How a Suicide Attempt Can Affect the Brain
The factors that induce someone to think about suicide, the ideators, and those who actually attempt suicide, the attempters, often depends upon numerous factors. 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 US, 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.
Following a failed suicide attempt, acute CO poisoning causes serious mental health problems due to the death of neurons in vulnerable brain regions, 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. Most of these neurological changes develop over a period of many days and occur due to extensive oxidative stress and brain inflammation induced by CO poisoning. The brain is particularly vulnerable due to its constant high demand for oxygen, which is denied to it by CO-enriched blood. 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.
Two therapies are often used for these patients. The first is hyperbaric oxygen therapy. The second is a drug that is commonly given to patients with Alzheimer’s disease, 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. One recent study discovered that survivors of CO poisoning also have reduced numbers of receptors for the drug nicotine in their brain. This knowledge about the role of acetylcholine neuronal damage may lead to the development of better therapies for survivors of CO poisoning related to a failed suicide attempt.