5-HIAA in cerebrospinal fluid. A biochemical suicide predictor?
ABSTRACT The incidence of suicidal acts was studied in 68 depressed patients and related to the level of 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid. The distribution of 5-HIAA levels was bimodal. Patients in the low 5-HIAA mode (below 15 ng/ml) attempted suicide significantly more often than those in the high mode, and they used more violent means. Two of the 20 patients in the low mode, and none of the 48 patients in the high mode died from suicide.
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- "Abnormalities in the serotonergic system have been pointed as a key factor in depression and other mental illness (Artigas, 2012). Clinical studies have demonstrated lower 5-HT metabolite concentrations in the CSF fluid of depressed patients which were correlated with suicide risk (Asberg et al., 1976). In agreement, most of the currently available antidepressants cause activation of serotonergic neurotransmission (Elhwuegi, 2004; Millan, 2004). "
ABSTRACT: Atorvastatin is a statin largely used in the treatment of hypercholesterolemia and recently revealed as a neuroprotective agent. The antidepressant-like effect of acute atorvastatin treatment in mice has been previously demonstrated by our laboratory. The purpose of this study was to explore the contribution of the serotonergic system in the antidepressant-like effect of atorvastatin in mice. Data demonstrate that the serotonin (5-HT) depleting agent p-chlorophenylalanine methyl ester (PCPA, 100 mg/kg, i.p.) completely abolished atorvastatin (0.1 mg/kg, p.o.) antidepressant-like effect. Besides atorvastatin, fluoxetine (10 mg/kg, p.o.), a serotonin selective reuptake nhibitor (SSRI) was able to exert an antidepressant-like effect, but any of them changed 5-HT content in hippocampus or frontal cortex. The 5H-T1A (WAY100635, 0.1 mg/kg, s.c) or the 5-HT2A/2C (ketanserin, 5 mg/kg, s.c.) receptor antagonists prevented atorvastatin antidepressant-like effect. In addition, a combinatory antidepressant-like effect was observed when mice received the co-administration of sub-effective doses of atorvastatin (0.01 mg/kg, p.o.) and the SSRI fluoxetine (5 mg/kg, p.o.), paroxetine (0.1 mg/kg, p.o.) or sertraline (1 mg/kg, p.o.). Taken together, these results indicate that the antidepressant-like effect of atorvastatin depends on the serotonergic system modulation.Pharmacology Biochemistry and Behavior 07/2014; DOI:10.1016/j.pbb.2014.04.005 · 2.82 Impact Factor
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- "sidered to be the main pathophysi - ological mechanisms in depressive disorders , i . e . , serotonergic , noradrenergic , and glutamatergic systems . It has been repeatedly demonstrated , in depressive patients , that there are decreased levels of serotonin metabolites in the cerebrospinal fluid , particularly in patients after suicide attempts ( Asberg et al . , 1976 ; Jokinen et al . , 2009 ; Chatzittofis et al . , 2013 ) . Tryptophan depletion ( a method of lowering brain serotonin , used as a model of depressive disorders ) not only worsens depres - sive symptoms ( Fields et al . , 1991 ; Booij et al . , 2005 ; van Steen - bergen et al . , 2012 ) and also can increase the sensation of pain ( Schwa"
ABSTRACT: Neither pain, nor depression exist as independent phenomena per se, they are highly subjective inner states, formed by our brain and built on the bases of our experiences, cognition and emotions. Chronic pain is associated with changes in brain physiology and anatomy. It has been suggested that the neuronal activity underlying subjective perception of chronic pain may be divergent from the activity associated with acute pain. We will discuss the possible common pathophysiological mechanism of chronic pain and depression with respect to the default mode network of the brain, neuroplasticity and the effect of antidepressants on these two pathological conditions. The default mode network of the brain has an important role in the representation of introspective mental activities and therefore can be considered as a nodal point, common for both chronic pain and depression. Neuroplasticity which involves molecular, cellular and synaptic processes modifying connectivity between neurons and neuronal circuits can also be affected by pathological states such as chronic pain or depression. We suppose that pathogenesis of depression and chronic pain shares common negative neuroplastic changes in the central nervous system (CNS). The positive impact of antidepressants would result in a reduction of these pathological cellular/molecular processes and in the amelioration of symptoms, but it may also increase survival times and quality of life of patients with chronic cancer pain.Frontiers in Behavioral Neuroscience 03/2014; 8:99. DOI:10.3389/fnbeh.2014.00099 · 4.16 Impact Factor
- "Fifty-three patients had a history of suicide attempt (mean AE SD, 2.3 AE 1.2 lifetime suicide attempts) and 42 did not. Suicide was defined as a conscious intent of the patient to end his/her own life, however ambivalent, through means that the patient thought could have lead to death (Asberg et al., 1976). Patients with a positive suicide history were then classified as: recent suicide attempters (n = 32), if the suicidal act occurred during the current depressive episode and had triggered their psychiatric hospitalization (neuroendocrine tests were performed 12—35 days after most recent suicide attempt); or past suicide attempters (n = 21), if the most recent suicide attempt had not occurred during the current depressive episode (neuroendocrine tests were performed 4—97 months after most recent suicide attempt). "
Dataset: PNEC Duval 2010