The Reptilian Brain

Language and the Human Reptile Brain

By Philip Lieberman
Department of Cognitive and Linguistic Sciences

My research concerns the biology and evolution of speech and language. Vocal language (or alternate forms such as manual sign language) allows us to act or think rapidly, transcending the limits on information flow imposed by the auditory and visual systems. My earlier work focussed on the evolution of speech anatomy; recent studies have explored some of the brain bases of language.

These studies suggest that neural substrate for vocal language evolved from systems that were "designed" to enable animals to produce timely motor responses in response to changing environmental challenges and opportunities. The basal ganglia, subcortical structures that are key parts of the neural systems regulating motor control in reptiles and humans and other mammals, appear to be key elements of the human neural system that regulates vocal language. Recent studies show that basal ganglia function is essential for the production and comprehension of spoken language and certain aspects of higher cognition. The central role of basal ganglia in these "higher" human attributes reflects the evolutionary mechanism noted by Charles Darwin, whereby "an organ originally constructed for one purpose ... may be converted into one for a wholly different purpose" (On the Origin of Species, 1859, p. 190).

The traditional view of the neural basis of human language is that it is cortical. Language is supposed to be regulated by Broca's and Wernicke's neocortical areas, linked by a cortical pathway. However, many independent studies that employ modern imaging techniques such as CT and MRI scans show that these cortical areas can be destroyed without permanent language loss (aphasia). For example, one of the studies that my colleagues and I are completing documents the retention of language in a 60-year-old male after complete destruction of Wernicke's area. Converging evidence shows that permanent aphasia occurs only after massive subcortical damage.

Moreover, language abilities can be lost without any major cortical damage. Over the past decade a series of studies of Parkinson's Disease (PD) subjects, directed by Dr. Joseph Friedman of the Brown University Medical Faculty and myself, have revealed speech and language deficits similar to those traditionally associated with Broca's aphasia. Parkinson's Disease affects the operation of subcortical basal ganglia, largely sparing neocortex. A speech production deficit first noted in Broca's aphasia by Sheila Blumstein and her colleagues occurs in some PD subjects. They are unable to sequence the lip, tongue, and larynx maneuvers necessary to correctly produce the initial consonants of words like "bad," "good," and "pad." We have found that many PD subjects are unable to comprehend distinctions in meaning conveyed by syntax. A highly significant correlation between syntax comprehension deficits and speech production sequencing deficits exists in PD subjects. The correlation may derive, in part, from impairment of short-term memory (verbal working memory); independent studies show that comprehending the meaning of a sentence involves maintaining its words in verbal working-memory by a process of "silent-speech" using the neural structures that regulate overt speech. Therefore, impaired neural regulation of speech production would also affect sentence comprehension. PD subjects are also frequently unable to solve cognitive problems that involve changing from one criterion to another. They instead "perseverate," clinging to an inappropriate mental operation. Motor perseveration also is a typical sign of basal ganglia dysfunction.

The data of many independent studies, including our own, thus suggest that basal ganglia constitute a neural "sequencing engine" that has two general functions. Studies of motor control in humans and other species show that basal ganglia circuits control the sequence in which the components of a complex act are executed. These studies also show that basal ganglia act to interrupt ongoing motor activity when sensory channels signal appropriate changes in the environment. It has become evident that basal ganglia perform similar operations when animals or humans think through neural circuits that are anatomically segregated. In short, thinking can be regarded as mental motor activity.

Studies of patients who have suffered damage to specific parts of basal ganglia and cerebellum (another subcortical structure) after strokes or coma have found similar effects. Emily Pickett, one of our former graduate students, showed profound motor and cognitive sequencing deficits in a subject who had suffered damage localized to basal ganglia. Similar deficits have been noted in independent studies. For example, the genetically transmitted neurological deficit of the London family "KE", which according to Steven Pinker demonstrated the existence of a "language gene," is remarkably small basal ganglia structures. The behavioral deficits of afflicted members of this family again involve impaired sequencing of tongue, lip, and larynx maneuvers, as well as difficulties comprehending language and thinking.

Although the general pattern of behavioral deficits associated with basal ganglia damage can be specified, the particular behavioral deficits that may occur in a particular PD subject, member of family KE, or individual suffering other brain damage usually vary somewhat. This variability reflects the "computational" architecture of biological brains. Although various parts of the brain can be identified that perform particular "computations," such as storing visual information for a brief period or sequencing motor commands, complex behaviors generally are not regulated in one isolated part of the brain. Complex behaviors generally are regulated by neural circuits linking many neuroanatomical structures throughout the brain. A neural circuit is formed by a segregated neuronal population in one neuroanatomical structure that projects to a neuronal population in another neuroanatomical structure. A particular neuroanatomical structure can be implicated in different aspects of behavior since it can support many independent, segregated, neural circuits that each transmit information to other neuroanatomical structures. Therefore, although we can predict the "menu" of possible behavioral deficits that can occur with damage to a subcortical structure like the putamien which supports different segregated circuits, the particular damage pattern in an individual will affect particular circuits and behaviors from this menu.

We have been able to replicate these findings in Chinese-speaking PD subjects in studies at the Academica Sinica in Taiwan. Other independent studies have replicated some of our findings in English- and Greek-speaking PD subjects. We also have found similar effects induced by hypoxia, oxygen deprivation. We monitored climbers on Mount Everest using radios from Base Camp. As the climbers ascended to higher altitudes where less oxygen was present, we administered language comprehension and cognitive tests. The climbers' speech motor control deficits were correlated with increases in the time that was necessary to comprehend simple sentences. Deficits in judgment also occurred in the climber-subjects -- the high death rate on Everest reflects cognitive losses as well as the weather and technical difficulties. These behavioral deficits most likely derive from impairment of globus pallidus, a basal ganglia structure that can be damaged by low oxygen levels. Many aircraft disasters have been attributed to hypoxia; speech-monitoring procedures sensitive to hypoxic cognitive loss could be developed to monitor pilots. We also hope to develop speech measures that will predict susceptibility to acute mountain sickness, which can result in death, as well as procedures that may be useful in the treatment of Parkinson's Disease and other neurodegenerative diseases.


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