This disorder is usually acquired in one of four ways: One cause is benzodiazepine drugs such as midazolam, flunitrazepam, lorazepam, temazepam, nitrazepam, triazolam, clonazepam, alprazolam, diazepam, and nimetazepam; all of these are known to have powerful<unk>  effects. This has also been recorded in non-benzodiazepine sedatives or "z-drugs" which act on the same set of receptors; such as zolpidem (also known as Ambien), eszopiclone (also known as Lunesta), and zopiclone (also known by brand names Imovane and Zimovane). A second cause is a traumatic brain injury in which damage is usually done to the hippocampus or surrounding cortices. It may also be caused by a PTSD, a shocking event, or an emotional disorder. Illness, though much rarer, can also cause<unk>  if it causes encephalitis, which is the inflammation of brain tissue. There are several types of encephalitis: one such is herpes simplex encephalitis (HSV), which, if left untreated, can lead to neurological deterioration. How HSV gains access to the brain is unknown; the virus shows a distinct predilection for certain parts of the brain. Initially, it is present in the limbic cortices; it may then spread to the adjacent frontal and temporal lobes. Damage to specific areas can result in reduced or eliminated ability to encode new explicit memories, giving rise to<unk> . Patients suffering from<unk>  may have episodic, semantic, or both types of explicit memory impaired for events after the trauma that caused the<unk> . This suggests that memory consolidation for different types of memory takes place in different regions of the brain. Despite this, current knowledge on human memory is still insufficient to "map out" the wiring of a human brain to discover which parts of which lobe are responsible for the various episodic and semantic knowledge within a person's memory.<unk>  is seen in patients who, for the reason of preventing another more serious disorder, have parts of their brains known to be involved in memory circuits removed, the most notable of which is known as the medial temporal lobe (MTL) memory system, described below. Patients with seizures originating in the MTL may have either side or both structures removed (there is one structure per hemisphere). In addition, patients with tumors who undergo surgery will often sustain damage to these structures, as is described in a case below. Damage to any part of this system, including the hippocampus and surrounding cortices, results in<unk>  syndromes. This is why people who suffer from strokes have a chance of developing cognitive deficits that result in<unk> , since strokes can involve the temporal lobe in the temporal cortex, and the temporal cortex houses the hippocampus. Alcohol intoxication<unk>  can also be caused by alcohol intoxication, a phenomenon commonly known as a blackout. Studies show rapid rises in blood alcohol concentration over a short period of time severely impair or in some cases completely block the brain's ability to transfer short-term memories created during the period of intoxication to long-term memory for storage and later retrieval. Such rapid rises are caused by drinking large amounts of alcohol in short periods of time, especially on an empty stomach, as the dilution of alcohol by food slows the absorption of alcohol. Alcohol-related<unk>  is directly related to the rate of consumption of alcohol (and is often associated with binge drinking), and not just the total amount of alcohol consumed in a drinking episode. Test subjects have been found not to experience<unk>  when drinking slowly, despite being heavily intoxicated by the end of the experiment. When alcohol is consumed at a rapid rate, the point at which most healthy people's long-term memory creation starts to fail usually occurs at approximately 0.20% BAC, but can be reached as low as 0.14% BAC for infrequent drinkers. The exact duration of these blackout periods is hard to determine, because most people fall asleep before they end. Upon reaching sobriety, usually after waking, long-term memory creation is completely restored. Chronic alcoholism often leads to a thiamine (vitamin B1) deficiency in the brain, causing Korsakoff's syndrome, a neurological disorder which is generally preceded by an acute neurological condition known as Wernicke's encephalopathy (WE). The memory impairment that is pathognomonic to Korsakoff's syndrome predominantly affects the declarative memory, leaving non-declarative memory that is often procedural in nature relatively intact. The disproportionate severity in<unk>  episodic memory processes in contrast to other cognitive processes is what differentiates Korsakoff syndrome from other conditions such as alcohol-related dementia. Evidence for the preservation of certain memory processes in the presence of severe<unk>  episodic memory serve as experimental paradigm to investigate the components of human memory.
Anterograde amnesia
Retrograde amnesia
Psychogenic amnesia
Semantic amnesia
Transient global amnesia
Childhood amnesia
Transient loss of consciousness
Confusion