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Book description

The merger of behavioral neurology and neuropsychiatry into a single medical subspecialty, Behavioral Neurology & Neuropsychiatry, requires an understanding of brain-behavior relationships and a clinical approach that transcends the traditional perspectives of neurology and psychiatry. Designed as a primer of concepts and principles, and authored by a multidisciplinary group of internationally known clinical neuroscientists, this book divides into three sections:Structural and Functional Neuroanatomy (Section I) addresses the neuroanatomy and phenomenology of cognition, emotion, and behaviorClinical Assessment (Section II) describes neuropsychiatric history taking, neurological and mental status examinations, neuropsychological assessment, and neuroimaging, electrophysiologic, and laboratory methodsTreatment (Section III) discusses environmental, behavioral, rehabilitative, psychological, social, pharmacological, and procedural interventions for cognitive, emotional, and behavioral disorders.By emphasizing the principles of Behavioral Neurology & Neuropsychiatry, this book will improve your understanding of brain-behavior relationships and inform your care of patients and families affected by neurobehavioral disorders.

Reviews

'This superb book is the most complete and comprehensive publication on this subject to date. It is essential reading for all who call themselves behavioral neurologists or neuropsychiatrists. It is also an essential reference for the care of patients who suffer from neuropsychiatric disorders.'

Source: Doody's Reviews

'This book is likely to become the standard textbook for programs offering subspecialty training in behavioural neurology and neuropsychiatry. I consider it to be an excellent volume and would strongly recommend it to psychiatrists with subspecialty interest in the interface between neurology and psychiatry.'

Source: The Canadian Journal of Psychiatry

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Contents

Page 1 of 2

Contents
  • 8 - Attention
    pp 115-133
  • View abstract

    Summary

    Neurology and psychiatry are securely established medical specialties with well-demarcated areas of clinical and research expertise. Behavioral neurology (BN) is widely held to have begun with the work of Norman Geschwind in the mid-twentieth century. A neuropsychiatric approach to patient care began to reemerge and steadily gain momentum as physicians increasingly appreciated the neurologic bases of psychiatric disease and the psychiatric aspects of neurologic disease. The prospect of BN and neuropsychiatry (NP) drawing together finds considerable support in academia. Annual scholarly meetings are held conjointly by the Society for Behavioral and Cognitive Neurology and the American Neuropsychiatric Association in order to disseminate new research findings and educate practitioners. Traumatic brain injury occupies a major portion of the practice of many subspecialists in BN&NP and additional studies are needed to better define the best methods of neurorehabilitation.
  • 9 - Motivation
    pp 134-143
  • View abstract

    Summary

    This chapter focuses on aspects of structural and functional neuroanatomy relevant to Behavioral Neurology & Neuropsychiatry (BN&NP). It considers the general structure of the brain from the brainstem through the cerebral cortex, including a review of white matter anatomy, the cerebral vasculature, and the ventricular system. The brainstem comprises the medulla oblongata, pons and cerebellum, and midbrain. Each of these areas and the neurobehaviorally salient structures they contain are reviewed briefly in the chapter. The reticular formation (which is contributed to by several brainstem substructures) and the cranial nerves (some, but not all, of which are located within the brainstem) also are discussed in the chapter. The diencephalon includes the thalamus, metathalamus (medial and lateral geniculate nuclei), epithalamus (habenula, stria medullaris, and pineal body), and subthalamus. The chapter considers briefly the thalamus, hypothalamus (and pituitary), and the epithalamus.
  • 11 - Memory
    pp 161-173
  • View abstract

    Summary

    This chapter presents an overview and practical approach to conceptualize manifestations of cerebellar lesions and outlines the principles that govern the cerebellar contribution to cognition and emotion as well as to sensorimotor function. Lesions of the cerebellum have been regarded as producing motor impairments. The cerebellar motor syndrome is characterized by wide-based and unsteady, or ataxic, gait; incoordination, or dysmetria, of the arms and legs; articulation impairment, or dysarthria; and eye movement abnormalities that disturb vision. The cerebellar cognitive affective syndrome (CCAS) results from lesions of the posterior lobe, characterized by clinically relevant deficits in executive function, visual spatial performance, linguistic processing, and dysregulation of affect. The connections of the cerebellum with brain circuits are implicated in psychiatric illness. Applying repetitive transcranial magnetic stimulation (TMS) to the limbic cerebellum in the vermis improves psychiatric disorders such as schizophrenia by upregulating cerebellar modulation of cerebrocerebellar circuits engaged in cognition and emotion.
  • 12 - Language
    pp 174-183
  • View abstract

    Summary

    White matter was first depicted as a neuroanatomic structure by the great anatomist Andreas Vesalius in 1543. The anatomy of white matter is fundamental to understand its role in brain-behavior relationships. The major function of white matter can be conceived as the transfer of information within the nervous system. The development of magnetic resonance imaging (MRI) in the early 1980s has proven to be a pivotal event in the understanding of white matter and its impact on higher brain function. Ten categories of white matter disorder are: genetic, demyelinative, infectious, inflammatory, toxic, metabolic, vascular, traumatic, neoplastic, and hydrocephalic. Three major groups of syndromes emerge that capture the variety of cognitive and emotional impairments related to cerebral white matter disorders: focal neurobehavioral syndromes, white matter dementia, and neuropsychiatric syndromes. The treatment of cerebral white matter disorders depends on the specific problem disclosed by the diagnostic search.
  • 13 - Affective prosody
    pp 184-198
  • View abstract

    Summary

    This chapter reviews the neuroanatomy and neurochemistry of frontal-subcortical circuits (FSCs) and outlines the signature syndromes of FSC circuit dysfunction. The oculomotor circuit originates in the frontal eye field as well as prefrontal and posterior parietal cortex and connects sequentially to the central body of the caudate nucleus, dorsomedial GP interna (GPi) and ventrolateral SN pars reticulata (SNr), ventral anterior and medial dorsal thalamic nuclei, and back to the frontal eye field. Emotional, motivational, and affective information processed by the basal ganglia is represented in the rostromedial limbic circuitry arising from the orbital and medial prefrontal cortex. Processing of the detailed information contained in the FSCs is modulated by input from dopaminergic, cholinergic, noradrenergic, and serotonergic systems. The orbitofrontal (OF) cortex is the neocortical representation of the limbic system and involved in the determination of the appropriate time, place, and strategy for environmentally elicited behavioral responses.
  • 14 - Praxis
    pp 199-213
  • View abstract

    Summary

    The arousal system involves multiple distributed neural networks working in harmony to permit normal sleep-wake cycles, satisfy internal drive states, and respond to environmental demands. Disorders of arousal involve pathology of the brainstem, thalamus, or widespread areas of both cerebral hemispheres. A parallel series of distinct neural networks using dopamine, histamine, serotonin, acetylcholine, and norepinephrine as neurotransmitters originates in the brainstem. Brain death represents the most severe disturbance of arousal, with total and irreversible cessation of any brain function. Coma is the state of neurological unconsciousness exhibited by unarousable unawareness of the external environment that is due to extensive damage to or depressed function of both cerebral hemispheres, bilateral diencephalic structures, or the ascending reticular activating system. A specific rehabilitative strategy is coma stimulation, in which structured sensory stimulation is administered for the purposes of improving sensory awareness and facilitating improvements in arousal and awareness.
  • 15 - Visuospatialfunction
    pp 214-224
  • View abstract

    Summary

    This chapter discusses the organization of human sleep by the brain mechanisms and specific sleep disorders that lead to disturbances in the brain mechanisms. Non-rapid eye movement (NREM) sleep is controlled by brainstem oscillators whose activation leads to the multiple physiological accompaniments of the NREM state. The dream is the unusual mental content that often accompanies REM sleep. As humans transition from wakefulness to sleep, characteristic physiological changes include decreases in respiratory rate, heart rate, and blood pressure. The domain of the insomnias benefits from thoughtful differential diagnosis, as the causation may be both multiple and obscure. The insomnia complaints that are comorbid with medical disorders include both sleep disturbances caused by medical symptoms, and also those sleep disturbances caused by the pathophysiology underlying the medical condition. Restless leg syndrome (RLS) and periodic limb movements of sleep (PLMS) are considered as sleep disorders.
  • 16 - Executivefunction
    pp 225-249
  • View abstract

    Summary

    This chapter outlines behavioral measures related to the control of attention and functional theories of attention based on such measures. It focuses on the control of visual attention in both normal and neurologically impaired individuals. The major types of attention are: spatial attention, in which stimuli are selected based on their position in space; object-based attention, in which stimuli are selected based on their identity; attentional selection in visual working memory, in which attention selects items that will be remembered; and executive attention, in which attention is involved in choosing which task or behavior an observer will perform. The chapter provides evidence for a number of cerebral sites that appear to be involved in the overall control of attention. Understanding how these sites interact and how they relate to functional theories of attentional control increases understanding of normal and disordered attentional control processes.
  • 17 - Comportment
    pp 250-265
  • View abstract

    Summary

    Motivation implies activation of the organism by external or internal stimuli resulting in goal-directed behaviors. Loss of motivation constitutes the core symptom of apathy, a syndrome frequently found among patients with acute or chronic neurological conditions such as stroke, traumatic brain injury, and dementia. The mechanism of motivated behavior is based on neural structures that attach salience and valence to a given stimulus, and activate and direct an appropriate behavior in response to that stimulus. Dopamine (DA) is considered to play a central role in the mechanism of motivation and regulation of effort-related processes. The classical studies linking DA to motivation were based on stereotaxic injections of neurotoxin into the afferent projections of the mesolimbic and mesocortical pathways, which produced severe aphagia and adipsia. The nucleus accumbens seems to mediate the primary motivational characteristics of feeding and reproductive behavior as well as reward-motivated behaviors.
  • 18 - Emotion
    pp 266-298
  • View abstract

    Summary

    This chapter discusses the processes by which one comes to know the environment, namely sensation, perception, and recognition. Perception builds upon basic sensation by extracting more complex attributes from sensory elements. For example, visual perception includes the ability to detect motion, differentiate colors, and distinguish basic forms. Recognition involves identification of a sensory stimulus via access to and integration of stored representations of previously encountered stimuli. Acquired brain damage and developmental abnormalities may affect each level of processing, including primary sensation, cortically mediated perception, or higher-order aspects of perception or recognition. Negative perceptual symptoms involving hearing may affect primary sensory processes, secondary perceptual abilities, or recognition. Cortical auditory disorder or auditory agnosia refers to a non-specific loss of the ability to discriminate both speech and environmental auditory stimuli. Sensory loss may arise from damage at any point within the somatosensory system.
  • 19 - Personality
    pp 299-309
  • View abstract

    Summary

    This chapter reviews the clinical context and describes the functional-anatomic architecture of multiple memory systems including working memory (WM), declarative memory, and non-declarative memory. The anatomical substrates of memory include distributed networks of cortical and subcortical nuclei interconnected by white matter projection pathways. Memory impairments are comorbid with other cognitive and neurobehavioral problems. Disorders such as herpes encephalitis, which has a predilection for limbic and paralimbic cortical regions, may cause an amnestic syndrome associated with other neurobehavioral features, such as personality change and seizures. WM refers to the retention of information over brief intervals of time. Neuropsychological evidence suggests that there are two main types of dysexecutive syndrome, each reflecting dysfunction in the central executive system. One type involves marked perseveration, indicating decreased ability to disengage and shit attention, whereas the other is characterized by excessive distractibility, which reflects impairments in attentional inhibition.
  • Section II - Neurobehavioral and Neuropsychiatric Assessment
    pp 310-497
  • View abstract

    Summary

    This chapter describes the neuroanatomy of language beginning with the foundation in the classical lesion model and concludes with an updated view of language-brain organization. Clinical aphasia or language impairments from brain lesions have been the window to localization of language in the brain. The neuropathologic lesion underlying transcortical sensory aphasia is in the left angular gyrus in the parietal region or in the left posterior superior or middle temporal gyri. Language impairment from the basal ganglia may resemble transcortical motor aphasia. Individuals with Paul Broca's aphasia demonstrate comprehension impairments and difficulty integrating words into the context of a sentence. In Karl Wernicke's aphasia, content words tend to be absent or replaced by general terms or associations based on context. Current information modifies the classical Wernicke-Geschwind model of language to incorporate the contributions of perisylvian processing hubs that participate in sequential, neurocomputational operations on language-related information.
  • 21 - Neurologicalexamination
    pp 319-332
  • View abstract

    Summary

    This chapter considers the topic of affective prosody as an important aspect of language that appears to be lateralized to the right hemisphere. Kinesics refers to facial, limb, and body movements associated with language and communications. Monrad-Krohn divided prosody into four major components: intrinsic, intellectual, emotional, and inarticulate. Intrinsic prosody enhances and clarifies the linguistic aspects of a language through judicious use of stress pauses and intonation without altering words. Emotional prosody infuses speech with primary types of emotions such as fear and anger. Monrad-Krohn also described various clinical disorders of prosody caused by brain injury or disease. Hughlings Jackson suggested that the emotional aspects of language and communication might be dominant functions of the right hemisphere. The specific combinations of affective-prosodic deficits following localized lesions in the right hemisphere appeared to be reasonably analogous to the functional-anatomic relationships of aphasic deficits observed after focal left brain damage.

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