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.

This chapter suggests that the dysexecutive syndrome associated with vascular dementia (VaD) is caused by impairment in separate but related cognitive concepts; that is, pathological inertia, mental bradyphrenia, disengagement, and temporal reordering. During the late 19th and early 20th centuries, cerebrovascular dementia was a well-established clinical syndrome. Multi-infarct dementia (MID) generally became associated with all types of vascular syndromes. Recent research suggests the presence of considerable overlap between the neuropathology underlying Alzheimer’s disease (AD) and VaD. Patients diagnosed with VaD tend to produce hyperkinetic/interminable perseverations, suggesting an inability to appropriately terminate a motor response. Other aspects of the dysexecutive syndrome associated with VaD revolve around constructs related to interference inhibition, flexibility of response selection, and sustained attention. From the view point of diagnosis, the neuropathology of VaD often differentially impacts the frontal lobes, whereas the neuropathology associated with AD revolves more around circumscribed temporal lobe involvement.

Dementia pugilistica (DP) is a form of chronic traumatic encephalopathy (CTE) that involves gross impairment of cognitive and motor functioning due to repetitive blows to the head from boxing. Rapidly increasing in popularity among fight fans and fighters is mixed martial arts (MMA). In the area of sport-related concussion, there are two other frequently used terms that are necessary to distinguish from DP and CTE: postconcussion syndrome (PCS) and second impact syndrome (SIS). The classical clinical signs and symptoms of DP include combinations of dysarthria, incoordination, gait disturbance, pyramidal and extrapyramidal dysfunction, and cognitive impairment. Some media reports about concussion and the potential link between repetitive concussions and long-term problems include eye-catching and emotionally provocative titles. This chapter has provided an overview of the many complex issues surrounding the effects of repeat concussive trauma, particularly in sports.

The Transmissible spongiform encephalopathies (TSEs) form a group of illnesses, characterized by a pathological form of the native prion protein, which results in a rapidly progressive neurodegenerative illness. They also are responsible for Gerstmann-Strâussler-Scheinker (GSS) syndrome and fatal familial insomnia (FFI), and they have been produced experimentally in several other animals. Creutzfeldt-Jakob disease (CJD) is the most common TSE in humans. Human prion diseases have three etiologies: (a) sporadic, (b) genetic, and (c) acquired. Human prion diseases are important to understand because of their underlying pathophysiology, public health implications, and clinical features that often result in misdiagnosis. This chapter reviews the historical discovery of prion diseases and the formulation of the prion hypothesis. It explores prion hypothesis and the neuropathogenesis of prion diseases. The chapter ends with a description of the diagnosis, prognosis, and experimental treatment of human prion diseases.

Dementia with Lewy bodies (DLB) is a clinical syndrome characterized by progressive dementia, cognitive fluctuations, visual hallucinations (VH), and parkinsonism. In 1961, Okazaki, Lipkin, and Aronson reported two patients with dementia and parkinsonism with cortical neuronal inclusions similar to the brain-stem Lewy bodies (LB) seen in Parkinson’s disease (PD). LBs are intra-cytoplasmic neuronal inclusions containing α-synuclein and ubiquitin. There are other associated pathological features in DLB such as spongiform change neuronal loss, and Alzheimer’s disease (AD) pathology includes amyloid plaques and neurofibrillary tangles (NFTs). DLB and other entities such as PD and multiple system atrophy (MSA) have been grouped under the term synucleinopathies due to the existence of &#945-synuclein inclusions in the brain. The central feature required for a diagnosis of DLB is the presence of dementia: a progressive cognitive decline of sufficient magnitude to interfere with normal social or occupational function.