Neurocognitive Disorders Case 3 Background Mr. Charles Winga

Case 3neurocognitive Disordersbackgroundmr Charles Wingate Is A 76 Y

Examine Case 3 above: You will be asked to make three decisions concerning the diagnosis and treatment for this client described above. Be sure to consider co-morbid physical as well as mental factors that might impact the client’s diagnosis and treatment. At each decision point, stop to complete the following: Decision Point 1 BASED ON THE INFORMATION PROVIDED IN THE SCENARIO ABOVE, WHICH OF THE FOLLOWING DIAGNOSES WOULD THE PSYCHIATRIC/MENTAL HEALTH NURSE PRACTITIONER (PMHNP) GIVE TO MR. WINGATE? In your write-up of this case, be certain to link specific symptoms presented in the case to DSM–5 criteria to support your diagnosis. OPTIONS to CHOOSE FROM BELOW: Major frontotemporal neurocognitive disorder (FTNCD) Major neurocognitive disorder due to Alzheimer’s disease Major neurocognitive disorder with Lewy bodies Decision #1 ANSWER: Differential Diagnosis 1) Which Decision did you select? Major neurocognitive disorder with Lewy bodies 2) Why did you select this Decision? Support your response with evidence and references to the Learning Resources. 3) What were you hoping to achieve by making this Decision? Support your response with evidence and references to the Learning Resources. 4) Explain any difference between what you expected to achieve with Decision #1 and the results of the Decision. Why were they different? Decision Point 2 BASED ON THIS DIAGNOSIS, SELECT YOUR CHOICE OF ACTIONS: OPTIONS to CHOOSE FROM BELOW: Begin Rivastigmine 1.5 mg orally twice a day Begin Olanzapine 5 mg orally at bedtime Begin Ramelteon 8 mg at bedtime Decision #2 ANSWER: Treatment Plan for Psychotherapy 1) Why did you select this Decision? Begin Rivastigmine 1.5 mg orally twice a day 2) Support your response with evidence and references to the Learning Resources. 3) What were you hoping to achieve by making this Decision? Support your response with evidence and references to the Learning Resources. 4) Explain any difference between what you expected to achieve with Decision #2 and the results of the Decision. Why were they different? RESULTS OF DECISION POINT TWO · Client returns to clinic in four weeks · Upon his return to your office, Mr. Wingate’s son reported that Mr. Wingate seems to be tolerating the medication well, but he has not noticed any improvement in his father’s memory. He denies any worsening of other symptoms, but also reports no improvement either. · Mr. Wingate’s son does report that Mr. Wingate’s nightmares appear to be getting worse in that he seems to “act out” his nightmares more. Decision Point 3 BASED ON THE ABOVE INFORMATION IN THE RESULT OF DECISION POINT TWO, SELECT YOUR NEXT ACTION. BE CERTAIN TO DISCUSS THE RATIONALE FOR YOUR DECISION. OPTIONS to CHOOSE FROM BELOW: Begin Clonazepam 0.5 mg orally at bedtime Begin Seroquel 25 mg orally at bedtime Educate Mr. Wingate and his son regarding the fact that it will take time for the Rivastigmine to stop the nightmares Decision #3: Treatment Plan for Psychopharmacology 1) Why did you select this Decision? Begin Clonazepam 0.5 mg orally at bedtime 2) Support your response with evidence and references to the Learning Resources. 3) What were you hoping to achieve by making this Decision? Support your response with evidence and references to the Learning Resources. 4) Explain any difference between what you expected to achieve with Decision #3 and the results of the decision. Why were they different? Decision #4 Also write and include how ethical considerations might impact your treatment plan and communication with clients and their family. Guidance to Student In the case of Mr. Wingate, he meets the diagnostic criteria for major neurocognitive disorder as evidenced by a decline from a previous level of performance in more than one cognitive domain—in this case, complex attention and executive function. The decline is based on a knowledgeable informant, as well as a clinician (the patient’s primary care provider) who referred him to you, as well as substantial impairment in another quantified clinical assessment (the MMSE). Cognitive deficits that Mr. Wingate demonstrates interfere with independence in everyday activities and he requires help with complex IADLs such as medication management and paying bills. Nothing in the scenario suggests that delirium could be responsible for the cognitive decline, nor is anything in the scenario suggestive of another mental disorder. While one may be initially inclined to consider major neurocognitive disorder due to Alzheimer’s disease, probable Alzheimer’s would require evidence of a causative genetic mutation either from family history or genetic testing; and/or decline in memory and learning and at least one other cognitive domain; steadily progressive, gradual decline in cognition without extended plateaus; and no evidence of mixed etiology (i.e., absence of other neurodegenerative or cerebrovascular disease, or another neurological, mental, or systemic disease or condition likely contributing to the cognitive decline). Similarly, while there is some evidence of mild apathy, and decline in executive abilities, there is insufficient evidence of three or more behavioral symptoms that would be needed to make a diagnosis of major frontotemporal neurocognitive disorder (e.g., behavioral disinhibition, loss of sympathy or empathy, perseverative, stereotyped or compulsive/ritualistic behavior, hyperorality and dietary changes, or prominent decline in social cognition and/or executive abilities) nor is there evidence of prominent decline in language ability, in the form of speech production, word finding, object naming, grammar, or word comprehension that would suggest major frontotemporal neurocognitive disorder. In Mr. Wingate’s case, there is clear evidence of fluctuating cognition, and spontaneous features of Parkinsonism, which had their onset subsequent to the development of cognitive decline. These symptoms, coupled with the presence of a rapid eye movement sleep behavior disorder, are suggestive of major neurocognitive disorder with Lewy bodies. Diagnostic testing should focus on determining the presence of a synucleinopathy. Since Mr. Wingate’s symptoms are more consistent with MNDLB, the addition of Seroquel may result in severe side effects that could be life threatening and include severe sedation, muscle rigidity, delirium, neuroleptic malignant syndrome, and depending on the source of the study reviewed, neuroleptics may be associated with a 2- to 3-fold increase in mortality, including cerebral vascular accident. Also, although Seroquel can be used off-label to induce sleep in some patients, there is an FDA warning against the use of antipsychotics in older adults with dementia as they have been associated with an increase in mortality. Acetylcholinesterase inhibitors may be useful in the treatment of NDAD, but there is limited data of their efficacy with MNDLB. If the PMHNP decides to try an acetylcholinesterase inhibitor, the PMHNP should always begin with the lowest starting dose, and then slowly titrate upward, being mindful of the development of side effects. The addition of low-dose Clonazepam (0.25 or even 0.125 mg) may be considered as a treatment for REM sleep disorders in individuals with MNDLB. Since Clonazepam has a long half-life, the PMHNP should begin at a low dose, and slowly titrate upward, being mindful to educate the client and family about potential side effects and therapeutic end-goals. Remember that safety is always the first priority with prescribing. PLEASE DO NOT FORGET INTRODUCTION, CONCLUSION AND REFERENCES LESS THAN 5 YEARS OLD.

Paper For Above instruction

Introduction

Neurocognitive disorders present complex clinical challenges, especially in elderly populations where multiple factors influence diagnosis and management. Mr. Charles Wingate, a 76-year-old male experiencing progressive cognitive decline, exemplifies these challenges. Accurate diagnosis is essential for targeted treatment, but overlapping symptoms and comorbidities complicate this process. This paper discusses the decision-making process regarding diagnosis and treatment, considering the clinical presentation, differential diagnosis, appropriate pharmacologic strategies, and ethical considerations.

Decision Point 1: Differential Diagnosis

Based on Mr. Wingate’s presentation, the most fitting diagnosis according to DSM-5 criteria appears to be Major Neurocognitive Disorder with Lewy Bodies (MNDLB). The key symptoms supporting this diagnosis include fluctuating cognition, parkinsonian features such as resting tremors, visual hallucinations (nightmares and acting out dreams), and REM sleep behavior disorder (RBD). These features align with Parkinson's disease dementia or Lewy body dementia, which are characterized by early fluctuations in cognition and prominent motor symptoms (McKeith et al., 2017). Another crucial aspect is that his cognitive decline is not purely memory-based, with deficits in attention, executive function, and visuospatial abilities, consistent with Lewy body pathology.

Alternative diagnoses such as Alzheimer’s disease were considered, but the presence of early motor symptoms and fluctuating cognition point more towards Lewy body dementia. Frontotemporal neurocognitive disorder was less likely given the absence of significant behavioral disinhibition or language decline. The clinical evidence of Parkinsonism, sleep disturbances, and visual hallucinations are definitive cues supporting MNDLB diagnosis (Hansen et al., 2019).

The selection aims to guide appropriate treatment and avoid the pitfalls of misdiagnosis, such as the adverse effects of antipsychotics in Lewy body dementia (Ballard et al., 2018). Confirmatory testing, such as dopamine transporter imaging (DaTscan), can be helpful but was not initially performed in this scenario. The diagnosis influences therapeutic choices, especially medication sensitivity and safety.

Decision Point 2: Treatment Plan

The cornerstone of pharmacologic management for MNDLB involves acetylcholinesterase inhibitors like rivastigmine. This choice is supported by evidence demonstrating modest cognitive benefits and reduction in neuropsychiatric symptoms in Lewy body dementia (Gao et al., 2018). Starting rivastigmine at 1.5 mg twice daily aligns with clinical guidelines emphasizing low-dose initiation to mitigate gastrointestinal and other side effects (Emre et al., 2017).

The rationale is to improve cognitive function, reduce fluctuations, and possibly slow disease progression. Care should be taken to monitor for adverse effects, given the increased sensitivity of Lewy body patients to anticholinergic and dopaminergic drugs (Hansen et al., 2019).

The patient’s lack of observable improvement after four weeks highlights that response to these medications can be variable and may take longer. Additionally, symptom worsening such as nightmares acting out may necessitate adjunct treatment but using antipsychotics like Seroquel (quetiapine) in Lewy body dementia is contraindicated due to potential severe extrapyramidal side effects and increased mortality (Ballard et al., 2018). Therefore, non-pharmacological interventions and symptom-specific approaches are preferable initially.

Decision Point 3: Management of Nightmare Symptoms

Given the worsening nightmares and acting out behavior, introducing clonazepam at a low dose (0.5 mg at bedtime) may help manage REM sleep behavior disorder. Clonazepam is considered first-line treatment for RBD and has evidence supporting its efficacy (Schenck et al., 2018). However, in Lewy body dementia, benzodiazepines must be prescribed cautiously due to their sedative effects, fall risk, and potential worsening of cognitive impairment.

The rationale for choosing clonazepam lies in its targeted effect on abnormal REM behavior without the significant antipsychotic risks associated with drugs like quetiapine. It is important to educate the patient and family that medication effects may take time to fully manifest, and adjustments may be necessary.

Potential side effects, such as excessive sedation, confusion, and increased fall risk, necessitate close monitoring. This approach balances symptom relief with safety considerations, acknowledging that treatment responses can vary and require ongoing assessment.

Decision Point 4: Ethical Considerations and Communication

Ethical considerations significantly impact treatment decisions and communication with Mr. Wingate and his family. Respect for autonomy involves ensuring informed consent, especially given cognitive impairment that affects decision-making capacity. Clear, honest communication about therapeutic goals, potential side effects, and prognosis is essential to uphold beneficence and non-maleficence.

Additionally, considerations around medication safety—particularly in the context of Lewy body pathology—must guide prescribing practices to avoid harm. Family involvement is crucial, but clinicians must also respect the patient’s dignity and preferences, tailoring interventions to their values and cultural context.

Informed consent, ongoing assessment of decision-making capacity, and documentation of discussions uphold ethical standards. Moreover, facilitating shared decision-making promotes trust and aligns treatment with the patient’s best interests.

Conclusion

The management of Mr. Wingate’s neurocognitive and motor symptoms requires an accurate diagnosis, cautious pharmacologic intervention, and ethical clinical practice. The diagnosis of Major Neurocognitive Disorder with Lewy Bodies is supported by clinical features, guiding tailored treatment such as rivastigmine and clonazepam, with vigilant monitoring for side effects. Ethical considerations, including informed consent and safety, underpin all aspects of care, emphasizing a patient-centered approach. Ongoing assessment and collaboration with caregivers will be essential to optimize quality of life and functional independence in this complex clinical scenario.

References

• Ballard, C., et al. (2018). Neuroleptic sensitivity in Lewy body dementia. The Lancet Neurology, 17(10), 845-854.
• Emre, M., et al. (2017). Rivastigmine for dementia associated with Parkinson's disease: A randomized controlled trial. Neurology, 78(4), 247–253.
• Gao, S., et al. (2018). The efficacy of acetylcholinesterase inhibitors in Lewy body dementia: A systematic review. Journal of Alzheimer's Disease, 63(3), 893–900.
• Hansen, L. A., et al. (2019). Lewy body dementia: Diagnostic challenges and management. Journal of Geriatric Psychiatry and Neurology, 32(3), 127–135.
• McKeith, I. G., et al. (2017). Diagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium. Neurology, 89(1), 88–100.
• Schenck, C. H., et al. (2018). Pharmacological management of REM sleep behavior disorder. Sleep Medicine Reviews, 36, 270–278.