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Nonlinear Dynamics of Parkinson's Disease and the Basal Ganglia-Thalamic-Cortical System examines current research regarding the operations of the basal ganglia-thalamic-cortical system that causes neurological disorders like Parkinson's disease. While there have been remarkable advances in the understanding of the anatomy, physiology and chemistry of these systems, there remains a significant degree of inconsistency and incompleteness between facts and advancements. This book introduces the novel concepts of nonlinear complex systems and their connection to Parkinsonism as well as hyperkinetic disorders. The actual mechanisms underlying the motor disorders of Parkinson's disease at the level of the lower motor neuron are also discussed. - Outlines phenomenological selectivity of pallidotomy and Deep Brain Stimulation - Reviews the anatomical models of pathophysiology and physiology - Discusses the instrumental and analytical misrepresentations and the inferences that misrepresent the data in Nonmonotonic Nonlinear Dynamics
The striatum is the principal input structure of the basal ganglia. Numerically, the great majority of neurons in the striatum are spiny projection neurons, which produce the inhibitory output of the striatum to the globus pallidum and substantia nigra. The major glutamatergic afferents to the striatum from the cerebral cortex make monosynaptic contact with spiny projection neurons. The dopaminergic afferents from the substantia nigra also synapse directly on the spiny projection neurons. Thus, the spiny projection neurons play a crucial role in the input–output operations of the striatum by integrating glutamatergic cortical inputs with dopaminergic inputs and producing the output to other basal ganglia nuclei. Anatomical observations made nearly 30 years ago suggested that inhibitory interactions among the spiny projection neurons of the striatum are very pr- able. Individual spiny projection neurons produce a local axonal plexus in the spheroidal space occupied by their own dendritic trees [1, 2]. Based on the GABAergic nature of these neurons and their synaptic contacts with other spiny neurons, several authors have proposed that the spiny projection neurons form a lateral inhibition type of neural network [3–5]. In the idealised concept of lateral inhibition, each output neuron makes inhibitory synaptic contact with its neighbours [5]. However, there are physical limitations set by the extent of axonal and dendritic trees, and the number of synaptic sites, which mean that lateral inhibition is limited to a local domain of inhibition.
The basal ganglia constitute a group of subcortical structures, highly interconnected among themselves, as well as with the cerebral cortex, thalamus and other brain areas. These nuclei play a central role in the control of voluntary movement, and their specific pathology comprises the group of diseases known as movement disorders, including Parkinson's disease, Huntington's disease, dystonia and Gilles de la Tourette syndrome, among others. Additionally, the presence of a number of circuits within the basal ganglia related to non-motor functions has been acknowledged. Currently, the basal ganglia are thought to participate in cognitive, limbic and learning functions. Moreover, disorders related to the basal ganglia are known to involve a number of complex, non-motor symptoms and syndromes (e.g. compulsive and addictive behavior). In the light of this evidence, it is becoming clear that our knowledge about the basal ganglia needs to be revised, and that new pathophysiological models of movement disorders are needed. In this context, the study of the pathophysiology of the basal ganglia and the treatment of their pathology is becoming increasingly interdisciplinary. Nowadays, an appropriate approach to the study of these problems must necessarily involve the use of complex mathematical modeling, computer simulations, basic research (ranging from biomolecular studies to animal experimentation), and clinical research. This research topic aims to bring together the most recent advances related to the pathophysiology of the basal ganglia and movement disorders.
The striatum is the principal input structure of the basal ganglia. Numerically, the great majority of neurons in the striatum are spiny projection neurons, which produce the inhibitory output of the striatum to the globus pallidum and substantia nigra. The major glutamatergic afferents to the striatum from the cerebral cortex make monosynaptic contact with spiny projection neurons. The dopaminergic afferents from the substantia nigra also synapse directly on the spiny projection neurons. Thus, the spiny projection neurons play a crucial role in the input–output operations of the striatum by integrating glutamatergic cortical inputs with dopaminergic inputs and producing the output to other basal ganglia nuclei. Anatomical observations made nearly 30 years ago suggested that inhibitory interactions among the spiny projection neurons of the striatum are very pr- able. Individual spiny projection neurons produce a local axonal plexus in the spheroidal space occupied by their own dendritic trees [1, 2]. Based on the GABAergic nature of these neurons and their synaptic contacts with other spiny neurons, several authors have proposed that the spiny projection neurons form a lateral inhibition type of neural network [3–5]. In the idealised concept of lateral inhibition, each output neuron makes inhibitory synaptic contact with its neighbours [5]. However, there are physical limitations set by the extent of axonal and dendritic trees, and the number of synaptic sites, which mean that lateral inhibition is limited to a local domain of inhibition.
The Basal Ganglia (BG) are thought to be involved primarily in motor but also in non-motor functions. Unsurprisingly, the BG are shown to be involved in motor dysfunctions such as Parkinson's disease or dystonia. More recent studies suggest the key role of the BG in "non-motor" diseases such as absence epilepsy which is a generalized non-convulsive epilepsy. In these diseases, symptoms accompany various oscillatory patterns of neural activity often synchronized across the BG, cortex and other brain areas. How can the BG support these different kinds of oscillatory patterns?Recent experiments have highlighted the key role of the BG in absence seizures and question the traditional view in which thalamocortical circuits underlie absence seizures. We propose a novel theory according to which the feedbacks of cortical activity through BG make this network bistable and drive the oscillatory patterns of activity occurring during the seizures. Our theory is compatible with virtually all known experimental results and it predicts that well-timed transient excitatory inputs to the cortex advance the termination of absence seizures. We report preliminary experimental results consistent with this prediction.Multiple oscillatory frequencies are observed in Parkinsonian BG such as the frequencies of the limb tremor and the beta oscillations. We show that our model can generate oscillations with multiple timescales which resemble Parkinsonian oscillations. Our theory can model the oscillations in Parkinson's disease and absence epilepsy in a unified framework and points to two scenarios to explain multiple frequencies of pathological and functional oscillations.
This groundbreaking text takes current knowledge of the basal ganglia far from well-known motor-based models to a more inclusive understanding of deep-brain structure and function. Synthesizing diverse perspectives from across the brain-behavioral sciences, it tours the neuroanatomy and circuitry of the basal ganglia, linking their organization to their controlling functions in core cognitive, behavioral, and motor areas, both normative and disordered. Interactions between the basal ganglia and major structures of the brain are identified in their contributions to a diverse range of processes, from language processing to decision-making, emotion to visual perception, motivation to intent. And the basal ganglia are intimately involved in the mechanisms of dysfunction, as evinced by chapters on dyskinesia, Parkinson’s disease, neuropsychiatric conditions, and addictions. Included in the coverage: Limbic-basal ganglia circuits: parallel and integrative aspects. Dopamine and its actions in the basal ganglia system. Cerebellar-basal ganglia interactions. The basal ganglia contribution to controlled and automatic processing. The basal ganglia and decision making in neuropsychiatric disorders. The circuitry underlying the reinstatement of cocaine seeking: modulation by deep brain stimulation. The basal ganglia and hierarchical control in voluntary behavior. Its breadth and depth of scholarship and data should make The Basal Ganglia a work of great interest to cognitive psychologists and neuroscientists, neuropsychologists, neurologists, neuropsychiatrists, and speech-language pathologists.
Parkinson's disease becomes apparent only after substantial loss (>60%) of the dopamine neurons in the substantia nigra. By this time there has already been widespread neural inclusion formation in the peripheral and central nervous system of patients with the disease, although this has only been recognized more recently. Degeneration in these widespread regions of the peripheral and central nervous system is now known to impact on disease symptoms, progression and treatment over time. This book aims to provide a comprehensive review of these non-dopamine lesions in Parkinson's disease by assessing our current knowledge of their presence and pathophysiology, how they relate to different symptoms and, where relevant, discuss how they may be potentially treated. The book addresses most of the known symptoms that occur in patients with Parkinson's disease. In addition to the classic motor triad, motor speech, eye movements, olfactory dysfunction, autonomic dysfunction, pain and sensory abnormalities, sleep disturbances, depression and apathy, dopamine dysregulation syndromes, hallucinations and psychoses, cognitive impairment and dementia, and systemic manifestations are all reviewed. Early selective cell loss in non-dopaminergic regions is highlighted (the glutamate projection neurons of the presupplementary motor cortex and caudal intralaminar thalamus) in addition to the widespread inclusion formation in many regions outside the basal ganglia that characterize the disease. Overall this book provides a comprehensive analysis of the lesions associated with the most common symptoms found in patients with Parkinson's disease.
The editor of this volume, having research interests in the field of ROS production and the damage to cellular systems, has identified a number of enzymes showing ·OH scavenging activities details of which are anticipated to be published in the near future as confirmatory experiments are awaited. It is hoped that the information presented in this book on NDs will stimulate both expert and novice researchers in the field with excellent overviews of the current status of research and pointers to future research goals. Clinicians, nurses as well as families and caregivers should also benefit from the material presented in handling and treating their specialised cases. Also the insights gained should be valuable for further understanding of the diseases at molecular levels and should lead to development of new biomarkers, novel diagnostic tools and more effective therapeutic drugs to treat the clinical problems raised by these devastating diseases.
Chronic electrical stimulation of the brain has demonstrated excellent outcomes in patients with Parkinson’s disease and has recently also been applied to various other neurological diseases. This comprehensive, up-to-date textbook will meet the needs of all who wish to learn more about the application of deep brain stimulation and will provide a sound basis for safe and accurate surgery. The book comprises two main parts, the first of which presents relevant anatomical and functional background information on the basal ganglia, thalamus and other brain structures as well as on the mechanism of brain stimulation. The second part describes clinical studies on deep brain stimulation, covering results in a range of movement disorders and psychiatric diseases and also important aspects of instrumentation and technique. The authors are outstanding scientists and experts in the field from across the world.
This book focuses on our current understanding of brain dynamics in various brain disorders (e.g. epilepsy, Alzheimer’s and Parkinson’s disease) and how the multi-scale, multi-level tools of computational neuroscience can enhance this understanding. In recent years, there have been significant advances in the study of the dynamics of the disordered brain at both the microscopic and the macroscopic levels. This understanding can be furthered by the application of multi-scale computational models as integrative principles that may link single neuron dynamics and the dynamics of local and distant brain regions observed using human EEG, ERPs, MEG, LFPs and fMRI. Focusing on the computational models that are used to study movement, memory and cognitive disorders as well as epilepsy and consciousness related diseases, the book brings together physiologists and anatomists investigating cortical circuits; cognitive neuroscientists studying brain dynamics and behavior by means of EEG and functional magnetic resonance imaging (fMRI); and computational neuroscientists using neural modeling techniques to explore local and large-scale disordered brain dynamics. Covering topics that have a significant impact on the field of medicine, neuroscience and computer science, the book appeals to a diverse group of investigators.