Brain Evolution, Language and Psychopathology in Schizophrenia

Paolo Brambilla, Andrea Marini, Paolo Brambilla, Andrea Marini

• Publisher: Routledge
• Year: 2013
• ISBN:
  9781134694426
• Edition: 1
• Topic: Psychologie
• Subtopic: Psychotherapie

This book provides a comprehensive review of new developments in the study of language processing and related neural networks in schizophrenia by addressing the complex link between psychopathology, language and evolution at different levels of analysis.

Psychopathological symptoms in schizophrenia are mainly characterized by thought and language disorders, which are strictly intertwined. In particular, language is the distinctive dimension of human beings and is ontologically related to brain development. Although normal at the levels of segmental phonology and morphological organization, the speech of patients suffering from schizophrenia is often characterized by flattened intonation and word-finding difficulties. Furthermore, research suggests that the superior temporal gyrus and specific prefrontal areas which support language in humans are altered in people with schizophrenia.

Brambilla and Marini bring together international contributors to explore the link between brain evolution and the psychopathological features of schizophrenia, with a focus on language and its neural underpinnings.

Divided into three sections the book covers:

• brain evolution and language phylogenesis
• brain abnormalities in schizophrenia
• psychopathology and schizophrenia.

This theoretical approach will appeal to professionals including clinical psychologists, cognitive neuroscientists, neuropsychiatrists, neuropsychologists, neurolinguists, and researchers considering the links between brain evolution, language and psychopathology in schizophrenia.

Part I

Brain evolution and language phylogenesis

1 Genes and the evolution of language

Philip Lieberman

It is clear that the traditional theory developed in the nineteenth century that localized speech production to a discrete frontal region of the cortex, Broca’s area, is wrong. Wernicke’s area, located in the posterior cortex, likewise does not appear to be the speech perception “organ” of the human brain. Current research instead points to neural circuits that link “local” activity in different cortical and subcortical structures as the agents involved in learning and carrying out the motor acts involved in talking. Similar neural circuits play a role in language and cognitive acts. Consistent with the fact that 99 percent of our genes are shared with chimpanzees, our closest living “cousins”, we share similar neural circuits. Claims for humans having unique neural circuits linking cortex to the larynx that somehow confer linguistic ability (Deacon 1997; Fitch 2010) do not hold up. This leads to an apparent mystery, since no chimpanzee, or other living species, can talk or command the complexities of human language.

Fortunately, recent independent studies have provided a starting point in understanding some of the genetic events that confer human linguistic and cognitive capabilities. The assessment of the motor, syntactic and some of the cognitive deficits of a large extended family led to the discovery of the FOXP2^human transcriptional factor. Further studies identified the neural structures affected by the anomalous form of FOXP2 present in this family. Genetic studies show that the human form of this gene spread throughout the extent human population some 260,000 years ago (Enard et al. 2002), and that its neural sequelae, which appear to enhance the efficiency of the subcortical basal ganglia and other structures, are linked in the neural circuits that regulate speech motor control and cognition, including language. Ongoing research has identified other transcriptional factors unique to humans that also act on the brain. Thus, what follows is an account of work in progress.

The Broca-Wernicke theory is wrong

In light of almost ubiquitous references to two discrete areas of the human cortex constituting “organs” that confer human language, a brief discussion of why this is not the case is in order. Paul Broca published in 1861 the study that relocated the “seat” of language to the lower left side of the frontal cortex (the left inferior frontal gyrus). Broca’s theoretical framework was phrenological. Phrenology is often described as an exercise in “quack” science. However, in the early decades of the nineteenth century, it was a plausible explanation of why some people are more capable at music, others at mathematics, why some people are pious, and so on. The phrenological solution was that some particular part of our brain is the “faculty” of mathematics, morality, piousness, language, and so on. Johann Spurzsheim published his treatise in 1815; it divided the surface of the brain into areas – “seats” that each yielded a particular aspect of behavior. Larger areas conferred greater capabilities or behavioral tendencies.

It was not unreasonable to suppose that discrete regions of the neocortex, the outermost region of the brain that seemed to differ most when apes and humans were compared, were conferring these complex human capabilities and behavior. The heart, for example, is a discrete organ whose primary function is pumping blood, although subsequent studies showed that it also contains sensors that monitor the level of CO₂ in the bloodstream and produces hormones. The external ear enhances localizing sounds, and so on. Phrenology was not a crank theory. But Broca thought that Spurzsheim had erroneously located the language organ between the eyes. If you accept the phrenological model, excising the cortical area that is the “seat” of talking should preclude or at least impede talking. This was ethically impossible, so Broca instead studied two patients who had extreme difficulty talking after suffering brain damage from strokes.

The study of patient “Tan” is Broca’s better-known case. Tan was a 51-year-old man who could not produce any recognizable words other than the syllable “tan”. Tan died soon after Broca saw him. The autopsy showed damage to the surface of the left frontal lobe of the patient’s brain, but Broca never examined the subcortical structures of Tan’s brain. A few months later, Broca examined a second patient, who could only say five words after suffering a stroke. An autopsy showed brain damage at approximately the same part of the surface of the brain, and so thereafter that part of the neocortex, Broca’s area, became the seat of expressive vocal language. Fortunately, the brains of both patients were carefully preserved in alcohol, and more than a century later, high-resolution magnetic resonance imaging (MRI) were performed (Dronkers et al. 2007). The MRI scans showed that in both patients massive damage had occurred to the neural circuits that link cortex with other parts of the human brain. The basal ganglia, structures deep within the brain that date back to species that lived before the age of the dinosaurs, other subcortical structures, and the pathways that connect cortical and subcortical neural structures were damaged. Moreover, the cortical area commonly labeled “Broca’s area” – the left inferior frontal gyrus, was not damaged in Paul Broca’s first two patients. Instead, anterior prefrontal areas (to the front of Broca’s area) were damaged.

In 1874, Carl Wernicke studied a patient who had difficulty comprehending speech after a stroke damaged part of the posterior temporal region of his cortex. Following the phrenological model, Wernicke decided that language comprehension was located in this area. Since language entails both talking¹ and comprehending speech, Lichtheim thus claimed in 1885 that a cortical pathway must link Broca’s and Wernicke’s areas. Thus, you can still read that Broca’s and Wernicke’s cortical areas are the neural bases of human language, as well as attempts to decide whether the skull of an extinct hominin (a primate thought to be in or related to species ancestral to present day humans) shows that its brain may have had Broca’s area.

Doubts had been expressed early in the twentieth century concerning the Broca-Wernicke theory, but in the closing decades of the twentieth century independent studies (e.g. Naeser et al. 1982) using computer-augmented tomography scans and MRI to examine the brains of stroke patients had already shown that permanent language loss does not occur unless subcortical structures, primarily the basal ganglia and/or pathways to them, are damaged. Patients having brain damage limited to the cortex typically recovered after a period of months. Dronkers and her colleagues (2007) demonstrated that the Broca-Wernicke theory was flawed from the start.

Neural circuits linking cortex and the basal ganglia

Around the same period as doubts were being raised concerning Broca’s and Wernicke’s areas being the human brain’s language organs, studies using highly invasive “tracer” techniques were mapping out neural circuits that regulated various aspects of behavior in animals. Clinical studies of neurological diseases such as Parkinson’s disease were coming to the same conclusion. Tracer techniques generally involve injecting a substance into a particular part of an animal’s brain. The animal is left alive for a period of time while the tracer moves up for certain substances, or down the pathways that link different neural structures. The animal is then sacrificed, its brain is suffused with a dye that attaches itself to the tracer, sliced up and microscopically examined. Alexander et al. (1986) mapped out a class of parallel, segregated neural circuits, some of which linked areas of the motor cortex with the basal ganglia. Other circuits linked prefrontal regions of the cortex with the basal ganglia and other subcortical structures. Other invasive experiments in which microelectrodes that directly recorded neural activity were inserted into an animal’s brain showed that these structures were active when some motor act was performed or when animals performed cognitive tasks such as keeping the location of an object in short-term memory.

Studies of Parkinson’s disease established in broad terms some of the operations that the basal ganglia perform in these circuits. In Parkinson’s disease, basal ganglia functions deteriorate owing to a decrease in output of the neurotransmitter dopamine (Jellinger 1990). The behavioral deficits that are first noted usually involve motor control. Tremor, rigidity and problems executing internally guided acts occur. Neurosurgery once was the only way to mitigate the disease’s effects and still is employed. Marsden and Obeso, in their 1994 review, noted that the basal ganglia carry out several “local operations”. The basal ganglia call out and link the sub-movements, stored in motor cortex, that constitute a willed, internally guided action such as walking or picking up a glass of water. Through a set of complex neural links the linked sub-movements ultimately activate the muscles that enable a person to walk or pick up the glass of water. The basal ganglia, in effect, act as sequencing “engine” that enables an animal or human to carry out routine motor acts. The basal ganglia complex (it consists of a number of structures, including the caudate nucleus, putamen, and globus pallidus) receives a flow of sensory information, and acting on contingencies that are either innate or learned can shift to different action. For example, frogs that lack a cortex will abort attempting to catch flies when they sense a predator approaching, and initiate a different action – jumping into the nearest pond.

Marsden and Obeso (1994) presciently suggested that, in humans, the basal ganglia may be a critical element of the neural machinery that confers cognitive flexibility – shifting thought processes. They took into account the cognitive inflexibility that often marks Parkinson’s disease – the “subcortical dementia” observed by Flowers and Robertson (1985). My research group noted similar effects in Parkinson’s disease, as well as deficits in comprehending the meaning of English sentences that have even moderately complex syntax (Lieberman et al. 1990, 1992). Our findings were replicated in subsequent studies (e.g. Natsopoulos 1993; Grossman et al. 2001; Hochstadt et al. 2006). Similar effects occurred in a subject who had bilateral focal lesions in the caudate nucleus and putamen (Pickett et al. 1998), and to a lesser degree in mountain climbers ascending Mount Everest, where the low oxygen content of air at extreme altitudes degrades basal ganglia activity (Lieberman et al. 2005).

Diffusion tensor imaging (DTI), a noninvasive technique based on MRI imaging that can map out neural circuits in humans, has revealed hundreds of circuits in the human brain, including circuits that connect different parts of the cortex. They show that humans have cortical-basal ganglia circuits similar to those found in monkeys discerned using traditional tracer techniques (Lehericy et al. 2004). DTI analyses support the finding reported by Cummings (1993) in his review article based on clinical findings and animal tracer studies. Human neural circuits channel the flow of information from dorsolateral prefrontal cortex, lateral orbitofrontal cortex, and the anterior cingulate cortex, as well as from the motor cortex. Cummings noted that the anterior cingulate circuit regulates attention and also controls laryngeal phonation. Patients become mute and apathic when the circuit is damaged. Clinical evidence suggested that the orbitofrontal circuit was implicated in emotional regulation – patients became disinhibited.

Neuroimaging studies

Neuroimaging studies have added to our knowledge of the operations performed in circuits linking cortex and the basal ganglia when humans perform cognitive tasks. Functional magnetic resonance imaging (fMRI) is a variant of MRI imaging that tracks the level of deoxygenated blood flow, reflecting metabolic activity in specific neural structures. Data from independent fMRI studies (e.g. Postle 2006; Badre and Wagner, 2006; Miller and Wallis 2009) indicate that ventrolateral, dorsolateral and other prefrontal cortical areas, in circuits involving the basal ganglia, direct attention to information used to carry out seemingly different tasks such as comprehending the meaning of a sentence (Kotz et al. 2003), mental arithmetics (Wang et al. 2005), or when selecting words according to their meaning or sound structure (Simard et al. 2011). The fMRI studies of Monchi and his colleagues have monitored the local operations carried in specific parts of the basal ganglia in tasks that entail cognitive flexibility and language. The Wisconsin card sorting test (WCST), which has been in use since the 1960s, is a standard instrument for assessing cognitive flexibility. Subjects are presented with a sequence of cards that each have images that vary according to shape, number and color. The task is to sort out the cards as the sorting criterion shifts arbitrarily from time to time. The subject, for example, may start by sorting out cards according to color, and then having to change to sorting by shape and then number, and then back to color, and so on. The Monchi research group adapted the WCST so that it could be used in fMRI studies. Monchi et al. (2001) reported the involvement of a cortical-basal ganglia loop involving the ventrolateral prefrontal cortex, the caudate nucleus, and the thalamus when a subject was told to change his or her sorting criterion. The posterior prefrontal cortex and putamen were active when applying the new sorting criterion for the first time. Dorsolateral prefrontal cortex was involved whenever subjects received any information as they performed the task, apparently monitoring whether their responses adhered to the chosen criterion. In another fMRI study, Monchi et al. (2006) showed that ventrolateral prefrontal cortex is active in planning ahead when a subject has to compare the card that is to be selected and the criterion. The basal ganglia’s caudate nucleus uses this information when any novel action needs to be planned. The Monchi fMRI studies point to the caudate nucleus being involved in the selection and planning, and the putamen in the execution of a self-generated action among different alternatives. The subthalamic nucleus (another basal ganglia structure) was only involved when a new motor action was required, whether planned or not. Other neuroimaging studies confirm the role of dopamine and the basal ganglia in cognitive flexibility (Monchi et al. 2007).

Contrary to the claims of widely cited books such as Pinker (1994), the operations performed in particular neural structures and circuits are not necessarily domain specific. Humans do not, as Noam Chomsky claims, have...

Table of contents

• Cover Page
• Half Title page
• Series page
• Title Page
• Copyright Page
• Contents
• List of illustrations
• About the editors
• List of contributors
• Introduction
• Part I Brain evolution and language phylogenesis
• Part II Brain abnormalities in schizophrenia
• Part III Psychopathology and schizophrenia
• Part IV Conclusion
• Glossary and abbreviations
• Index