brain area to as the “mammalian brain” in a nod to our similarity to other mammals. Much of the middle brain landscape serves as a relay station, collecting signals from elsewhere in the body and directing them to the upper levels of cerebral cortex for more intensive processing. The hypothalamus regulates our endocrine system, which is comprised of glands that secrete hormones into the bloodstream. The master endocrine gland, the pituitary, is nestled near the brain and responds from directions generated by the hypothalamus in response to bodily stimuli. The limbic system makes up most of the midbrain real estate, which includes the amygdala and hippocampus. Our amygdala is primarily responsible for basic emotions, especially primal ones such as fear and anger, and is crucial for storing our implicit memory. Our hippocampus plays a role in the formation, processing, and storage of explicit memories. The midbrain area serves as the connection between the upper and lower brains, which is why we can voluntarily control our breathing, and indirectly our heart rates, to a certain extent (consider yoga, mindfulness, and meditation). We refer to the uppermost area of the brain as the cerebrum, with the outer layer described as the cortex. This is the part we refer to as our higher brain, in that is more developed than the analogous structures in other animals. Four functional lobes, on two distinct sides of the cortex known as hemispheres, comprise this level. The temporal lobes are situated on the sides above the ears, and they play a role in interpreting information gathered from auditory stimuli. The back lobes are the occipital, and they receive information coming in from vision. Top middle lobes are the parietal, and these collect data from nerve cells responsible for touch and muscular movement. At the front of the brain are the two large frontal lobes. These are the primary association areas, responsible for logical thought, analysis, problem solving, and decision making. The corpus callosum, a dense collection of neuronal fibers, connects the right and left cerebral hemispheres. In general, the left hemisphere communicates with the right side of the body, while the right hemisphere is wired to the left side. This explains why a person suffering a stroke in the right hemisphere may have impairments in use of the left hand. We must keep in mind that this description is a simplistic view of brain anatomy and physiology, but it is enough to help us understand how children’s brains form and how negative experiences can impact a maturing central nervous system (Kolb & Whislaw, 2003; Lawrence, 2015; Santrock, 2017).

The cerebral cortex is the least mature of the three layers at birth. The brain stem functions by necessity; infants have a heartbeat, respiration, and sleep/wake cycles. Neonates primarily react on impulse. They do not yet think rationally by activating the highly advanced parts of their brains. One way to illustrate this phenomenon is by considering infant reflexes. Newborn infants have a set of specific, innate reflexes such as rooting, grasping, startling, and sucking. Babies and young toddlers react to stimuli by enlisting the lower parts of the brain. These primitive reflexes secure survival by allowing for food and safety. These reactions are not consciously controlled; they are automatic. As the child gets older, the brain and nervous connections mature, and the upper levels of the brain take over and allow for decision making (Kolb & Whislaw, 2003). As a result, the reflexes cease. An older child doesn’t automatically suck or grab onto things; he first considers what he is doing. This implies higher-order analysis. As we mature, we get better at solving our problems and contemplating our actions. This is the cerebral cortex at work.

When we are first confronted with threatening or traumatic circumstances, we react unconsciously by using our lower- and middle-level brain areas. When we reflect on a major stressor in our lives, we are familiar with the fight-or-flight response originated by an autonomic nervous system. In times of stress, the sympathetic nervous system activates, creating an excitatory reaction. Our pulse races, blood pressure increases, respiration rate rises, sweating accelerates, muscles tense, and eyes dilate in acknowledgment of something we find dangerous. This quick response to an external threat requires little conscious thought, as it is the body’s way of preparing for danger. When we hear an unexpected loud noise, for example, we jump in anticipation of the fight-or-flight mode. In other cases, conscious ideas can stimulate the perception of jeopardy, such as when our pre-sleep awareness drifts to the concern that the IRS may be examining our tax returns. Although animals exhibit signs of sympathetic nervous system activation primarily, if not exclusively, to external threats, humans trigger similar responses to mere stressful thoughts originating in our frontal lobes. In other words, we not only prepare to fight true dangers, but our bodies are primed to combat imaginary and potential threats, too. Since there is no immediate resolution in these situations, our sympathetic nervous system remains activated for long periods of time. When we are not in danger, the para-sympathetic branch of the autonomic nervous system dominates, creating a sense of physiological calm. Our heart rate is slow and steady, our breathing regulates, our muscles relax, and sweating ceases. When our frontal lobes are working overtime and generating worrisome thoughts, the parasympathetic system is overridden by the activation of the fight-or-flight response. The result is chronic anxiety.

This stress reaction is part of the hypothalamic pituitary adrenal (HPA) axis. A threatening stimulus evokes an emotional reaction in our amygdala, which signals our hypothalamus to let the pituitary gland know that we are potentially under attack and stress hormones are required. The pituitary then signals the adrenal glands, located on top of each kidney, to crank out stress hormones into our blood stream. The primary hormones involved in this response are short-acting adrenalin and cortisol, a longer-acting chemical messenger. These hormones circulate through the body, stimulating the physiological responses we associate with fear and anxiety (Cozolino, 2006). A few of these responses, like pulse and breathing rates, are under the primary control of the brainstem. Higher in the midbrain, the amygdala continues to process the threat and perpetuates the corresponding emotional response. The hippocampus becomes involved in the formation and storage of long-term memories. The intense emotionality triggers the amygdala to dominate the response, which can lead to powerful, exaggerated emotional reactions that are frequently irrational. The amygdala may become permanently hyper-responsive to anxiety-producing triggers. Likewise, evidence suggests that increased stimulation of the amygdala, such as what occurs during a crisis, may inhibit formation of memory (Jenkins & Oatley, 1998; Perry & Pollard, 1998). The hippocampus may become less efficient in controlling the influx of elevated levels of stress hormones, particularly cortisol, further impairing memory storage (Cozolino, 2006; Shonkoff et al., 2012). Sometimes, memory consolidation is inhibited, while in other cases, recall may be problematic. Anxiety and other negative emotions may color the memories (Jenkins & Oatley, 1998). Context may be fuzzy, further contributing to biased recall and irrational interpretations (Shonkoff et al., 2012). This mechanism can explain everything from test anxiety, in which stress may block memorized knowledge, to episodes of dissociative amnesia, in which a person remembers little to nothing about a specific traumatic event. Since the hippocampus and amygdala are linked, emotions can affect memory and vice versa. Theoretically, as we increase in age and developmental maturity, our ability to think logically should improve. However, when confronting a stressor, adults, too, may respond on an emotional or instinctual level.

Researchers have studied the response to traumatic experiences, discovering that individuals exposed to extreme and chronic stress react viscerally to triggers. Moreover, this learned response becomes imprinted within the neurological network as neurons create corresponding connections with their neighbors. In other words, a person, especially a young one whose brain is highly plastic, becomes accustomed to tension and learns to react accordingly, even when the sources of the stress are no longer present. An individual becomes primed, or predisposed, to anxiety. This tension generates anticipation of negative outcomes at every turn as the HPA axis is caught up in a feedback loop and stress hormones are secreted abnormally (Cozolino, 2006). Weiss, Longhurst, and Mazure (1999) collected data from numerous studies that suggest that early childhood stressors not only trigger the HPA axis in the short term but also chronically. Stressors cause the release of corticotropin-releasing hormones (CRH), which in turn, initiates the HPA reaction. When these stress responses occur in childhood, they may create a biological vulnerability to depression or anxiety later in life. In fact, elevated levels of CRH are found in depressed patients, and the evidence suggests that early experiences can increase production of CRH and subsequently, generate a hyperactive HPA axis (Coplan et al., 1996; Nemeroff et al., 1984; Heim, Newport, Mletzko, Miller, & Nemeroff, 2008; Weiss et al., 1999). These stressful reactions can become hard-wired in the brain, perhaps increasing the susceptibility to depressive and anxiety disorders in adulthood (Ladd, Owens, & Nemeroff, 1996; Nemeroff, 1996; Perry & Rosenfelt, 2013). Research demonstrated that the earlier in development an impactful event occurs, the more devastating the potential effects (Hambrick et al., 2018).

Studies have indicated that chronic and extreme stress reactions can affect the brain’s structure as well as its neurochemical functioning, especially in a young person’s brain. Imaging has shown that parts of the amygdala, hippocampus, and prefrontal cortex can decrease in size and neuronal complexity after exposure to traumatic stress (O’Doherty, Chitty, Saddiqui, Bennett, & Lagopoulus, 2015; Shonkoff & Garner, 2012). The prefrontal cortex is the foremost section of the brain. In this area, executive functions such as decision making, problem solving, goal setting, and self-control take place. If a person’s prefrontal cortex is damaged, he may demonstrate impulsive behaviors and immature responses to complex situations (Kolb & Whislaw, 2003; Shonkoff & Garner, 2012). The decreased hippo-campal volume indicates the potential for memory dysfunction (O’Doherty et al., 2015; Shonkoff & Garner, 2012). Reacting to a traumatic stressor requires making reasonable choices, rational planning, and recalling past experiences. If these areas are negatively affected by chronic activation of the fight-or-flight response, the consequences may not be conducive to effective coping.

There is evidence that early trauma can specifically influence the right hemisphere’s maturation, with dramatic results. This side of the cerebral cortex rarely engages in language tasks, responding on a nonverbal, guttural level. This side may be dominant in creativity and emotional intelligence. Studies have suggested that early trauma may impact this hemisphere, leading to weaker attachments, difficulty with emotional regulation, and higher rates of mental illness (Schore, 2001). Details aside, we can assume that experiences in infancy and early childhood can become ingrained in the plastic brain, programming the nervous system for a lifetime if adaptations are not made.

Obvious triggers can stimulate these reactions, but so can anything reminiscent of the original traumatic event. Even when memories appear to have faded or forgotten, impressions may be present on an unconscious level. When the child encounters a triggering stimulus, he may react with fear, anxiety, or panic (Perry & Pollard, 1998). For example, when 5-year-old Brynn learned of her father’s death, a song was playing on the radio. The association may not register consciously but occurs somewhere in the unconscious recesses of Brynn’s mind. When she once again hears this specific song, she becomes anxious without knowing why. Odors are also common triggers. For instance, we may associate pungent hospital odors with negative events that occurred within its walls and may react with panic at a whiff of the characteristic antiseptic smell. Any sensory experience can trigger emotional reactions. The flood of memory and concurrent emotions from the mid-brain may persist throughout the life span, and it may take patience and a little detective work to uncover the true nature of the associations.

Perry and Rosenfelt (2013) distinguish between our reactions to trauma and grief. They believe that the neurological pathways formed from these two different experiences may lead to two different emotions—sadness in grief and anxiety in trauma. This may be true with adults, but we must remember that children are egocentric and inexperienced. An incident that might cause sadness to a grown-up, such as a grandmother’s death after a long-term illness, may create apprehension, fear, and even terror to a young child. A young person’s imperfect understanding of such events may generate feelings of anxiety along with sadness. Moreover, certain losses are objectively traumatic, such as when a person dies suddenly, violently, or painfully. Children take losses personally, focusing on the death in egocentric terms. They may worry they are in danger of being the next victim, and this apprehension can magnify to paralyzing fear. When a young person dies, the event may drive home the suggestion to a child that he, too, can lose his life. Viewing events through egocentric eyes may lead to phobias or despondency (Brohl, 2007; Lawrence, 2015).

Individuals meeting the criteria for complicated grief, a condition characterized by prolonged, severe reactions to a loss, showed small but significant differences in cognitive functioning and smaller brain volume than controls experiencing normal grief (Perez et al., 2015). Imaging studies, including fMRIs, have demonstrated abnormal neuronal communications in subjects labeled with complicated grief (Arizmendi, Kaszniak, & O’Connor, 2016). While more research is necessary, early indications suggest that severe grief reactions can create biological and neurological changes in the brain. These physiological responses can then present as personality traits, as the developing person’s brain is organized around the stress response (Perry, Pollard, Blaicley, Baker, & Vigilante, 1995). Stress that accumulates overtime becomes toxic as the individual’s physical and psychological set point is high on the anxiety scale (Toxic Stress, n.d.). The term toxic stress refers specifically to prolonged, repeated, or severe physiological reactions to stress without the buffering effect of a close attachment with another individual (Shonkoff & Garner, 2012). Without the security of a support system, the affected person becomes hypervigilant and quick to jump into action mode at the mere hint of a threat.

If panic, anxiety, fear, and grief can become embedded in the neurological network of the brain, why are a few children more susceptible to this reaction than others? Why do some kids rebound quickly from a traumatic event while others struggle for longer periods of time? While there are a host of reasons for the variety of responses (including social factors, emotional maturity and intensity of attachment), one source of this discrepancy may lie in the brain’s genetic composition. In My Age of Anxiety, Scott Stossel (2013) describes how a biological predisposition to anxiety may be a contributing factor in a person’s ability to handle stress. He writes how research on genetic markers that may indicate susceptibility to anxiety-related disorders, including posttraumatic stress disorder. Research has suggested a link between specific gene sequences and posttraumatic stress disorder (PTSD) (Bharadwaj et al., 2016). Other studies have focused on epigenetics, which involves mechanisms that control a gene’s function without altering the actual DNA. These mechanisms vary in detail, but it will suffice to say that environmental factors can potentially influence them. Epigenetics explains why the genes of identical twins, who share the same DNA, may be expressed in different ways. Researchers are still studying the ways in which epigenetic factors influence genes, including ones that dictate responses to severe trauma (Klengel & Binder, 2015). Although Stossel (2013) admits th...

Table of contents

• Cover
• Half Title
• Title
• Copyright
• Dedication
• Contents
• Preface
• Acknowledgments
• Author Biography
• Introduction: Why Educators Should Be Knowledgeable About Grief
• SECTION 1 Defining Grief Within a Developmental Context
• SECTION 2 Reactions to Grief and Loss During Early and Middle Childhood
• SECTION 3 How to Help Grieving Students
• Appendices
• References
• Index