TY - CHAP M1 - Book, Section TI - Aphasia A1 - Volpe, Darren A2 - Salardini, Arash A2 - Biller, José PY - 2016 T2 - The Hospital Neurology Book AB - Aphasia is defined as a disturbance of language processing caused by damage to the brain. It can be one of the most devastating consequences of structural or functional damage to the dominant hemisphere of the brain, that is, the hemisphere dominant for language. The left hemisphere is dominant for language in over 90% of all individuals—in virtually all persons who are right-handed, and in a majority of persons who are left-handed. Aphasia has long been recognized as a consequence of brain damage in the medical literature, and variants thereof were most clearly described by Broca and Wernicke in the 19th century. These were based on pathological studies and were the basis for the localization-based approach that has largely persisted to this day. During the 20th century, other variants of aphasia were identified and described, and in the dawning of the 21st century, a more systems-based approach has come into favor. This chapter will set out to accomplish the following:Define terminology important for understanding language-based discussions.Define basic neuroanatomic regions in the dominant (usually the left) hemisphere, which are important in primary language processing and output; and the corresponding regions in the nondominant (usually the right) hemisphere related to the processing and output of the emotional or nonverbal aspects of language.Outline aphasic syndromes in their classic localization-based descriptions, as they remain essential to understand the “input and output” aspects of language, with the understanding that many different cortical–subcortical, and even inter-hemispheric, networks are activated in parallel, which allow for the comprehensive experience of “language.”Discuss pitfalls and pearls in the evaluation of the patient with language deficits. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/03/28 UR - neurology.mhmedical.com/content.aspx?aid=1127045666 ER -