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Suicidal thoughts, also known as suicidal ideation are thoughts about how to kill oneself, which can range from a detailed plan to a fleeting consideration and does not include the final act of killing oneself. The majority of people who experience suicidal ideation do not carry it through. Some may, however, make suicide attempts. Some suicidal ideations can be deliberately planned to fail or be discovered, while others might be carefully planned to succeed.
What Are the Signs and Symptoms of Suicidal Thoughts?
A symptom is something the patient senses and describes, while a sign is something other people, such as the doctor notice. For example, drowsiness may be a symptom while dilated pupils may be a sign.
� Appearing to feel trapped or hopeless
� Appearing to have an abnormal preoccupation with violence, dying and/or death
� Being in a heightened state of anxiety
� Being very moody
� Changing personality
� Changing routine
� Changing sleeping patterns
� Consuming (more) drugs
� Consuming more alcohol
� Engaging in risky behavior, such as driving carelessly or taking drugs
� Getting affairs in order
� Getting hold of a gun, medications, or substances that could end a life
� Giving stuff away
� Having depression
� Having panic attacks
� Impaired concentration
� Increased self-criticism
� Isolating oneself
� Psychomotor agitation - such as pacing around a room, wringing one's hands, taking off clothing and putting it back on, and other such actions
� Saying goodbye to others as if it were the last time
� Seeming to be unable to experience pleasurable emotions from normally pleasurable life events such as eating, exercise, social interaction or sex
� Seeming to have severe remorse
� Talking about killing oneself, expressing regret about being alive or ever having been born.
A direct relationship between alcoholism, suicidal behavior and specific changes in cerebral areas is not easily traceable. Recent studies of brain functioning in alcohol-dependent adults have produced varied results. However, it is well known that alcoholism is associated with dysfunctions in multiple neurotransmitter systems, and alcoholics are at significantly higher risk for suicide than individuals in the general population.
The main neurotransmitter systems involved in the action of alcohol are the GABAergic, the serotonergic and the glutamatergic systems but, secondarily, other bioaminergic transmissions may be involved, such as the dopaminergic and the noradrenergic systems [120,121]. The effects of ethanol, either acute or chronic, are due to the interplay of these neurotransmitters. These neurochemical actions need to be carried-out in specific brain nuclei for the multiple and fleeting alcohol-induced symptoms to occur. Combined brain imaging and neurochemical techniques may aid in assessing which molecules, which brain areas and which brain activities are affected. To see whether suicidal ideation, suicide attempts or having completed suicide might be associated with the same mechanism, the combined imaging-neurochemical techniques or post-mortem investigations should focus on the same target. At the neurochemical level, alcohol increases the activity of GABA, the brain’s principal inhibitory neurotransmitter , and other central brain mechanisms related to behavioral activation such as increased serotonin . The well-known action of ethanol on GABAergic transmission is brought forth through various mechanisms and is region-specific [124,125], dose-related , and linked to both alcohol-induced behavioral inhibition and reward . The activation of corticotropin-releasing factor type 1 (CRF1) receptors in the central amygdala appear to be crucial for the potentiation of GABAergic activity . In this site, ethanol promotes the expression of new functional opioid receptors on both glutamatergic and GABAergic synapses which mediate ethanol-induced conditioned place preference  and inhibits acutely, but enhances chronically, non-NMDA pre- and post-synaptic glutamatergic activity possibly related to reward . Another nucleus which is important in reward is the nucleus accumbens, which is rich in dopaminergic nerve endings and appears to constitute a final common target of most recreational drugs. In this nucleus, ethanol inhibits the presynaptic release of glutamate through opioid mechanisms and reduces post-synaptic glutamatergic transmission through inhibition of both NMDA-mediated and kainate-mediated currents .
Generally, it is believed that the sedative effects of ethanol are mediated by its combined action of both GABA transmission enhancement and glutamate transmission attenuation . However, this is not always the rule. In the nucleus accumbens, core, metabotropic mechanisms enhance ethanol-mediated GABA activation , indicating complex interactions at that level. The nucleus accumbens is the terminal area where ethanol may interact with dopaminergic activity and reward, but an action on the origin of these neurones in the ventral tegmental area has also been described. This is mediated through the enhancement of local GABAergic transmission . GABAergic enhancement is brought about by ethanol by stimulating sensitive neurones which bear GABA receptors with a alpha4/6/beta3delta channel structure, which are sensitive to the benzodiazepine analog Ro15-4513 .
Ethanol-induced NMDA inhibition in the cerebral cortex results in the reduction of noradrenaline and acetylcholine , and this might be related to the development of depression. This has been proposed as an explanation of the association between alcohol and depression, but may be also relevant to suicide. Glutamate in the cerebellum increases the levels of BDNF via NMDA, and this in turn reduces apoptosis. Ethanol decreases the effect of glutamate on BDNF  and may thus indirectly be related to the increased apoptosis and movement disorder found in chronic alcoholism. Interestingly, suicidal behavior has been found in a man with cerebellar agenesis . Reduced serotonin function has been identified in suicides and possibly in serious suicide attempters (see  for a review) and alcohol dependent patients . Serotonin depletion was also found in individuals displaying aggressive and impulsive behavior  and was a predictor of both early-onset al.cohol use disorders  and suicide attempts among alcoholics [142,143]. Koob and LeMoal  suggested that the changes in hedonic tone that accompany substance use are central aspects of the addictive process, and the maintenance of substance use in the dependent person is driven by attempts to regulate the affective disturbance that results from substance use. Ethanol has been shown to potentiate acutely 5-HT3 receptor function and to modulate chronically 5-HT3-augmented mesolimbic dopaminergic function, but also to regulate alcohol drinking and its reinforcing properties at the ventral tegmental area level [145,146]. However, 5-HT3 receptors were not found to be altered postmortem in suicides . An association between suicide attempts, impulsiveness, alcohol dependence and serotonin neurotransmission deficiency has been proposed [148–151], but the possibility that impulsive suicide attempts may reflect mood disturbance-related low serotonin activity in alcohol-dependent individuals is currently only speculative.
Neurobiological, including serotonergic mechanisms may play a role in the higher suicidality of depressed individuals with comorbid alcohol dependence compared to depressed subjects without comorbid alcohol dependence [152–155]. A study of prolactin responses to fenfluramine administration in patients with comorbid major depression and alcohol dependence, patients with major depression only and healthy controls found that controlling for gender, prolactin responses were lower in the comorbid group compared to the major depression only group or the health control group . Controlling for gender and aggression, prolactin responses in the comorbid group remained significantly lower compared to the control group but the difference between the two patient groups disappeared which indicates that the difference in prolactin responses between the patient groups could be attributed to higher aggression scores in the comorbid group compared to the major depression only group. Another study found an anterior medial prefrontal cortical area where subjects with comorbid major depression and alcohol dependence had more severe hypofrontality than patients with major depression only . This area encompassed the left medial frontal and left and right anterior cingulate gyri. This group difference disappeared after fenfluramine administration which suggests that serotonergic mechanisms play a role in the observed differences between the groups. Reduced serotonin input in the prefrontal cortex may underlie decreased behavioral inhibition in individuals with alcoholism and a greater probability of acting on suicidal feelings. A comparison of high- and low-lethality drug-free depressed suicide attempters with comorbid alcoholism showed that CSF 5-HIAA levels were lower in high-lethality attempters compared to low-lethality attempters which suggests that higher lethality of suicidal behavior in depressed patients with alcoholism is related to lower serotonergic activity . Higher suicidality in depressed patients with alcohol dependence compared to depressed persons without comorbid alcohol dependence may also be related to the differences in dopaminergic regulation between the two groups. It has been observed that depressed subjects with a history of alcohol dependence had lower CSF HVA levels, compared with depressed subjects without a history of alcoholism .
Underwood et al. , using quantitative autoradiographic experiments in human postmortem brain tissue, found that binding to 5-HT1A receptors is lower in both alcoholic suicides and nonsuicides; so they suggested that this effect might be related to alcoholism and not to suicide. In nonalcoholic suicides, there is a localized increase in 5-HT1A binding in ventral prefrontal cortex, hypothesized to be a response to less serotonin input which had been hypothesized to be related to increased impulsivity and emotional dysregulation . Recently, Oscar-Berman et al.  reported that alcoholics exhibit behaviors associated with prefrontal brain dysfunction in a study of 345 subjects in whom alcoholism and specific drinking variables (amount and duration of heavy drinking) significantly predicted frontal system and affective abnormalities.
Alcoholic suicides may fail to up-regulate ventral prefrontal 5-HT1A receptors in response to decreased serotonergic transmission increasing the risk of suicidal behavior. Binding to the serotonin transporter is low only in alcoholic suicides, suggesting an association with suicide. Evidence of impaired serotonergic innervation associated with alcoholism is also confirmed by less 5-HT1D terminal autoreceptor binding in alcoholics.
Furthermore, Storvick et al.  reported a decrease of the serotonin transporter density in the perigenual anterior cingulate cortex in the Cloninger type 1 alcoholics (prone to anxiety) using postmortem whole-hemisphere autoradiography. They also found that the 5-HT(1A) density was significantly decreased in the upper level of the perigenual anterior cingulate cortex.
Regarding the noradrenergic system, alcoholics had less alpha2 and beta1 adrenergic binding but more alpha1 adrenergic binding in the ventrolateral and orbital cortex . Tapert et al.  found that alcohol-dependent women showed less differential response to working memory than controls in frontal and parietal regions, especially in the right hemisphere.
Regarding other receptors involved in the action of ethanol, genetic polymorphisms have been found in suicidal persons for both the CRF1  and CRF2 receptors , but the latter is not apparently involved in the action of ethanol . However, mRNA for CRF1, but not CRF2 receptors, were found to be reduced in the frontal cortex of suicides, along with mRNA for the alpha1, alpha3, alpha4, and delta receptor subunits of the GABAA-benzodiazepine receptor cortex . It has to be mentioned, however, that CRF receptor numbers and affinity have been reported to be either reduced  or unchanged by different groups of investigators .
Altered glutamatergic receptors in the brains of people who died from suicide comprise reduced NMDA receptors  and increased caudate metabotropic receptors . These findings are interesting in pointing to alcohol-suicide commonalities in neurochemical alterations but, unfortunately, these post-mortem findings in the brains of suicides are only partially matched by alterations found in brains of non-suicidal people with chronic alcoholism. Notably, GABAA receptors were reduced [172–174], but the subunit compositions only partly overlap with those found in suicides.
Regarding functional or structural neuroimaging studies, there is no overlap, with structural imaging in alcohol-abusing or -dependent people focusing on gross alterations such as ventricular enlargement and cortical thickness and research on suicidality consisting mainly of the detection of subtle abnormalities, such as white matter volume and hyperintensities [175,176]. Taken together, these results remain highly suggestive, but not conclusive, for a neurobiological link between alcohol misuse and suicidal behavior.
A state of intoxication may trigger self-inflicted injuries, not only by increasing impulsivity, but also by promoting depressive thoughts and feelings of hopelessness, while simultaneously removing inhibiting barriers to hurting oneself . Indirect mechanisms, including alcohol consumption as a form of self-medication for depression, or alcohol use as a marker for other high-risk behaviors, may also be relevant. Although we are far from understanding the relationships between alcohol use and suicidal behavior, a number of possible direct mechanisms for the association have been proposed.
Additionally, cognitive constriction (narrowed attention which reduces perceived potential solutions to a dichotomy—finding an immediate solution or committing suicide) is frequently observed prior to a suicide attempt . Alcohol produces cognitive constriction through alcohol myopia , and this process has been confirmed by research showing that inhibition conflict (weighing pros and cons and identifying alternative solutions) mediates the relation between intoxication and social behavior .
Once a decision has been made to attempt suicide, alcohol use may serve several functions. Alcohol expectancies play an important role in determining alcohol use and behavior  and, consequently, it is reasonable to hypothesize that suicide-related alcohol expectancies relevant to gaining courage, numbing fears or anesthetizing the pain of dying may lead to the incorporation of alcohol use into a suicide plan. Alcohol may also serve as a “means to an end” as the suicide method itself [182–184].
There is a vulnerability to the neurotoxic effects of alcohol, and adolescent substance use has adverse consequences on brain development and executive functioning . Some mood disorders may be alcohol induced (and remit after a period of abstinence) , and alcohol withdrawal is often associated with affective disturbance .
Sociological interpretations include the hypothesis that acute alcohol use leads to increased social deterioration and anomie , unemployment, debts, and social isolation [188–190]. Biological interpretations of the association include impaired physical and mental functioning  and interactions with other psychotropic drugs . Disinhibition, in which alcohol acts to remove psychological and even physiological barriers to self-harm, has also been proposed as a relevant factor .
Hufford  summarized four psychological pathways for the proposed relationship between acute alcohol use and suicidal behaviour: (1) increasing psychological distress, including hopelessness, loneliness and depression; (2) enhancing or facilitating aggressive behaviour, including self-aggression; (3) changing an individual’s expectations and helping to propel suicidal ideation into action; and (4) constricting attention and inhibiting effective coping strategies that would facilitate avoiding suicidal behaviour. Rossow  has also reviewed a number of possible mechanisms in individual and aggregate level studies. However, these mechanisms are presented as post hocinterpretations of findings rather than as hypotheses tested in carefully designed studies, and so the evidence supporting these proposed pathways is limited.