Stahl's Essential Psychopharmacology: Neuroscientific Basis and Practical Applications

Stahl's Essential Psychopharmacology: Neuroscientific Basis and Practical Applications

Stephen M. Stahl

Language: English

Pages: 626

ISBN: 1107686466

Format: PDF / Kindle (mobi) / ePub


With this fully revised fourth edition, Dr Stahl returns to the essential roots of what it means to become a neurobiologically empowered psychopharmacologist, expertly guided in the selection and combination of treatments for individual patients in practice. Embracing the unifying themes of 'symptom endophenotypes', dimensions of psychopathology that cut across syndromes, and 'symptoms and circuits', every aspect of the text has been updated to the frontiers of current knowledge, with the clarity of explanation and illustration that only Dr Stahl can bring. Integrating much of the basic neuroscience into the clinical chapters, and with major additions in the areas of psychosis, antipsychotics, antidepressants, impulsivity, compulsivity and addiction, this is the single most readily readable source of information on disease and drug mechanisms. This remains the essential text for all students and professionals in mental health seeking to understand and utilize current therapeutics, and to anticipate the future for novel medications.

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schizophrenia. The stages of schizophrenia are shown here over a lifetime. The patient often has full functioning (100%) early in life and is virtually asymptomatic (stage I). However, during a prodromal phase (stage II) starting in the teens, there may be odd behaviors and subtle negative symptoms. The acute phase of the illness usually announces itself fairly dramatically in the twenties (stage III), with positive symptoms, remissions, and relapses but never a complete return to previous levels

anxiety disorder (Figure 9-1) or one anxiety disorder into another (Figures 9-2 through 9-5). From a therapeutic point of view, it may matter little what the specific diagnosis is across this spectrum of disorders (Figures 9-1 through 9-5). That is, first-line psychopharmacological treatments may not be much different for a patient who currently qualifies for a major depressive episode plus the symptom of anxiety (but not an anxiety disorder) versus a patient who currently qualifies for a major

potentially raise plasma levels sufficiently in the case of clozapine, zotepine, duloxetine, or theophylline to increase side effects, including possibly increasing the risk of seizures. Thus, the dose of clozapine or zotepine (or olanzapine and asenapine, as well as duloxetine) may need to be lowered when administered with fluvoxamine, or an antidepressant other than fluvoxamine may need to be chosen. Figure 2-17. Consequences of CYP 1A2 inhibition. Numerous drugs (theophylline, duloxetine,

parvalbumin-containing GABA interneurons fail to function properly, they do not adequately inhibit key glutamatergic pyramidal neurons in the prefrontal cortex, causing those glutamate neurons to become hyperactive (Figure 4-29B box 3; compare Figure 4-29A box 3). This hypothetically disrupts the functioning of downstream neurons, especially dopamine neurons (Figures 4-30B, 4-31B, and 4-32B, explained below). So, one sick synapse in a neuronal circuit can affect the whole circuit, from GABA

counts, the use of clozapine is low in clinical practice, perhaps too low. It is important not to lose the art of how to prescribe clozapine and for whom, as clozapine remains a powerful therapeutic intervention for many patients. OlanzapineAlthough this agent has a chemical structure related to clozapine and is also an antagonist at both serotonin 5HT2A and dopamine D2 receptors, olanzapine is more potent than clozapine, and has several differentiating pharmacologic (Figure 5-46) and clinical

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