Pathophysiological processes in the brain has been the subject of many research.
The aim of our study,
was to assess the contribution of pathological changes in the carotid arteries in advanced age patients with patchy periventricular hyperintensities on MR compatible with leukoaraiosis.
Failure of the vascular system is believed to cause leukoaraiosis in the white matter of the brain (2),
but the pathogenesis is not fully cleared.
Recent studies show that brain vascular structures significant differences between,
leukoaraiosis observed patients and healthy people.
leukoaraiosis patients,
are more prone to ischemic and hemorrhagic stroke.
Also patients with leukoaraiosis show weakness,
depression,
fecal incontinence,
mental disorders and an increased incidence of dementia (5,6,7,8,16).
For this reason it’s important to determine the risk factors associated with leukoaraiosis.
Cerebral blood flow is thought to diminshed by Extracranial carotid artery stenosis.
This reduction in blood flow may be a factor in the development of leukoaraiosis (18).
Our data suggest that the atherosclerotic stenosis and arterial system disorders in carotid vessels were found to be statistically more frequent in leukoaraiosis of patients compared to the control group.
Diffuse white matter demyelination associated with atherosclerosis is detected in patients with leukoaraiosis.
Brain hyperintensities consistent with periventricular leukoaraiosis detected in advanced stage of atherosclerotic changes.
Many studies support leukoaraiosis is associated with atherosclerotic changes in cardiac,
peripheral arteries and carotid arteries.
According to the results in our study in the presence of leukoaraiosis there are atherosclerotic carotid artery intima-media layer thickening and stenosis.
These results suggest the hypothesis (Fazekes et al) that the development of the leukoaraiosis is secondary to ischemic process (21,22,23).
this hypothesis assume that,
Leukoaraiosis occur as a result of reactive gliosis secondary to chronic ischemia,
induced by occlusion of small arterioles supplying the white matter.
Correlation between the Carotid artery stenosis,
atherosclerotic intima-media thickness and plaque types in patients with leukoaraiosis were examined.
Leukoaraiosis is more commonly observed in elderly.
This also suggests that a significant correlation between age and leukoaraiosis.
Previous studies also support this data; age-related brain atrophy and Wallerian degeneration contribute to the process of developing leukoaraiosis (23,24).
Several studies are available demonstrating the connection between leukoaraiosis and cerebrovascular diseases (hypertension,
diabetes,
dyslipidemia,
smoking) (4,25,26,27).
Our data suggest a statistically significant correlation between leukoaraiosis and the age distribution,
atherosclerosis,
carotid artery stenosis and plaque types (Figure 17).
Previous studies submit data that carotid arteries with fatty plaques (Type 1,
Type 2) contribute to leukoaraiosis,
the data in our study also supports this.
In summary,
recent studies reveal structural changes in the white matter the parenchyma of the aging brain.
Addition to T2 signal changes on MR imaging,
further investigation is needed in the functional sense.
However,
we believe that these factors may be linked to each other.
Greater number of participants will contribute to a clearer understanding of the pathophysiology of leukoaraiosis.