Neurocognitive Disorders Example Paper

Neurocognitive Disorders Example Paper

You will be asked to make three decisions concerning the diagnosis and treatment for this client. Be sure to consider co-morbid physical as well as mental factors that might impact the client’s diagnosis and treatment Neurocognitive Disorders Example Paper.

At each Decision Point, stop to complete the following:

Brief introduction with purpose of the assignment

  • Decision #1: Differential Diagnosis

o             Which Decision did you select? Major Cognitive Neurocognitive Disorder due to Alzheimer’s Disease

o             Why did you select this Decision? Support your response with evidence and references to the Learning Resources.

o             What were you hoping to achieve by making this Decision? Support your response with evidence and references to the Learning Resources.

o             Explain any difference between what you expected to achieve with Decision #1 and the results of the Decision. Why were they different?

  • Decision #2: Treatment Plan for Psychotherapy: Begin Memantine 5 mg orally daily

o             Why did you select this Decision? Support your response with evidence and references to the Learning Resources.

o             What were you hoping to achieve by making this Decision? Support your response with evidence and references to the Learning Resources.


o             Explain any difference between what you expected to achieve with Decision #2 and the results of the Decision. Why were they different?

  • Decision #3: Treatment Plan for Psychopharmacology: Begin Clonazepam 0.25 mg orally at bedtime

o             Why did you select this Decision? Support your response with evidence and references to the Learning Resources.

o             What were you hoping to achieve by making this Decision? Support your response with evidence and references to the Learning Resources.

o             Explain any difference between what you expected to achieve with Decision #3 and the results of the decision. Why were they different Neurocognitive Disorders Example Paper?

  • Also include how ethical considerations might impact your treatment plan and communication with clients and their family.


Mr. Charles Wingate is a 76-year-old Caucasian male who presents to your office for an initial psychiatric evaluation. He is accompanied by his eldest son, Mark, who lives with Mr. Wingate. Mr. Wingate was referred to you by his primary care provider who has performed an extensive diagnostic workup to rule out an organic basis for his changes in cognition. Mr. Wingate’s son Mark has verbalized a concern that Mr. Wingate may have Alzheimer’s disease. When questioned, Mr. Wingate states that he is unaware of anyone in his family ever having been diagnosed with Alzheimer’s disease.


Mr. Wingate states that he has always been “a little bit forgetful,” but he noticed that in his 60s and 70s, it got worse. Mark states that “for the past 2 years, it has been getting worse. He doesn’t even notice how bad his memory has become.” On at least two occasions, Mr. Wingate has gotten lost when he was driving to the grocery store. Mr. Wingate protested his disagreement with this accusation stating, “but they were doing road construction, anyone could have gotten mixed up!” While his son conceded to this, he pointed out that Mr. Wingate’s memory has caused some other problems, such as errors with paying his monthly utility bills (at one point, the electric company threatened to shut off his electricity due to his nonpayment of the bill). His son Mark also pointed out that the family is concerned for Mr. Wingate’s safety as he twice left his keys hanging in the door and just two evenings ago, put food in oven and forgot about it until the smoke detector in the kitchen began to alarm. Mr. Wingate also has had a few issues with managing his medications. Specifically, he took too many Norvasc tablets a few months ago, which resulted in hypotension and a fall. Since that time, Mark’s wife has been setting up Mr. Wingate’s pills in pill boxes, but recently, multiple “missed doses” have been noted. Mr. Wingate states: “but those are my night pills that I miss—I’m always better at remembering things in the morning.” Mark agrees, stating that Mr. Wingate’s cognition does vary throughout the course of the day and appears to worsen in the evening. He also reports that his father seems much less alert in the evenings, and more alert in the mornings. Mr. Wingate reports that he has had poor sleep for “a long time now.” He does report that over the past few months, he has been having what he describes as “very vivid nightmares.” His son states that sometimes he is awakened by his father’s yelling during nightmares, and enters his father’s room, and sees his father swinging or kicking in his sleep. He reports that his appetite is “alright” and that his energy levels do fluctuate throughout the course of the day. He states: “sometimes, I can concentrate really well; other times I can’t … it is very frustrating!” Specific to substance use, Mr. Wingate notes that he used to enjoy a glass of wine or two with dinner, but states that it just doesn’t interest him, anymore. Plus, he stated that he notices that when he does drink, he develops slow muscle contractions. Mr. Wingate’s son also shares a concern about his father’s abnormal movements. He states that for about the last 6 months, his father has had problems with coordination. He states that he raised these concerns with the family doctor who suggested it may be “late onset Parkinson’s disease.” However, he was not treated because the symptoms were “not that bad.”


Mr. Wingate was overall calm and pleasant during the clinical interview. Throughout the clinical interview, you notice that Mr. Wingate is not really involved in the discussion. He seems somewhat indifferent to the assessment and does not seem very concerned with what is being discussed. He only protested when discussing how he got lost on his way to the supermarket and his evening medication dose. Review of systems and screening physical assessment were unremarkable, with the exception of fine resting tremors noted in both of Mr. Wingate’s hands. The psychiatric/mental health nurse practitioner (PMHNP) also reviewed laboratory studies that were sent from Mr. Wingate’s primary care provider; they were within normal limits with the exception of a serum sodium level of 130


Mr. Wingate is alert. He is oriented to person, place, and partially oriented to time (he knows that it is morning, but cannot tell the hour). His speech is clear, coherent, goal directed, and spontaneous. Mr. Wingate’s self-reported mood is “ok.” Affect is somewhat constricted. His eye contact is fleeting throughout the clinical interview. He denies visual or auditory hallucinations, no overt delusional or paranoid thought processes appreciated. Judgment seems well preserved, but insight appears impaired as he is having trouble understanding why his son brought him to this appointment. Concentration and attention also appear impaired, which prompts the PMHNP to perform a minimental status exam (MMSE) on Mr. Wingate.


This essay entails the following; a briefcase description of Mr. Charles Wingate, a patient who presents with the neuro-cognitive disorder. Secondly, it will describe three decisions made for the care plan of the patient, one, the diagnosis assigned to the patient explaining why the specific diagnosis was chosen. Two, a decision on the psychotherapy treatment plan. a description of the reason behind the decision will be explained. Three, another decision will be made after assessing the patient in the next four weeks. An explanation of the psychotherapy treatment plan chosen at this point will be explained basing it on the literature evidence. Lastly, a conclusion to summarize this essay Neurocognitive Disorders Example Paper.

Case study

Patient Charles Wingate, a 76-year male presents memory loss, he says that it has worsened in his 60s and 70s although his son Mark, says that it has worsened in the last two years. The patent has a history of getting lost twice and has forgotten to pay his bills. His safety is in danger as he has forgotten keys outside the door twice, has forgotten food in the oven and he overdosed. His sleeping pattern has been altered as he gets nightmares. His appetite is normal and his energy levels do not fluctuate. He has the poor concentration at times and it is made worse when he drinks. In addition to this when he drinks his muscle contraction becomes slow. On physical exam, it is noticed that he has tremors on his hands. On the mental status exam, it is noted that he is oriented although cannot specify the hour/time, his affect is constricted, he is indifferent, he has impaired insight, concentration, and attention.

Decision point one.

The patient’s presentation directs the diagnosis to the major cognitive neurocognitive disorder as a result of Alzheimer’s disease. Alzheimer’s or senile dementia is a chronic, progressive and degenerative brain disorder (Albert et al., 2014). It is accompanied by very profound effects on cognition, memory and the ability of self-care. in most cases, it affects people above 60 years. It is a spectrum disorder as it starts with early memory loss and progresses to functional dependence which later on translates to death (Castellano et al., 2015).

Alzheimer disease is a (Diagnostic and Statistical Manual of Mental Disorder- fifth edition) DSM-5 disorder under dementia (Diagnostic, D. S. M. V. 2013). There two categories of the effects of this disorder, it can either cause major or mild neurocognitive disorder. The DSM-V dictates that for its diagnosis there have to be effected on the cognitive function. It further gives six cognitive domains; the complex attention, executive functioning, learning, and memory, language, perceptual motor functioning and social cognition. In major neurocognitive disorder, one or more of the cognitive domains are adversely affected causing impairment in function which dependence. In mild neurocognitive disorder, these conditions are treatable restoring the patients cognitive functioning (Sachdev et al., 2014; Sperling et al., 2014).


In patient Charles Wingate, his presentations point to the major neurocognitive disorder as a result of Alzheimer’s disease as he has cognitive impairment in different domains. Firstly, he has issues with the complex attention, he had selective and divided attention during the assessment. Secondly, the executive function, which includes planning, the working memory, and decision making. He forgot to pay his bills and he has been lost twice. Thirdly, his social cognition is affected as his insight is altered. he does not why he soon booked this appointment.  Fourthly his learning and memory have greatly been impaired as he has forgotten food in the oven, keys on the doors and to pay bills and also his concentration is impaired Neurocognitive Disorders Example Paper.

Decision point two

Selected decision

Begin Memantine 5 mg orally daily

Reasons for this choice

Memantine has a low to a moderate affinity of the N-Methyl-D-aspartate receptor (NMDAR) as an antagonist. It was approved as a psychotherapy drug in both moderate and severe Alzheimer’s diseases by two bodies, the European Agency for the Evaluation of Medicinal Products (EMEA), as well as the Food and Drug Administration (FDA) in 2002 and 2003 respectively. Memantine is a glutamine antagonist. Glutamine is one of the major excitatory neurotransmitters in the central nervous system. An increased concentration of glutamate causes an increase in the NMDAR which in turns causes increased Ca+2 influx which in turn causes excitotoxicity. To avoid this Memantine is neuroprotective, blocks the excessive NMDAR without causing a disruption of the normal activity. The most important/primary endpoint of Memantine is to improve the cognitive functioning the behavioral changes are considered to be secondary (Cummings, 2016; Peskind, et al., 2016).

Expected outcome

There are expectations on the cognitive functioning, behavioral, activity of daily living and global functioning. In cognition, there is an expectation of improved memory and concentration. On behavioral change, it is expected that his appetite will improve, his sleeping pattern will normalize by eliminating nightmares. On the ADLs and the global functioning, it is expected that he will be more independent.

The following side effects are expected; in the nervous system dizziness, gait abnormal and seizures. In the gastrointestinal disorders, constipation, vomiting, and pancreatitis. Expected to get a fungal infection, hypertension or/and venous thrombosis. It is can also cause psychotic disorders; somnolence, confusion, hallucination. It generally causes fatigue and headache (Cummings, 2016; Peskind, et al., 2016).

Differences from the expected outcome and the actual results

After four weeks of using Memantine, Mr. Wingate’s son reports that his father has been tolerating the drugs well although there has been no improvement in his memory and nightmare. he actually thinks that he is getting worse. In addition to this, he reports that his father has developed a visual hallucination which is vivid.

It is clear that the treatment plan has not improved the patient’s cognitive, behavior, ADLs and global functioning as expected. Despite this, the drug side effects are being manifested as he gets vivid visual hallucinations.

Decision point three

Selected decision

Begin Clonazepam 0.25 mg orally at bedtime.

Reasons for this choice

Clonazepam is a benzodiazepine that primarily acts by facilitating the GABAergic transmission in the GABA receptors that are on the dorsal raphe neurons. GABA acts by inhibiting raphe cell firing. Clonazepam does not affect serotonin production although it affects its utilization (Jenner, Pratt, & Marsden, 2016).

The above mode of action causes improvement in the cognitive functioning, improves on the behavior of the patient and specifically the sleeping patterns. It reduces agitation and improves the quality of sleep the patient gets. It also has an antimyclonus effect which will reduce the patient hand tremors (Ancill, Carlyle, Liang, & Holliday, 2016) Neurocognitive Disorders Example Paper.

Expected outcome

There is an expectation that the cognitive functioning, behavioral, sleeping patterns will be improved while agitation and the hand tremors will be reduced. In addition to this the following side effects will be expected; muscle weakness, dizziness, drowsiness, slurred speech, confusion, reduced judgment, and syncope (Ancill, Carlyle, Liang, & Holliday, 2016).

Differences from the expected outcome and the actual results

The cognitive functioning, the behavioral and sleeping patterns improve. The patient’s hallucinations and nightmares are lost although the patient experiences confusion, dizziness and syncope.


In summary, the patient experiences Alzheimer’s disease, a major neurocognitive has greatly affected his cognitive, behavior, ADLs and global functioning. His treatment plan starts with Memantine which causes more harm than good causing a change of therapy to clonazepam which causes an improvement.


Albert, M. S., DeKosky, S. T., Dickson, D., Dubois, B., Feldman, H. H., Fox, N. C., … & Snyder, P. J. (2014). The diagnosis of mild cognitive impairment due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimer’s & Dementia, 7(3), 270-279.

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders; DSM-V. Washington DC.

Ancill, R. J., Carlyle, W. W., Liang, R. A., & Holliday, S. G. (2016). Agitation in the demented elderly: a role for benzodiazepines? International clinical psychopharmacology.

Castellano, C. A., Nugent, S., Paquet, N., Tremblay, S., Bocti, C., Lacombe, G., … & Cunnane, S. C. (2015). Lower brain 18F-fluorodeoxyglucose uptake but normal 11C-acetoacetate metabolism in mild Alzheimer’s disease dementia. Journal of Alzheimer’s Disease, 43(4), 1343-1353.

Cummings, J. L., Schneider, E., Tariot, P. N., Graham, S. M., & Memantine MEM-MD-02 Study Group. (2016). Behavioral effects of Memantine in Alzheimer disease patients receiving donepezil treatment. Neurology, 67(1), 57-63.

Diagnostic, D. S. M. V. (2013). statistical manual of mental health disorders: DSM-5. 5.

Jenner, P., Pratt, J. A., & Marsden, C. D. (2016). Mechanism of action of clonazepam in myoclonus in relation to effects on GABA and 5-HT. Advances in neurology, 43, 629-643.

Peskind, E. R., Potkin, S. G., Pomara, N., Ott, B. R., Graham, S. M., Olin, J. T., … & Memantine MEM-MD-10 Study Group. (2006). Memantine treatment in mild to moderate Alzheimer disease: a 24-week randomized, controlled trial. The American journal of geriatric psychiatry, 14(8), 704-715.

Sachdev, P. S., Blacker, D., Blazer, D. G., Ganguli, M., Jeste, D. V., Paulsen, J. S., & Petersen, R. C. (2014). Classifying neurocognitive disorders: the DSM-5 approach. Nature Reviews Neurology, 10(11), 634.

Sperling, R. A., Aisen, P. S., Beckett, L. A., Bennett, D. A., Craft, S., Fagan, A. M., … & Park, D. C. (2014). Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimer’s & Dementia, 7(3), 280-292 Neurocognitive Disorders Example Paper.




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