Select one of the following discussion prompts to address. In the subject line of your post, please identify which prompt you are responding to, for example, choice #2 vitamin deficiencies.

Consider the impact of spinal cord injury and the potential scope of lifetime disability and sequelae associated with spinal cord injury. The greatest challenge facing the neuroscience community involves developing therapy that will allow damaged nerve tissue to be regrown and regenerated. Reflect on this article (Links to an external site.)and discuss the importance of Schwann cells and their impact on damaged axons.

Describe the genetic components, pathophysiology, and major neurologic features of neurofibromatosis, Cri du chat syndrome, Tay-sachs disease, and Parkinson disease (early onset).

Define dementia of Alzheimer type (DAT) and describe the pathophysiology, clinical manifestations, evaluation and treatment.

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Solution

Week 5 Nurs 530

Choice 3: Dementia of Alzheimer type

Alzheimer’s disease (AD) is a gradual degenerative disorder affecting the neurologic system. It is insidious and presents with a progressive cognitive function loss causing dementia and alterations in affect and behavior (Weller & Budson, 2018). AD is a common neurodegenerative disorder that causes dementia. The onset of AD occurs in middle age, and thus it is not found exclusively in the elderly.

Pathophysiology

AD dementia occurs when the number of neurons and synapses reduces in the cerebral cortex and various subcortical area. The reduced number of neurons causes atrophy of the affected brain regions (Silva et al., 2019). The pathophysiology of AD dementia is complex and involves various cellular, molecular, and physiological pathologies. The most affected brain regions in AD are the neurons in the hippocampus, amygdala, neocortex, and the basal forebrain cholinergic system (Silva et al., 2019). Patients with AD dementia present with specific neuropathologic and biochemical changes. They comprise neurofibrillary tangles which is a knotted mass of non-functioning neurons, and neuritic plaques, which are amyloid protein deposits in the brain. The damage of neurons in AD dementia take place mainly in the cerebral cortex and causes a decreased brain size.

Clinical Manifestations

The clinical manifestations of AD progress from the early stages to the terminal stages. Signs and symptoms in the initial stages include mild memory loss (Weller & Budson, 2018). An individual may encounter mild challenges in occupational and social activities but has ample cognitive function to conceal the memory loss and functions independently. Late clinical manifestations include increasing memory loss that is evident in most daily activities. Individuals lose their capacity to identify familiar faces, objects, and places and may get lost in familiar places (Weller & Budson, 2018). There are repetitions and diminished ability to create concepts and think abstractly. In addition, individuals become depressed, paranoid, hostile, and even combative. Physical activity and agitation increase, and the individual may wander at night. In the terminal stage, the individual is usually immobile and needs total nursing care due to a lack of bladder and bowel control (Weller & Budson, 2018). They experience significant weight loss, difficulty swallowing, skin infections, grunting, and increased sleeping.

Evaluation

The diagnosis of AD dementia is made by taking a patient history and conducting mental status examination. Diagnostic studies are used to aid in the diagnosis, including blood studies such as Complete blood count, chemistry profile, HIV testing, VDRL test for syphilis, vitamin B12 to assess hematologic disease, and thyroid-stimulating hormone test to rule out thyroid disorder (Silva et al., 2019). Brain CT scan or MRI are performed in the initial evaluation of persons with dementia to visualize lesions that lead to cognitive impairment such as stroke and brain tumor (Silva et al., 2019). A lumbar puncture is performed to examine the cerebrospinal fluid and rule out disorders such as CNS infections and normal-pressure hydrocephalus.

Treatment

The standard pharmacological treatment for AD dementia includes partial N -methyl-D-aspartate (NMDA) antagonists and cholinesterase inhibitors (ChEIs). ChEIs are used to treat mild to moderate AD dementia (Zucchella et al., 2018). The FDA-approved ChEIs include Rivastigmine, Donepezil, and Galantamine, which block the breakdown of acetylcholine. ChEIs exhibit a modest impact on aspects of cognitive function and performing activities of daily living (Zucchella et al., 2018). Moderate to severe AD dementia is managed using NMDA antagonist memantine, an FDA-approved agent to treat moderate and severe AD.

References

Silva, M. V. F., Loures, C. D. M. G., Alves, L. C. V., de Souza, L. C., Borges, K. B. G., & das Graças Carvalho, M. (2019). Alzheimer’s disease: risk factors and potentially protective measures. Journal of biomedical science, 26(1), 1-11. https://doi.org/10.1186/s12929-019-0524-y

Weller, J., & Budson, A. (2018). Current understanding of Alzheimer’s disease diagnosis and treatment. F1000Research, 7, F1000 Faculty Rev-1161. https://doi.org/10.12688/f1000research.14506.1

Zucchella, C., Sinforiani, E., Tamburin, S., Federico, A., Mantovani, E., Bernini, S., … & Bartolo, M. (2018). The multidisciplinary approach to Alzheimer’s disease and dementia. A narrative review of non-pharmacological treatment. Frontiers in neurology, 9, 1058. https://doi.org/10.3389/fneur.2018.01058