Currently, the pathophysiological mechanisms which produce<unk>  are not completely known. The most common research strategy to clarify these mechanisms is the examination of the impaired functional capabilities of people with<unk>  <unk>  after a<unk>  brain injury. Neurological mechanisms Hippocampus (animation) Research on the effect of emotional trauma on memory retention and amnesic symptoms has shown that exposure to prolonged levels of extreme stress has a direct effect on the hippocampus. Elevated stress levels can lead to an increase in the production of enkephalins and corticosteroids, which can produce abnormal neural activity and disrupt long-term potentiation (a neural mechanism associated with learning) in the hippocampus. Individuals who have been subjected to repeated sexual abuse during childhood or who have experienced combat show significant impairment and atrophy of the hippocampal region of the brain. The amygdala, an area of the brain involved in emotional regulation, may be involved in producing remembrance for some aspects of the trauma. Even though the trace of a memory for trauma may be lost from the hippocampus, it may remain partially encoded in the form of an emotional memory in the amygdala where it can be subsequently recalled in the form of a flashback or partially recovered memory. Diaschisis Diaschisis refers to the sudden dysfunction of portions of the brain due to lesions in distant but connected neurons. Diaschisis is implicated as playing an important role in<unk> , more particularly in the declarative memory impairments observed in patients experiencing an episode of<unk> . The loss of function observed after<unk>  brain injuries, as well as the resulting loss of consciousness, was thought to be mediated by the 'neural shock' associated with diaschisis. Diaschisis was originally believed to be a result of disruption to neural tissue, but more recent evidence implicates increased activity levels of choline acetyltransferase, the enzyme responsible for the production of acetylcholine, as a major cause. Based on these findings, diaschisis could be helped through the use of drugs that would reduce cholinergic (acetylcholine) activity, and reduce the levels of acetylcholine in the brain. This idea is supported by the fact that there is an increase in acetylcholine concentrations in the brain after head injury. Animal studies have shown that concussive injuries in rats lead to changes in the central nervous system's cholinergic system. This increase in acetylcholine levels has also been tied to behavioral suppression and unconsciousness, both symptoms of<unk> . In long-term recovery, acetylcholine levels associated with diaschisis may continue to play a role in maintaining memory deficits. Brain-imaging studies Brain imaging techniques are useful for examining the changes in the brain that occur as a result of damage. Metting et al. (2001) used CT scans to examine the pathophyiological damage in patients currently experiencing an episode of<unk> , patients with resolved<unk> , and a control group that had not experienced<unk> . Bloodflow to the occipital lobe, the caudate nucleus, and the grey matter of the frontal lobe was significantly reduced in patients who were scanned during the episode of<unk> . No differences were seen between patients with resolved<unk>  and the control group. This encouraging finding points to the positive long term prognosis of<unk> ; most patients return to normal levels of functioning. The frontal lobes are associated with explicit memory retrieval, and deficits on explicit memory tasks are often found with patients experiencing<unk> . Working memory deficits are a common symptom in patients with<unk> . The duration of an episode of<unk>  was correlated with reduced bloodflow to the right hemisphere, a finding which was consistent with functional MRI studies that link working memory with right frontal activity. The prefrontal cortex, which plays an important role in explicit memory retrieval, was also found to have decreased neural activation in patients scanned during the episode of<unk> . Researchers noted that the damage was related to vascularization and neural functionality, but not to structural injury, suggesting that the resolution of<unk>  is dependent on functional changes. Memory and new learning involve the cerebral cortex, the subcortical projections, the hippocampus, the diencephalon and the thalamus, areas that often suffer damage as a result of TBI. Frontal lobe lesions may also play a role in<unk> , as damage to these areas is associated with changes in behavior, including irritability, aggressiveness, disinhibition, and a loss of judgment. Damage to this area may account for the uncharacteristic behavior often exhibited in<unk>  patients. Accelerated forgetting Researchers have also found that individuals experiencing<unk>  show accelerated forgetting. This contrasts with the normal forgetting observed by patients with normal amnesia related to brain damage. The temporal lobes are often the most vulnerable to the diffuse (widely distributed) and focal (more specifically localized) effects of TBI and it is possible that temporal lobe lesions may account for the accelerated forgetting observed in patients with<unk> . These predictions were supported by the finding that most of the patients who showed rapid forgetting also had lesions to the temporal lobe. Bilateral damage to the temporal lobes also causes severe anterograde amnesia, making it likely that lesions to this area would be involved in<unk> . Patients exhibit a temporal gradient with memory loss, meaning that older memories are preserved at the expense of newer memories. Temporal lobe damage has been linked to a temporal gradient of this sort, because older memories are less dependent on the hippocampus and thus are less influenced by its damage. There is a significant link between individuals currently suffering from<unk>  and their performance on the Wechsler Adult Intelligence Scale (WAIS). The scores of those currently experiencing an episode of<unk>  were compared to individuals who had previously suffered a<unk>  brain injury resulting in<unk> . Those still suffering from<unk>  performed significantly worse on both the performance and the verbal subscales of the WAIS. Also, people in early stages of<unk>  have substantial impairment to anterograde memory function. For example, in the case report of a patient referred to as "JL", Demery et al. noted that his memory impairments were so severe following his injury that he had forgotten that he had attended a Major League Baseball game less than 30 minutes after returning to the center where he was being treated. The majority of neuropsychological studies available have suggested that the medial temporal lobes are the most important system in the pathophysiology of<unk> . However, there is little research done on this topic, and as new research is done, more information should come forth concerning functionality in these areas in<unk>  patients. One MRI study showed that a long duration of<unk>  was correlated with damage in the hemispheric and central areas, regardless of whether the duration of the coma was relatively short. In patients who had a longer coma duration, deeper lesions in the central area were observed without extensive damage to the hemispheric area.
Post-traumatic amnesia
Excited delirium
Drug-induced amnesia
Childhood amnesia
Transient global amnesia
Memory distrust syndrome
Psychogenic amnesia
Emergence delirium