Okay, so few people need help damaging their brains. Unless you're doomed to spend the rest of your life working as a clerk at a convenience store, all that excess capacity might be useful at some point. But then again, the average human brain has 100 billion neurons, and when you die, any left living will die with you. Why let so many perfectly good brain cells go to waste? Here are some ideas of what to do with them. If you've got any additions, or if I've screwed up somewhere, /msg me and I'll add them to the list.

I am not a doctor; I'm a high school student who has, as of now, taken only one neuroscience course. If you need medical advice, please do not rely on this list. Special thanks to paraclete for his help in ensuring that I haven't made any grave errors.

Violence

  • Concussion - Imagine a bouncy ball in a very small jar of syrup. Under normal conditions, the ball will never hit the edge of the jar, but if you give the jar a good shake, it very well might. The brain floats in a pool of blood and cerebrospinal fluid. When this fluid cannot cushion an impact, the brain bounces against the skull, resulting in a concussion, and producing neuronal death.
  • Contusion - A cerebral contusion is a bruise within the brain. In a coup-contrecoup injury, contusions occur on both sides of the brain. The injury on one side occurs from the blow itself, while the injury on the opposite side occurs as the brain bounces against the opposite side of the skull.
  • Diffuse axonal injury - When the brain is rotated or shaken extremely quickly, shearing forces can cause axons, the parts of brain cells that send messages to other brain cells, to tear, resulting in cell death.
  • Increased intracranial pressure - An increase in pressure on the brain results in tissue damage. The most common cause of increased intracranial pressure is subdural hematoma, in which ruptured blood vessels leak blood into the subdural space between the dura matter and archanoid membrane.
  • Penetration injury - Recently, a man went to his doctor complaining of persistent toothache. As it turned out, he had been unknowingly shot with a nail gun, and a nail had forced itself into his brain. When an object, such as skin, bone, or a bullet, penetrates the brain, a penetration injury results. As the celebrated case of Phineas Gage shows, severe penetration injuries can occur without producing death.
  • Second injury syndrome - If the brain is injured before a previous injury has healed, the brain may swell, resulting in permanent damage and death. Fun.
See http://www.biausa.org/Pages/types_of_brain_injury.html or Wikipedia for more information on these types of injury.

Drugs

  • Absinthe - besides exceedingly high amounts of ethanol, absinthe also contains thujone, a GABA receptor antagonist. Effectively, thujone is the opposite of benzodiazepine anticonvulsant/tranquilizers (such as Xanax and Valium). Unsurprisingly, in high doses, thujone has been proven to cause seizure and death. Fortunately (or unfortunately, if you're looking to damage your brain cells), the European Union places restrictions on thujone content in absinthe, ensuring the drink's psychoactive and neurotoxic qualities arise from the high alcohol content, and not the thujone.
  • Alcohol - while the greatest ethanol-induced brain damage results from vitamin deficiencies (see Wernicke-Korsakoff Syndrome below), alcohol itself can also result in structural changes within the brain. Since ethanol has a variety of pharmacological effects, it's difficult to tell exactly how the damage arises, but MRI evidence shows decreased brain volume in alcoholic patients.
  • Dissociatives (DXM, MK-801, PCP, Ketamine) - A study by J.W. Olney showed that in rat models, administration of normal doses NMDA receptor antagonist drugs resulted in over-excitation and death of neurons as a result of malfunction of intracellular organelles (specifically, the mitochondria and endoplasmic reticulum). Since then, additional studies have shown many kinds of cognitive deficits in chronic ketamine users.
  • MDMA (Ecstasy) - MDMA has been proven to produce damage to serotonin neurons in rats and mice due to oxidative stress and free radical damage. Some have claimed that fMRI evidence demonstrates similar damage in humans, although many have disputed these studies. There have also been several studies showing memory deficits in those who abuse MDMA. Administration of a SSRI such as fluoxetine (Prozac) within 4-6 hours of MDMA use may reduce the risk of damage. The media has hyped MDMA's relationship to dehydration, which can also produce brain damage (see below).
  • Methamphetamine (speed, meth, ice, way too many Vicks Vapor Inhalers, etc.) - like MDMA, methamphetamine appears to produce oxidative stress, but damages dopamine rather than serotonin neurons. As a result, chronic methamphetamine abusers often show early-onset symptoms of Parkinson's disease and other cognitive deficits. Recent research has shown that prior administration of a free radical scavenger such as N-acetylcysteine can attenuate damage. Like any other stimulant, methamphetamine can also produce stroke (see below).
  • MPTP - MPTP results from improper synthesis of MPPP, a synthetic opioid. A single dose can result in severe damage to dopamine neurons, producing symptoms resembling those of Parkinson's disease. MPTP is often used to produce animal models of the disease to test new treatments.
Notably absent from this list are marijuana and the 5-HT2A agonist psychedelics (LSD, psilocybin mushrooms, mescaline, etc.). That doesn't mean that these drugs are safe, just that according to the research I was able to find, they are not neurotoxic in and of themselves. On the other hand, there is well-established evidence that these drugs can damage the brain in other ways. Psychedelics can produce HPPD or PTSD, and early-onset marijuana use increases the probability an individual will develop schizophrenia. See PubMed, Erowid, or Wikipedia for more on the effects of drugs.

Other

  • Dehydration - without sufficient levels of water, the ion concentration gradient within the brain is disrupted, resulting in permanent damage to the brain. See also water toxicity below.
  • Disrupted sleep schedule - a recent study demonstrated that flight attendants who frequently traveled between time zones showed significantly decreased right temporal lobe volume, along with spatial cognitive deficits. Researchers proposed chronically increased levels of the stress hormone cortisol, which usually follows a circadian rhythm, as the cause of the damage. Sleep deprivation also results in elevated cortisol levels, suggesting that chronic sleep deprivation may result in the same damage. Luckily, parts of the temporal lobe can regenerate, so this damage may not be permanent.
  • Stroke - a cerebrovascular accident, or stroke, results from temporary interruption of blood flow to the brain, as a consequence of ischemia (blockage of blood vessels) or hemorrhage (rupture of blood vessels). Usually, damage is localized to one side of the brain. The extent of the damage ranges from barely noticeable lesions in specific structures to widespread cell death.
  • Water toxicity - water toxicity arises from rapid consumption of a large amount of water, unaccompanied by a sufficient quantity of sodium, resulting in swelling of the brain. An individual on a low sodium diet may die from the damage caused by water toxicity if he or she consumes as little as 1.8 litres of water in one sitting. For an individual on a normal diet, as few as 3 litres may be fatal.
  • Wernicke-Korsakoff syndrome - chronic deficiency of thiamin (Vitamin B1) results in this debilitating disease. First, Wernicke's encephalopathy results in damage to nerves in the central and peripheral nervous systems; then, Korsakoff's psychosis results in permanent retrograde or anterograde amnesia. It is most often found in alcoholics, since chronic consumption of large quantities of alcohol interferes with thiamin metabolism.
See WebMD or Wikipedia for more on these sources of neurotoxicity.

Log in or registerto write something here or to contact authors.