Odds are, you know of somebody who has suffered a stroke. After all, approximately 795,000 Americans have one each year; it has been consistently ranked the fourth leading cause of death in the United States, and the leading cause of long term disability (CDC, 2016). Strokes affect individuals of all ages, ethnicities, and health statuses (albeit with different susceptibility); thus, it’s relevance has rendered it one of the most thoroughly studied neurological disorders today. That being said, how much do you really know about what a stroke actually is? Despite the relatively large body of research that exists, chances are you aren’t aware of the actual impact of a stroke on your body and brain. The reality is that strokes can produce profound and long-lasting cognitive and motor deficits.
A stroke occurs when the brain is deprived of blood flow for an extended period of time. Roughly 87% of all strokes are classified as ischemic, which occurs when the vessels supplying blood to the brain are blocked. The two separate categories of ischemic stroke are: cerebral thrombosis and cerebral embolism. A thrombosis occurs when a blood clot (or thrombus) develops at the vessel it blocks, whereas an embolism refers to a blood clot that forms at another location and travels throughout the bloodstream until it reaches a vessel too small to let it pass. The secondary form of stroke is referred to as hemorrhagic stroke, in which blood vessels burst and cause bleeding into brain tissue.
Examining the neurobiological impact of a stroke can be complicated, because nothing in the brain occurs independently. First and foremost, our brain cells need oxygen to stay alive and to do all the things we expect it to do… circulation of blood is how that oxygen gets around! Prolonged lack of oxygen and glucose to brain cells can lead to a cascade of detrimental effects. The diagram below illustrates the ways in which ischemic strokes at varying severities can impact the brain at a cellular level.
As shown, advanced ischemic episodes tend to result in the destruction of cell components, as well as the death of cell clusters. This is because neurons in the brain require a constant supply of glucose and oxygen in order to function; without maintenance of specific ion concentrations they are unable to send and receive nerve impulses from surrounding neurons, rendering them virtually useless. Certain bodily functions are localized in specific brain regions; for example, neuronal connections in a specific region of the brain may control the muscles involved in moving your upper right leg, whereas a separate but nearby cluster of neurons may control the acuity at which you can control your fingers. Thus, a single ischemic episode can result in loss of motor function of several parts of the body.
Much of the research regarding strokes has been focused on how to best treat individuals after the fact. Neuroscientists and clinicians alike are interested in developing treatment plans that maximize recovery and minimize long-term detriment. This isn’t an easy task because recovery after stroke can be contingent on so many disparate factors. For example, how long the brain was deprived of blood, where the clot was in relation to other brain structures, and the pre-existing health of the individual are all factors with direct implications on recovery outcomes. Unfortunately the brain is unlike other organs that have the capacity to replace large numbers of damaged or dead cells (such as the skin or the liver), but it has something else going for it: nervous tissue has the remarkable ability to adapt its function rather than regenerate its structure in response to a changing environment. This ability to adapt and learn from experiences is called neural plasticity. Neural plasticity essentially allows the brain to remap dendritic and axonal connections between neurons, meaning that to a certain degree, healthy neurons can take over in areas where neurons degraded past the point of function (Pekna, et al., 2012) . In fact, studies show that brain injury leads to increased neural plasticity in the spared regions!! Plasticity peeks roughly one to three months after injury, and as such, several researchers have focused on how to utilize specific therapeutic tasks in this time frame to maximize healing (Hara, 2015; Murphy & Corbett, 2009).
Evidence from animal models suggest that plasticity is best enhanced through activity-dependent and synapse strengthening mechanisms. The upper image below is from a paper in which researchers examined the impact of targeted stroke and subsequent neural plasticity in the the somatosensory and motor cortices of the brain involved in mouse forelimb and hindlimb activation (Zhang, 2007). They found that in rats who did not experience a targeted stroke, the synapses were tightly coupled to small brain blood vessels only 13 micrometers away. In contrast, in rats who underwent a stroke showed looser coupling, and the synaptic structure was maintained by flowing blood vessels at a much greater distance of 80 micrometers. In simpler terms, the rats who experienced a stroke showed far less synaptic plasticity relative to those who did not, supporting the idea that the brain has this self protective mechanism of neural plasticity that ramps up when needed.
Despite the speed at which stroke research is progressing, better long-term rehabilitation treatment plans are still very much a necessity. Strokes can impact any area of the brain, from motor function of major extremities to speech production. It’s a neurological disorder that impacts everyone in one way or another, and alleviating the often debilitating outcomes are of the upmost importance.
Hara, Y. (2015). Brain plasticity and rehabilitation in stroke patients. Journal of Nippon Medical School, 82(1), 4-13.
Pekna, M., Pekny, M., & Nilsson, M. (2012). Neural plasticity as a basis for stroke rehabilitation. L.M. Carey, (Ed.), Stroke Rehabilitation: Insights from Neuroscience and Imaging (pp. 24-34). New York, NY: Oxford University Press.
“Stroke Facts.” Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 30 Dec. 2016. Web. 07 Apr. 2017.
Zhang, S., & Murphy, T. H. (2007). Imaging the impact of cortical microcirculation on synaptic structure and sensory-evoked hemodynamic responses in vivo. PLoS Biol, 5(5), e119.