Abstract
Decline in memory function.
7.1 Primary Problem
Decline in memory function.
7.2 Clinical History
A 65-year-old retired administrative assistant was referred by her family doctor to investigate reduced memory function. Her partner was also present during the consultation. On his referral letter, the family doctor mentioned a decline in the patient cognition, without abnormalities on the laboratory tests or brain CT. During the consultation, the patient described difficulties in keeping track of conversations when she was playing golf. She was definitively more dependent on her notes and on her smartphone to remember appointments out of her routine. She mentioned a lack of attention and memory lapses were causing some level of embarrassment during her social activities. She also noticed that she was getting easily fatigued and not as fast as before in performing her domestic duties. Although the partner expressed some concerns regarding the patient’s emotional independence, she confirmed that the patient remains independent regarding personal and financial affairs.
7.3 General History
The patient had normal blood pressure, lipid profile, glycemia, and practiced daily exercises as a routine for many years. The couple followed a Mediterranean-like diet and there was no clinical history of recent sleep abnormalities and cardiovascular, respiratory, or urinary problems. From the neuropsychiatric perspective, there was no clinical history of disinhibition, reduced impulse control, substance-related disorders, stereotypical or ritualistic symptoms, hallucinations, or delusions.
7.4 Examination
The blood pressure and the cardiac rhythm were normal, as well as the carotid auscultation. Her MoCA score was 23/30 (impairment confined to delayed recall). From a cognitive perspective, she had a normal executive function as well as speed of processing, visual attention, working memory, and social cognition. The cranial nerves, reflexes, motor, cerebellar, and sensory examinations were normal. Her gait and stance were unremarkable.
7.5 Laboratory Tests
Laboratory tests were all normal. Apolipoprotein E genotype revealed that this patient was a double E4 carrier. The patient decided to engage in research protocols and had amyloid and tau scans conducted with [18F]AZD4694 and [18F]MK6240, respectively (Figure 7.1a and b). The amyloid scan revealed high uptake of amyloid in the precuneus, anterior and posterior cingulate, inferior parietal, basolateral temporal, and occipital cortices. Tau images also reveal abnormal uptake in the mesial temporal cortex, lateral temporal cortex, anterior and posterior cingulate, as well as prefrontal cortices in a topology compatible with Braak stages 4–5. Brain magnetic resonance imaging (MRI) showed a bilateral reduction of volumes in the hippocampus (R > L; Scheltens scale = 4). No acute ischemic changes were seen in DWI or ADC.
Figure 7.1 Images represent in vivo quantification of brain amyloid and tau aggregates obtained using the [18F]MK6240 (a) and [18F]AZD4694 PET imaging agents (b). T1-weighted structural MRI (c) shown at the same levels as the PET images indicate the brain regions affected by amyloid and tau deposition in this patient as well as right hippocampal atrophy (c, red arrow). FLAIR MRI sequence before (d) and after the anti-amyloid therapy (e) shows the hyperintensity (ARIA, e) in the left temporal neocortex (red arrow) suggestive of vasogenic edema. (f) Frontal area with hypointensity observed on the GRET2* sequence (red arrow).
7.6 Family History
The patient’s mother died with complications of Alzheimer’s disease (AD) at the age of 81 years. She had two out of five maternal siblings affected by AD. There was no information regarding the paternal side of her family. None of her younger brothers were affected.
7.7 Follow-Up
Nearly 2 years later, the patient scored 23/30 (memory and serial 7s) on MoCA. The patient now needs her partner’s assistance to manage her financial affairs. She started with cholinesterase inhibitors, and a few months later, she decided to volunteer in a clinical trial with an experimental therapy for AD. In a subsequent visit, she mentioned that, unfortunately, she decided to withdraw from the study due to the presence of a side effect detected by the safety MRIs. A new MRI confirmed the presence of increased white matter signal in the right temporal lobe (Figure 7.1e) in the fluid-attenuated inversion recovery (FLAIR) sequences. There were also various 1–3 mm dark spots in the frontal and temporal regions on the susceptibility sequence (GRE T2*; Figure 7.1f).
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