Abstract
An 85-year-old woman with hypertension and hyperlipidemia presented with gradual and progressive cognitive impairment for more than 2 years, involving cognitive domains of memory, executive function, visuospatial and mood. She has short-term memory loss such as forgetting whether she has eaten or showered. She will also ask the same questions repeatedly. However, her long-term memory remains intact. She has forgotten how to cook and has recently burnt the pot while cooking on the stove. She is also unable to manage finances and often gives the wrong change while buying her usual groceries. She has lost her way a few times in places where she is familiar with. In addition, she started having mood swings, low mood, and poor sleep. Physical examination reveals mild bilateral bradykinesia, absence of postural or rest tremors, normal limb power, tone and tendon reflexes. She has lower limb apraxia and mild postural instability. Her Mini-Mental State Examination (MMSE) was 16. While she scored 0 for delayed recall, she was able to recall all 3 objects with either category or lexical cueing.
26.1 Case Presentation
An 85-year-old woman with hypertension and hyperlipidemia presented with gradual and progressive cognitive impairment for more than 2 years, involving cognitive domains of memory, executive function, visuospatial and mood. She has short-term memory loss such as forgetting whether she has eaten or showered. She will also ask the same questions repeatedly. However, her long-term memory remains intact. She has forgotten how to cook and has recently burnt the pot while cooking on the stove. She is also unable to manage finances and often gives the wrong change while buying her usual groceries. She has lost her way a few times in places where she is familiar with. In addition, she started having mood swings, low mood, and poor sleep. Physical examination reveals mild bilateral bradykinesia, absence of postural or rest tremors, normal limb power, tone and tendon reflexes. She has lower limb apraxia and mild postural instability. Her Mini-Mental State Examination (MMSE) was 16. While she scored 0 for delayed recall, she was able to recall all 3 objects with either category or lexical cueing.
Her brain magnetic resonance imaging (MRI) shows confluent periventricular and deep white matter T2 hyperintensities, chronic tiny infarcts in the left lentiform nucleus and pons, and chronic microhemorrhages in the left thalamus and right pons. While there are global involutional changes, there is no disproportionate hippocampal atrophy (Figure 26.1). She is diagnosed with moderate dementia, due to vascular dementia and concomitant Alzheimer’s disease (AD). She is treated with cholinesterase inhibitors and her cardiovascular risk factors are optimized.
Figure 26.1 MRI showing confluent periventricular and deep white matter T2 hyperintensities, chronic tiny infarcts in the left lentiform nucleus and pons, and chronic microhemorrhages in the left thalamus and right pons.
26.2 Discussion
This case illustrates a patient with cerebrovascular risk factors, who presents with gradual and progressive decline in cognition, mainly affecting her executive function, visuospatial, and mood/behavior cognitive domains. While she had short-term memory loss, this improved when given cues. Her MRI brain shows extensive small vessel cerebrovascular disease (CVD).
Vascular cognitive impairment (VCI), which encompasses all forms of cognitive impairment with CVD contributing to the symptoms, is the second most common cause of dementia after AD. VCI makes up 10–20% of dementia in North America and Europe, and in a longitudinal, population-based study looking at the pathological correlates of dementia, the estimates of adjusted population attributable risk of dementia due to cerebral microinfarcts is 33%. VCI also often coexists with other neurodegenerative pathologies, such as Alzheimer’s pathology. From our Asian cohorts, we found that 28.3% of mild AD and 39.7% of moderate-severe AD have severe white matter hyperintensities (WMH).
26.2.1 Diagnostic Criteria for VCI
There are a number of clinical diagnostic criteria for VCI. The Hachinski Ischemic Score (HIS) was first proposed to distinguish multi-infarct dementia from AD. Subsequent diagnostic criteria for VCI include the following:
1. International Classification of Diseases, Tenth Revision (ICD-10)
2. National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche et l’Enseignement en Neurosciences (NINDS-AIREN)
3. State of California Alzheimer’s Disease Diagnostic and Treatment Centers (ADDTC)
4. American Heart Association/American Stroke Association (AHA/ASA)1
5. International Society of Vascular Behavioural and Cognitive Disorders (Vas-Cog)2
6. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5)
These criteria require cognitive impairment to be present together with evidence of a contribution of CVD to the symptoms, supported by clinical history, physical examination, neuropsychological assessment, and neuroimaging. While the NINDS-AIREN and ADDTC require the presence of memory impairment as one of the criteria, the AHA/ASA, Vas-Cog, and DSM-5 allow a decline in any of the cognitive domains.
The AHA/ASA, Vas-Cog, and DSM-5 also acknowledge that VCI may present as poststroke VCI or nonstroke forms of VCI, such as that caused by subcortical ischemic disease. In this regard, neuroimaging and neuropathology studies play an important role in identifying CVD associated with cognitive impairment in individuals who do not present with a clinical history of stroke.
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