New York Physical Therapy 36-Hour Ebook Continuing Education

A diagnosis of vascular dementia is made based on clinical presentation, neurocognitive testing, and brain imaging studies. Magnetic resonance imaging (MRI) of the brain may show characteristic abnormalities associated with vascular damage, but it may not be conclusive. Some changes in the brain that are consistent with vascular dementia can coexist with the distinct brain changes seen in AD, leading to a diagnosis of mixed dementia (i.e., evidence of any two or more dementias

are present). Because vascular dementia is closely tied to other cardiovascular conditions, managing risk factors associated with heart disease can play a role in preventing later cognitive decline. Preventive treatment may include monitoring blood pressure, weight, blood sugar, and cholesterol and maintaining a high level of physical activity. Active management of risk factors, even after diagnosis, is essential to comprehensive care. The progressive courses of the three most common types of dementia are distinctly different and are depicted in Figure 1. Alzheimer’s dementia shows a slow, somewhat steady progression, vascular dementia progresses in a stepwise fashion, and LBD often shows significant fluctuations over time. Figure 1: Progressive Course of the Most Common Dementias

Dementia with Lewy bodies and Parkinson’s disease dementia Dementia with Lewy bodies is the third most common cause of dementia and is often considered to include two types of presentations: Lewy body dementia (LBD) and Parkinson’s disease dementia (PDD). The pathology and clinical picture of these two dementias are similar, and their diagnoses are generally related to the timing of the onset of symptoms. If parkinsonian motor symptoms precede cognitive symptoms by 1 year or more, the dementia is classified as PDD, but if cognitive symptoms precede or are concurrent with Parkinson’s motor symptoms, LBD is diagnosed. Lewy bodies are abnormal deposits of the protein alpha- synuclein that form inside nerve cells within the brain. Alpha- synuclein is normally present in a healthy brain, but abnormal clumps of this protein in central nervous system neurons are a hallmark of LBD and PDD. A definitive differentiation among AD, LBD, and PDD can be difficult because the neuropathology of AD can coexist with Lewy bodies. Lewy body pathology leads to patterns of decline similar to those seen in AD, including problems with memory, judgment, and behavior changes; although memory impairment is the hallmark symptom of AD, it may not be the first symptom to appear in LBD. Daily fluctuations in cognitive symptoms (e.g., level of arousal, attention, facility of speech) may be apparent in LBD, but they are not as common in AD. People with LBD may also experience visual hallucinations, sleep disorders, and autonomic dysregulation. Finally, parkinsonian motor symptoms of tremor, bradykinesia, rigidity, and postural instability are seen with PDD and can develop with LBD.

Note. From Western Schools, 2020.

Mixed dementias More common than previously thought, mixed dementias present with pathology and symptoms of two or more types of dementia – most commonly Alzheimer’s and vascular dementia, but sometimes LBD or other dementias. Patients with mixed dementias often present with the classic memory Frontotemporal dementia Frontotemporal dementias (FTDs) are a group of conditions affecting the nerve cells in the frontal and temporal lobes of the brain with hallmark symptoms related to personality, behavior, and emotional and language disorders. FTD is the most common type of dementia in individuals younger than age 60. The early onset and the usual relative sparing of memory until late in the disease can result in a misdiagnosis of a psychiatric disorder prior to an accurate diagnosis of FTD. FTD is characterized by the early and rapid onset of severe personality and behavior disturbances, including impairments in personal interactions, Less common types of dementia There are other less common types of dementia, some of which present with unique clinical characteristics. HIV-associated dementia HIV can cause an encephalopathy (also called AIDS dementia complex ), which presents as widespread destruction of the brain’s white matter. Unlike other sequelae of HIV, this condition is related to the presence of the virus itself, as opposed to being the result of an opportunistic infection. Individuals with HIV-associated dementias present with memory and learning impairment, confusion, and difficulty with executive functions. Over time, they may develop motor problems as well.

and cognitive impairment seen with AD, but they may have a stepwise progression of clinical deterioration (as seen in vascular dementia) or more fluctuation of cognitive impairment (as seen in LBD).

judgment, planning, and social functioning. Inappropriate comments to others and irrational decision making regarding finances or personal matters are common. Individuals with FTD may present as disconnected from a situation and appear either apathetic and disinterested or manic. The microscopic brain changes in FTD appear to be related to accumulation of abnormal tau protein (tauopathy) and scarring (gliosis). There are several subtypes, including variant FTD, primary progressive aphasia, progressive supranuclear palsy (PSP), and Pick’s disease. Huntington’s disease dementia Huntington’s disease is a fatal brain disorder caused by a faulty gene for the protein huntingtin. The gene destroys nerve cells, beginning in the basal ganglia, causing a typical triad of symptoms: motor, cognitive, and psychiatric. Huntington’s disease is an autosomal dominant trait, so anyone with a parent who has Huntington’s disease has a 50% chance of inheriting the gene and a 100% chance of developing Huntington’s disease if he or she inherits the gene. Symptoms typically surface between age 30 and 50 years, with progressive and significant disability. Death usually occurs 15 to 25 years after symptom onset. Motor symptoms of Huntington’s disease include involuntary choreiform (rapid, jerky, dyskinetic) movements of the trunk

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