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.
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Old age brings with it unique challenges in diagnosis, treatment, and care; dementia complicates these issues even more. Improving the management and care of persons with dementia has positive implications for patients, caregivers, and physicians alike. Two types of secondary complications can be analyzed in relation to dementia: conditions that arise outside of the dementia and then conditions that appear to develop due to the neurological degeneration inherent in dementia. Examples of psychiatric complications include depression, anxiety, and psychosis. Medical problems consist of issues such as stroke, cardiovascular problems, cancer, infections, orthopedic issues, diabetes, nutritional disorders, vision and hearing problems, as well as general pain. The high comorbidity of dementias with other psychiatric and medical issues can complicate the diagnosis and treatment of patients with dementia. Issues in the central nervous system (CNS) have long been looked at as possible predictors of dementia.
Dementia is chronic and causes widespread dysfunction in multiple neuropsychological domains. While cognitive symptoms vary across different types of dementia based on their underlying neuropathology, impairments in attention, memory, and comprehension predominate. This chapter briefly discusses the research on the efficacy of various cognitive and behavioral interventions aimed to improve the neuropsychological symptoms in patients with dementia. Cognitive reserve has been shown to be influenced by various premorbid factors. Cognitive training refers to nonpharmacological interventions aimed to improve a patient’s cognitive function and is specifically designed to improve the patient’s functional capacity. Cognitive training generally includes a combination of cognitive stimulation, memory rehabilitation, reality orientation, and neuropsychological rehabilitation. Cognitive interventions have been shown to improve global cognitive functioning and abilities of daily living, reduce behavioral disturbances, and have positive effects on quality of life in patients with dementia.
Vascular dementia (VaD) is an umbrella term representing a clinical grouping with inherent heterogeneity in its clinical manifestations reflecting a variability in its underlying etiology. This chapter discusses specific presentations that can fall under the VaD heading. It includes discussion of multi-infarct dementia (MID) and dementia associated with lacunar states (LSs), as well as Binswanger’s disease (BD), which remains embroiled in controversy. The chapter discusses cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) and moyomoya disease due to their clinical overlap. The etiology of MID is in many ways the same as the etiology of cerebrovascular disease (CVD) in general and even late-life dementia. The term MID itself is used to describe a disorder characterized by a stepwise deterioration of cognitive functioning associated with strokes or accumulated transient ischemic attacks (TIAs).
Chronic alcohol use has been related to various linked disorders when used in excess, particularly when this excessive use becomes chronic. It is important for clinicians to clarify the amount and type of alcohol being consumed and the frequency of this consumption when considering its potential role in any neuropsychological profile. The most commonly reported terms found in the literature include alcohol-induced persisting dementia (APA), alcohol-related dementia, and Korsakoff’s syndrome (KS). This chapter provides some synthesis of this literature to offer some clarity on cognitive dysfunction as it relates to alcohol and the manifestation of dementia as a result of chronic use, including discussion of the classic KS and related presentations. Alcohol dependency is commonly associated with a number of neurological impairments including deficits in abstract problem solving, visuospatial and verbal learning, memory function, perceptual-motor skills, and even motor function.