This chapter addresses the key principles of sport, exercise, and performance psychology. It reflects the broadening of sport psychology studies to encompass more widespread human performance research. It provides Dr. Sachs’s honest and open remarks along with interspersed additions from the authors to introduce the field and its accompanying issues. In explaining his career trajectory, Dr. Sachs recalls earning his undergraduate degree in psychology and then applying to graduate programs in applied behavioral analysis. Dr. Sachs’s somewhat zigzagged trajectory in the field demonstrates the important sport and exercise psychology principle that explains the benefits of focusing on the process rather than the outcome when setting goals. Dr. Sachs added that the United States leads the way in research and writing with regard to sport and exercise psychology, while other countries may be more advanced in the application of that knowledge at the professional levels.
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This chapter addresses the key principles of sport, exercise, and performance psychology. It reflects the broadening of sport psychology studies to encompass more widespread human performance research. The topic of decision making has been covered in psychology, economics, and motor learning but addressed very sparsely in sport, exercise, and performance psychology. Rational decision making requires defining the problem, identifying criteria, weighing those criteria, generating alternative solutions, and ultimately computing the optimal decision. The chapter introduces the literature on decision making and provides examples of factors that influence the choices people make. The decision to act, move, or what move to make is decided in the response selection stage, and the final stage is when one’s brain and muscles are organized to make the actual move. The key to improve the decision-making over time is to increase personal awareness of own limitations and keep learning and collecting information from reliable sources.
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.
One of the most important findings from the original battered woman syndrome (BWS) research was the existence of a three-phase cycle of violence that could be described and measured through careful questioning of the battered woman. This chapter describes the cycle, updates it by adding information from the courtship period, and divides the third phase into several different sections where appropriate so that there may not be any loving contrition or even respites from the abuse at times during the relationship. Teaching the woman how her perception of tension and danger rises to an acute battering incident after which she experiences feelings of relief and then gets seduced back into the relationship by the batterer’s loving behavior, often similar to what she experienced during the courtship period, has been found to be helpful in breaking the cycle of violence that keeps the woman in the relationship.Source:
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 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.Source:
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.Source:
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.