Aphasia Syndromes

Abstract

The assessment of language is an essential component to neuropsychological evaluations. One that is often quickly summarized as “speech was fluent and articulate, with normal rate, rhythm, intonation, and prosody.” While this may describe some aspects of speech, it by no means offers clinicians enough information to determine if language functions are impaired.

This chapter will approach the assessment of language from more of a diagnostic perspective. That is, we will approach language disorders based on well-described aphasia syndromes which are familiar to many. While this can be helpful, some readers uncertain of aphasia syndromes, but observing some disruption of language, are encouraged to review Chap. 7, which explores diagnosis of language disorders from a symptomatic (behavioral observation) perspective.

Aphasia syndromes denote an acquired language dysfunction due to neurological injury or disease. Aphasia syndromes are generally described by three language domains first detailed by Bensen and Geschwind: (1) fluent or nonfluent, (2) language comprehension, and (3) repetition. Additional components for assessing aphasia have been added, including naming, reading, and writing. Maintaining consistency with Chap. 7, reference to “dominant hemisphere” will refer to left hemisphere, since greater than 90% of people are left hemisphere dominant for language. Approximately 90–95% of the general population is right-handed.

Rule of thumb: Left hemisphere dominance for language

Right handed – 90–95%

Left handed – 60–70%

The clinical features of each aphasia syndrome are reviewed below along with neuroanatomical correlates. For rapid review, please see Tables 12.1 and 12.2 and Appendix. For more detailed discussion, please see Heilman and Valenstein (Clinical neuropsychology, 4th edn, Oxford University Press, New York, 2004), Kolb and Whishaw (Fundamentals of human neuropsychology, 6th edn, Worth, New York, 2008), Goodglass et al. (The assessment of aphasia and related disorders, 3rd edn, Pro-Ed, Austin, 2001), Lezak et al. (Neuropsychological assessment, 4th edn, Oxford University Press, New York, 2004), Mesulam (Principles of behavioral and cognitive neurology, 2nd edn, Oxford University Press, New York, 2000), and/or Victor and Ropper (Adams and Victor’s principals of neurology, 7th edn, McGraw-Hill, New York, 2001) for reviews.

Appendix: Rapid Review Summary for Classic Aphasia Syndromes

	Neuroanatomical correlates	Figure
Aphasia syndrome
Global	Lesion affecting anterior and posterior language areas (perisylvian or lateral fissure region)	Fig. 12.1
Expressive (Broca’s)	Anterior language area, posterior left frontal region, including Brodmann’s area 44	Fig. 12.3
Transcortical Motor	Left anterior frontal sparing Broca’s area (Brodmann’s 44)	Fig. 12.4
Receptive (Wernicke’s)	Temporoparietal damage affecting Wernicke’s area (Brodmann’s area 22, and often 39, 41, and 42)	Fig. 12.5
Transcortical Sensory	Posterior temporal and parietal dysfunction, sparing Wernicke’s area	Fig. 12.6
Mixed Transcortical	Lesion damaging frontal and temporoparietalregions, but Broca’s and Wernicke’s areas spared	Fig. 12.2
Conduction	Lesion of the supramarginal gyrus and arcuate fasiculus, but sparing both Broca’s and Wernicke’s areas.	Fig. 12.7
Anomic	Acute syndrome classically associated with a lesion posterior to Wernicke’s area involving either the angular gyrus (not shown) or inferior temporal region (shown). However, other aphasia syndromes may clinically resolve to an anomic aphasia. Finally, diffuse head trauma and neurodegenerative diseases can present with an anomic aphasia.	Fig. 12.8