Related Experiment Videos
A review on blood pressure and ischaemic white matter lesions
1Institute of Clinical Neuroscience, Section of Psychiatry, Sahlgrenska Hospital, Göteborg University, Sweden. Ingmar.Skoog@psychiat.gu.se
Insights
High blood pressure is a primary risk factor for white matter lesions (WMLs). Both high and low blood pressure can contribute to WMLs through various vascular and neurological pathways.
Area of Science:
- Neurology
- Vascular Biology
- Pathophysiology
Background:
- Hypertension is a major risk factor for ischemic white matter lesions (WMLs).
- WMLs are characterized by demyelination and axonal loss in subcortical structures.
- The pathogenesis involves vascular changes and potential blood-brain barrier disturbances.
Purpose of the Study:
- To explore the complex relationship between hypertension and ischemic white matter lesions (WMLs).
- To elucidate the multifactorial pathways contributing to WMLs in the context of blood pressure dysregulation.
Main Methods:
- Review of existing hypotheses on hypertension-induced WMLs.
- Discussion of vascular mechanisms like lipohyalinosis and hypoperfusion.
- Exploration of blood-brain barrier integrity and the renin-angiotensin system's role.
Main Results:
- Long-standing hypertension can lead to lipohyalinosis, vessel wall thickening, and lumen narrowing in small arteries supplying white matter.
- Hypotension episodes can cause white matter hypoperfusion and hypoxia-ischemia.
- Hypertension may also disrupt the blood-brain barrier, leading to edema and cellular damage via various mediators.
Conclusions:
- Hypertension is a key risk factor for WMLs, acting through vascular damage and potentially altered blood-brain barrier function.
- Both elevated and low blood pressure levels are implicated in WML development.
- The renin-angiotensin system and potential links to Alzheimer's disease warrant further investigation in WML pathogenesis.
Abstract:
Hypertension or high blood pressure is constantly reported to be the main risk factors for ischaemic white matter lesions (WMLs). These lesions show the histopathological picture of diffuse demyelination and moderate loss of axons in subcortical structures. The main hypothesis regarding the association between high blood pressure and ischaemic WMLs is that long-standing hypertension causes lipohyalinosis of the media and thickening of the vessel walls with narrowing of the lumen of the small perforating arteries and arterioles which nourish the deep white matter. Episodes of hypotension may then lead to hypoperfusion and hypoxia-ischaemia in the white matter. In line with this, low blood pressure has also been reported to be a risk factor for WMLs. However, also other pathogenetic mechanisms may be involved. Hypertension may cause disturbances in the blood-brain barrier, which may cause lesions in the white matter by cerebral oedema, by activation of astrocytes or by destructive enzymes or other poisons which pass through the damaged vessel walls. The renin-angiotensin system is an example of a system that may be involved in the pathogenesis of both hypertension and arteriosclerosis. Its effector peptide angiotensin II has several blood-pressure-increasing effects, such as direct vasoconstriction and activation of the sympathetic nervous system. It also promotes hyperplasia and hypertrophy in vascular smooth muscle cells. Recently an association between hypertension and Alzheimer's disease has been reported. It is not clear whether this may be the reason for the common occurrence of WMLs in cases of late-onset Alzheimer's disease, as Alzheimer's disease may also cause lesions in the cerebral microvasculature. The association between WMLs and hypertension may thus be mediated through several different pathogenetic pathways.