The Frontal Lobes

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• Publisher: Elsevier
• Year: 2019
• Print ISBN: 9780128042816
• eBook ISBN: 9780128043264
• Topic: Medicine
• Subtopic: Neurology

The Frontal Lobes, Volume 163, updates readers on the latest thinking on the structure and function of the human frontal lobe. Sections address methodology, anatomy, physiology and pharmacology, function, development, aging and disorders, and rehabilitation. Patients with focal lesions in the frontal lobes have long been studied to reveal the organization and function of the frontal lobes. Over the last two decades, studies of patients with neurodegenerative diseases and developmental disorders have increased, with new findings discussed in this volume. In addition, the book includes discussions on genetics and molecular biology, optogenetics, high-resolution structural and functional neuroimaging and electrophysiology, and more.Lastly, new knowledge on the biology, structure and function of the frontal lobes, new treatment targets for pharmacology, non-invasive brain stimulation, and cognitive/social remediation are presented. The last section covers new efforts that will hopefully lead to better outcomes in patients with frontal lobe disorders.- Provides an overview of the structure, function, disorder and rehabilitation of the frontal lobes- Addresses a wide variety of methodologies – from genetics and molecular biology, to optogenetics and hi-res fMRI, and more- Contains content of interest to advanced students, junior researchers and clinicians getting involved in research- Features the input of leaders in neuroanatomical research from around the globe – the broadest, most expert coverage available

Section IV

Function of the frontal lobes

Chapter 8

Frontal lobe syndromes

Justin Reber^1,3; Daniel Tranel^2,* ¹ Department of Psychological and Brain Sciences, University of Iowa, Iowa City, IA, United States
² Department of Neurology, University of Iowa College of Medicine, Iowa City, IA, United States
³ Department of Psychiatry, University of Iowa College of Medicine, Iowa City, IA, United States
* Correspondence to: Daniel Tranel, Ph.D., Neuroscience PhD Program Director, Associate Dean of Graduate and Postdoctoral Studies, Department of Neurology, University of Iowa Hospitals and Clinics, 200 Hawkins Drive, 2155 RCP, Iowa City, IA 52242, United States. Tel: + 1-319-384-6050, Fax: [phone] email address: [email protected]

Abstract

The frontal lobes contain a complex set of diverse anatomic regions that form multiple distinct, complex networks with cortical and subcortical regions. Damage to these cortical–subcortical networks can have dramatic behavioral consequences, ranging from apathy to impairments in executive functioning. This chapter provides a brief overview of the common syndromes caused by damage to the mediodorsal and dorsolateral prefrontal circuits, followed by a more detailed review of the syndrome—sometimes referred to as pseudopsychopathy or acquired sociopathy—associated with damage to the ventromedial prefrontal circuit.

Keywords

Prefrontal; Apathy; Abulia; Perseveration; Pseudopsychopathy; Acquired sociopathy; Ventromedial; Orbitofrontal; Dorsolateral

Introduction

The frontal lobes make up over one-third of the human cerebral cortex and comprise several diverse anatomic units with distinct and highly complex connections (unidirectional and bidirectional) to other cortical and subcortical regions and to each other. Despite major progress over the past couple of decades in cognitive neuroscience and neuropsychology, clinicians (especially clinical neuropsychologists, behavioral neurologists, neuropsychiatrists, and neurosurgeons) who evaluate and treat frontal lobe dysfunction still face many of the challenges and limitations encountered by prior generations. Acquired damage can disrupt in myriad ways the varied and complex neuroanatomic and functional systems in the frontal lobes, systems which for the most part remain incompletely understood. Challenges presented by the anatomic complexity of the frontal lobes are paralleled by the equally daunting array of signs and symptoms of frontal lobe damage, and in particular by the fact that such signs and symptoms do not lend themselves easily to quantitative analysis in a laboratory setting (including clinical neuropsychologic evaluation, e.g., Lezak et al., 2012). Thus, although the central role of the frontal lobes in higher cognitive functions is not in question, and there is similarly little question that frontal dysfunction contributes to many prominent psychiatric disorders, the precise characterization and measurement of cognitive and behavioral manifestations of frontal lobe dysfunction remain elusive. In this chapter, we review salient cognitive and behavioral changes that result from focal damage to the frontal lobes. To keep the scope of our review tractable, we focus on the prefrontal cortex and on cognitive and behavioral manifestations that are most commonly encountered in clinical practice with patients who have focal, acquired damage to the prefrontal cortex (readers are referred to other chapters in this volume for other perspectives).

Prefrontal Syndromes

Damage to the prefrontal lobes can have widely varying behavioral consequences, depending upon the location, extent, and etiology of the lesion or degeneration. Furthermore, damage to the prefrontal lobes is rarely limited to a single region, but often affects multiple areas and disrupts their connections with other cortical and subcortical structures (Cummings, 1993). Damage to white matter tracts can also disrupt these circuits, causing far more severe impairments than would be expected from the extent of cortical damage. It is important, therefore, to consider lesions in the prefrontal lobes not as isolated neurologic injuries, but as disruptions in complex anatomic and functional networks.

Despite the complexity of prefrontal networks, the majority of symptoms resulting from prefrontal dysfunction can be sorted into three broad categories, each closely linked with one of three parallel yet relatively segregated frontal–subcortical circuits. The first category generally involves disruptions in motivation and willful behavior, including the striking manifestations of apathy, abulia, and akinetic mutism. Such manifestations typically occur with lesions to the medial frontal circuit and the anterior cingulate gyrus and underlying white matter (Fig. 8.1). The second category, hallmarked by impairments in executive functioning, is associated with damage to the dorsolateral prefrontal circuit. The final category of symptoms, often labeled pseudopsychopathy or acquired sociopathy, involves disturbances in personality, affect, social conduct, and behavioral regulation, and typically follows lesions to the orbitofrontal circuit and the associated ventromedial cortex and white matter. This chapter will provide a brief overview of the first two categories, followed by a more detailed review of the last category.

Fig. 8.1 Stylized three-dimensional renderings of the brain depicting the major cortical areas involved in the medial frontal, dorsolateral, and ventromedial circuits.

Diminished Motivation: Medial Frontal and Anterior Cingulate Lesions

Disruption and damage to the anterior cingulate or the medial frontal circuit can cause a spectrum of impairments in motivation and willful behavior. The mildest form, apathy, derived from the Greek root pathos, is marked behaviorally by limited spontaneous activity, such as speech, movement, and gesture, with unaffected consciousness, attention, and mood (Marin, 1990; Marin and Wilkosz, 2005; Filley, 2011). Patients with apathy are capable of planning and initiating behavior, but they do so less frequently than normal individuals. In striking contrast to their impoverished outward behavioral expressions, the patients tend to have normal emotional experiences. Abulia is often used to describe a more severe version of apathy, accompanied by psychomotor slowing, long latency to speech, and a further dampening of initiative, cognition, and emotion. Neither apathy nor abulia entail a complete lack of affect—in fact, apathetic and abulic patients may experience intense bouts of irrational anger or euphoria, but these emotional experiences are rare. Furthermore, apathy and abulia resulting from damage to the medial frontal circuit is distinguished from major depressive disorder by the lack of distress and negative cognitions predominant in the latter.

In the most severe cases, both unilateral and bilateral lesions to the anterior cingulate or the dorsomedial prefrontal circuit can cause akinetic mutism, a condition wherein patients display a complete loss of spontaneous speech and motor behavior. While they retain consciousness and continue to track their environment, patients with akinetic mutism lack any other overt behaviors, a condition described by Cairns et al. (1941) as “motionless, mindless wakefulness” (Marin and Wilkosz, 2005). These patients will not groom themselves, eat and drink only when fed, and often lack bowel and bladder control. Although the conditions can have similar behavioral profiles, akinetic mutism may be differentiated from locked-in syndrome by the fact that the lack of movement in akinetic mutism is not due to paralysis, but rather due to lack of volition. Unlike patients with locked-in syndrome, patients with akinetic mutism can make significant recoveries, regaining their mobility, speech, and goal-directed behavior once their motivation returns (Yang et al., 2007). Although akinetic mutism is rare and often transient, varying degrees of apathy and abulia are among the most common symptoms of traumatic brain injury, with studies recording incidence of apathy between 41% and 71% in patients (Craig et al., 1996; Kant et al., 1998; Ciurli et al., 2011). Notably, Parvizi et al. (2013) observed that direct electrical stimulation of the dorsomedial circuit by way of the anterior cingulate can produce a sort of reverse apathy, a sense of increased motivation that they dubbed “the will to persevere.”

Anatomy and common etiologies

The medial frontal circuit includes the cingulate gyrus and the dorsomedial surface of the prefrontal cortex, including the supplementary motor area, and the white matter subjacent to these regions. Thes...

Table of contents

• Cover image
• Title page
• Table of Contents
• Copyright
• Handbook of Clinical Neurology 3rd Series
• Foreword
• Preface
• Contributors
• Section I: History
• Section II: Methods
• Section III: Anatomy, physiology and pharmacology
• Section IV: Function of the frontal lobes
• Section V: Development, aging, and disorders
• Section VI: Rehabilitation