A Multifactor Approach to Mild Cognitive Impairment

Taha Qarni, BHSc; Arash Salardini, MD

Disclosures

Semin Neurol. 2019;39(2):179-187. 

In This Article

Our Practice

We perform some form of brain imaging on most patients who present to our clinic with memory or other cognitive complaints who have not had a scan in the year preceding their visit. We use MRI unless contraindicated. We ask the radiology department for a high-resolution series (often T1-weighted), as well as T2-weighted, susceptibility-weighted imaging (SWI), fluid-attenuated inversion recovery (FLAIR), and DWI sequences. We also ask for coronal and sagittal reconstructions. We find volumetric studies to be useful as well. These are now commercially available, but are not always covered by insurance. We use the T1-weighted image sequence to look for focal and regional atrophy. For example, atrophy of the frontal or temporal lobes argue more for frontotemporal dementia, whereas parietal and temporal atrophy are more indicative of AD. Additionally, we find the size of the hippocampus is a good indicator of neurodegeneration in individuals with suspected AD. If quantification is not available, we use the medial temporal lobe atrophy score.[48] Briefly, this is a visual rating scale which uses coronal MRI images at the level of the pons. Descriptively, score are as follows: no atrophy (0), widening of the choroid fissure only (1), widening of the inferior horn of the lateral ventricle (2), loss of hippocampal height (3), and severe atrophy (4). Visual guides for reference are available, and we reproduced one with permission in Figure 1.

Figure 1.

Magnetic resonance imaging (MRI) exemplars for the visual rating of mesial temporal atrophy using Schelten's scale. Reproduced with permission from Velickaite V, Ferreira D, Cavallin L, et al. Eur Radiol 2018;28:1739.57

DWI can show cytotoxic edema in the setting of either a very recent stroke or a rapidly degenerative process. Classically, it leads to cortical ribboning or increased basal ganglia signal in prion diseases. SWI is useful in identifying microhemorrhages seen in both cerebral amyloid angiopathy and arteriosclerotic disease. We use a combination of T2-weighted and FLAIR imaging to identify evidence of white matter disease. FLAIR is used to evaluate for white matter hyperintensities. Enlarged perivascular spaces and lacunar infarcts are more easily identifiable on T2-weighted images.

We also perform a laboratory panel which includes thyroid-stimulating hormone, B12, folate, and, if not recently performed, a comprehensive metabolic panel and complete blood count. Other testing including immunological testing, infectious workup, or metabolic disease will be considered on case-by-case basis. The most important part of the testing, in our opinion, is the neuropsychological testing which, when done well, not only presents age- and education-normalized data we can use in our diagnostic deliberation, but also provides another clinical opinion for diagnosis. In individuals with a strong family history of dementia or who have early onset dementia, we make a referral to our neurogeneticist who provides both excellent interpretation and counseling, but is also sometimes able to combine whole exome sequencing with selected commercial tests to reduce the cost to the patient.

Testing using other modalities depends on several factors, the most important of which is the degree of diagnostic certainty a patient demands from us. As a rule, younger patients who continue to work and may need to make drastic changes to their life plans often require a higher level of diagnostic certainty. Preliminary reports from the Imaging Dementia- Evidence for Amyloid Scanning study which studies the behavior of clinicians after ordering amyloid PET scans (18,488 scans nationwide) indicated that amyloid imaging made a significant contribution to clinical decision making by physicians. We do offer further testing to all our patients, but are guided by their preferences. Presently, most insurance companies do not cover amyloid PET scanning. Although CSF studies of amyloid and tau are more readily available.

Once a patient is diagnosed with MCI, we determine whether a patient is interested in participating in clinical trials or not. If so, we will give contact numbers for various centers near their place of residence who may be offering clinical trials. We also discuss with the patient the fact that once in the trial, they will not have the opportunity to change their medications for the duration of it unless they decide to withdraw from the study. For this reason, we offer to start a cholinesterase inhibitor in anticipation of being enrolled in a trial if the patients are amenable.

For these patients and all others, we explore the possibility of coexisting mood disorders which we then treat. We provide extensive counseling aimed at giving information about progression, the evidence behind the various treatments offered in the commercial space, and how to maximize function. We also enquire about driving safety. At later stages of disease, we may comanage with a geriatrician. We find the skill sets complementary. We encourage involvement in patient and caregiver groups, Alzheimer's association events, and community programs.

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