Memory consultation

We have covered memory disorders. We have also looked at cognitive disorders, the psychobehavioural disorders experienced by patients who have symptoms of Alzheimer’s disease. We have looked at the assessment carried out by the general practitioner and now let’s see what happens when they come to the short-term memory consultation. 

This is when we explore their disorder more precisely and we confirm Alzheimer’s disease. This is an important slide that we’ve already seen, in which we explained that there are two stages in early Alzheimer’s disease. The prodromal phase linked to damage in the hippocampus, and then a secondary phase which is associated with the spread of lesions outside the hippocampal regions, which gradually comes with various other disorders: cognitive, behavioural, and ultimately what has been called the dementia stage, which means the loss of autonomy, with an impact on daily activities. In the memory consultation, we will explore the various sectors. 

This is about memory, of course, and then executive functions, those which are organised in the frontal lobe, and then language, which is an instrumental function, overall cognitive efficiency and also the person’s independence, their autonomy as well as their attentional disorders. We will look at the various sectors, the different areas of cognitive and behavioural activity. We have tests to do this. For example the FAB, Frontal Assessment Battery, which, in six different areas, will give a fairly general idea of how the frontal regions are working. These regions are involved in conceptualisation, mental flexibility, programming, environmental dependence, and sensitivity to interference or inhibitory control. Language will be explored, speech, quite simply the naming of images or objects on the desk or on more specific catalogues, for example the Boston catalogue, which is widely used, verbal influence, the number of animals that the subject can give in a given time, 1 to 2 minutes of words starting with the letter ‘s’, repeating words or sentences of varying length and simple or complex understanding. “Show me the window, give me the pen that’s on the table”, etc. 

These things are relatively easy for the doctor to do. But in memory consultations, there are obviously very standardised tests which, depending on the age and cultural level, give an idea of the subject’s ability to carry out the request. These disturbances can be observed in neurodegenerative diseases such as Alzheimer’s. And as far as language is concerned, primary progressive aphasia, PPA; gestural praxis: the ability to perform gestures, either relatively automatic gestures like motor sequences, or reflexive gestures based on imitation, we ask the subject to imitate the gestures that are made in front of them, for example butterfly wings, etc. or symbolic gestures “What would you do to show there was a bad smell in here, a military salute, the V for victory, how you hammer in a nail” and so on. 

These disturbances can be observed in Alzheimer’s disease, Benson syndrome or corticobasal degeneration, in particular. Once these cognitive assessments and behavioural assessments have been run using standardised and calibrated tests and have given a precise idea of how much damage there is in the various areas and how overall efficiency is affected, we can explore in more depth. An MRI, which we have already talked about, showed atrophies, see for example on the left, there is atrophy in the frontal part of the brain, but especially the PET-scan with FDG. I’ll explain how this works. A sugar substance is injected into the bloodstream. 

The sugar is radioactive, and this radioactivity lasts a few minutes. The sugar will be consumed by the cells, depending on how active they are. All the cells in the body will consume the sugar that has been injected. Here we are focusing on the brain. The way we read this scan is very simple, there are regions that consume a lot of sugar because they are very active, those are red. 

And then there are regions that are less active, they are green or yellow, for example, on the bottom row on the left, part of the cerebral cortex is red, on the bottom left and on the right and at the top, it is yellow and even green. There are fixation holes, regions of the brain that don’t consume sugar. This is what we call a cortical hypometabolism located here in the frontal region, and in the frontal region on the right side. We can probably say that there is localised frontal degeneration in this patient. 

We now have biomarkers that allow us to observe the presence of Alzheimer’s disease. In a subject who has the cognitive or behavioural disorders that we talked about, who perhaps has abnormalities on neuroimaging, we still might wonder if it really is Alzheimer’s disease. To find out, we can use these pathophysiological biomarkers, those that are at the top of this slide, by a simple lumbar puncture, we can now measure in the cerebrospinal fluid the concentration of proteins responsible for the disease of Alzheimer’s that we talked about during the first capsule, which are beta amyloid lesions and tau lesions. 

We can measure the cerebrospinal fluid and in this way, we will be able to formally link the disorders observed during the cognitive assessment in the presence of Alzheimer’s disease. This is done in certain fairly specialised memory consultations. It is not always performed, of course, but it is something we may be required to do when we want to confirm Alzheimer’s disease or another disease, it might be important. It might also be important if the doctor wants to prescribe drugs which are currently in development and which are reserved for patients in whom Alzheimer’s disease has been confirmed. These are the things we usually do. Now, in specialised centres, a lumbar puncture is done to confirm the presence of Alzheimer’s disease in patients with cognitive disorders.