NR 507 Week 7 CNS; Sensory and Motor Disorders

vessels over 琀椀me (high blood pressure, hyperlipidemia, and diabetes) Incidence of vascular demen琀椀a increases with age and cardiovascular risk factors. 3. Lewy body demen琀椀a (15-20%): Refers to abnormal protein clumps found in neurons. The earliest and most prominent feature is a sleep behavior disorder where pa琀椀ents physically and some琀椀mes violently act out their dreams (sleep walking, screaming, laughing, kicking, punching). It is a REM sleep disorder with failure to inhibit movement during sleep. There can also be visual hallucina琀椀ons; memory loss may not be no琀椀ceable un琀椀l later stages. Demen琀椀a caused by advanced Parkinson’s disease demen琀椀a belongs in this group and will be discussed later in more detail. 4. Frontotemporal demen琀椀a: is another common type of progressive demen琀椀a. It is characterized by neuronal cell death in the frontal and temporal lobes of the brain. The areas associated with this relates to behaviors and language. Common signs and symptoms include changes in behaviors (social inappropriateness, impulsivity, apathy, emo琀椀onal indi昀昀erence) and language de昀椀cits This type has a strong gene琀椀c component and tends to occur earlier between the ages of 40-50 years. More than one type of the demen琀椀as men琀椀oned above may co-exist in one pa琀椀ent (mixed demen琀椀a). Less common causes of demen琀椀a include Hun琀椀ngton’s disease, Creutzfeldt-Jakob disease and trauma琀椀c brain injuries. Demen琀椀as may also develop from metabolic and endocrine processes such as thyroid disorders and vitamin de昀椀ciencies (B1, B6, B12) or infec琀椀ons like Lyme disease and neurosyphilis. For these types of demen琀椀as, symptoms can be reversed. Alzheimer’s Disease Alzheimer’s disease is the most common neurogenera琀椀ve disease in the world. Ten percent of individuals over the age of 65 have Alzheimer’s disease. Alzheimer’s, like demen琀椀a, is a progressive disorder associated with impaired cogni琀椀ve func琀椀on and impaired cor琀椀cal skills. The speed by which it develops varies among individuals and can occur over many years (4, 8 or 20 years). It is associated with neuronal loss (dying or atrophy of the neurons). This results in a smaller brain. In the brain of a pa琀椀ent with Alzheimer’s disease as compared with the normal brain in the diagram below, there is cor琀椀cal atrophy and overall reduc琀椀on in brain size and weight which causes an overall reduc琀椀on in cor琀椀cal mass. There is also enlargement of the ventricles and reduc琀椀on in size of the hippocampus. Another theory on what causes Alzheimer’s disease involves glutamate excitotoxicity. Glutamate is another excitatory neurotransmi琀琀er of the CNS. It works on the neuron. If we have a neuron and we want that neuron to 昀椀re o昀昀 an ac琀椀on poten琀椀al, star琀椀ng at the cell body and send it to the neurotransmi琀琀ers, we need to excite it. Glutamate can be given. Glutamate comes down to the cell body to bind with glutamate receptors. Once this occurs, the ac琀椀on poten琀椀al is sent. Remember that neurons are nega琀椀ve on the inside of the cells. Posi琀椀ve ions located on the outside rush into the cell in a domino e昀昀ect. Glutamate s琀椀mulates this by binding to receptors to open the calcium channels that allows calcium to rush inside the cell. When