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.

First, it is important to understand the difference between a “speech” impairment and a “language” impairment. A deficit of speech is one that affects the articulatory and phonetic aspects of verbal expression. A language deficit is one which reflects an abnormality of the brain that causes impairments in the comprehension and/or generation of language.¹ There are several terms that will be important to define before proceeding with any discussion of aphasia:^1–3

• 
  

  Phoneme: smallest individual speech sounds

  
  
• 
  

  Morpheme: the joining of individual speech sounds, which become the units of words

  
  
• 
  

  Mutism: lack of any verbal output

  
  
• 
  

  Dysphonia: production of crude vowels only

  
  
• 
  

  Dysarthria: a problem of motor speech execution. Production of poorly articulated consonants, often with a slow pace, resulting in “slurring” of speech

  
  
• 
  

  Dyspraxia: altered motor planning of speech—faulty phrasing, faulty stress on words or syllables. In itself, is not an aphasia because it is not a “language” impairment, but usually coexists with aphasia

  
  
• 
  

  Dysprosodia: altered intonation and rhythm of speech

  
  
• 
  

  Paraphasias:

  
  
  
  
  • 
    

    Phonemic (literal) paraphasia: substitution of an unintended sound into a word, for example, syllable or consonant substitutions within a word

    
    
  • 
    

    Semantic (verbal) paraphasia: substitution of one word (often related) for another

  
  
  
  
• 
  

  Neologistic: utterances that sound like words but are not real words

  
  
• 
  

  Anomia: deficit in word retrieval

  
  
  
  
  • 
    

    Simple retrieval deficit

    
    
  • 
    

    Long latency of retrieval (usually subcortical deficits)

    
    
  • 
    

    Substitutions of less specific general words (“thing,” “it”)

    
    
  • 
    

    Substitutions of descriptive phrases (circumlocutions)⁴

  
  
  
  
• 
  

  Fluency: generally defined as the number of correctly ordered words per unit time

  
  
• 
  

  Syntax: general sentence structure

While the classic “Broca’s” and “Wernicke’s” localizations remain useful concepts to understand the basic subdivision of language impairments (expressive versus receptive), lesion locations do not always respect the exact expectations of the classic literature in clinical settings.^1,3,4 What follows is a description of the regions of the language-dominant hemisphere that clearly have prominent roles in the production and comprehension of language.

The perisylvian region

The perisylvian region (figure 23-1) in the dominant and nondominant hemispheres has a clear role in the formation and comprehension of language, of both verbal (usually left hemisphere) and nonverbal (usually right hemisphere) information. Damage to this region in the dominant hemisphere leads to the aphasia syndromes, which are most common and well known, causing difficulty in either expressing language or comprehending language, or sometimes a combination of both. Interestingly, damage to the analogous regions in the nondominant hemisphere leads to difficulty in expressing or comprehending “body language” and the emotional content of speech,² which are important aspects of language but are less easily recognized, and not as disabling. Similarly, a portion of the right inferior frontal gyrus roughly analogous to Broca’s area on the left is preferentially activated during expression of music.

Anterior perisylvian cortex

Broca’s area

Broca’s area is located in the posterior portion of the inferior frontal gyrus. It includes an inverted triangular fold of cortex (pars triangularis) and an opercular portion. The operculum is the region of cortex that directly bridges the posterior-most part of the inferior frontal gyrus to the anterior insula. Interestingly, Broca’s area is in very close proximity to the lateral-most part of the precentral gyrus, which contains areas that control the movement of the mouth, tongue, and larynx, all the movements required to form motor programs for speech sounds. However, it is important to note that Broca’s area is not just involved in forming motor programs for speech—it allows for fluent language with proper ordering of words and syllables, grammatical constructs, and even the comprehension of grammar.^2,5

Posterior perisylvian cortex

Wernicke’s area

Wernicke’s area is located in the posterior portion of the superior temporal gyrus, which is involved in processing the input of language, and therefore in the comprehension of language. It allows us to ultimately extract meaning from speech sounds (phonemes), gestures (as in sign language), and in part visual symbols (further processing of visual symbols such as letters and words for reading comprehension has a locus in the dominant angular gyrus, part of the inferior parietal lobule). To understand verbal/spoken language, the elementary processing of auditory information first occurs in Heschl’s gyrus, located on the transverse temporal gyrus, which is the medial border of the superior temporal gyrus, and is part of the temporal operculum. This auditory information is then further processed in Wernicke’s area, which is considered a lexicon for the recognition of auditory word-forms which then has a role in processing their meanings and contexts.⁸

White matter connections

The arcuate fasciculus is a large white matter tract that connects Wernicke’s area to Broca’s area (figure 23-2), lesions of which are classically thought to cause impairment in repetition.

Stroke and perisylvian language cortex

Damage to the primary language regions of the brain can occur from virtually any structural lesion bordering the dominant perisylvian region, including tumors, abscesses, vascular malformations, and intracranial hemorrhage. However, the most common cause of aphasia is infarction to the territory of the left middle cerebral artery (MCA). If, for example, an embolism lodges in the MCA in its superior division within the Sylvian fissure proximal to its branches to Broca’s area, a Broca’s type language disturbance would be expected. If an embolism lodges in the inferior division of the MCA proximal to branches to Wernicke’s area in the posterior aspect of the superior temporal gyrus, a Wernicke’s-type receptive aphasia would be expected. The variability in aphasic syndromes seen in individuals with similar lesions may be due to the variations of neuroanatomic loci of language in those individuals, different branching patterns of their vasculature, or perhaps variations in the ability to form alternate pathways for language.