Neurocircuitry and Neuroautonomic Disorders
Karger, S (Verlag)
978-3-8055-7413-6 (ISBN)
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The authors of this book developed the only clinical neurochemistry laboratory equipped routinely to assay all circulating neurotransmitters. These parameters have been measured in more than 20,000 normal, severely diseased, depressed, stressed and psychosomatic patients. The results obtained have been published in more than 100 scientific papers. The authors postulated the existence of at least three well-defined types of pathophysiologic profiles: (1) endogenous depression, (2) dysthymic depression, and (3) uncoping (maladapted) to stress. Being aware of them, clinicians can prescribe distinct neuropharmacological therapies. The first and third profiles are also registered in Th1 and Th2 autoimmune diseased patients, respectively.
The first part of the book is devoted to the outline of these central neurocircuitry functions during the wake-sleep cycle in normal subjects as well as depressive states, uncoping stress, psychotics, bipolar disorders and panic attacks. Due to these neuroautonomic and neuroimmune interactions being noticed, various neuropharmacological therapeutic approaches can be referred to. In a second part the authors present treatments able to cure or help improve diseases presenting with a Th1 autoimmune profile as well as a Th2 autoimmune profile.
A Karger 'Publishing Highlights 1890-2015' title The authors of this book developed the only clinical neurochemistry laboratory equipped routinely to assay all circulating neurotransmitters. These parameters have been measured in more than 20,000 normal, severely diseased, depressed, stressed and psychosomatic patients. The results obtained have been published in more than 100 scientific papers. The authors postulated the existence of at least three well-defined types of pathophysiologic profiles: (1) endogenous depression, (2) dysthymic depression, and (3) uncoping (maladapted) to stress. Being aware of them, clinicians can prescribe distinct neuropharmacological therapies. The first and third profiles are also registered in Th1 and Th2 autoimmune diseased patients, respectively. The first part of the book is devoted to the outline of these central neurocircuitry functions during the wake-sleep cycle in normal subjects as well as depressive states, uncoping stress, psychotics, bipolar disorders and panic attacks. Due to these neuroautonomic and neuroimmune interactions being noticed, various neuropharmacological therapeutic approaches can be referred to. In a second part the authors present treatments able to cure or help improve diseases presenting with a Th1 autoimmune profile as well as a Th2 autoimmune profile.
1;Contents;5
2;Preface;8
3;Overview;10
4;Introduction;11
5;Central Neurocircuitry Functioning during the Wake- Sleep Cycle;13
6;Some Neuroautonomic and Neuroendocrine Changes Registered during the Wake and Sleep Periods;24
7;Stress;28
8;Depression;33
9;Stress versus Depression;38
10;Bipolar Syndrome;57
11;Psychotic Syndrome;61
12;Panic Attacks;64
13;Neuroautonomic, Neuroendocrine and Neuroimmune Interactions;67
14;Neuroendocrine-Immune Interactions;70
15;Stress, Depression and Immunity;72
16;Bronchial Asthma;76
17;Concluding Remarks;79
18;Illustrations of Some Therapeutic Results;85
19;References;105
20;Subject Index;141
Chapter 8: Panic Attacks
We have carried out the only scientific research dealing with this syndrome in which all plasma neurotransmitters were assessed during both resting and stimulated conditions. We also tested the effects of buspirone, a drug which is able to trigger the increase of both central NA activity + central DA activity. The LC noradrenergic neurons and the ventral tegmental (VTA) or A10 DA neurons are both excited by buspirone. In addition, this drug depresses central 5HT activity. In effect, buspirone is a 5HT1A agonistic drug that inhibits the firing activity of those serotonergic neurons endowed with 5HT1A inhibitory somatodendritic autoreceptors. 5HT2 inhibitory autoreceptors which are located at 5HT-terminal axons also exist.
Considering that 5HT1A autoreceptors are located mainly at the DR 5HT nucleus, these serotonergic neurons are the main target of the low doses of buspirone we used in our research. In effect, MR 5HT neurons are not crowded with 5HT1A receptors. Finally, caudal serotonergic nuclei (raphe magnus, raphe obscurus and raphe pallidus) are inhibited by buspirone only when great doses of this drug are microinjected directly onto these nuclei. In light of all the above, the oral dose of buspirone (10 20 mg) we administered to panic patients would act mainly at the DR-5HT nucleus. These buspirone doses were able to trigger panic attacks in all our patients. It is a very well-stated fact that panic attacks are associated with disinhibition of the periaqueductal gray (PAG-5HT)-amygdala pathway. Furthermore, this pathway is bridled by 5HT axons arising from DR-5HT neurons, thus, panic attacks have been associated with the failure of the DRPAG inhibitory pathway. Our finding that TRP plasma levels are very low in panic patients is consistent with the above. The low TRP plasma levels were registered both during the attack and during the nonattack periods.
Many authors have reported that NA and/or Ad are raised in panic patients, thereby originating great confusion among readers. These plasma catecholamines have been investigated during both panic and nonpanic periods. However, we have shown, throughout the last 20 years, that only systematic assessment of all plasma neurotransmitters during both resting and stressed situations (orthostasis, exercise, glucose, buspirone, etc.) can reveal the particular participation of both central (neural) and peripheral (adrenal) sympathetic activity. We and many other researchers have exhaustively demonstrated that these two branches of the sympathetic system can act independently or in associated or dissociated ways. It is a great mistake to continue dwelling on sympathetic activity as if it were self-contained. For a start, central sympathetic activity depends on firing by the LC A6 group of NA neurons, whereas peripheral (adrenomedullary) sympathetic activity is dependent on C1 Ad neurons located at the rostral ventral lateral area of the medulla. Further, it has been shown that ACh preganglionic axons innervating the adrenal medulla, located at the thoracic segments of the intermediolateral spinal column, receive modulatory axons arising from the C1-Ad neurons. In effect, stimulation of C1-Ad neurons triggers adrenaline release from the adrenomedullary glands.
| Erscheint lt. Verlag | 19.6.2002 |
|---|---|
| Zusatzinfo | 72 fig., 28 in color, 12 tab. |
| Verlagsort | Basel |
| Sprache | englisch |
| Gewicht | 622 g |
| Themenwelt | Medizin / Pharmazie ► Medizinische Fachgebiete ► Neurologie |
| Schlagworte | gastroenterology • HC/Medizin/Klinische Fächer • immunology • Neurologie • Neurology • Oncology • pharmacology • Physiology • pneumology • Psychiatry |
| ISBN-10 | 3-8055-7413-4 / 3805574134 |
| ISBN-13 | 978-3-8055-7413-6 / 9783805574136 |
| Zustand | Neuware |
| Informationen gemäß Produktsicherheitsverordnung (GPSR) | |
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