Stroke: The Silent Killer
Stroke or cerebrovascular accident (CVA) is the most common cause of brain damage. More specifically, a stroke is the rapid loss of brain function due to the disruption of blood supply to the brain. In turn, a significantly reduced amount of oxygen and glucose flowing to the brain results in the death of brain cells and brain damage. This often results in speech, movement and memory impairment.
About 75% of all strokes are due to ischemia and occurs when a blood clot or thrombus forms, which retards or stops blood flow to parts of the brain. When a clot forms in the body and breaks to be free-floating , it is called an embolus.
The clot may be carried throughout the bloodstream where it is likely to cause an ischemic stroke. A stroke is considered hemorrhagic when, blood vessels on the surface of the brain ruptures and the space between the brain and the skull is filled with blood entering the brain tissue(subarachnoid hemorrhage) or when a defective artery to the brain and skull with blood ruptures and brain tissue again starts to fill with blood (cerebral hemorrhage). Both result in a lack of blood flow to the brain and a buildup of blood that puts too much pressure on the brain.
Signs and Symptoms of Stroke
After having a stroke, the brain cells quickly begin to die and symptoms become apparent in the individual. It is important to note these symptoms, as recovery from a stroke is more likely the earlier you notice the signs and begin treatment. Common symptoms include but are not limited to:
• Dizziness, difficulty walking, imbalance and coordination
• Speech impediments
• Numbness, weakness, or paralysis on one side of the body
• Impaired vision (blurred, darkened or double)
• Acute onset of severe headaches
• Smaller strokes (or silent strokes), however, they may not cause any symptoms, but can still damage brain tissue.
One of the tell tale signs that a stroke is about to occur is a transient ischemic attack (TIA) – a temporary interruption in blood flow to part of the brain. TIA symptoms are similar to that of a stroke but the period of time they last are much shorter and the damage done is neither noticeable nor permanent.
How do strokes occur?
In the case of a cerebral blood vessel being blocked by a clot or rupturing, the brain tissue that is supplied by that vessel loses nutrients vital to it’s survival i.e., glucose and oxygen. This usually results in damage to and the death of the deprived tissue.
On a side note, just to peak your interest, new research has found that neural damage (and the subsequent loss of neural function) extends far beyond the blood-deprived area as a result of a neurotoxic effect that leads to the death of additional nearby cells. The cells deprived of blood die initially by necrosis (unintentional cell death), but the ill-fated neighbors undergo apoptosis (deliberate cell suicide).
In excitotoxicity, the initial O2-starved cells secrete amounts of glutamate, a common excitatory neurotransmitter. Due to the overdose of glutamate from the damaged brain cells, glutamate binds with other nearby neurons causing them to be overexcited as well. Glutamate binds specifically to excitatory receptors known as NMDA receptors, they function as channels for Calcium cations.
The activation of these channels by toxic neurotransmitter causes the channel to be accessible for an abnormally long period of time, allowing excessive amounts of Ca2+ to flood in to the affected neurons nearby. This increased amount of intracellular Ca2+ sets off a signal to the cells for them to self-destruct, producing free radicals in the process.
Radicals, which are a highly reactive electron-deficient particle furthers the damage by drawing electrons to it from other molecules. These highly reactive, electron-deficient particles cause further damage by snatching electrons from other molecules. It is speculated by researchers that the calcium ion apoptotic signal spreads to healthy cells via the gap junction allowing calcium and other small ions to diffuse as they please between cells with no restriction, effectively killing even more neurons.
Therefore, most neurons that die following a stroke are originally healthy cells that commit suicide in response to the chain of reactions released by the toxic secretion of glutamate from the original site of low O2 levels.