Dr. McNamara has undertaken the goal of presenting a new, innovative “top-down” model for understanding the cognitive, personality, and mood disorders that are commonly associated with Parkinson's Disease (PD). In general, he proposes that the major non-motor impairments associated with PD are related to deficiencies in what he terms the “agentic self.” The agentic self, according to his argument, is a neurologic system (related to different neural pathways, networks, and chemicals) that is responsible for planning for the future, setting goals, and acting on these goals. He then proceeds to describe how impairments in these future oriented cognitive skills are the cause of PD's specific cognitive, personality, and mood disorders.
After reading the book it is clear that this agentic self, as Dr. McNamara has suggested, is analogous to what is commonly referred to as the executive system of the brain. However, based on his expertise in PD, Dr. McNamara has proposed a speculative model that is likely to be of interest to serious PD researchers, as well as individuals interested in the study of different models of the neurologic and psychiatric basis of the “self” and its various manifestations (e.g., Decety & Sommerville, Reference Decety and Sommerville2003).
Let's Start with the Title
First things first. The title appears to be misleading as it suggests that the book will focus on the “cognitive neuropsychiatry” of PD (e.g., the cognitive impairments associated with PD, the neuropsychiatric foundations of these impairments, and the various neuropsychiatric treatments for them). In reality, only several chapters focus on the basic neuropsychiatric foundations of PD. Instead, the focus of the book is presenting Dr. McNamara's novel conceptualization of an “agentic self,” with the majority of chapters focusing on describing the model, neurologic correlates of the agentic self, and the manner in which disorders of the agentic self affect the ability of persons with PD to engage in intentionality (i.e., goal direction), forethought, self-reactiveness, and self-reflectiveness. Dr. McNamara hypothesizes that neurologically based impairments in the agentic self (or executive skills) cause the cognitive, personality, and mood disorders that are common to PD. These chapters are clearly the highlight of the book.
The variable emphases of the chapters provide insight into the somewhat ambiguous structure of the book. For example, the first chapters (On Parkinson's Disease; Dopamine and Parkinson's Disease Neuropsychiatry) provide basic information regarding PD and will be of use to individuals with limited knowledge of the disorder. The subsequent chapters (The Nature and Function of the Agentic Self; Impairment of the Agentic Self in PD: Cognitive Deficits in PD; The Agentic Self and Personality Changes in PD; Evolutionary Perspectives on the Agentic Self, Its Neural Networks, and PD) are novel, interesting, and the main focus of the book. In proposing his theory of the agentic self and its impact on functioning in PD, Dr. McNamara cites related research that suggests the manner by which the agentic self (or executive skills) are impaired in PD (i.e., “…cognitive, mood, and personality changes of Parkinson's Disease are essentially due to the inability to activate fully agentic aspects of the self…”). He also offers his thoughts regarding how his theory of the agentic self interacts with other theories of the self (e.g., simple self) based on the PD disease process, which may be of interest to researchers of the neurological basis of the self (and it's various proposed manifestations).
After these comprehensive chapters on the agentic self, the next several chapters (Speech and Language Deficits of PD; Sleep Disorders of PD; Mood Disorders and Apathy in PD; Psychosis and Dementia in PD; Impulse Control Disorders in PD) have little to say about the role of the agentic self in the manifestation or treatment of these PD-related impairments. They may be best placed in a general book on the neuropsychiatry of PD. The last chapter, Rehabilitation of the Agentic Self, provides general information about the rehabilitation of executive, behavioral, or social impairments associated with PD, but little if any actual suggestions for therapies regarding the agentic self. The organization of the chapters suggests that the editors and author compromised on a book that would present more general information regarding the neuropsychiatric presentation of PD, as well as a novel model regarding the agentic self and PD. Focusing solely on the agentic self and PD would have been more interesting (i.e., numerous other books are available regarding basic neuropsychiatric impairments and treatments for PD), but none present a new conceptualization of an agentic self for consideration. Focusing on one area or the other would have made sense, but combining them leads for a somewhat disjointed presentation.
Novelty
The primary strength of the book is its ability to make the reader think about PD related impairments in a new light. The book is novel in its supposition that PD impairments are related to disorder of the agentic self, which has four basic properties: 1) intentionality; 2) forethought; 3) self-reactiveness; and 4) self-reflectiveness. In general, the agentic self acts with intention of future goals, which Dr. McNamara hypothesizes has six basic serial cognitive causal operations: 1) identifies values; 2) prioritizes them into long term goals; 3) decides which goals to pursue; 4) develops plans to attain those goals; 5) initiates goal pursuit by inhibiting valuation and responding on impulse alone; and 6) monitors and adjusts such plans. Problems in any one of these causal operators, which Dr. McNamara proposes all have neurologic foundations, and particularly the fifth one, lead to the common PD impairments such as apathy, lack of initiation, depression, anxiety, and personality changes (e.g., novelty seeking). The chapters on the agentic self are thought provoking and may prove to be worthwhile when planning future and specific research in this area.
Besides the competing emphasis on the neuropsychiatry of PD and the agentic self, another weakness relates to the book's attempt to differentiate between the agentic self and the “minimal self” (a less planful but more impulsive self). To bolster the conceptualization of an agentic self, it would also have been helpful for a chapter to discuss how other brain disorders/injuries, and not just PD, would affect the agentic self and its related impairments for other disorders (maybe such a book is in the works?). For example, do psychiatric disorders associated with depletion of dopamine or dysfunctional basal ganglia, frontal lobes, and substantia nigra lead to similar impairments (and not just in PD). In addition, it would have been interesting for him to compare his model of the agentic self with other more commonly accepted neurologic models of the self which are based on research that has demonstrated that the right hemisphere injury, and particularly right parietal lobe dysfunction, are associated with “disorders of the self” (Feinberg, Reference Feinberg2001; Feinberg & Keenan, Reference Feinberg and Keenan2005). Specifically, after reading his book questions arise as to whether or not impairments in the agentic self are related to anosagnosia, left sided neglect, Capgras syndrome, for example, and how so? Comparing and contrasting his model of the agentic self to other conceptualizations of the self would help bolster his argument that an agentic self exists.
As to whether or not to read the book, the answer depends on one's interest. If one is solely interested in learning the basic neuropsychiatric causes, impairments, and treatments of PD, as the title of the book suggests, then this book is not for you and other common texts will meet your needs. However, if one is interested in considering a novel model of the self for understanding the manner in which individuals with PD demonstrate common cognitive, personality, and mood impairments, then this is likely to be a rewarding and intellectually stimulating book.
