Phonology, Neural Basis of

PHONOLOGY refers to the sound structure of language. As such, the study of phonology includes investigation of the representations and organizational principles underlying the sound systems of language, as well as the exploration of the mechanisms and processes used by the listener in speech perception or by the speaker in speech production. The study of the neural basis of phonology is guided by an attempt to understand the neural mechanisms contributing to the perception and production of speech. This domain of inquiry has largely focused on investigations of adult aphasics who have language deficits subsequent to brain damage, exploring their language impairments and accompanying lesion localization. These "experiments in nature" provide the traditional approach to the study of the neural bases of phonology. More recently, neuorimaging techniques, such as POSITRON EMISSION TOMOGRAPHY (PET) and functional MAGNETIC RESONANCE IMAGING (fMRI), have provided a new window into the neural mechanisms contributing to phonology, allowing for investigation of neural activity in normal subjects as well as brain- damaged patients.

It has been long known that the left hemisphere is dominant for language for most speakers, and that the peri-sylvian regions of the left hemisphere are most directly involved in LANGUAGE PRODUCTION and SPEECH PERCEPTION. The classical view has characterized speech/language deficits in APHASIA in terms of broad anatomical (left anterior and left posterior) and functional (expressive and receptive) dichotomies (Geschwind 1965). In this view, expressive language deficits occur as a result of damage to the motor (anterior) areas, and receptive language deficits occur as a result of damage to the auditory association (posterior) areas. Nonetheless, the processing components involved in both speech production and perception are complex and appear to involve more extensive neural structures than originally proposed.

In order to produce a word or group of words, a speaker must select the word(s) from the set of words in long-term memory, encode its phonological form in a short-term buffer in order to plan the phonetic shape, which will vary as a function of the context ( articulatory phonological planning), and convert this phonetic string into a set of motor commands or motor programs to the vocal tract (articulatory implementation). Results from studies with aphasic patients show that all patients, regardless of clinical syndrome and accompanying lesion localization, display deficits in the processes of selection and planning (Blumstein 1994). That is, they may produce the wrong sound segment, a selection error, such as "keams" for "teams", or they may produce the wrong sound segment because of the influence of a neighboring sound, a planning error, such as "rof beef" for "roast beef." The patterns of errors that occur show that the sounds of speech are organized in terms of smaller units called phonetic features (cf. DISTINCTIVE FEATURES), and that patients tend to make errors involving a change in the value of a phonetic feature. For example, the production of "keams" for "teams" reflects a change in the place of articulation of the initial stop consonant. Of importance, phonetic features are not "lost," but the patterns of errors reflect statistical tendencies. Sometimes the patients produce a word correctly, sometimes not; and sometimes they may make one type of error on a word, and other times a different type of error on the same word. These phonological deficits arise in nearly all aphasic patients including Broca's aphasics who may have brain damage in Broca's area and other anterior brain structures such as the precentral gyrus and the BASAL GANGLIA, and Wernicke's aphasics who may have brain damage in the third temporal gyrus and other posterior structures such as the second temporal gyrus and the supramarginal gyrus.

Although speech-production deficits that relate to selection and planning may not have a distinct neural locus, speech-production impairments that relate to articulatory implementation processes do. Such deficits seem to stem from impaired timing and coordination of articulatory movements (Ryalls 1987). The correct sound may be selected, but the articulatory system cannot implement it normally. For example, for "teams" the patient may produce an overly aspirated initial /t/. Lesion data from aphasic patients and evoked potential and PET data from normal subjects implicate the left inferior frontal gyrus (including Broca's area), the precentral gyrus, the basal ganglia, the precentral gyrus of the insula, and the supplementary motor areas, in the articulatory implementation of speech (Baum et al. 1990; Dronkers 1996; Petersen et al. 1989). Interestingly, although the speech musculature is bilaterally innervated, speech-production deficits emerge only as a consequence of left-brain damage and not right-brain damage to these structures.

Speech perception processes are also complex. They require a transformation of the auditory input from the peripheral auditory system to a spectral representation based on more generalized auditory patterns or properties, followed by the conversion of this spectral representation to a more abstract feature (phonological) representation, and ultimately the mapping of this sound structure onto its lexical representation. Presumably, the word is selected from a set of potential word candidates that are phonologically similar. Speech perception studies support the view that the neural basis of speech perception is dominant in the left hemisphere. However, they challenge the classical view that these deficits underlie the auditory comprehension impairments of Wernicke's aphasics and that speech perception impairments are restricted to patients with temporal lobe pathology. Nearly all aphasic patients, regardless of their lesion localization, display some deficits in perceiving the sounds of speech, as demonstrated by discrimination experiments with words, "pear" versus "bear," or nonwords, "pa" versus "ba." These patients do not seem to have impairments in transforming the auditory input into a phonological form nor do they show impairments in phonological structure. Differences among aphasic patients relate to the quantity of errors, not the patterns of errors. The basis for the different quantity of errors might reflect a greater involvement of posterior structures in such speech processing tasks. Nonetheless, differential patterns of performance do emerge in studies exploring the mapping of sound structure onto lexical representations, implicating lexical processing deficits for Broca's and Wernicke's aphasics rather than speech processing impairments (Milberg, Blumstein, and Dworet-zky 1988).

PET and fMRI studies provide converging evidence consistent with the results from studies with aphasic patients. These studies have shown activation in a number of posterior and anterior structures when passively listening to words or in making phonetic judgments. These structures include the first and second temporal gyri, the supramarginal gyrus, the inferior frontal gyrus, as well as premotor areas. Nonetheless, direct comparisons between the behavioral/lesion studies and the neuroimaging studies are difficult because the experimental tasks used have not been comparable. For example, patients may be required to listen to pairs of words and make same/different judgments, whereas normal subjects may be required to listen to pairs of words and determine whether the final consonant of the stimuli is the same. Even so, it seems clear that the processes involved in the perception of speech are complex and invoke a neural system that encompasses both anterior and posterior brain structures.

See also


-- Sheila E. Blumstein


Blumstein, S. E. (1994). The neurobiology of the sound structure of language. In M. Gazzaniga, Ed., Handbook of the Cognitive Neurosciences. Cambridge: MIT Press.

Baum, S. R., S. E. Blumstein, M. A. Naeser, and C. L. Palumbo. (1990). Temporal dimensions of consonant and vowel production: An acoustic and CT scan analysis of aphasic speech. Brain and Language 39:33-56.

Dronkers, N. F. (1996). A new brain region for coordinating speech articulation. Nature 384:159-161.

Geschwind, N. (1965). Disconnexion syndromes in animals and man. Brain 88:237-294, 585 - 644.

Milberg, W., S. E. Blumstein, and B. Dworetzky. (1988). Phonological processing and lexical access in aphasia. Brain and Language 34:279-293.

Petersen, S. E., P. T. Fox, M. I. Posner, M. Mintun, and M. E. Raichle. (1989). Positron emission tomographic studies of the processing of single words. Journal of Cognitive Neuroscience 1:153-170.

Ryalls, J., Ed. (1987). Phonetic Approaches to Speech Production in Aphasia and Related Disorders. Boston: College-Hill Press.

Further Readings

Binder, J. R., J. A. Frost, T. A. Hammeke, R. W. Cox, S. M. Rao, and T. Prieto. (1997). Human brain language areas identified by functional magnetic resonance imaging. Journal of Neuroscience 171:353-362.

Binder, J. R., S. M. Rao, T. A. Hammeke, Y. Z. Yetkin, A. Jesmanowicz, P. A. Bandettini, E. C. Wong, L. D. Estkowski, M. D. Goldstein, V. M. Haughton, and J. S. Hyde. (1994). Functional magnetic resonance imaging of human auditory cortex. Annals of Neurology 35:662-672.

Binder, J. R., J. A. Frost, T. A. Hammeke, S. M. Rao, and R. W. Cox. (1996). Function of the left planum temporale in auditory and linguistic processing. Brain 119:1239-1247.

Damasio, H. (1991). Neuroanatomical correlates of the aphasias. In M. T. Sarno, Ed., Acquired Aphasia. 2nd ed. New York: Academic Press.

Demonet, J. F., J. A. Fiez, E. Paulesu, S. E. Petersen, and R. J. Zatorre. (1996). PET studies of phonological processing: A critical reply to Poeppel. Brain and Language 55:352-379.

Gandour, J., and Dardarananda, R. (1982). Voice onset time in aphasia: Thai, I. Perception. Brain and Language 1:24-33.

Gandour, J., and R. Dardarananda. (1984). Voice-onset time in aphasia: Thai, II: Production. Brain and Language 18:389-410.

McAdam, D. W., and H. A. Whitaker. (1971). Language production: Electroencephalographic localization in the normal human brain. Science 172:499-502.

Petersen, S. E., P. T. Fox, M. I. Posner, M. Mintun, and M. E. Raichle. (1988). Positron emission tomographic studies of the cortical anatomy of single-word processing. Nature 331:585-589.

Poeppel, D. (1996). A critical review of PET studies of phonological processing. Brain and Language 55:317-351.

Posner, M. I. and M. E. Raichle. (1994). Images of Mind. New York: W. H. Freeman and Co.

Price, C. J., R. J. S. Wise, E. A. Warburton, C. J. Moore, D. Howard, K. Patterson, R. S. J. Frackowiak, and K. J. Friston. (1996). Hearing and saying: The functional neuro-anatomy of auditory word processing. Brain 119:919-931.

Rosenbek, J., M. McNeil, and A. Aronson, Eds. (1984). Apraxia of Speech. San Diego, CA: College-Hill Press.

Zatorre, R. J., A. C. Evans, E. Meyer, and A. Gjedde. (1992). Lateralization of phonetic and pitch discrimination in speech processing. Science 256:846-849.

Zatorre, R. J., E. Meyer, A. Gjedde, and A. C. Evans. (1996). PET studies of phonetic processes in speech perception: Review, replication, and re-analysis. Cerebral Cortex 6:21-30.