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.
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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:
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.
This chapter shows the importance, for older persons, of support groups. In spite of the changes that have occurred in the American family, and all the negative things that fill the popular press concerning family relationships, the family is still the backbone of support for most older people. To some extent, the type of family support older people obtain depends on whether they are living in the community or in an institutional setting such as a group home, retirement village, or nursing facility. Whether a person is married, has great impact on that person’s support within a family setting including emotional, financial, and physical support, particularly in times of illness or infirmity. The success of a second marriage depends to a considerable extent on the reaction of the adult children of the elderly couple. Older grandparents, no matter how motivated, can find caring for grandchildren to be very tiring.
Delirium, also known as acute confusional state, organic brain syndrome, brain failure, and encephalopathy, is a common occurrence among medical and surgical patients and causes extensive morbidity and mortality. This chapter provides an updated review of delirium, including pathophysiological correlates, clinical features, diagnostic considerations, and contemporary treatment options. The defining features of delirium include an acute change in mental status characterized by altered consciousness, cognition, and fluctuations. The chapter explores the risk factors for delirium. These can be divided into two categories: predisposing factors and precipitating factors. Imbalances in the synthesis, release, and degradation in gamma-aminobutyric acid (GABA), glutamate, acetylcholine, and the monoamines have also been hypothesized to have roles in delirium. GABA is the primary inhibitory neurotransmitter in the central nervous system (CNS) and medications such as benzodiazepines and propofol have known actions at GABA receptors and have been associated with delirium.
This chapter shows how the United States and the world are experiencing an aging evolution we are growing older. America is going through a revolution. As a whole, Americans are becoming older, and there are many more older people among people than ever before in our history. Obviously all cohorts of the population youth, young adults, middle-aged, young-old, oldest-old are heterogeneous. When some people think about the elderly as a whole, they picture frail, weak, dependent persons, some in nursing homes and many confined to their homes. The chapter demonstrates the differences the various age categories have in relation to selected chronic health conditions that cause limitations of activity. Widowhood is much more common for elderly American women than for older men. The aging of Baby Boomers will solidify the shift America is experiencing with the aging of its population. Centenarians make up a small percentage of the total U.S. population.
Primary progressive aphasia (PPA) is the term applied to a clinical syndrome characterized by insidious progressive language impairment that is initially unaccompanied by other cognitive deficits. This chapter describes several variants of PPA and more than one etiology. It explains three main variants of PPA, namely, semantic Variant of PPA (svPPA), nonfluent/agrammatic variant of PPA (nfvPPA) and logopenic variant of PPA (lvPPA), and also describes criteria for their diagnoses. The defining symptom of PPA is the presence of a language impairment for at least 2 years in the absence of any other significant cognitive problem. Assessment of other cognitive domains is challenging because many tests of memory, attention, executive functioning, and visual-spatial skills rely on language processes in some manner. There are no drug therapies proven to arrest progression of signs and symptoms of PPA due to frontotemporal lobar dementia (FTLD) or Alzheimer’s disease (AD) pathologies.
Dementia is an umbrella term for conditions such as Alzheimer’s disease (AD), dementia with Lewy bodies (DLB), vascular dementia (VaD), and frontotemporal dementia (FTD). Under that umbrella, FTD, also known as frontotemporal lobar degeneration (FTLD), can be further categorized to define a group of neurodegenerative disorders resulting from a progressive deterioration of the cells in the anterior temporal and/or frontal lobes of the brain. More specifically, ventromedial-frontopolar cortex is identified with metabolic impairment in FTD. This chapter elaborates on the history, epidemiology, pathophysiology, clinical features, treatment, and outcomes of FTD. The history and background section of each of the FTD categories highlights the evolution of the disease conceptualization. The FTD subtypes are conceptualized in three categories: neurobehavioral variant, motor variant, and language variant. The chapter illustrates the features of all three categories of FTD.
The concept of Mild cognitive impairment (MCI) makes a lot of sense in that individuals are typically not “normal” one day and “demented” the next. In theory, especially for progressive neurodegenerative conditions, such as Alzheimer’s disease (AD), frontotemporal dementia (FTD), the development of dementia may take months or years. The clinical syndrome of MCI due to AD can be identified via a neuropsychological evaluation or less-sensitive cognitive screening measures. Much of what we are learning about MCI, and therefore refining its diagnostic criteria, is coming from two large-scale studies of cognition and aging: Alzheimer’s Disease Neuroimaging Initiative (ADNI) and Australian Imaging, Biomarkers and Lifestyle (AIBL). According to the most recent research diagnostic criteria for MCI due to AD, evidence of beta-amyloid deposition, neuronal injury, and/or other biochemical changes needs to be seen to increase confidence of the etiology of MCI. Cholinesterase inhibitors remain the primary pharmacological treatment for AD.