Alzheimer`s Dementia: Managing Psychosis and Agitation

Alzheimer’s disease, along with Pick disease, thyroid dysfunction, vascular disorders, tumors, normal-pressure hydrocephalus, and vitamin B12 deficiency, is one of the leading causes of dementia. Alzheimer’s dementia patients exhibit gradual memory loss, odd behavior, altered thinking, and an inability to execute daily tasks. Alzheimer’s dementia has been linked to hereditary and environmental variables such as age, vascular disease, and decreasing brain size (Duthey, 2013).

Because environmental factors play a role in the development and progression of Alzheimer’s dementia, I will incorporate many non-pharmacological measures in the management plan in addition to drugs. Cessation of smoking, support groups, alcohol, weight reduction, controlled diet and light physical exercise were highlighted by Reitz et al., (2014) as environmental factors that can hinder progression and worsening of symptoms.

Medication

The primary objectives of treating the 69-year-old patient include; improve patient`s quality of life, restore patient`s functional status and prevent progression of signs and symptoms.

Cholinesterase Inhibitors

Acetylcholine is an important neurotransmitter as far as the pathophysiology of AD is concerned. Reitz et al., (2014), alluded to the fact that low levels of acetylcholine worsen AD. Cholinesterase inhibitors inhibit the breakdown of acetylcholine in the synaptic junction leading its accumulation and improved brain function. Examples of drugs include donepezil and tacrine.

Antiglutamatergic Therapy

The physiological effects of an excitatory neurotransmitter, glutamate, on N-methyl-D-aspartate receptors in AD lead to neuronal loss and worsening of the signs and symptoms of Alzheimer`s dementia. Use of anti glutamatergic agents such as memantine is therefore justified since the drug ensures glutamate does not bind to the NMDA receptors (Reitz et al., 2014).

Managing Depression

Depression in AD patient presents as anorexia, fatigue, irritability, and insomnia. Selective serotonin reuptake inhibitors such as paroxetine and fluoxetine are preferred due to their selective nature and decreased side effects. Other agents such as tricyclic antidepressants (Amitriptyline and Nortriptyline) and monoamine oxidase inhibitors (Phenelzine) can be used in managing depression.

Managing Psychosis and Agitation

According to Dubois et al., 2014, benzodiazepines (diazepam), carbamazepine and valproate are effective in controlling behavioral disorders in AD. Antipsychotic Clozapine and Risperidone are used in managing psychosis and agitation. Unlike the typical antipsychotics, Clozapine and Risperidone do not have extrapyramidal side effects.

Other treatment approaches in special population include use of estrogen in post-menopausal women, anti-inflammatory drugs such as diclofenac in lowering risk of AD, lipid-lowering agents such atorvastatin to maintain brain vascular health.

Comorbidities

Comorbidities in AD lead to decreased self-care, lower recognition, increased morbidity and mortality (Duthey, 2013). Comorbidities become a critical issues if they affect the brain directly and if they predispose to increased adverse effects from concomitant medications. Vascular diseases such as diabetes mellitus, hypertension, and coronary artery disease enhance dementia and influence the presenting signs and symptoms. Managing these comorbidities positively impact on AD management. Use of anticholinergic drugs for respiratory and cardiovascular conditions lead to pharmacological antagonism, therefore, worsening AD symptoms.

Lab tests to monitor progress

Biomarkers indicate a pathological condition (Reitz et al., 2014). Magnetic resonance imaging (MRI) is used to visualize the structure of the brain. In AD, the area involved in memory retention and processing (hypothalamus) is reduced in size. Other features such as decreased brain metabolism can be assessed by Functional MRI and computer-aided tomography and positron emission tomography.

Levels of biomarkers in the CSF can be used in monitoring and diagnosis. Features such as increased phosphorylated tau, decreased amyloid-B and increased total tau indicate presence r deterioration of AD. CSF biomarkers of inflammation such as C-reactive protein, interleukins 6 and tumor necrosis factors can be used for diagnosis.

Biomarkers linked to RNA and DNA can also be used. However, this is limited by the complexity of obtaining RNA from blood and the nucleotide polymorphism among individuals. Depending on the financial ability of my patient, I will monitor his/her progress using the above-discussed methods.

References

Duthey, B. (2013). Background paper 6.11: Alzheimer disease and other dementias. A Public

Health Approach to Innovation, 1-74.

Dubois, B., Feldman, H. H., Jacova, C., Hampel, H., Molinuevo, J. L., Blennow, K., ... &

Cappa, S. (2014). Advancing research diagnostic criteria for Alzheimer’s disease: the

IWG-2 criteria. The Lancet Neurology, 13(6), 614-629.

Reitz, C., & Mayeux, R. (2014). Alzheimer disease: epidemiology, diagnostic criteria, risk

factors and biomarkers. Biochemical pharmacology, 88(4), 640-651.