Baz
07 May 2020Wolfzx12r
Baz - Wolfzx12rAVMs become symptomatic only when the damage they cause to the brain or spinal cord reaches a critical level. This is one of the reasons why a relatively small fraction of people with these lesions experiences significant health problems related to the condition. AVMs damage the brain or spinal cord through three basic mechanisms: by reducing the amount of oxygen reaching neurological tissues; by causing bleeding (hemorrhage) into surrounding tissues; and by compressing or displacing parts of the brain or spinal cord.
AVMs compromise oxygen delivery to the brain or spinal cord by altering normal patterns of blood flow. Arteries and veins are normally interconnected by a series of progressively smaller blood vessels that control and slow the rate of blood flow. Oxygen delivery to surrounding tissues takes place through the thin, porous walls of the smallest of these interconnecting vessels, known as capillaries, where the blood flows most slowly. The arteries and veins that make up AVMs, however, lack this intervening capillary network. Instead, arteries dump blood directly into veins through a passageway called a fistula. The flow rate is uncontrolled and extremely rapid—too rapid to allow oxygen to be dispersed to surrounding tissues. When starved of normal amounts of oxygen, the cells that make up these tissues begin to deteriorate, sometimes dying off completely.
This abnormally rapid rate of blood flow frequently causes blood pressure inside the vessels located in the central portion of an AVM directly adjacent to the fistula—an area doctors refer to as the nidus, from the Latin word for nest—to rise to dangerously high levels. The arteries feeding blood into the AVM often become swollen and distorted; the veins that drain blood away from it often become abnormally constricted (a condition called stenosis). Moreover, the walls of the involved arteries and veins are often abnormally thin and weak. Aneurysms—balloon-like bulges in blood vessel walls that are susceptible to rupture—may develop in association with approximately half of all neurological AVMs due to this structural weakness.
Bleeding can result from this combination of high internal pressure and vessel wall weakness. Such hemorrhages are often microscopic in size, causing limited damage and few significant symptoms. Even many nonsymptomatic AVMs show evidence of past bleeding. But massive hemorrhages can occur if the physical stresses caused by extremely high blood pressure, rapid blood flow rates, and vessel wall weakness are great enough. If a large enough volume of blood escapes from a ruptured AVM into the surrounding brain, the result can be a catastrophic stroke. AVMs account for approximately 2 percent of all hemorrhagic strokes that occur each year.
Even in the absence of bleeding or significant oxygen depletion, large AVMs can damage the brain or spinal cord simply by their presence. They can range in size from a fraction of an inch to more than 2.5 inches in diameter, depending on the number and size of the blood vessels making up the lesion. The larger the lesion, the greater the amount of pressure it exerts on surrounding brain or spinal cord structures. The largest lesions may compress several inches of the spinal cord or distort the shape of an entire hemisphere of the brain. Such massive AVMs can constrict the flow of cerebrospinal fluid—a clear liquid that normally nourishes and protects the brain and spinal cord—by distorting or closing the passageways and open chambers (ventricles) inside the brain that allow this fluid to circulate freely. As cerebrospinal fluid accumulates, hydrocephalus results. This fluid buildup further increases the amount of pressure on fragile neurological structures, adding to the damage caused by the AVM itself.
Hi guys, I've had a horrible time but at least I'm still here thanks to Walton Neurosurgery Clinic and Dr Eldridge. I had a bleed last June 2010 which I hear go pop behind my left ear and the left side of my body went numb and speech difficulties, being a man I tried to shrug it off but the pain got so bad I went to see me GP the next day who sent me for the first of many scans, the scan came back showing that I'd had a bleed and a stroke, my GP referred me over to Walton where I had a Angiogram which showed I not only had I had a bleed from the AVM but I had another AVM on the right side front temple area.
Two and a half years from my first AVM hemorrhage and stroke, then a second hemorrhage just before Christmas 2010 resulted in an emergency coil and embolization of one of two AVM's I have this caused an AF of my heart (back pressure) and horrendous tinnitus, second AVM was embolized in March 2011, since the op's I've had very bad pain all the way through recovery and now on the 24th December 2012 I suffered a seizure, head pain has reduced along with the tinnitus in my left ear, I have now been told by the Doc's that I will lose my driving license for a year. I have spent the last 8 months getting my business back up and running and as a sole trader will have to shut it down again, having AVM's is a total life changing disability and will rule your life forever.
Thank god it's been very quiet on here, just an update to where I am, still waiting for my driving license back after the seizure on December 24 2012 no further seizures since that one, I am back to Walton Nero on the 13th Jan for another angiogram, that will make number 4. The upside to the seizure I have had very little pain from AVM number 1 op site, just get the occasional bubbling and pulling sensation and the tinnitus in my left ear has dropped dramatically but still really bad still really bad in my right ear again very little pain from AVM number
Baz Emptage
Shaz Emptage