Stroke, also called cerebrovascular accident, is the sudden onset of neurological deficit resulting from interference of blood supply to the central nervous system. Stroke is common among older people, especially above 65 years of age (McCance& Huether, 2019). Additionally, it is estimated to occur more in blacks than in whites. The incidence of stroke in the black community is 150% more than in the white community (McCance& Huether, 2019). This shows not only a racial predisposition but also a familial predisposition. There is an increased chance of an individual suffering from stroke if they have a family member with the same history. An ischemic stroke causes about 85% of the incidences of stroke while the remainder occurs due to hemorrhagic stroke.
Ischemic stroke occurs when an area of the brain loses blood supply and can be caused by either sudden occlusion, gradual occlusion or due to vessel stenosis causing narrowing. When blood vessel to a particular part of the brain is occluded, a central core with ischemia develops (McCance& Huether, 2019). That central core is an area with no blood supply and undergoes necrosis. The center is surrounded by an area of borderline ischemia, which is usually called the ischemic penumbra (McCance& Huether, 2019). The cells within the penumbra do not undergo enough oxygen deprivation to cause cell death. Instead, these cells can be restored with the restoration of blood supply within a few hours (Mir et al., 2014). Prevention of cellular death within the penumbra is possible if thrombolytic agents are administered within three hours of the accident (McCance& Huether, 2019). After ischemia has occurred, necrosis develops, with subsequent swelling around the insult, followed by mushy disintegration within two to three days (McCance& Huether, 2019). Macrophages infiltrate the area and phagocytose any necrosed tissues, leading to a resolution of the necrosis within two weeks. The result is a cavity with surrounding glial scarring.
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Hemorrhagic stroke occurs when there is bleeding from a vessel into the brain tissue (Woodruff et al., 2011). When bleeding occurs, the surrounding brain tissue is often compressed and displaced, leading to ischemia, edema, increases intracranial pressure and cellular necrosis (McCance& Huether, 2019). Bleeding can occur either massively, in small amounts, in slits or as petechial hemorrhages (McCance& Huether, 2019). Massive hemorrhages are extensive, while petechial hemorrhages can be as small as pinheads. When there is massive hemorrhage, cerebral perfusion can halt, leading to massive cellular death. More minor hemorrhages can cause surrounding neuronal ischemia leading to cellular edema (McCance& Huether, 2019). The major challenge in hemorrhagic stroke is the development of cellular ischemia, which can be fatal. However, with moderate ischemia, hemorrhage can resolve through reabsorption, macrophage clearance and development of a glial scar.
At the cellular level, the key pathophysiological process is cellular ischemia leading to cellular damage. When ischemic or hemorrhagic necrosis occurs, neurons lose their oxygen and nutrient supply (Mir et al., 2014). Often, neurons undergo aerobic metabolism, and in the absence of oxygen, the disruption of aerobic necrosis leads to a failure of the sodium/potassium ATPase pump (Tadi &Lui, 2019). The pump fails due to a lack of ATP production. The result is an accumulation of sodium intracellularly and potassium extracellularly (Tadi &Lui, 2019). Intracellular sodium accumulation leads to cellular depolarization with subsequent release of glutamate (Mir et al., 2014). Glutamate is responsible for opening N-Methyl-D aspartate(NMDA) and AMPA receptors, allowing the inflow of calcium ions into neurons (Mir et al., 2014). The continued inflow of calcium ions leads to increased neuronal firing leading to cellular death from excitotoxicity.
Another mechanism that leads to cellular death in stroke is the production of reactive oxygen species. When blood supply is reduced, reactive oxygen species are produced from the mitochondria during the electron transport process (Woodruff et al., 2011). Other free radicals are also derived from ischemic neurons as they process arachidonic acid or during reperfusion injury (Woodruff et al., 2011). Reactive nitrogen species, derived from the monocytes, also contribute to neuronal damage during ischemia (Woodruff et al., 2011). Both reactive oxygen species and reactive nitrogen species have a role in activating inflammatory processes and apoptosis, leading to cell death (Woodruff et al., 2011). These free radicals produced in cells, combined with other proinflammatory mediators secreted by brain cells, lead to inflammation (Mir et al., 2014). Brain inflammation worsens cellular damage.
The musculoskeletal system is usually significantly affected during a stroke. Often, patients become hemiparetic or develop spasticity (Gray et al., 2012). Hemiparesis is the paralysis of one side of the body and can last for years after stroke. Hemiparesis in stroke has been linked to decreased muscle excitability, decreased muscle firing rates, and decreased muscle length (Gray et al., 2012). Following a stroke, most patients become immobilized or inactive. As a result, their muscles length decreases, and muscle strength reduces (Gray et al., 2012). Reduced muscle mass, length and strength are worsened by ageing in most stroke patients. The mechanical properties of muscle play a role in the generation of force by a muscle. A larger fiber diameter in a longer muscle generates more force (McCance& Huether, 2019). Additionally, the more muscle mass found in a muscle, the higher the firing power (McCance& Huether, 2019). Hence, the reduction in muscle mass and length that follows stroke leads to weakness in the muscles.
Spasticity that develops after a stroke occurs due to increased excitation of the stretch reflex. Following a stroke, there is a decrease in cortical disinhibition (Li & Francisco, 2015). This leads to an imbalance between inhibitory impulses and facilitatory impulses of the stretch reflex in muscle (Li & Francisco, 2015). Stroke often affects the cortex, affecting corticospinal and corticoreticular pathways that often inhibit the excitation of the stretch reflex (Li & Francisco, 2015). Hence, with decreased inhibition, the reticulospinal tract's excitation goes uncontrolled, leading to increased excitation of the stretch reflex and resulting spasticity in muscles (Li & Francisco, 2015). The result is often spastic hemiplegia in patients with a history of stroke. These motor deficits that occur from stroke usually decrease the functional abilities of most patients and require further treatment and rehabilitation.
References
Gray, V., Rice, C. L., & Garland, S. J. (2012). Factors that influence muscle weakness following stroke and their clinical implications: a critical review. Physiotherapy Canada , 64 (4), 415-426.
Li, S., & Francisco, G. E. (2015). New insights into the pathophysiology of post-stroke spasticity. Frontiers in human neuroscience , 9 , 192.
McCance, K. L. & Huether, S. E. (2019). Pathophysiology: the biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.
Mir, M. A., Al-Baradie, R. S., & Alhussainawi, M. D. (2014). Pathophysiology of Strokes. Recent Advances in Stroke Therapeutics. Retrieved from https://www. researchgate. net/publication/273061843_Pathophysiology_of_Strokes .
Tadi, P., & Lui, F. (2019). Acute stroke (cerebrovascular accident).
Woodruff, T. M., Thundyil, J., Tang, S. C., Sobey, C. G., Taylor, S. M., & Arumugam, T. V. (2011). Pathophysiology, treatment, and animal and cellular models of human ischemic stroke. Molecular neurodegeneration , 6 (1), 11.
