Brain haemorrhage

Eight days later, however, on the catastrophic 11th of September, my father was struck by a bad brain haemorrhage from which he did not recover. He died on 27th of October 2001. 

PI. Palsdottir, A., Abrahamson, M., Thorsteinsson, L., Arnason, A., Olafsson, I., et al., Mutation in cystatin C gene causes hereditary brain haemorrhage. Lancet 2(8611), 603-604 (1988). 

A 53-year-old woman who had been taking acenocoumarol for 2 years after a heart valve replacement died after a massive brain haemorrhage about 3 weeks after starting to take tamoxifen 20 mg daily for a benign breast condition. ... 

Barlow, J. J., Baruah, J. K. and Davison, A. N. (1977). D-Aminolaevulinic acid dehydratase activity and focal brain haemorrhages in lead-treated rats. Acta Neuropathol. (Berlin), 39, 219... 

Another condition in which energy stress plays a role in disturbance of neural activity is stroke. In stroke, either haemorrhagic or ischaemic, the oxygen supply to parts of the brain is reduced. Since ATP generation is totally aerobic in neurones, this results in complete failure of ATP generation. 

These result from over-stimulation of the sympathetic nervous system anxiety, sweating, tachycardia, arrhythmia, hypertension, myocardial ischaemia, headache, cerebral haemorrhage, pulmonary oedema. Adrenaline may cause pupillary dilatation which must be distinguished from pupillary dilatation due to other causes, e.g. severe brain injury. 

Grontoft, O. 1964. Intracranial haemorrhage and blood-brain barrier problems in the newborn. Acta Pathol Microbiol Scand Suppl. C l. 

White blood cells readily traverse the blood-brain barrier 12-24 hours after ischaemia and contribute to the excessive production of oxygen free radicals. Eventually the infarcted zone becomes infiltrated with lymphocytes, polymorphs and macrophages. The cytokines released from the macrophages contribute to the injury of the vessel walls and to the consequent oedema, haemorrhage and necrosis. Thus the function of the anti-inflammatory agents is to reduce the initial adhesion of the white blood cells and thereby limit the extent of the inflammatory response. 

M6. Mantle, D., Siddique, S., Eddeb, F., and Mendelow, A. D., Comparison of protein carbonyl and antioxidant levels in brain tissue from intracerebral haemorrhage and control cases. Clin. Chim. Acta 312, 185-190 (2001). 

Q1 A stroke involves significant reduction in blood flow to a part of the brain. It can be caused either (i) by an embolus or by intravascular clotting, which blocks blood flow to an area (approximately 85% of strokes), or (ii) by haemorrhage from a ruptured blood vessel, which compresses the brain tissue (approximately 15% of strokes). Patients with extensive atherosclerosis are at risk of intravascular coagulation and blockage of cerebral blood flow, but a vessel can be blocked by a thrombus originating in another part of the circulation. This cause of stroke is common in elderly patients >60 years of age. Aneurysms which rupture suddenly are a more common cause of stroke in younger patients. 

Regulation of anti-diuretic hormone secretion is primarily through the plasma osmolarity. Osmolarity is sensed in the hypothalamus by neurons known as osmoreceptors, which in turn stimulate secretion from those neurons that produce anti-diuretic hormone. Secretion of antidiuretic hormone is also simulated by decreases in blood pressure and volume, conditions sensed by stretch receptors in the heart and large arteries. Changes in blood pressure and volume are not nearly as sensitive a stimulator as increased osmolarity, but are nonetheless potent in severe conditions. For example, loss of 15-20% of blood volume by haemorrhage results in a massive secretion of anti-diuretic hormone. Another potent stimulus of anti-diuretic hormone is nausea and vomiting, both of which are controlled by regions in the brain with links to the hypothalamus. 

Bornebroek M, Westemdorp RGJ, Haan J et al. (1997). Mortality from hereditary cerebral haemorrhage with amyloidosis Dutch type. The impact of sex parental transmission and year of birth. Brain 120 2243-2249 Brott T, Broderick J, Kothari R et al. (1997). Early haemorrhage growth in patients with intracerebral haemorrhage. Stroke 28 1-5 Brown RD, Wiebers DO, Torner JC et al. (1996). Incidence and prevalence of intracranial vascular malformations in Olmsted, County Minnesota 1965 to 1992. Neurology 46 949-952... 

Haemorrhagic lesions are characteristic of experimental thiamine deficiency and WE in humans indicative of a breakdown of the blood-brain barrier (BBB). A study using immunoglobulin G (IgG) as an indicator of BBB integrity in thiamine-deficient rats revealed increased IgG immunoreactivity in the inferior colliculus and inferior olive prior to the onset of cell death in these regions (Calingasan et al.,... 

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