Brain aneurism, also known as cerebral aneurism is a localized swelling condition of the brain’s blood vessels. The affected vessel is dilated at a localized point and may go unnoticed for a long time. People suffering from this condition experience symptoms such as sudden headaches and general discomfort. Severe aneurism may rupture a blood vessel at the point of dilation. Aneurism occurs randomly among patients with a history of heart disease (Milunsky 8). This is because the genetic causes of heart ailments are also likely to result in brain vessels’ disorders. The relationship between the heart conditions and brain aneurism is an issue under research and the suggested links are a result of probabilistic analysis. Since the term aneurism refers to dilation of any blood vessel, the cerebral aneurism is also referred to as intracranial aneurism.
A receptor gene in the human chromosome 9 is the causative agent of most blood vessel disorders (Milunsky 9). Moreover, blood vessel disorders are the major cause of heart ailments. The endothelin receptor gene controls the ability of the vessel’s tissue to stretch, the diameter of the blood vessels and reconstructive activity of the endothelium. Due to constant movement of the human body and blood, abrasion to the inner surface of blood vessels is inevitable. The gene, which controls the reconstruction of the inner layer, the endothelium, may inhibit quick recovery. The vessels then slowly stretch with the weak points swelling or bulging into aneurism. This condition of the blood vessels may occur in all parts of the body, but might go unnoticed in most of the cases. The body organs that are sensitive to the deformation of blood vessels such as the brain and the heart may become significantly affected. Aneurism in the cardiac arteries may signify an imminent cardiac arrest. Cerebral aneurism often results in the rapture of the dilated blood vessel especially in a case whereby the concerned person has hypertension. The endothelin receptor gene is responsible for the abnormal constriction of the blood vessels resulting in high blood pressure. High blood pressure often causes cardiac disorders in most people (Chung 29). In addition, high blood pressure causes abnormal dilation of brain vessels posing a risk of aneurism at weak points especially at the point where the vessels branch out. The bulge of the vessel may cause trauma to the brain consequently inducing headache. Sometimes, the bulge may burst resulting in a stroke. Stroke is usually fatal and may result to death if professional medical care is not availed immediately.
In addition, the endothelin receptor gene controls the deposit of cellulose material and fat in the anterior walls of the blood vessels. Progressive and localized deposit of fat in a blood vessel may cause thrombosis or blocking of the vessel. If the blocking or narrowing of the vessel reaches below the minimum, a condition known as coronary thrombosis or cardiac arrest occurs. Similarly, the depositing of cellulose and a material known as arteriosclerosis may cause hypertension. The pressure on the blood vessel’s walls may cause forceful dilation resulting into cerebral aneurism. This gene causes its effect through the control of building of proteins. Furthermore, the protein structure and concentration determines the physical properties of blood vessels, and the deposit of the cellulose material on the endothelium. The gene is also a determinant of the outcome of the growth of the heart (Adams 238). Consequently, the malfunctioning of this gene leads to disorders or malformation of the heart and the blood vessels leading to the occurrence of heart disorders and cerebral aneurisms simultaneously.
Works Cited
Adams, Harold P.. Principles of cerebrovascular disease. New York: McGraw-Hill Medical, 2007. Print.
Chung, Ka Young. Physiological and pathological function of enothelin receptor type A in adult ventricular myocytes. Madison: University of Wisconsin, 2008. Print.
Milunsky, Aubrey. Your genes, Your health. Manchester: Oxford University Press, 2008. Print.