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42 m a s s a g e & b o d y w o r k m a y / j u n e 2 0 1 7 Treatment for vascular dementia can slow or halt its progression, so it is important to distinguish between this condition and other forms of dementia as early as possible. Lewy Body Dementia Lewy bodies are protein deposits that accumulate inside certain cells in the brain. They are a part of the pathophysiology of Parkinson's disease, and they are the main feature in the cognitive disorder called Lewy body dementia (LBD). This condition is still not well understood, but it appears to be related to a disruption in the flow of neuron signals between the frontal lobe (where we make decisions) and a section of the basal ganglia (where voluntary movement is initiated). LBD looks a little different from Alzheimer's disease because the dementia it causes seems to fluctuate: sometimes people can seem fine, and at other times they are definitely not. And because it affects movement centers, it can also affect voluntary muscle control: myoclonus, or a sudden involuntary jerking contraction OTHER FORMS OF DEMENTIA Dementia and memory loss are the leading indicators in early Alzheimer's disease, but other conditions involve dementia as well. It can be important to identify the cause of mental changes, because treatment options vary. That said, it is possible for a person to have multiple, or mixed, causes of dementia; of course, this makes treatment much more challenging. Vascular Dementia Vascular dementia is a collection of conditions that comprise this second most common form of dementia in the United States, accounting for up to 20 percent of all dementia cases. As we might surmise from its name, it has to do with blood vessels and is strongly correlated to a history of hypertension, cardiovascular disease, high cholesterol, and strokes. A typical pattern seen in vascular dementia patients is that they experience a specific neurological event followed by progressive cognitive impairment. Their function tends to decline in a stepwise pattern: it stabilizes at a certain level, then suddenly declines and re-stabilizes at a lower level, and then declines again, and so on. This reflects new sites of brain damage from vascular disease. Tangles Neurofibrillary tangles are a different signature lesion associated with Alzheimer's disease. The neurons in our brain must be in the right spatial relationship to each other for their synapses to function. These cells are held up with an internal scaffolding made partly of a protein called tau. For reasons that are not clear, the tau proteins degenerate in Alzheimer's disease patients. This causes the neurons to collapse. Long fibers become snarled and twisted together: these are the neurofibrillary tangles. Both plaques and tangles interfere with functioning synapses. The consequences of this are complex and serious: not only do important signals get lost, but those postsynaptic neurons are no longer stimulated by neurotransmitters from the damaged presynaptic neurons. Unstimulated neurons degenerate, healthy levels of neurotransmitters decline, and the problem progresses throughout the brain. In particular, we see that Alzheimer's disease leads to shrinking and reduced function at the hippocampus—the part of the brain that processes and stores new information and short-term memory. Over time, all the brain tissue shrinks, and function is lost—first with memory, but then with other aspects of cognition as well. In the long run, even the most basic autonomic functions of the brain are interrupted. Most patients with Alzheimer's disease succumb to other causes of death before this happens, however. If we can add just a little improvement to the life of someone who lives with these conditions, then we are having a positive impact not just on the client, but also on their loved ones and caregivers.