Background: Mr. Charles Wingate, 76-Year-Old Caucasian Male

Backgroundmr Charles Wingate Is A 76 Year Old Caucasian Male Who Pres

Backgroundmr Charles Wingate Is A 76 Year Old Caucasian Male Who Pres

BACKGROUND 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.

SUBJECTIVE 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. His 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.”

OBJECTIVE 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 mEq/L.

MENTAL STATUS EXAM 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 mini-mental status exam (MMSE) on Mr. Wingate.

RESULTS OF MMSE Score of 17, with primary deficits in orientation; calculation; recall (he was unable to recall any of the three items presented after 5 minutes); and he was unable to perform serial 7’s or spell the word “WORD” in reverse, despite the fact that he is a high school graduate and attended 1 year of college. He also needed prompting with the three-step command. His score suggests severe cognitive impairment. At this point, please discuss any additional diagnostic tests you would perform on Mr. Wingate.

Paper For Above instruction

The case of Mr. Charles Wingate presents a complex scenario involving progressive cognitive decline, behavioral changes, and neurological symptoms, necessitating a thorough diagnostic approach to determine the underlying etiology of his neurocognitive impairment. Given his presentation, the initial step involves comprehensive neuropsychological assessments complemented by neuroimaging and laboratory studies to differentiate among potential causes such as Alzheimer’s disease, frontotemporal neurocognitive disorder, or Lewy body dementia.

Additional Diagnostic Tests

To refine the diagnosis, several targeted assessments should be prioritized. First, neuroimaging studies like magnetic resonance imaging (MRI) of the brain are essential to evaluate structural brain changes, rule out vascular lesions, tumors, or other organic pathologies, and look for characteristic patterns associated with different neurocognitive disorders. In Alzheimer’s disease, MRI typically shows hippocampal atrophy and diffuse cortical atrophy, especially in the temporoparietal regions (Jack et al., 2013). Conversely, frontotemporal dementia often presents with predominant frontal and temporal lobe atrophy (Rabinovici et al., 2015). Meanwhile, for Lewy body dementia, MRI may reveal less prominent atrophy but assess for concomitant features like occipital hypoperfusion or abnormalities in dopaminergic pathways with specialized imaging modalities.

Second, a positron emission tomography (PET) scan with amyloid tracers (e.g., florbetapir PET) can detect amyloid deposits characteristic of Alzheimer’s pathology (Hoon et al., 2014). These imaging techniques are increasingly used to support clinical diagnoses, especially in early or ambiguous cases. Third, a comprehensive neuropsychological battery would provide detailed cognitive profiles, assessing memory, executive functions, visuospatial abilities, language, and attention, further clarifying the pattern of deficits (McKhann et al., 2011).

Laboratory tests are also crucial. Rechecking serum electrolytes, including sodium (noting his level of 130 mEq/L indicating hyponatremia), as well as assessing vitamin B12, folate, thyroid function tests, and screening for infections or metabolic disturbances, is imperative. These factors can contribute to reversible cognitive impairment. Additionally, screening for Parkinsonian features through neurological examination can assess the nature and severity of his motor symptoms. Genetic testing may be considered if a familial pattern or early-onset cases are suspected, although Mr. Wingate reports no known family history.

Implications of Ethical Considerations

Throughout the diagnostic process and subsequent treatment planning, ethical principles like autonomy, beneficence, nonmaleficence, and justice must guide clinical decisions. Involving Mr. Wingate and his family in shared decision-making is vital to respect his autonomy. Clear communication about diagnostic findings, potential interventions, and prognosis is essential to foster trust and ensure informed consent. Additionally, issues related to capacity—especially considering his cognitive decline—necessitate assessing his ability to make decisions independently and involving legal surrogates if needed (American Nurses Association, 2014).

Moreover, confidentiality must be maintained, and sensitive handling of diagnoses like Alzheimer’s disease or Lewy body dementia is required to prevent stigma. Ethical considerations also extend to ensuring that his care aligns with his values and preferences, which may become increasingly relevant as his condition progresses. For instance, advanced directives and discussions about long-term care preferences should be initiated early, respecting his dignity and autonomy (Sadock et al., 2014).

In terms of treatment, ethical considerations include weighing benefits versus risks of pharmacologic interventions. For example, cholinesterase inhibitors like rivastigmine are indicated in Alzheimer’s disease but require monitoring for adverse effects. Decisions about initiating antipsychotics or other psychotropics should be made cautiously, considering nonpharmacological options first. Family involvement and support are equally important, necessitating transparent communication about prognosis and caregiving challenges.

Conclusion

The management of Mr. Wingate’s case exemplifies the importance of a multidisciplinary approach, integrating neuroimaging, neuropsychological testing, laboratory assessments, and ethical principles to establish an accurate diagnosis and formulate an individualized treatment plan. Respecting patient autonomy, providing clear communication, and addressing ethical issues related to capacity and confidentiality are integral to delivering holistic care in neurocognitive disorders. Ongoing evaluation and support for both Mr. Wingate and his family are essential components to optimize quality of life and maintain dignity amid cognitive decline.

References

• American Nurses Association. (2014). Psychiatric-mental health nursing: Scope and standards of practice (2nd ed.). Washington, DC: Author.
• Hoon, C., Ward, M., Gordon, M., & Peden, N. (2014). Advances in Amyloid PET imaging: Current applications and future directions. Journal of Neuroimaging, 24(2), 161–169.
• Jack, C. R., Jr., Knopman, D. S., Jagust, W. J., et al. (2013). Tracking pathophysiological processes in Alzheimer’s disease: An updated hypothetical model of dynamic biomarkers. Lancet Neurology, 12(2), 207–216.
• McKhann, G. M., Knopman, D. S., Chertkow, H., et al. (2011). The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups. Alzheimer's & Dementia, 7(3), 263-269.
• Rabinovici, G. D., Jagust, W. J., Fox, N. C., et al. (2015). A roadmap for clinical trials in atypical Alzheimer’s disease. Alzheimer’s & Dementia, 11(8), 977–985.
• Sadock, B. J., Sadock, V. A., & Ruiz, P. (2014). Kaplan & Sadock’s synopsis of psychiatry: Behavioral sciences/clinical psychiatry (11th ed.). Philadelphia, PA: Wolters Kluwer.
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