Multi-infarct dementia, sometimes called vascular dementia, is a form of progressive cognitive decline that results from accumulating lesions in the brain, usually as a result of a disruption in the blood supply.
Multi-infarct dementia presents similarly to other forms of dementia. It is, nonetheless, distinguishable through its time course and progression. It tends to worsen progressively but in sudden, discrete steps with a worsening of intellectual performance followed by mild recovery. Some forms of multi-infarct dementia are associated with more gradual progression. This occurs particularly when subcortical structures are involved in lacunar infarctions and Binswanger dementia.
Focal neurologic findings become more apparent with disease progression. Patients tend to develop abnormalities in gait, muscular weakness in specific extremities, extrapyramidal dysfunction, Babinski reflex, increased deep tendon reflexes and hemiplegia.
Cognitive damage in multi-infarct dementia is usually more specific than generalized. Short-term memory may be more strongly present than other features of cognition. In addition, patients with multi-infarct dementia are at a higher risk of depression because they are more likely to be aware of their condition, especially in patients with partial aphasia.
Workup of multi-infarct dementia generally consists of laboratory and imaging studies. Laboratory and blood tests are performed to exclude certain conditions that may also result in dementia. A range of blood tests are performed. These generally are a complete blood count, assessment of liver function tests, creatinine and urea for assessment of kidney function, thyroid hormones, vitamin B12, ESR to detect the presence of any infection, VDRL for syphilis and folate levels within the red blood cells. It may also be necessary to perform additional testing in certain patients such as HIV testing, ANA (antinuclear antibody), ANCA (antineutrophil cytoplasmic antibody), antiphospholipid antibody and lupus anticoagulants.
Imaging studies are necessary to diagnose the disease. Both CT and MRI can be very important diagnostic tools. Lesions that target blood vessels appear on both modalities. Characteristic features of CT and MRI scans in patients with multi-infarct generally are the presence of a number of bilateral infarcts in the limbic cortex, lesions in the white matter around the ventricles and lacunar strokes.
Multi-infarct dementia may also be differentiated from Alzheimer's disease with MRI. The prodromal phase of multi-infarct dementia will generally show lacunar infarcts within the white matter, in addition to leukoaraiosis. In contrast, the prodromal phase of Alzheimer's disease usually targets the limbic cortex, with frequent involvement of the hippocampus and the entorhinal cortex.
Positron emission tomography can also help in distinguishing multi-infarct dementia from Alzheimer's disease. Multi-infarct dementia is associated with hypoperfusion in the frontal lobes, especially in the superior frontal gyrus and the cingulate cortex. On the other hand, patients with Alzheimer's disease will exhibit decreased perfusion along a parietotemporal spread. CT accompanied by single-photon emission will generally show similar findings.
Cerebral angiography is not necessary to establish the diagnosis. Nonetheless, it may be performed prior to surgery of the carotid artery. In addition, it can help diagnosing cerebral vasculitis, in which vascular beading is prominent.
Additional tests are useful in assessing frequently associated disorders. These include Doppler scanning of the carotid arteries, Holter monitoring and echocardiography.
Treatment of multi-infarct dementia is generally targeted to decrease future occurrences and lessen complications. Antiplatelet drugs are particularly important in preventing further cerebrovascular accidents. Evidence points out that the progression of multi-infarct dementia is significantly delayed by aspirin.
Furthermore, it is critically important to control risk factors that are directly associated with the occurrence and progression of the disease. Pharmacotherapy is targeted at chronic vascular and metabolic diseases such as diabetes mellitus, hypertension and hyperlipidemia. Other drugs act to increase cerebral blood flow. These include ergoloid mesylates, also known as hydergine, and pentoxifylline. The latter was shown to be beneficial in patients in a large multicentric, double blinded and placebo controlled European study, especially in regards to overall cognitive and intellectual ability.
Other potential drugs with neuroprotective effects include propentofylline, posatirelin and dihydropyridine calcium channel blockers such as nimodipine and nicardipine. The latter were found to delay cognitive and intellectual damage, not only in patients with multi-infarct dementia, but also those diagnosed with cerebrovascular conditions more generally.
Cholinergic neurotransmission may be of particular importance to multi-infarct dementia. Alzheimer's disease has been also linked to abnormalities in the cholinergic system. Clinical trials have already shown some benefit for cholinesterase inhibitors in multi-infarct dementia, although they are yet to be employed in the treatment of the disease.
Aside from pharmacotherapy, patients also require social and psychological support. All patients should be referred to community services. Their decision-making and rational judgment capacities should be adequately assessed, in addition to their ability to perform the basic functions of living such as driving and taking care for themselves.
In addition to cognitive deterioration, patients with dementia may frequently show irritability, agitation and even psychotic episodes. Selective serotonin inhibitors (SSRIs) seem to have a beneficial effect on agitation and psychosis, even though they have not been systematically studied in these patients. Patients also seem to tolerate SSRIs better than typical or atypical antipsychotics. It will be important to conduct large scientific studies to exactly assess their beneficial advantages.
Diet also plays an important role in the progression of the disease. Fish intake was correlated with decreased risk of dementia, in contrast to increased fat intake, which showed increased association. In addition, high homocysteine levels are also related to an increased risk of multi-infarct dementia. The latter usually results from decreased levels of vitamin B6, vitamin B12 and folic acid.
Decreases in life expectancy are associated with multi-infarct dementia in around half of all male patients. Individuals with a lower educational status as well as those who do not perform as well on neuropsychological tests also suffer from worse outcomes.
Multi-infarct dementia may also be complicated by death, but this generally results from associated conditions such as heart disease and malignancy.
Smoking is one of the most important associated risk factors. One study on 21,123 individuals found that heavy smokers have more than double the risk compared to the general population to develop dementia after 2 decades. Heavy smokers were defined as those who smoke more than 2 packs per day and mean smoking period was around 23 years. The risk is not limited to multi-infarct dementia but also includes Alzheimer's disease and other forms of dementia. It is independent of gender and race .
Multi-infarct dementia may sometimes follow strokes. This scenario may more frequently be present in aged patients, those with a family history, and those who have a lower educational status. In addition, particular strokes may increase the risk, especially those that involve white matter around the ventricles, regions supplied by the thalamic artery, the hippocampus, the inferomedial temporal lobes and watershed areas between the parietal and superior frontal areas .
Prevalence of dementia varies with age. In the United States, around 5% of all individuals between 71 and 79 years of age develop dementia with the risk increasing exponentially in patients older than 90. Among this population, around 40% of all individuals are ultimately diagnosed with this disease. Alzheimer's dementia is the most common form, affecting approximately 70% of all individuals with dementia. On the other hand, multi-infarct dementia is responsible for 17% of call cases although it is important to note that the two conditions may frequently overlap .
Incidence of multi-infarct dementia is estimated at 3.8 cases in every 1000 individuals per year, although this varies depending on the criteria employed. Incidence also increases greatly with age, from 0.3 to 2.2 cases in patients between 65 and 60 years of age and up to 15.9 in patients older than 90 . The disease is more likely to affect men than women, in contrast to Alzheimer's dementia . Multi-infarct dementia has greater predilection for particularly ethnic groups, especially individuals with Asian and African lineage  .
The pathophysiological mechanisms underlying multi-infarct dementia generally include infarcts, leukoaraiosis, hemorrhage and mixed forms.
Infarctions can lead to dementia when they are multiple and target a large number of brain regions, affecting the brain's ability to compensate for loss of localized function . Nonetheless, small infarcts can be sufficient to lead to dementia, especially when they target the thalamus and the basal ganglia . Small infarcts generally result from arteriosclerosis and are usually less than 1.5 cm in size. They are termed lacunar infarcts, and involve small arteries and arterioles. Lacunar infarcts have a predilection for the basal ganglia, the pons, the thalamus and the internal capsule .
Leukoaraiosis describes pallor of the white matter. It is the eventual result of accumulating loss of white matter constituents such as oligodendrocytes, axons and myelin sheath. Tissue around blood vessels is especially affected and there is concomitant damage to the blood-brain barrier . Although ischemia is thought to underlie the development of leukoaraiosis, classical infarction may not be present. It has been hypothesized that excessive pulsation of the small vessels may ultimately lead to the pathophysiological manifestations .
Hemorrhage may also lead to brain damage. Hypertension is a principle causative factor, and results in a large number of small bleeding sites. They occur most commonly in the basal ganglia. On the other hand, amyloid deposition can lead to sites of limited hemorrhage in the white matter and the cortex . Excessive accumulation of amyloid beta protein weakens the walls of the arteries and makes them particularly susceptible for rupture.
Mixed dementia consists of a combination between multi-infarct and Alzheimer's dementia. Patients suffering from both conditions are expected to be more strongly affected than those affected by one form only .
Multi-infarct dementia is a particular form of dementia associated with small lesions in the brain . It tends to follow a progressive course with incremental deterioration. It is strongly associated with risk factors for cerebrovascular and cardiovascular disease, such as hypertension, diabetes mellitus, dyslipidemia and smoking. Smoking is a particularly important risk factor, with heavy smoking resulting in more than the doubling of the risk. Pathophysiological mechanisms underlying multi-infarct dementia include small infarcts, leukoaraiosis and small hemorrhages. Small infarcts generally result from arteriosclerosis and tend to have a predilection for subcortical structures. Hypertension is an important risk factor for limited bleeding in the basal ganglia. On the other hand, leukoaraiosis results from progressive loss of white matter, especially in perivascular spaces.
Workup of multi-infarct dementia is broad and is generally targeted at excluding other potential causes of dementia, such as hypothyroidism and B12 hypovitaminosis. Imaging studies with CT and MRI are necessary to diagnose multi-infarct dementia, and show distinctive findings. MRI and PET are particularly useful in differentiating multi-infarct dementia from Alzheimer's disease.
Treatment of multi-infarct dementia is principally with pharmacotherapy to decrease the occurrence of future strokes and slow the progression of the disease. Aspirin is particularly useful in preventing future cerebrovascular accidents and is associated with better intellectual functioning of patients with multi-infarct dementia.
Multi-infarct dementia is a form of dementia that targets older individuals and results from accumulating small lesions in the brain. These lesions are caused by a disruption of blood perfusion into specific areas of the brain. It is strongly associated with risk factors that affect the functioning of the heart and blood vessels, such as smoking, hypertension, diabetes and elevated lipid levels. Patients with vascular dementia progressively worsen, but unlike in Alzheimer's disease, deterioration is incremental and not continuous.
Workup is usually targeted at excluding other potential causes of dementia, such as deficiencies in folate and vitamin B12 and dysfunction in the thyroid gland. Imaging testing with MRI and CT are necessary to establish the diagnosis and can help distinguish multi-infarct dementia from Alzheimer's disease.
Treatment of multi-infarct dementia is aimed at decreasing future occurrences of cerebral lesions and delaying progression. Prevention and elimination of risk factors such as smoking, hypertension and diabetes is of paramount importance.