Psychopharmacology of Neurologic Disease

Handbook of Clinical Neurology Series

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• Publisher: Elsevier
• Year: 2019
• Print ISBN: 9780444640123
• eBook ISBN: 9780444640130
• Topic: Medicina
• Subtopic: Neurología

Psychopharmacology of Neurologic Disease, Volume 165 in the Handbook of Clinical Neurology series, provides clinicians with an up-to-date, critical review of the best approaches to treatment of neurologic disease as discussed by experienced clinical investigators. The book is organized into sections on dementia, delirium, movement disorders, hereditary degenerative disease, epilepsy and psychogenic seizures, brain vascular disease, pseudobulbar affect, traumatic brain injury, neuro-oncology, multiple sclerosis and other demyelinating disorders, chronic fatigue syndrome/fibromyalgia, pain, headache, sleep disorders, autoimmune encephalitis/anti- NMDA encephalitis, functional sensory neurologic symptom disorders and neurodevelopmental disorders.Each of these diagnostic categories has a significant incidence of behavioral symptomatology that is secondary to the neurologic diagnosis that can serve to complicate other therapeutic interventions, alter the course of illness, and cause distress in patients and family caregivers.- Provides a systematic, evidence-based compendium of best practices in the treatment of behavioral symptomatology relating to neurologic conditions- Integrates state-of-the-art approaches in treating all behavioral symptomatology across all major neurologic disorders- Explores psychopharmacological intervention, non-pharmacological strategies, behavioral symptomatology, and therapeutic interventions

Chapter 1

Psychiatric manifestations of neurologic diseases: Etiology, phenomenology, and treatment

Victor I. Reus^1,*; Daniel Lindqvist^{2 1} Department of Psychiatry, University of California, San Francisco (UCSF) School of Medicine, San Francisco, CA, United States
² Department of Psychiatry, Lund University, Lund, Sweden
^* Correspondence to: Victor I. Reus, MD, Distinguished Professor of Psychiatry, University of California, San Francisco, School of Medicine, UCSF Weill Institute for Neurosciences, Langley Porter Psychiatric Institute, Box 0990, 401 Parnassus Avenue, San Francisco, CA 94143, United States. Tel: + 1-415-476-7478, Fax: [phone] email address: [email protected]

Abstract

Understanding the etiology and meaning of behavioral symptomatology in the context of neurologic disease, and choosing the most effective intervention is a vexing task. This introduction summarizes the history of our understanding of the relationship between behavioral symptoms and primary neurologic conditions, and considers the ways in which both psychiatric and neurologic disorders occurring simultaneously may inform both knowledge of etiology and treatment decisions.

Keywords

Psychiatric; Neurologic; Behavioral; Psychopharmacology; Treatment; Etiology

A comprehensive and practical review of the behavioral symptoms and syndromes associated with neurologic diseases and their etiology and treatment has not appeared in over a decade (Lyketsos et al., 2008). Why this should be the case, given their acknowledged prevalence and impact on quality of life and psychosocial functioning, treatment adherence, and outcome is not entirely clear. The history of the relationship between psychiatry and neurology in the 20th century is partly to blame, with neurology focusing more on structure and localization in the central nervous system (CNS) (bottom up), and psychiatry more on functional disturbances and holistic formulations of disease (top down) (Reynolds, 1990; Cunningham et al., 2006; Taylor et al., 2015; Frisch, 2016). Dysfunction at the circuit level, the focus of this volume, sits at the middle of this pyramid, the interface, and reflects each discipline's conceptual discomfort in addressing the meaning of comorbid behavioral disorders of unknown etiology in the context of neurologic diseases of known causation (Krakauer et al., 2017; Azuar and Levy, 2018). How should such symptoms be assessed and quantified? How do symptoms change over time, and what is the influence of an individual's premorbid state and circumstance in the emergence of symptoms? What is the role of environment and social support, and will interventions developed to treat one type of syndrome, e.g., major depressive disorder, also be effective in treating a similar presentation deriving from a different etiology, e.g., poststroke depression (Lyketsos et al., 2007)? Are the principles of treating agitation associated with psychosis in schizophrenia applicable to the treatment of agitation associated with psychosis in dementia?

The authors of the various chapters in this volume, each an expert in his or her respective area, have done a masterful job summarizing what has been learned and have provided succinct treatment guidelines based on our current knowledge; but it is clear that the current state of affairs is far from satisfactory. Data from controlled clinical trials and case controlled epidemiologic investigations remain the exception, and many of the recommendations necessarily stem from expert consensus based on case series and naturalistic observations rather than empirical findings. One regulatory reason for this likely stems from the US Food and Drug Administration (FDA)'s requirement in 2007 that psychotropic agents previously found effective for a given nonspecific symptom or condition, such as psychosis or agitation, would henceforth be required to show efficacy in the neurologic disorder of interest to receive approved labeling (Cummings and Jeste, 2007). It is likely, however, when this domain of clinical practice is once again reviewed in another decade, that the guidelines will rest on more solid ground (Silbersweig, 2017).

Advances in understanding the pathophysiology and genetic underpinnings of both psychiatric and neurologic disorders have been progressive and substantial, and it is increasingly clear that there is a significant overlap in the neural circuitry and neural anatomic substrates involved in the symptomatic expression of many of these separately defined conditions (Martin, 2002; Taber et al., 2010). Cross-species approaches have demonstrated that structural and functional components of biologic systems subserving neurologic and psychiatric conditions are highly conserved across vertebrate species and can be used to identify relevant mechanistic networks (Devinsky et al., 2018; Scarpa et al., 2018). It is interesting and somewhat surprising, however, that the genetic architecture of neurologic and psychiatric conditions has been shown to be somewhat distinct, suggesting that the pathways leading to this overlap may also be somewhat different (Antilla et al., 2018). Nevertheless, therapeutic agents and interventions that were initially developed for neurologic conditions have shown efficacy in psychiatric disorders, and vice versa (Grunze, 2008; Narang et al., 2015). Similarly, it is increasingly recommended that individuals presenting with serious mental illness receive a comprehensive neurologic evaluation at their initial presentation and that individuals with neurologic diseases be systematically screened for behavioral symptomatology that might otherwise go unrecognized (Canevelli et al., 2017). Bechter and Diesenhammer (2017), for example, have suggested that cerebrospinal spinal fluid (CSF) should routinely be obtained in acute psychiatric patients, while others have encouraged more defined and sophisticated neuroimaging procedures to capture regional- and disorder-specific brain changes at the onset of psychiatric conditions (Lui et al., 2016; Vieira et al., 2017).

Interpreting the specific meaning of behavioral symptoms in the context of known neurologic diseases is complex and will differ according to the individual history and the disorder involved. In some cases, the behavioral symptoms may represent a direct expression of the core pathophysiology of the neurologic disorder, sometimes as the initial precursor of the yet-to-be-developed full syndrome (Herrera et al., 2018; Kessler et al., 2018). In others, the behavioral changes may emerge as indirect collateral damage to the requisite circuitry involved in the emotional or behavioral process from a more pervasive and progressive degenerative condition (Rubin, 2018). Complicating both of these assessments is the possibility that any medication used to treat the primary neurologic disorder may itself have behavioral side effects.

Historically, it was frequently the case that behavioral symptoms were seen as bearing no direct or indirect relationship to the underlying neurologic pathology but rather served as an emotional response on the part of the individual to the burdens of the illness process and prognosis itself (Tucker and Neppe, 1988; Price et al., 2000). The origin and character of the behavioral pathology in both psychiatric and neurologic conditions is, in turn, affected by social experience and the environment and epigenetic effects on germline expression, an awareness that has resulted in the new field of “social neuroscience” (Cameron et al., 2017; Crossley et al., 2019; Famitafreshi and Karimian, 2019). What this means clinically is that the observed variance in prevalence, severity, and course of behavioral symptoms both within and between individual neurologic syndromes may be due as much to developmental events as to preexisting genetic risk factors and the subsequent unfolding of the disease process. None of these formulations is mutually exclusive, of course, and from a clinical perspective, it seems desirable that all be considered in understanding the patient's presentation and in treatment planning decisions.

The extent to which obse...

Table of contents

• Cover image
• Title page
• Table of Contents
• Copyright
• Handbook of Clinical Neurology 3rd Series
• Foreword
• Preface
• Contributors
• Chapter 1: Psychiatric manifestations of neurologic diseases: Etiology, phenomenology, and treatment
• Chapter 2: Behavioral and psychological symptoms in Alzheimer's dementia and vascular dementia
• Chapter 3: Frontotemporal dementia
• Chapter 4: Therapies for prion diseases
• Chapter 5: Behavioral symptomatology and psychopharmacology of Lewy body dementia
• Chapter 6: Comorbid depression and apathy in HIV-associated neurocognitive disorders in the era of chronic HIV infection
• Chapter 7: Neuropsychiatric aspects of Parkinson disease psychopharmacology: Insights from circuit dynamics
• Chapter 8: Tourette disorder and other tic disorders
• Chapter 9: Progressive supranuclear palsy, multiple system atrophy and corticobasal degeneration
• Chapter 10: The psychopharmacology of Huntington disease
• Chapter 11: The psychopharmacology of Wilson disease and other metabolic disorders
• Chapter 12: The psychopharmacology of epilepsy
• Chapter 13: The psychopharmacology of brain vascular disease/poststroke depression
• Chapter 14: The psychopharmacology of pseudobulbar affect
• Chapter 15: Psychopharmacology of traumatic brain injury
• Chapter 16: The psychopharmacology of primary and metastatic brain tumors and paraneoplastic syndromes
• Chapter 17: Psychiatric manifestations and psychopharmacology of autoimmune encephalitis: A multidisciplinary approach
• Chapter 18: Psychopharmacology of multiple sclerosis
• Chapter 19: Psychopharmacology of chronic pain
• Chapter 20: Psychopharmacology of headache and its psychiatric comorbidities
• Chapter 21: Psychopharmacology of sleep disorders
• Chapter 22: Sensory neurologic disorders: Tinnitus
• Chapter 23: Psychopharmacology of neurobehavioral disorders
• Chapter 24: The psychopharmacology of autism spectrum disorder and Rett syndrome
• Chapter 25: The psychopharmacology of catatonia, neuroleptic malignant syndrome, akathisia, tardive dyskinesia, and dystonia
• Index