Abstract
An 80-year-old man came to the consultation with problems in writing a thesis.
6.2 Clinical History
This retired teacher came alone to the first consultation mentioning that he was having difficulties writing a thesis at a local educational institution. He described that his thoughts were not as clear as before and that he struggled to focus on a specific idea during the process of drafting his thesis. As an example, he experienced difficulties in articulating his thoughts into meaningful sentences and noticed delays in finding words to appropriately complete them. Indeed, similar word-finding difficulties became apparent, particularly during conversations with his peers and advisor. Regarding memory, he mentioned that, in order to prevent problems, he became more dependent on his agenda, calendars, and notes as compared to a few years ago. In spite of these symptoms, he was capable of taking all the courses and requirements for graduating. He denied problems related to drawing abilities, visual problems, anxiety, or depression. He was managing his financial affairs, and he was driving safely. At home, he used to help his wife with simple tasks such as setting the table and doing the dishes. He denied past medical history of neurological conditions, including brain trauma, stroke, or neuropsychiatric conditions. On his first examination, he obtained 27 on the Montreal Cognitive Assessment (MoCA) (−3 on delayed recall), 29 on the Mini-Mental State Examination (MMSE) (−1 on copy design), and 18 on the Frontal Assessment Battery (FAB). The rest of the neurological examination was normal. His MRI showed few white matter hyperintensities (Fazekas = 1) and hippocampal atrophy (Scheltens = 3). He had an inconclusive [18F]fluorodeoxyglucose (FDG) PET scan, not fully compatible with Alzheimer’s disease (AD).
Nearly 5 years later, after a successful thesis defense, this man returned to the consultation, now accompanied by his spouse, describing exacerbation of previous symptoms. He also started noticing inability to maintain the thread of a conversation as he used to do previously. In fact, he stopped speaking in public, due to frequent pauses since words were not becoming available while speaking the way they used to previously. He continued to use his computer but not as fast as before. His wife remarked that he started forgetting names of friends and familiar people. She also highlighted the patient’s difficulties to retain the content of conversations. The wife also noticed some degree of social withdrawal, possibly due to language difficulties. Apart from reduced motivation to conduct his tasks at home, the wife denied significant behavioral changes such as hallucinations, delusions, mood alterations, repetitive behaviors, or reduced empathy. His wife and other family members started to manage the patient’s financial affairs. The patient and his wife denied the presence of disorientation, motor symptoms, or falls.
6.3 General History
The patient had 21 years of education with a doctoral degree. He was taking daily doses of vitamin B12, ramipril 10 mg, atorvastatin, and insulin.
6.4 Examination
On his second visit, the physical examination was unremarkable. During the mental status exam, he was cooperative, attentive, and responsive and oriented in time and space. However, his Clinical Dementia Rating (CDR) was 1, MoCA progressed to 19/30, and the MMSE was 24/30, with normal immediate recall. The reverse order tests were abnormal. He made a few mistakes on the serial 7. Copy and clock drawing were normal. Anterograde memory evoked by a delayed recall showed deficits, which were partially corrected by cueing. Judgment and abstract thoughts were appropriated. The language assessment revealed an abnormal Boston naming test score of 6/25. The semantic fluency was reduced; however, the phonemic-letter fluency (FAS) was normal. The Boston Aphasia Examination test showed normal reading and comprehension. The rest of the neurological examination was normal. A second MRI ruled out brain infarcts and confirmed white matter hyperintensities (Fazekas = 1) and mild progression of hippocampal atrophy (Scheltens = 3–4). A second [18F]FDG PET scan showed mild reduction on the FDG uptake in the posterior cingulate, suggesting early AD. Amyloid PET was negative and tau PET was positive on the temporal lobe (mesial, basal, and neocortical) precuneous, inferior parietal cortex, orbitofrontal cortex, and amygdala (Braak stage 5; see Figure 6.1).
