Approach
Vascular dementia is classically assumed to be a stepwise progression in cognitive symptoms, although a gradual progression is also possible. It is useful to identify patients with atherosclerotic ischemic disease and those with cardioembolic disease.
Atherosclerotic disease refers to disease without a definitive cardiac source for cerebral emboli and suspected pathogenesis of artery-to-artery embolism.
Cardioembolic disease refers to disease with a definitive cardiac source for cerebral emboli (e.g., atrial fibrillation, valvular heart disease, left ventricular thrombus).
History
It is important to talk to a family member or caregiver, in addition to the patient, in order to establish an accurate history of cognitive symptoms and impairment in daily activities.[63]
Temporal relation of cognitive symptoms to a clear clinical stroke event or multiple stroke events may strongly suggest a vascular cause for cognitive impairment.[63]
A lack of prestroke cognitive symptoms may further support a vascular cause for cognitive impairment.
Cognitive symptoms may include impaired memory, difficulty in problem solving or using familiar equipment, slowed processing, difficulty initiating activity, perseveration in behavior, disinhibition, and difficulty in managing finances.
Slowing of gait, shuffling, feet "stuck to the floor" when starting to walk, increasing loss of balance, falls, and incontinence may all suggest vascular brain disease. A decline in ability to perform activities of daily living associated with cognitive history may be apparent.
Risk factors should be sought. A full medication history to exclude an effect of psychotropic drugs should be taken. History alone may be insufficient for diagnosis.
Examination
Usually a specialist referral to a geriatrician or neurologist with expertise in cognitive disorders is recommended. Signs listed below may occur in isolation or in any combination. The presence of these signs does not necessarily exclude the presence of a coexistent degenerative dementia such as Alzheimer disease (AD). Occasionally such symptoms may also be present in other neurologic diseases such as Steele-Richardson syndrome, multisystem atrophy, and normal pressure hydrocephalus.
Signs include the following:
Frontal signs such as apathy, disinhibition, and frontal release reflexes (grasp, glabella tap, jaw-jerk)
Depression and altered mood secondary to vascular disease
Focal hemispherical or bulbar signs (e.g., hemiparesis, dysarthria, dysphagia)
Impairment in multiple cognitive domains usually detected by cognitive testing - see below. Memory may be impaired secondary to executive or attentional impairment, and may manifest as a retrieval memory deficit (helped by cues) rather than rapid forgetting (not helped by cues). The patient may require detailed neuropsychologic testing beyond a physician's expertise
Difficulty initiating gait, short shuffling steps, poor postural control while walking
Cognitive testing
There are a number of possible tests used to identify the presence, nature and severity of vascular dementia.[63] They cover several cognitive domains which broadly tend to include: attention, memory, fluency, language, and visuo-spatial awareness.
Montreal Cognitive Assessment (MoCA) test is widely used and can be used to assess mild cognitive impairment, including when there is executive dysfunction. It is a 30-point test which takes around 10 minutes to administer.
Addenbrooke’s Cognitive Examination-III (ACE-III) is a 100-point test which takes around 15 minutes to administer and incorporates the well-known Mini Mental State Examination (MMSE) so that a score for both tests can be derived.
The MMSE, which was first published in 1975, is usually insufficient alone to detect attentional deficits and frontal executive impairment commonly seen in vascular cognitive impairment. It is therefore rarely used for specialist assessment in secondary care, where the MoCa or ACE-III are likely to be favored.
Laboratory investigations
Routine investigations are indicated to exclude modifiable contributors to cognitive decline, such as hypothyroidism, B12 deficiency, hyponatremia, and anemia, that may add to symptoms. Lupus anticoagulant, antiphospholipid, and antinuclear testing should be performed in selected patients with atypical presentations or at increased risk for these conditions (e.g., young people with recurrent strokes). Investigations routinely performed at baseline should include:
Complete blood count
Erythrocyte sedimentation rate
Basic metabolic panel including renal and liver function tests and blood glucose
Vitamin B12 and folate
Thyroid function
Serologic testing for syphilis (Venereal Disease Research Laboratory [VDRL]) in high-risk patients
Neuropsychologic testing
Neuropsychologic assessment is required for most patients to identify patterns of strengths and weaknesses in cognitive performance. Such information can be used to establish a baseline for future assessment of cognitive retention and decline.[63] For patients in whom the temporal relation between stroke onset and onset of cognitive symptoms is definite from the history, formal neuropsychologic evaluation may not be necessary.
Neuroimaging
Brain imaging is important for diagnosis and is required in all patients approaching a diagnosis. A magnetic resonance imaging brain scan should be performed to detect the presence of infarcts and assess the severity of white matter lesions.[10][63] The presence of these infarcts supports a vascular component to the dementia but does not necessarily exclude coexistent AD.
An absence of cerebrovascular lesions is usually taken as evidence against a vascular etiology for the dementia. Imaging is also useful to exclude other potentially treatable etiologies such as hydrocephalus or tumor. The yield, however, is low, being variously described as between 1% and 10% of cases having a potentially treatable cause found.[64][65]
A positron emission tomography scan may help differentiate AD from vascular dementia, but it is not used in the diagnosis of vascular dementia.
Other tests
ECG is used to check for the presence of atrial fibrillation, which increases the risk for embolic cerebral ischemia. Other, more nonspecific, abnormalities may suggest underlying cardiac disease that may reflect common risk factors for atherosclerotic disease.
Carotid duplex ultrasound is indicated for patients with dementia caused by cortical infarction, to rule out carotid stenosis as the source of embolism. Carotid stenosis of >70% is generally thought to be significant, but lower-grade stenoses (50% to 70%) may be important if the patient is symptomatic and especially if ulcerated plaques are present. In the absence of acute focal neurologic symptoms, there is no value in doing a carotid duplex.
Echocardiography is indicated for patients with dementia who are perceived to be at high risk for cardioembolism. These are the patients who have brain imaging suggesting multiple infarcts consistent with embolism, including those with multiple cortical bilateral stroke, cardiac arrhythmia, or cardiac failure. In the absence of these, an echocardiogram is usually not helpful.
Suicide risk assessment needs to be included in the diagnostic process within both primary and secondary care settings as risk is increased in the first 3 months post diagnosis of dementia, particularly in younger patients under 65 and in those with psychiatric comorbidities.[66]
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