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 demonstrates how social work ethics apply to ethical and legal decision making in forensic social work practice. It discusses the context of social work practice in legal systems. The chapter also details the basic structures of the United States (U.S.) civil and criminal legal systems. It lays the foundation for the criminal and civil court processes in the United States and introduces basic terminology and a description of associated activities and progression through these systems. The chapter focuses on providing an introductory, and overarching, picture of both civil and criminal law in the U.S. and introduces the roles social workers play in these systems. It focuses on the ETHICA model of ethical decision making as a resource and tool that can be used to help forensic social workers process difficult and complex situations across multiple systems.

This chapter explains the theoretical basis for motivational interviewing (MI). It reviews the empirical evidence for the use of MI with diverse populations in forensic settings. MI involves attention to the language of change, and is designed to strengthen personal motivation and commitment to a specific goal by eliciting and exploring the person’s own reasons for change within an atmosphere of acceptance and compassion. It is now internationally recognized as an evidence-based practice intervention for alcohol and drug problems. MI involves an underlying spirit made up of partnership, acceptance, compassion, and evocation. The chapter discusses four key processes involved in MI: engaging, focusing, evoking, and planning. It also describes five key communication microskills used throughout MI: asking open-ended questions, providing affirmations, offering summarizing statements, providing information and advice with permission, and reflective statements.

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.