Journal•ISSN: 1067-3229
Harvard Review of Psychiatry
Lippincott Williams & Wilkins
About: Harvard Review of Psychiatry is an academic journal published by Lippincott Williams & Wilkins. The journal publishes majorly in the area(s): Mental health & Medicine. It has an ISSN identifier of 1067-3229. Over the lifetime, 1114 publications have been published receiving 46699 citations.
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TL;DR: Clinical observations and empirical studies that focus on painful affects and subjective states of distress more consistently suggest that such states of suffering are important psychological determinants in using, becoming dependent upon, and relapsing to addictive substances.
Abstract: The self-medication hypothesis of addictive disorders derives primarily from clinical observations of patients with substance use disorders. Individuals discover that the specific actions or effects of each class of drugs relieve or change a range of painful affect states. Self-medication factors occur in a context of self-regulation vulnerabilities--primarily difficulties in regulating affects, self-esteem, relationships, and self-care. Persons with substance use disorders suffer in the extreme with their feelings, either being overwhelmed with painful affects or seeming not to feel their emotions at all. Substances of abuse help such individuals to relieve painful affects or to experience or control emotions when they are absent or confusing. Diagnostic studies provide evidence that variously supports and fails to support a self-medication hypothesis of addictive disorders. The cause-consequence controversy involving psychopathology and substance use/abuse is reviewed and critiqued. In contrast, clinical observations and empirical studies that focus on painful affects and subjective states of distress more consistently suggest that such states of suffering are important psychological determinants in using, becoming dependent upon, and relapsing to addictive substances. Subjective states of distress and suffering involved in motives to self-medicate with substances of abuse are considered with respect to nicotine dependence and to schizophrenia and posttraumatic stress disorder comorbid with a substance use disorder.
2,169 citations
TL;DR: For instance, this article found that failure of declarative memory may lead to organization of the trauma on a somatosensory level (as visual images or physical sensations) that is relatively impervious to change.
Abstract: Ever since people's responses to overwhelming experiences have been systematically explored, researchers have noted that a trauma is stored in somatic memory and expressed as changes in the biological stress response. Intense emotions at the time of the trauma initiate the long-term conditional responses to reminders of the event, which are associated both with chronic alterations in the physiological stress response and with the amnesias and hypermnesias characteristic of posttraumatic stress disorder (PTSD). Continued physiological hyperarousal and altered stress hormone secretion affect the ongoing evaluation of sensory stimuli as well. Although memory is ordinarily an active and constructive process, in PTSD failure of declarative memory may lead to organization of the trauma on a somatosensory level (as visual images or physical sensations) that is relatively impervious to change. The inability of people with PTSD to integrate traumatic experiences and their tendency, instead, to continuously relive ...
1,135 citations
TL;DR: The current view of separate addictions is similar to the view espoused during the early days of AIDS diagnosis, when rare diseases were not distinguished between alcohol dependence and pathological gambling.
Abstract: “The important thing in science is not so much to obtain new facts as to discover new ways of thinking about them”Sir William Bragg (1862–1942)1It is common for clinicians, researchers, and public ...
568 citations
TL;DR: Dysregulation of glutamatergic neurotransmission may be particularly relevant to those forms of schizophrenia in which negative symptoms, cognitive deficits, and deterioration are prominent features.
Abstract: Schizophrenia is a syndrome, undoubtedly with multiple etiologies, that variably exhibits several features including positive and negative symptoms, cognitive deficits, onset in young adulthood, and deterioration from the previous level of function. This review will examine the growing evidence that dysfunction of corticolimbic glutamatergic neurotransmission may contribute to or account for the manifestations of schizophrenia. Glutamatergic neurons represent the primary excitatory afferent and efferent systems innervating the cortex, limbic regions, and striatum. The postsynaptic actions of glutamate are mediated by a family of glutamate-gated ion channels that permit the influx of sodium and calcium, thereby depolarizing (exciting) neurons. One of these receptors, the N-methyl-D-aspartate (NMDA) receptor, is the site of action of psychotomimetics such as phencyclidine and related anesthetics, which can reproduce in normal individuals most of the symptomatic features of schizophrenia. An endogenous antagonist at the NMDA receptor, N-acetyl-aspartyl glutamate, appears to have enhanced activity in the frontal cortex and hippocampal formation in persons with this disorder. Glutamatergic dysfunction may be particularly relevant to those forms of schizophrenia in which negative symptoms, cognitive deficits, and deterioration are prominent features. In support of this inference, clinical studies have shown that drugs that enhance NMDA-receptor function reduce negative symptoms and cognitive deficits in persons with chronic schizophrenia who are receiving neuroleptics. Thus, dysfunction of glutamatergic neurotransmission represents an important organizational focus for research on the complex manifestations of schizophrenia.
556 citations
TL;DR: Key conclusions are (1) human research with intranasal oxytocin has uniquely enhanced the authors' understanding of the microstructure and function of the human social brain, and (2) the Oxytocin system is a promising target for therapeutic interventions in a variety of conditions, especially those characterized by anxiety and aberrations in social function.
Abstract: Oxytocin is a neuropeptide involved in a wide variety of social behaviors in diverse species. Recent research on its effects in humans has generated an arresting picture of its role in the dynamic function of the social brain. This review presents a broad overview of this uniquely social peptide, with a particular focus on extant studies of its effects in humans. After a short discussion of the evolutionary history of the oxytocin system, critical aspects of its peripheral and central physiology, and several salient technical issues surrounding human oxytocin research, a systematic review of studies of the effects of intranasal oxytocin in humans is presented. These effects include alterations in social decision making, processing of social stimuli, certain uniquely social behaviors (e.g., eye contact), and social memory. Oxytocin's prosocial influence is then framed by an evolutionary perspective on its role in mammalian social bonding and attachment. Finally, limitations in current human oxytocin research and oxytocin's potential therapeutic applications are discussed. Key conclusions are (1) human research with intranasal oxytocin has uniquely enhanced our understanding of the microstructure and function of the human social brain, and (2) the oxytocin system is a promising target for therapeutic interventions in a variety of conditions, especially those characterized by anxiety and aberrations in social function.
547 citations