Cerebrospinal Fluid Amine Metabolites

Redmond, D. Eugene

doi:10.1001/archpsyc.1986.01800100028005

Cited by 73 publications

(9 citation statements)

References 63 publications

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“…A study that included a mix of MDD and bipolar depressed patients noted an association between elevated CSF levels of 3-methoxy-4-hydroxyphenylglycol (MHPG), a norepinephrine metabolite, and agitation and anxiety in depressed patients (242). Additionally, studies reported diminished immunoreactivity of locus coeruleus processes and decreased CSF MHPG in suicidal bipolar subjects compared with controls (243, 244).…”

Section: Alterations In Gaba Glutamate and Monoamine Transmissionmentioning

confidence: 99%

Integrated Neurobiology of Bipolar Disorder

2014

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From a neurobiological perspective there is no such thing as bipolar disorder. Rather, it is almost certainly the case that many somewhat similar, but subtly different, pathological conditions produce a disease state that we currently diagnose as bipolarity. This heterogeneity – reflected in the lack of synergy between our current diagnostic schema and our rapidly advancing scientific understanding of the condition – limits attempts to articulate an integrated perspective on bipolar disorder. However, despite these challenges, scientific findings in recent years are beginning to offer a provisional “unified field theory” of the disease. This theory sees bipolar disorder as a suite of related neurodevelopmental conditions with interconnected functional abnormalities that often appear early in life and worsen over time. In addition to accelerated loss of volume in brain areas known to be essential for mood regulation and cognitive function, consistent findings have emerged at a cellular level, providing evidence that bipolar disorder is reliably associated with dysregulation of glial–neuronal interactions. Among these glial elements are microglia – the brain’s primary immune elements, which appear to be overactive in the context of bipolarity. Multiple studies now indicate that inflammation is also increased in the periphery of the body in both the depressive and manic phases of the illness, with at least some return to normality in the euthymic state. These findings are consistent with changes in the hypothalamic–pituitary–adrenal axis, which are known to drive inflammatory activation. In summary, the very fact that no single gene, pathway, or brain abnormality is likely to ever account for the condition is itself an extremely important first step in better articulating an integrated perspective on both its ontological status and pathogenesis. Whether this perspective will translate into the discovery of innumerable more homogeneous forms of bipolarity is one of the great questions facing the field and one that is likely to have profound treatment implications, given that fact that such a discovery would greatly increase our ability to individualize – and by extension, enhance – treatment.

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Section: Alterations In Gaba Glutamate and Monoamine Transmissionmentioning

confidence: 99%

Integrated Neurobiology of Bipolar Disorder

2014

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“…See Table 1 for a summary (Malone and Mann 1993;Owens and Nemeroff 1994;Stoff and Mann 1997;Mann 1998). In major depression there are fewer platelet serotonin transporters (5-HTT), lower CSF 5-HIAA (Mendels et al 1972;Sjöström and Roos 1972;Ashcroft et al 1973aAshcroft et al , 1973bPost and Goodwin 1974;Bowers 1974;Goodwin and Post 1977;van Praag and de Haan 1979;Koslow et al 1983;Åsberg et al 1984;Gerner et al 1984;Roy et al 1985;Redmond et al 1986), as well as a reduced growth hormone (GH) response to 5-hydroxytryptophan (5-HTP) (Upadhyaya et al 1991) and a blunted prolactin (PRL) response to oral fenfluramine (Siever et al 1984;Coccaro et al 1989;O'Keane and Dinan 1991;Mann et al 1992) and to intravenous L-tryptophan (Heninger et al 1984;Cowen et al 1990;Price et al 1991;Upadhyaya et al 1991). The antidepressant efficacy of selective serotonin reuptake inhibitors (SSRIs) suggests the abnormality in depression probably includes impaired serotonergic function, because selective enhancement of serotonergic activity is therapeutic (Åsberg et al 1986a).…”

mentioning

confidence: 99%

The Neurobiology and Genetics of Suicide and Attempted Suicide: A Focus on the Serotonergic System

Mann

2001

Neuropsychopharmacology

356

208

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Neuro-receptors Major depression and suicidal behavior are independently related to altered serotonergic function (Mann and Stanley 1986). See Table 1 for a summary (Malone and Mann 1993;Owens and Nemeroff 1994;Stoff and Mann 1997;Mann 1998). In major depression there are fewer platelet serotonin transporters (5-HTT), lower CSF 5-HIAA (Mendels et al. 1972;Sjöström and Roos 1972; Ashcroft et al. 1973a Ashcroft et al. , 1973bPost and Goodwin 1974; Bowers 1974; Goodwin and Post 1977;van Praag and de Haan 1979;Koslow et al. 1983; Åsberg et al. 1984; Gerner et al. 1984;Roy et al. 1985;Redmond et al. 1986), as well as a reduced growth hormone (GH) response to 5-hydroxytryptophan (5-HTP) (Upadhyaya et al. 1991) and a blunted prolactin (PRL) response to oral fenfluramine (Siever et al. 1984; Coccaro et al. 1989;O'Keane and Dinan 1991;Mann et al. 1992) and to intravenous L-tryptophan (Heninger et al. 1984; Cowen et al. 1990;Price et al. 1991;Upadhyaya et al. 1991). The antidepressant efficacy of selective serotonin reuptake inhibitors (SSRIs) suggests the abnormality in depression probably includes impaired serotonergic function, because selective enhancement of serotonergic activity is therapeutic (Åsberg et al. 1986a). Depletion of serotonin by parachlorophenylalanine (PCPA) (Shopsin et al. 1976) or by reduction of brain tryptophan (Delgado et al. 1990), quickly reverses the antidepressant effect of serotonergic medication in patients (Åsberg et al. 1986a), suggesting that sustained enhancement of serotonergic function is a necessary requirement to sustain this SSRI-mediated antidepressant effect. It seems that the abnormality in serotonergic function may be a biochemical trait, because a blunted prolactin response to fenfluramine and a vulnerability to depression in response to tryptophan depletion are present during the 24 , NO . 5 period of remission between episodes (Flory et al. 1998). An intermorbid biological abnormality or trait implies a genetic or developmental origin, although enduring illness or treatment effects cannot be ruled out.Lower serotonergic activity is also independently associated with suicidal behavior. We have hypothesized that there is a serotonergic abnormality contributing to the diathesis or vulnerability for suicidal acts (Mann 1998). Lower levels of CSF 5-HIAA (Åsberg et al. 1986b) and a blunted prolactin response to fenfluramine (Mann et al. 1992) correlate with the presence and lethality of past suicide attempts in patients with major depression and can predict future suicide or suicide attempts (Roy et al. 1989;Träskman-Bendz et al. 1992;Nordström et al. 1994). The association between suicide attempts and low CSF 5-HIAA has also been reported in schizophrenia and personality disorders, indicating that this association is independent of diagnosis. Lower brainstem serotonin (5-HT) and/or 5-hydroxyindoleacetic acid (5-HIAA) levels, and alterations in binding kinetics of a number of serotonin receptor subtypes are reported postmortem in the brain of suicide victims compared...

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“…Myriad abnormalities in serotonin production and function have been described, including decreased serotonin platelet transporters, decreased cerebrospinal fluid serotonin precursors, and abnormal serotonergic responses to growth hormone and other ligands (Mendels et al, 1972;Redmond et al, 1986;Mann et al, 1992). Lower serotonergic activity has also been shown to be independently associated with suicidal behaviour.…”

Section: Understanding Suicidementioning

confidence: 99%

Interventions for postconcussion syndrome

Allen

2007

Trauma

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The World Health Organization estimates that in the year 2000, approximately one million people died from suicide worldwide. Over the last 45 years, suicide rates have increased by 60%, with a particularly precipitous rise among young people. The underlying psychology of suicide is complex and individual. However, certain themes emerge from studying individuals who have attempted or completed suicides. This paper will provide an overview of suicide and suicidal behaviour as it relates to trauma practitioners, detailing risk factors, biologic and genetic interactions, and opportunities for prevention and treatment.

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Cerebrospinal Fluid Amine Metabolites

Cited by 73 publications

References 63 publications

Integrated Neurobiology of Bipolar Disorder

Integrated Neurobiology of Bipolar Disorder

The Neurobiology and Genetics of Suicide and Attempted Suicide: A Focus on the Serotonergic System

Interventions for postconcussion syndrome

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