Traumatic brain injury (TBI) causes two injury types: primary and secondary. In infants and young children, nonaccidental TBI is an important etiology of brain injury and is commonly a repetitive insult. TBI is by far the most common cause of acquired brain injury (ABI) in children and is the most common cause of death in cases of childhood injury. In 2009, the Pediatric Emergency Care Applied Research Network (PECARN) issued validated prediction rules to identify children at very low risk of clinically important TBI, which is defined as TBI requiring neurosurgical intervention or leading to death. The range of outcomes in pediatric TBI is very broad, from full recovery to severe physical and/or intellectual disabilities. Children and adolescents who have suffered a TBI are at increased risk of social dysfunction. Studies show that these patients can have poor self-esteem, loneliness, maladjustment, reduced emotional control, and aggressive or antisocial behavior.

The electrical discharge of neurons associated with seizure activity stimulates a marked rise in cerebral metabolic activity. Estimates from animal experiments indicate that energy utilization during seizures increases by more than 200", while tissue adenosine triphosphate (ATP) levels remain at more than 95" of control, even during prolonged status epilepticus. The brain generally withstands the metabolic challenge of seizures quite well because enhanced cerebral blood flow delivers additional oxygen and glucose. Mild to moderate degrees of hypoxemia that commonly accompany seizures are usually harmless. However, severe seizures and status epilepticus can sometimes produce an imbalance between metabolic demands and cerebral perfusion, especially if severe hypotension or hypoglycemia is present. A marked increase in glutamate release, which occurs during a prolonged seizure, is likely to result in the activation of all types of glutamate receptors. Although kainic acid produces seizures in the immature brain, it produces little cytotoxicity.

This chapter presents an overview of the restorative justice movement in the twenty-first century. Restorative justice, on the other hand, offers a very different way of understanding and responding to crime. Instead of viewing the state as the primary victim of criminal acts and placing victims, offenders, and the community in passive roles, restorative justice recognizes crime as being directed against individual people. The values of restorative justice are also deeply rooted in the ancient principles of Judeo-Christian culture. A small and scattered group of community activists, justice system personnel, and a few scholars began to advocate, often independently of each other, for the implementation of restorative justice principles and a practice called victim-offender reconciliation (VORP) during the mid to late 1970s. Some proponents are hopeful that a restorative justice framework can be used to foster systemic change. Facilitation of restorative justice dialogues rests on the use of humanistic mediation.

This chapter describes some of the recent restorative justice innovations and research that substantiates their usefulness. It explores developments in the conceptualization of restorative justice based on emergence of new practices and reasons for the effectiveness of restorative justice as a movement and restorative dialogue as application. Chaos theory offers a better way to view the coincidental timeliness of the emergence of restorative justice as a deeper way of dealing with human conflict. The chapter reviews restorative justice practices that have opened up areas for future growth. Those practices include the use of restorative practices for student misconduct in institutions of higher education, the establishment of surrogate dialogue programs in prison settings between unrelated crime victims and offenders. They also include the creation of restorative justice initiatives for domestic violence and the development of methods for engagement between crime victims and members of defense teams who represent the accused offender.

This chapter aims to give the behavioral health specialist (BHS) a basic understanding of pain, knowledge about how to effectively evaluate chronic pain, and a description of effective pain management techniques. Knowledge of the biological and psychological basis of pain is important to understanding the experience of chronic pain. A biopsychosocial assessment is the foundation for providing behavioral health treatment to the chronic pain patient. Chronic pain is less responsive to treatments commonly used for acute pain such as opioid analgesia and avoiding physical activity. A multidisciplinary team approach can substantially improve outcomes in chronic pain treatment. Whatever the format of service provision, utilizing multiple interventions such as physical therapy/exercise, emotional management, pacing, and medication, rather than a single modality can substantially improve outcomes for chronic pain. Providing psychoeducation about chronic pain can be an important strategy.

Recent advancements in molecular genetics have expanded our understanding of the etiology of many neurological diseases and neurodevelopmental abnormalities. Having a comprehensive understanding of genetics is essential in treating patients with metabolic epilepsies. Genetic counseling has been defined as a process of helping people understand and adapt to the medical, psychological, and familial implications of genetic contributions to disease. Some of the components of a genetic counseling interaction include interpretation of family and medical histories to assess the chance of disease occurrence or recurrence; education about inheritance, testing, management, prevention, resources, and research; and counseling to promote informed choices and adaptation to the risk or condition. The genetic counselor may also educate patients and their families about the underlying genetics of their epilepsy and the relevance of a genetic cause of epilepsy for family members, including recurrence risk, reproductive options and the possible teratogenic effect of antiepileptic drugs.

This chapter presents a brief review of the enzymes, transporters, and cofactor producers of the urea cycle. Seizures have long been associated with urea cycle disorders (UCDs), thought to be caused by high levels of ammonia. Furthermore, the brain damage obtained during metabolic crisis has been thought to damage critical structures, leading to epilepsy after the conclusion of the crisis. The first and most critical step of successful treatment of UCDs is recognition. Neurologic monitoring is an essential part of the emergency management of UCDs. The neurological abnormalities observed in patients with urea cycle defects are vast. Controlling ammonia levels by dialysis and complementary medication are needed. EEG monitoring should be initiated early, as this may be very useful for clinical management and indication of untreated metabolic crises. Furthermore, aggressive treatment of clinical and subclinical seizure activity may be helpful in optimizing outcomes for these patients.

This chapter explores recent insights from preclinical and clinical studies of cancer induced bone pain (CIBP). There are various neuropathic, nociceptive, and inflammatory pain mechanisms that contribute to CIBP. Neuropathic pain can be induced as tumor cell growth injures distal nerve fibers that innervate bone and pathological sprouting of both sensory and sympathetic nerve fibers. These changes in the peripheral sensory neurons result in the generation and maintenance of tumor induced pain. CIBP is usually described as dull in character, constant in presentation, and gradually increasing in intensity with time. A component of bone cancer pain appears to be neuropathic in origin as tumor cells induce injury or remodeling of the primary afferent nerve fibers that normally innervate the tumor bearing bone. The treatment of pain from bone metastases involves the use of multiple complementary approaches including radiotherapy, chemotherapy, surgery, bisphosphonates, and analgesics.

Cancer can affect the autonomic nervous system in a variety of ways: direct tumor compression or infiltration, treatment effects (irradiation, chemotherapy), indirect effects (e.g., malabsorption, malnutrition, organ failure, and metabolic abnormalities), and paraneoplastic/autoimmune effects. This chapter focuses on a diagnostic approach and treatment of cancer patients with dysautonomia, with an emphasis on immune-mediated autonomic dysfunction, a rare but potentially highly treatable cause of dysautonomia. Autonomic dysfunction can be divided into nonneurogenic (medical) and neurogenic (primary or secondary) causes. Orthostatic hypotension is a cardinal symptom of dysautonomia. The autonomic testing battery includes sudomotor, vasomotor, and cardiovagal function testing and defines the severity and extent of dysautonomia. Conditions encountered in the cancer setting that are associated with autonomic dysfunction include Lambert-Eaton Myasthenic Syndrome, anti-Hu antibody syndrome, collapsin response-mediator protein 5, subacute autonomic neuropathy, neuromyotonia (Isaacs’ syndrome), and intestinal pseudo-obstruction. The chapter describes various pharmacologic and nonpharmacologic therapies for treatment of orthostatic hypotension.

Clinical neurophysiology (CNP) is a time-honored medical specialty that continues to make great strides, bolstered by rapid advances in neuroscience, biomedical engineering, and computer technology. It encompasses a wide range of methods and techniques for recording, presenting, and analyzing neurophysiologic signals in order to diagnose sensory, motor, autonomic, and central nervous system disorders. Testing performed in CNP or procedures used in current neurological practice include a variety of modality-specific and mixed-modality tests. Modality-specific CNP tests are performed to assess specific functional modalities using biomedical instruments that measure changes in neurophysiologic signals that occur spontaneously or with activation. Mixed-modality CNP tests utilize two or more test modalities to assess complex states (e.g., sleep, coma), to track multiple physiologic parameters, or to obtain more accurate results. CNP tests are classified based on functional anatomy or neural pathway tested. This chapter discusses artifact recognition and presents sources of artifacts in clinical neurophysiologic testing.