Aphasia is a disorder characterized by an acquired impairment in understanding and reproducing speech. Aphasia often develops following a stroke: stroke affects the blood supply to the left hemisphere, and subcortical structures experience prolonged hypoxia (Wang & Wiley, 2020). The capsule and caudate nucleus of the basal ganglia dominate the area of speech formation, so their lesion due to stroke, infectious disease, or traumatic brain injury (TBI) leads to the development of aphasia. Depending on the area of damage, aphasia is divided into different types, differing in the activity of brain structures (San Lee et al., 2020). Developing aphasia is manifested by varying degrees of speech and perception impairment, as the extent of the lesions affected directly correlates with the ability to perceive the cognitive load.
In addition to the apparent speech impairment, aphasia can affect the auditory areas, namely the temporal lobe. The auditory cortex is located in Brodmann 41 and 42, so head injuries in the temporal lobes result in partial or complete hearing loss. Due to the connection with the speech centers, aphasia develops (Swenson et al., 2022). Damage to the inner and outer ear leads to decreased hearing. Damage to the superior temporal gyrus impairs the perception of sounds.
TBI are a frequent cause of hearing impairment, and in the context of aphasia, they disrupt neural connections and the ability to regenerate subcortical structures. The types of aphasia differ in the degree of damage to the speech and hearing apparatus, as well as to the sense of action and decision-making center (Grossman & Irwin, 2021). Prolonged compression of brain structures leads to hypoxemia and impaired cerebral blood flow (Swenson et al., 2022). TBI increases the risk of infection and disrupts the cerebrospinal fluid and blood pH, thereby reducing oncotic and osmotic pressure. Hence, aphasia relates to the biological principles of onset and development depending on the agent acting on the auditory and speech subcortical centers.
References
Grossman, M., & Irwin, D. J. (2018). Primary progressive aphasia and stroke aphasia. Continuum (Minneapolis, Minn.), 24(3), 745–767. Web.
San Lee, J., Yoo, S., Park, S., Kim, H. J., Park, K. C., Seong, J. K., Suh, M. K., Lee, J., Jang, H., Kim, K. W., Kim, Y., Cho, S. H., Kim, S. J., Kim, J. P., Jung, Y. H., Kim, E. J., Suh, Y. L., Lockhart, S. N., Seeley, W. W., Na, D. L., … Seo, S. W. (2020). Differences in neuroimaging features of early- versus late-onset nonfluent/agrammatic primary progressive aphasia. Neurobiology of Aging, 86, 92–101. Web.
Swenson, T. L., Roehmer, C., Tran, R., & Plummer, C. (2022). Donepezil for aphasia after severe traumatic brain injury: A clinical vignette. American Journal of Physical Medicine & Rehabilitation, 101(4), e54–e56. Web.
Wang, R., & Wiley, C. (2020). Confusion vs Broca aphasia: A case report. The Permanente Journal, 24, 19-061. Web.