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How a failed suicide affects the brain

The numerous factors that induce someone to think about suicide, the “ideators,” are often different from those who actually attempt suicide, the “attempters.” For example, the traditional risk factors for suicide, such as depression, hopelessness, many psychiatric disorders, and impulsivity, strongly predict suicide ideation but weakly predict suicide attempts among ideators. Alternatively, a diminished fear of pain, injury, and death can increase one’s probability to attempt suicide and facilitate the progression from suicidal thoughts to suicidal acts.

Out of the approximately 120 successful suicides that occur each day in the United States, 70% are committed by white, mostly middle aged, males. Fifty percent of all successful suicides are achieved using firearms, which are chosen, mostly by males, for their extreme efficacy.

In contrast to the certainty of using a firearm, each year thousands of people deliberately inhale carbon monoxide (CO) in order to end their lives, usually via the exhaust fumes from their own cars while sitting at home in their own garage. For example, out of all of the fatal CO poisonings in Utah between 1996 and 2013, 70% were due to suicides. The incidence of successful CO-induced suicide has actually declined due to strict federal CO emissions standards for motor vehicles following the Clean Air Act of 1970 and the widespread presence of catalytic converters. One recent study examined the CO levels in a standard size garage after 20 minutes. The CO level was 253 PPM for a car without a catalytic converter and 30 PPM for the car equipped with one. Emissions controls on automobiles have thus significantly reduced the success rates of CO related suicides. Subsequently, although thousands of people every year attempt suicide by this widely familiar method, a greater percentage of them survive the attempt.

When the blood becomes enriched with CO it is much less capable of transporting adequate amounts of oxygen to the tissues of the body. Neurons in the brain are particularly vulnerable to hypoxia due to their constant high demand for oxygen. The hypoxia kills neurons when their energy demands, primarily for the production of the energy molecule ATP, outpace the ability of the blood to provide sufficient oxygen. When the oxygen supply via the blood falls below a critical level, energy failure occurs. The level of ATP can decline by 90% in less than five minutes! At this point, everything critical for normal neuronal function begins to fail and neurons rapidly begin to die. Interestingly, not all neurons are equally vulnerable to the consequences of the hypoxia. This may explain the consistent appearance of specific cognitive and motor symptoms.

In contrast to the certainty of using a firearm, each year thousands of people deliberately inhale carbon monoxide (CO) in order to end their lives

Following a failed suicide attempt, acute CO poisoning causes serious mental health problems due to the death of neurons in brain regions that are particularly vulnerable to hypoxia, such as the hippocampus, a brain structure that is critical for learning and memory abilities, and the basal ganglia, a brain region that controls normal movement. During the first few days and weeks after the failed attempt, the initial symptoms include headaches, dizziness, fainting with loss of consciousness and, following severe poisoning, seizures. Later, after many weeks, survivors often report significant learning and memory impairments, movement disorders that resemble Parkinson’s disease, depression, psychosis, and even symptoms of dementia. The degree and number of neurological symptoms depends upon the extent and location of the most severe oxygen deprivation inside the brain as well as the ability of some neurons to defend themselves from the consequences of the hypoxia.

Two therapies are often used for these patients. The first is hyperbaric oxygen therapy. This method remains somewhat controversial; some reports suggest that hyperbaric oxygen therapy can enhance recovery, while other reports suggest that hyperbaric oxygen therapy can induce greater brain injury. The second approach to therapy involves administration of a drug that is commonly given to patients with Alzheimer’s disease, donepezil, marketed under the name, Aricept. Aricept is an inhibitor of the enzyme acetylcholinesterase. The benefits provided by this drug suggest that neurons that release the neurotransmitter acetylcholine were likely injured by the CO poisoning. Aricept enhances the function of this neurotransmitter in the hippocampus and frontal lobes. In addition, Aricept may be able to induce the birth of new neurons, called neurogenesis, within the hippocampus and improve cognitive functioning. This knowledge about the role of acetylcholine neuronal damage, and the potential benefits of Aricept, may lead to the development of better therapies for survivors of CO poisoning related to a failed suicide attempt.

Featured image credit: “Nerve Cell” by ColiN00B. CC0 Public Domain via Pixabay.

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