Pharmacological Intervention for Major Neurocognitive Disorder Due to Alzheimer’s Disease


Mr. Akkad is a 76-year-old Iranian male who is brought to your office by his eldest son for “strange behavior.” Mr. Akkad was seen by his family physician, who ruled out any organic basis for Mr. Akkad’s behavior. All laboratory and diagnostic imaging tests (including a CT scan of the head) were normal.

According to his son, he has been demonstrating some strange thoughts and behaviors for the past two years, but things seem to be getting worse. Per the client’s son, the family noticed that Mr. Akkad’s personality began to change a few years ago. He began to lose interest in religious activities with the family and became more “critical” of everyone. They also noticed that things he used to take seriously had become a source of “amusement” and “ridicule.”

Over the course of the past two years, the family has noticed that Mr. Akkad has been forgetting things. His son also reports that sometimes he has difficulty “finding the right words” in a conversation and then will shift to an entirely different line of conversation.




During the clinical interview, Mr. Akkad is pleasant and cooperative and seems to enjoy speaking with you. You notice some confabulation during various aspects of memory testing, so you perform a Mini-Mental State Exam. Mr. Akkad scores 18 out of 30 with primary deficits in orientation, registration, attention & calculation, and recall. The score suggests moderate dementia.



Mr. Akkad is a 76-year-old Iranian male who is cooperative with today’s clinical interview. His eye contact is poor. Speech is clear and coherent but tangential at times. He makes no unusual motor movements and demonstrates no tic. The self-reported mood is euthymic. Affect, however, is restricted. He denies visual or auditory hallucinations. No delusional or paranoid thought processes were noted. He is alert and oriented to person, partially oriented to place, but is disoriented to time and event [he reports that he thought he was coming to lunch but “wound up here”- referring to your office, at which point he begins to laugh]. Insight and judgment are impaired. Impulse control is also impaired, as evidenced by Mr. Akkad’s standing up during the clinical interview and walking toward the door. When you asked where he was going, he stated that he did not know. Mr. Akkad denies suicidal or homicidal ideation.

Diagnosis: Major neurocognitive disorder due to Alzheimer’s disease (presumptive)



§ Folstein, M. F., Folstein, S. E., & McHugh, P. R. (2002). Mini-Mental State Examination (MMSE). Lutz, FL: Psychological Assessment Resources.

You will focus on neurological and musculoskeletal diseases.   Please make sure to include dosing and side effects in your assignment.

This week you will be assigned an interactive media piece that will help construct your assignment.

Please access the link for the week 8 decision tree.

There is a decision tree at the bottom to select from that says Decision Point 1.   Please select Razadyne 4 mg PO BID  You will then be taken through subsequent assessments based on your initial selection.


  •  The client returns to the clinic in four weeks
  •  The client is accompanied by his son, who reports that his father is “no better” from this medication
  •  He reports that his father is still disinterested in attending religious services/activities and continues to exhibit disinhibited behaviors
  •  You continue to note confabulation and decide to administer the MMSE again. Mr. Akkad again scores 18 out of 30 with primary deficits in orientation, registration, attention & calculation, and recall

Decision Point Two

Discontinue Razadyne and begin with Exelon (rivastigmine) 1.5 mg Orally BID


  •  The client returns to the clinic in four weeks
  •  The client’s son reports that the client is tolerating the medication well but is still concerned that his father is no better
  •  He states that his father is still not interested in attending religious services with the family, and he is still concerned that his father is still easily amused by things he once found serious

Decision Point Three

Continue the current dose of Exelon and reevaluate on the next office visit.

(above choice should be adjusted already instead of maintaining the dose, Please make a suggestion based on the guidelines below, I am considering adding Namenda on the course once the therapeutic level of Exelon is achieved without side effects.)

Cholinesterase inhibitors can take months to demonstrate any stabilization in the degenerative course of Alzheimer’s disease. Since the client has had no side effects, it would be prudent to consider increasing the Exelon dose to 3 mg orally BID. Recall that the target dose of Exelon is 12 mg orally daily in divided doses, or a transdermal patch delivering 9.5 mg daily could be used. Slow titration of the drug toward a therapeutic dose will decrease the risk of side effects. These should be teaching points directed toward the client and his son.

You could maintain the current dose of Exelon and reevaluate at the next office visit, but since the client is having no side effects and the client has been on the current dose for at least 4 weeks, it would probably be advisable to increase at this time to facilitate the goal of arriving at a therapeutic dose of the medication.

It may be early to augment with Namenda. Maximization of the Exelon dose should first occur, then augmentation with an NMDA receptor antagonist would be appropriate, but Namenda should be started at 5 mg orally daily and then titrated up to a maximum dose of 10 mg orally BID. Doses over 5 mg orally daily should be divided into two doses, or the drug can be switch to an extended release preparation.

Finally, it is important to note that changes in the MMSE should be evaluated over the course of months, not weeks. The absence of change in the MMSE after 4 weeks of treatment should not be a source of concern.


Pharmacological Intervention for Major Neurocognitive Disorder Due to Alzheimer’s Disease

Alzheimer’s disease (AD), the most prevalent cause of cognitive decline, is severe enough to impede daily activities. It is a neurodegenerative condition that often affects persons over 65, affecting reasoning, memory, judgment, language, comprehension, and attention (Kumar & Tsao, 2019). Insidious onset and gradual impairment of cognition and behavioral functioning characterize Alzheimer’s disease (Cummings, 2021). Although many medicines may alleviate the symptoms of Alzheimer’s disease, the disease itself is incurable. This assignment examines pharmaceutical therapies for significant neurocognitive dysfunction with a presumptive Alzheimer’s diagnosis.

Case Summary

Mr. Akkad, a 76-year-old Iranian man, exhibits dementia symptoms such as forgetfulness, difficulty finding the right words, and behavioral changes. His family doctor found no organic cause for his conduct after normal blood and imaging tests. Mr. Akkad cooperated during the clinical interview but showed confabulation during the memory assessment. On the Mini-Mental State Test, he scored 18 out of 30, indicating mild dementia. During his mental status evaluation, he demonstrated poor eye contact, poor judgment, tangential speech, impaired insight, restricted affect, disorientation to time and event, and poor impulse control. The presumptive diagnosis is Alzheimer’s disease-related significant neurocognitive dysfunction.

Decision Point One

Treatment started with Razadyne (galantamine) 4 mg BID orally. Galantamine belongs to the group of medicines known as acetylcholinesterase inhibitors (Kalola & Nguyen, 2021). It is advised to start the medication at the lowest dosage possible and gradually increase it after determining its clinical efficacy and tolerability. The initial dosage for treatment is 4 mg twice daily. After at least four weeks, the dosage can be increased to 16 mg/day and then further escalated to a maximum of 24 mg/day (Kalola & Nguyen, 2021). When the patient with his son revisited the clinic in a month, the son reported that the medication had not improved his father. I keep noticing confabulation, and when I repeat the MMSE, the patient got 18 out of 30, with a deficiency in orientation, registration, attention & calculation, and recollection.

Decision Point Two

We stop Razadyne and start Exelon (rivastigmine) 1.5 mg orally BID. When the client comes to the facility in four weeks, his son notes he tolerates the medication appropriately but is still anxious that his father is not improving. Rivastigmine belongs to the cholinesterase inhibitor category of medications. (Patel & Gupta, 2023). According to studies, long-term rivastigmine treatment at the highest dosage results in the most substantial improvement in cognitive performance (Eldufani & Blaise, 2019). However, MMSE scores between 26 and 24, or 10 to 11, qualify for therapy.

Decision Three

We maintain the current Exelon dosage and reassess at the subsequent doctor visit. It may take months for cholinesterase inhibitors to show any stabilization in the degenerative course of Alzheimer’s disease. The Exelon dose should be increased to 3 mg orally BID as the client has no adverse effects. Exelon’s recommended dose is 12 mg, taken twice a day by mouth, spaced out to reduce the chance of side effects.

Perhaps now is not the right time to add Namenda. The optimal dose of Exelon should be reached before considering the addition of an NMDA receptor antagonist. Namenda dosage should begin at 5 mg orally daily and titrate up to 10 mg orally BID. The above 5 mg used orally daily should be divided into two doses, or an extended-release medication can be used instead (Kuns et al., 2020). The healthcare provider should emphasize that they need to assess the changes in the MMSE over months rather than weeks. If the MMSE has not improved after four weeks of treatment, that is not necessarily a cause for concern. Patients, families, and caregivers should be aware of the condition’s progressive nature and have reasonable expectations for treatment.


Cummings, J. (2021). The role of neuropsychiatric symptoms in research diagnostic criteria for neurodegenerative diseases. The American Journal of Geriatric Psychiatry, 29(4), 375–383.

Eldufani, J., & Blaise, G. (2019). The role of acetylcholinesterase inhibitors such as neostigmine and rivastigmine on chronic pain and cognitive function in aging: A review of recent clinical applications. Alzheimer’s & Dementia: Translational Research & Clinical Interventions, 5, 175–183.

Kalola, U. K., & Nguyen, H. (2021). Galantamine. PubMed; StatPearls Publishing.

Kumar, A., & Tsao, J. W. (2019, August 18). Alzheimer disease.; StatPearls Publishing.

Kuns, B., Rosani, A., & Varghese, D. (2020). Memantine. PubMed; StatPearls Publishing.

Patel, P. H., & Gupta, V. (2023). Rivastigmine. PubMed; StatPearls Publishing.

Do you need help with you nursing essay or assignment? You are in the right place. We have expert nursing writers at your disposal. Message us today to get the best offers!