Background: Mr. Akkad Is A 76-Year-Old Iranian Male Who Is B

Backgroundmr Akkad Is A 76 Year Old Iranian Male Who Is Brought To Yo

Background: Mr. Akkad is a 76-year-old Iranian male brought to the clinic for “strange behavior.” He was evaluated by his family physician, who ruled out organic causes through laboratory tests and imaging, including a normal CT scan of the head. Over the past two years, his family has observed progressive changes such as increased forgetfulness, disinterest in religious activities, increased critical attitudes, and a shift from seriousness to amusement regarding formerly important matters. These symptoms have worsened, with noticeable cognitive decline and behavioral changes.

Subjective: During the clinical interview, Mr. Akkad appeared pleasant and cooperative, engaging well and showing some confabulation during memory tests. The Mini-Mental State Examination (MMSE) score was 18 out of 30, indicating moderate dementia, with deficits in orientation, registration, attention & calculation, and recall. He exhibited poor eye contact, clear but tangential speech, no motor abnormalities, and no hallucinations or delusions. His mood was euthymic, but affect was restricted. He was alert, oriented to person, partially oriented to place, but disoriented to time and events, exemplified by confusion about the location. Insight and judgment were impaired, and he demonstrated impaired impulse control, evidenced by attempting to leave during the interview. He denied suicidal and homicidal ideation.

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

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Alzheimer’s disease (AD) is the most common cause of dementia, characterized by progressive cognitive decline, behavioral changes, and functional impairment. The case of Mr. Akkad exemplifies typical features of AD, especially in the context of mild to moderate stages marked by memory deficits, disorientation, and behavioral changes. Management primarily involves pharmacologic therapy aimed at modifying disease progression and symptomatic control, along with supportive interventions for caregivers and families.

Pharmacological management for Alzheimer’s disease centers on cholinesterase inhibitors (ChEIs) such as rivastigmine (Exelon), donepezil (Aricept), and galantamine (Razadyne). These agents work by increasing the availability of acetylcholine in the brain, which is deficient in AD due to neuronal degeneration. The choice of medication often depends on patient tolerability, comorbidities, and clinician preference. In Mr. Akkad’s case, initiating a cholinesterase inhibitor was appropriate given his cognitive status and behavioral symptoms.

The initial decision was to start rivastigmine at 1.5 mg orally twice daily, with an increase to 3 mg after two weeks. This approach aligns with clinical guidelines advocating slow titration to minimize side effects such as gastrointestinal disturbances. As observed, after four weeks, no significant cognitive or behavioral improvements were noted, but tolerability was good. Increasing the dose to 4.5 mg BID was the logical next step, aiming to optimize therapeutic effects, as documented by clinical trials demonstrating dose-dependent improvements in cognition and activity engagement (Birks, 2006).

Further dose escalation to 6 mg BID was considered after another four weeks, provided the patient tolerated the previous dose well. It is important to note that medication effects on cognition and behavior often manifest over many months. The absence of immediate improvements does not indicate inefficacy; instead, clinicians must counsel families about the slow progression and gradual response profile. Additionally, combining cholinesterase inhibitors with other agents like memantine (Namenda)—which blocks glutamate-mediated excitotoxicity—may offer additional benefit in moderate to severe stages of AD (Howard et al., 2012).

The decision to continue or adjust medications must consider side effects, functional improvements, and caregiver feedback. In Mr. Akkad’s case, the increase to 4.5 mg BID resulted in tolerability and some behavioral stabilization, as evidenced by his increased social participation (attending religious services). This suggests some symptomatic benefits, although cognition remains stable or slightly fluctuating.

After assessing the response to the initial treatment, next steps could include increasing rivastigmine to 6 mg BID. This is based on evidence supporting dose escalation to maximize cholinergic transmission without undue adverse effects (Birks & Harvey, 2018). Alternatively, adding memantine at 10 mg BID could be considered if cognitive decline progresses or if behavioral symptoms persist or worsen. However, current guidelines recommend maximizing cholinesterase inhibitor dosage before introducing combination therapy (McKhann et al., 2011).

Monitoring through regular cognitive assessments, caregiver reports, and clinical observations is crucial. The MMSE score of 18 signifies moderate dementia, and although pharmacologic options can stabilize or slow progression, they do not reverse the disease process. Physicians should also emphasize non-pharmacological interventions, including cognitive stimulation, behavioral therapies, and caregiver support, to improve quality of life.

In conclusion, dementia treatment necessitates a comprehensive approach combining pharmacotherapy, psychosocial interventions, and ongoing assessment. The case of Mr. Akkad illustrates the typical progression and management challenges, highlighting the importance of medication titration, realistic expectations regarding improvements, and the need for tailored, patient-centered care strategies.

References

• Birks, J., & Harvey, R. J. (2018). Donepezil for dementia due to Alzheimer's disease. The Cochrane Database of Systematic Reviews, (6), CD001190.
• Birks, J. (2006). Cholinesterase inhibitors for Alzheimer's disease. Cochrane Database of Systematic Reviews, (1), CD005593.
• Howard, R., McShane, R., Lindesay, J., Ritchie, C. W., Reed, C., Cornes, M., ... & Wilcock, G. (2012). Memantine for Alzheimer’s disease and other dementias. The Cochrane Database of Systematic Reviews, (3), CD003154.
• McKhann, G. M., Knopman, D. S., Chertkow, H., Hyman, B. T., Jack Jr, C. R., Kawas, C. H., ... & Phelps, C. H. (2011). The diagnosis of dementia due to Alzheimer's disease: Recommendations from the National Institute on Aging and the Alzheimer’s Association workgroup. Alzheimer's & Dementia, 7(3), 263-269.
• Folstein, M. F., Folstein, S. E., & McHugh, P. R. (2002). Mini-Mental State Examination (MMSE). Psychological Assessment Resources.