Neurotransmitter Assessment in Neuropsychiatric Disorders of Childhood

Rasmusson, Ann M.; Riddle, Mark A.; Leckman, James F.; Anderson, George M.; Cohen, Donald J.

doi:10.1007/978-1-4613-0525-5_3

Cited by 5 publications

(6 citation statements)

References 164 publications

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“…Less is known about the involvement of the dopaminergic system in PTSD because, unlike 5-HT and NE peripheral measures of dopamine function do not correlate well with the central measures (A. M. Rasmusson, Riddle, M. A., Leckman, J. F., Anderson, G. M., & Cohen, D. J., 1990).…”

Section: Monoaminergic Systemmentioning

confidence: 99%

Posttraumatic stress disorder: An integrated overview of the neurobiological rationale for pharmacology.

Kelmendi¹,

Adams²,

Southwick³

et al. 2017

Clinical Psychology: Science and Practice

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Thirty years of research on the biology of posttraumatic stress disorder now provides a foundation for hypotheses related to the mechanisms underlying the pharmacotherapy of this disorder. Only two medications, sertraline and paroxetine, are approved by the U.S. Food and Drug Administration for the treatment of PTSD. While these medications are somewhat effective, other treatment mechanisms must be explored to address the unmet need for effective treatment. This article provides a concise summary of advances in our understanding of the neurobiology of PTSD that suggest novel approaches to pharmacotherapy.

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Section: Monoaminergic Systemmentioning

confidence: 99%

Posttraumatic stress disorder: An integrated overview of the neurobiological rationale for pharmacology.

Kelmendi¹,

Adams²,

Southwick³

et al. 2017

Clinical Psychology: Science and Practice

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“…Nonetheless, whatever the mechanism, this study illustrates that whole blood serotonin could become a useful measure for epidemiological research. Recent commentaries on the literature (Berman, Kavoussi, Coccaro, in press;Rasmusson, Riddle, Leckman, Anderson & Cohen, 1990;Stoff, Ieni, Friedman, Bridger, Pollock, & Vitello, 1991) have blamed failures to replicate relations between serotonin and behavior on small, idiosyncratic samples. These commentaries also advise us to address the developmental origins of links between serotonin and aggression by studying representative samples of children longitudinally with repeated behavioral and serotonin measures.…”

Section: Discussionmentioning

confidence: 99%

“…If replicated, our findings suggest that whole blood serotonin may be a useful measure for studying larger, more representative samples, and may allow repeated measures in developmental studies. Epidemiological research can complement clinical research by delineating the population parameters of the serotoninviolence relation first revealed by studies of inpatient samples (Rasmusson, Riddle, Leckman, Anderson & Cohen, 1990).…”

Section: Discussionmentioning

confidence: 99%

“…Not all studies of the serotonin/violence relation report consistent findings, and reviews implicate inconsistencies in samples (Berman, Kavoussi & Coccaro, in press;Coccaro, 1989). Analyses of variation within a patient sample can be distorted by the restricted range of scores, sometimes producing inaccurate estimates of the sensitivity ofa biological marker (Berk, 1983;Rasmusson, Riddle, Leckman, Anderson & Cohen, 1990). Clinical studies that use matched non-patient controls risk deductive error by failing to represent the healthy population as faithfully as they represent the population of patients (Mednick, 1978).…”

Section: Whole Blood Serotonin Relates To Violence In An Epidemiologimentioning

confidence: 99%

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Biosocial Bases of Violence

1997

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“…For instance, numerous animal studies suggest that function of the dopaminergic, serotonergic, and excitatory amino acid systems is altered in particular parts of the brain during stress or from previous exposure to stress. However, alterations in these systems are generally more challenging to detect in humans 27 . Clinical inquiries are also limited by logistical difficulties in organizing human studies of the scale and prospective design needed to answer many of the important scientific questions just outlined.…”

mentioning

confidence: 99%

Animal Models of Relevance to PTSD

Rasmusson

Charney

1997

Annals of the New York Academy of Sciences

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Posttraumatic stress disorder or PTSDI is a psychiatric disorder of considerable prevalence and morbidity and can affect persons of any age and ethnic or socioeconomic background.2-10 It is, unfortunately, a far too common outcome of participation in war, affecting 15.2% of Vietnam theater veterans 20 years after the war." Its prevalence may be even higher in inner city communities exposed to compound community trauma. In one small northeastern city, it was found to affect 67% of adolescents frequenting a community medical clinic for routine preventive health care.lz Reducing exposure to trauma would obviously be the most effective and immediate means of controlling the induction of PTSD and should be given the highest social priority. Beyond such efforts, understanding the means by which the extreme stress of trauma is neurobiologically transduced to produce PTSD may help in its prevention and treatment. Clinical studies have yielded, thus far, important empiric findings on ways in which the neurobiology of persons with PTSD differs from that of normal controls and from that of individuals with other psychiatric disorders. The most robust findings include apparent increased baseline activation of the noradrenergic system13 and exaggerated noradrenergic responses to pharmacologic perturbation of that system,I4 decreased 24-hour urine cortisol l e v e l~, l~'~ opiate antagonist-sensitive increases in stress-induced analgesia?' apparent enhanced negative feedback in the hypothalamic-pituitary-adrenal axis increased circulating thyroid hormone levels,22 increased cerebrospinal fluid corticotropin-releasing factor:3 and diminished hippocampal volume as measured by magnetic resonance imaging.w26These findings are invaluable in guiding further scientific studies. For example, it would be useful to know if these neurobiologic characteristics are sequelae of threshold trauma in all individuals or only in those individuals predisposed in some way to the development of PTSD. It would also be useful to know if any of these characteristics could be premorbid and thereby predispose to PTSD symptom formation on exposure to trauma. It is also not clear whether or how these findings relate to specific symptoms of PTSD. Also, are they early manifestations of PTSD or do they develop over time? Indeed, if these neurobiological stigmata of PTSD can be 'Address for correspondence: Ann M. Rasmusson, M.D., Psychiatry Service/l16A, Connecticut VA Healthcare System, West Haven Campus,

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Neurotransmitter Assessment in Neuropsychiatric Disorders of Childhood

Cited by 5 publications

References 164 publications

Posttraumatic stress disorder: An integrated overview of the neurobiological rationale for pharmacology.

Posttraumatic stress disorder: An integrated overview of the neurobiological rationale for pharmacology.

Biosocial Bases of Violence

Animal Models of Relevance to PTSD

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