The man you have just read about exhibits a phenomenon known as blindsight, which involves the retention of some visual capabilities without the conscious experience of seeing (Weiskrantz, 2009). What makes such cases so fascinating is that they raise a fundamental question: What does it really mean to “see”?

When you open your eyes, the visual world appears to you, seemingly without effort. The immediacy and apparent ease of visual awareness makes it hard to believe that a large proportion of your brain is working very hard to solve the complex problems of vision. In the brains of humans and other primates, visual processing is highly developed. The immense amount of brain tissue dedicated to sight enables us to have the exquisitely detailed color vision that is one of the hallmarks of being a primate.

In this chapter, we review work on a range of bilingual aphasias – the language impairments that occur due to a lesion or atrophy in the brain. We begin the chapter by discussing two theoretical approaches, namely the localizationist and dynamic accounts, which explain the extent to which one or both languages are affected. We see that the severity and type of aphasia that result from a lesion depends on its size and location. Additionally, a number of other nonlesion factors can affect the severity of the resulting aphasia. The premorbid variables that have been most studied are frequency of language use, AoA, and L2 proficiency. We then address how bilinguals are assessed for aphasia (e.g., the Bilingual Aphasia Test), and the possibilities for treatment and recovery. In this regard, the following important questions are discussed: In which language(s) should treatment be provided and what are the differential outcomes? If rehabilitation is given in only one language, is there cross-language generalization to the language not treated? We conclude that the most common pattern is parallel recovery in which both languages improve at a similar rate.

In this chapter, we reinforce the book’s aim to shed light on changes inflicted on language, cognition, and the brain rather than to focus on advantages and disadvantages of being bilingual. To obtain a more realistic picture of bilingualism, its assets (i.e., what is easier), and its difficulties (i.e., what is taxing and leads to high consumption of mental resources), we have drawn on research from various disciplines. We conclude the book by identifying complexity as the major issue for research on bilingualism. The complexity problem is fundamental to definitions of bilingualism and the characterization of bilingual participants in empirical studies, leading to discussions about its assessment as a dichotomous or continuous variable. Considering bilingualism as an experience and how such experience impacts overall language development, cognition, and the brain at different levels are related to usage-based approaches of examining bilingualism as well as a concern regarding confounding and moderating variables. The shift for designing research in the field of bilingualism seems to necessarily be more interdisciplinary in nature than in the past.

This chapter distinguishes studies on the mind from studies investigating the brain. By describing linguistic, psychological, and cognitive neuroscience approaches, some aspects which have been found to be relevant for bilingualism have only been studied in linguistic terms, leaving open whether certain findings are limited to the mind level only or whether there is any correspondence on the brain level. Other aspects, well researched in linguistic or psychological studies, have not yet been taken up in neuroscientific studies, leaving the question of whether certain variables would change the results or explain variance unanswered. We then look at details of learning in the brain and in particular at brain plasticity, a lifelong available characteristic of the brain. The chapter also addresses the notion that for linguists, acquisition and learning are not the same, since context in general and factors such as input quality and quantity must be taken into account. In brain terms, there is only learning. We then discuss different factors influencing language acquisition and learning and reveal that individual differences can be found among these factors to a great extent.

In this chapter, we explore neural representations and language processing in the bilingual brain. We begin by discussing key language areas and lateralization in bilinguals and look at some of the primary functions of the hemispheres, noting that, in fact, many brain functions – including bilingual language processing – are distributed across both hemispheres. We then consider the function of the four lobes of the brain and identify important regions for language, including Broca’s and Wernicke’s areas, which have been found to support language production and comprehension, respectively. The chapter then addresses how early or late exposure to a second language (L2) affects the cortical representation of the two languages. We then turn to specific processes of language use, namely how bilinguals comprehend and produce language. Overall, we have seen that the neural representations and processing of two languages are far from being fully understood. Nonetheless, we are gaining a clearer picture of the dynamic nature of two languages in one brain and the many individual differences that can affect this, such as age of acquisition (AoA) and proficiency.

So writes the neurologist and gifted observer of human behavior, Oliver Sacks, in discussing the remarkable case of Temple Grandin, possibly the world’s highest functioning person with autism. At the time of this writing, Grandin is an accomplished professor of animal science at Colorado State University, designer of facilities for managing cattle, and author of numerous books about her experience with autism. She has been the subject of a feature-length film (Temple Grandin, released in 2010 and starring Claire Danes), was selected as one of Time magazine’s 100 most influential people in the world in 2010, and was elected to the National Academy of Arts and Sciences in the United States in 2017.

Born in 1947 and diagnosed with autism at the age of 3, Grandin experienced a childhood quite different from most children. In addition to delayed language development, a tendency toward “sensory overload,” and an experience of the world that was highly visual, she also experienced significant social deficits.

For bilinguals, the use and knowledge of one language affects how they process the other. Various cross-linguistic influences (CLI) can be observed in both language production and comprehension across all domains of linguistics. We start by broadly exploring the concept of transfer, both negative and positive, and forward and reverse. In doing so, we identify various classifications of CLI. Following this, we review key studies on phonological, lexical, morphological, and syntactic transfer along with other types such as discursive, pragmatic, and sociolinguistic. We find that there are a number of factors that can determine the degree to which transfer emerges or whether it happens at all. We then review studies investigating the ability to switch between the two language systems. In doing so, we look at theoretical models that explain what facilitates language switching and what empirical studies tell us about the neural and electrophysiological activity that arises in language switching. Finally, we discuss dreaming and bilingualism and argue that dreaming in an L2, contrary to popular belief, does not necessarily imply fluency in that language.

The circadian system in mammals involves a hierarchy of clock regulators that entrain circadian rhythms in the periphery. The molecular circadian clock regulates all systems in the body, including the nervous and immune systems. Under healthy conditions, the circadian system enables effective function of the nervous and immune systems by promoting system vigilance during predicted daily active phases, and rejuvenation during rest phases. However, injury to the nervous system causes spiralling neuroimmune activation that exacerbates damage. Here, we will discuss how the circadian system regulates neuroinflammatory dynamics in the central nervous system during health and after neurotrauma. Traumatic brain injury or spinal cord injury dysregulate the circadian system, and circadian disruption is worsened during acute post-injury times by a suboptimal circadian environment in the hospital. In turn, circadian disruption unleashes immune activation and impairs reparative responses, thereby worsening damage. Given the intimate link between the circadian and neuroimmune systems, there are several levels of potential therapeutic intervention. Environmental interventions include improving light–dark amplitude between day and night and reducing nighttime interruptions acutely after neurotrauma. Pharmacologic interventions after injury could reinforce circadian rhythms or target clock genes to create a reparative neuroimmune milieu. Future studies should explore the circadian–neuroimmune axis, with a goal to use evidence-based chronotherapies to enhance repair and recovery after traumatic brain injury and spinal cord injury.

The circadian timing system has pronounced effects on learning and memory, with learning and recall regulated by time of day and the cellular mechanisms underlying learning and memory being under circadian control. Given this influence of the circadian system, studies across species, including humans, reveal that circadian disruption has pronounced negative effects on cognitive functioning. Circadian disruption leads to deficits in learning and memory by negatively affecting neurogenesis, synaptic plasticity, and epigenetic events required for acquisition and recall of memories. The present chapter describes the impact of circadian disruption on learning and memory while considering the mechanisms underlying circadian control of cognitive function. Given that the modern world is rife with temporal disruptions due to work requirements, limited exposure to sunlight during the day, and exposure to artificial lighting and blue light-emitting electronic devices at night, understanding the negative impact of circadian disruption on learning and memory and developing mitigating strategies are vital.

The immune system is a highly dynamic element of physiology, sensitive to both the external environment and organism-intrinsic factors. Inflammatory responses of sufficient magnitude are required to maintain homeostasis and protect from disease, but must be resolved on an appropriate timescale to prevent excessive damage and chronic inflammation. The circadian clock is a critical regulator of immune function and circadian disruption is a known risk factor in multiple diseases, disturbing physiological processes and exacerbating inflammation. Interactions between the circadian clock and immune system are bidirectional, as pathogens and inflammatory molecules can themselves disrupt local rhythms in cells and tissues. Here, we discuss the evidence linking circadian disruption with maladaptive immune function, including studies of shift work, sleep deficiency, genetic disruption of rhythms, and animal models of inflammatory diseases.

The brain and body work together to ensure survival. Under typical conditions, the endogenous circadian (daily) clock helps predict regularly occurring events, like the day–night cycle, to build a behavioral and physiological framework that optimizes use of resources while taking advantage of environmental opportunities. On the other hand, the stress system responds to emergencies, deploying countermeasures that promote survival in the face of threat. When the stress system is engaged inappropriately or for too long, factors that help promote adaptation (allostatic mediators) can cause damage to the biological systems they are meant to protect. This allostatic load can lead to allostatic overload, where a cascading set of failures in these systems lead to pathology. Here, I discuss the interplay between the stress and circadian systems, how disruption of the circadian clock can contribute to allostatic load and overload, and the negative health consequences that this can cause.

Circadian rhythms have a period of approximately 24 hours and are set to precisely 24 hours by various zeitgebers (time givers), light being the most prominent zeitgeber. The central pacemakers for mammalian circadian rhythms are the suprachiasmatic nuclei (SCN) in the anterior hypothalamus. Humoral and neural signals from the SCN help synchronize circadian clocks throughout the body. At the molecular level, cellular circadian rhythms are formed from interlocking transcriptional-translational feedback loops (TTFL) of circadian clock genes that drive spontaneous oscillations of gene and protein expression with an approximately 24-hour period. Remarkably, the molecular clock components are expressed rhythmically in nearly every cell of the body and are entrained by signals from the SCN. Disruption of clock genes either through genes or environment can impair optimal biological function. Circadian rhythms regulate myriad homeostatic systems including the cardiac, immune, metabolic, and central nervous systems. Circadian regulation of physiological and behavioral functions can be disrupted by several factors including the timing of light exposure and food intake. This chapter reviews circadian disruptors to set up the remainder of the book.

Circadian clocks in all tissues confer temporal organization to the physiology and behavior of organisms. Rhythms of the cardiovascular system have been scrutinized because of the morning peak of adverse cardiovascular events and because night and rotating shift work have been associated with heart disease and biomarkers of elevated cardiometabolic risk. Animal models support the important role that the clock plays in the heart. External disruptions such as jetlag and internal disruptions such as loss of clock function contribute to poor heart health. In this chapter, we review key findings from animal models of circadian disruption and from experiments in humans designed to isolate the effects of the circadian clock on cardiovascular physiology.

Circadian rhythms exhibit many alterations during the normal aging process and more severe disruptions are evident in age-related neurological conditions such as Alzheimer’s disease (AD). Indeed, evidence suggests that circadian rhythm alterations increase susceptibility to AD and conversely that the progressive neuropathological features of AD such as amyloid-beta accumulation further exacerbate circadian rhythm disruption. Impairments in neural function in the master circadian pacemaker in the hypothalamic suprachiasmatic nucleus underlie age- and AD-related alterations in circadian rhythms. Deficits in expression of the clock genes constituting the molecular pathways controlling circadian rhythms also contribute to circadian rhythm impairments and neurodegeneration in senescence and AD. This chapter describes the mechanisms underlying age- and AD-related alterations in circadian rhythms as well as their possible causes and potential strategies for their amelioration.