Post-traumatic amnesia
Post-traumatic amnesia is a state of confusion that occurs immediately following a traumatic brain injury in which the injured person is disoriented and unable to remember events that occur after the injury. The person may be unable to state their name, where they are, and what time it is. When continuous memory returns, PTA is considered to have resolved. While PTA lasts, new events cannot be stored in the memory. About a third of patients with mild head injury are reported to have "islands of memory", in which the patient can recall only some events. During PTA, the patient's consciousness is "clouded". Because PTA involves confusion in addition to the memory loss typical of amnesia, the term "post-traumatic confusional state" has been proposed as an alternative.
There are two types of amnesia: retrograde amnesia and anterograde amnesia. PTA may refer to only anterograde forms, or to both retrograde and anterograde forms.
A common example in sports concussion is the quarterback who was able to conduct the complicated mental tasks of leading a football team after a concussion, but has no recollection the next day of the part of the game that took place after the injury. Individuals with retrograde amnesia may partially regain memory later, but memories are not regained with anterograde amnesia because they were not encoded properly.
The term "post-traumatic amnesia" was first used in 1940 in a paper by Symonds to refer to the period between the injury and the return of full, continuous memory, including any time during which the patient was unconscious.
Symptoms
The most prominent symptom of post-traumatic amnesia is a loss of memory of the present time. As a result, patients are often unaware of their condition and may behave as if they are going about their regular lives. This can cause complications if patients are confined to a hospital and may lead to agitation, distress and anxiety. Many patients report feeling as though they were being "held prisoner" and being prevented from carrying on with their daily lives. Other symptoms include agitation, confusion, disorientation, and restlessness.Patients also often display behavioral disturbances. Patients may shout, swear and behave in a disinhibited fashion. There have been cases in which patients who do not recognize anyone will ask for family members or acquaintances that they have not seen in years. Some patients exhibit childlike behavior. Other patients show uncharacteristically quiet, friendly and loving behavior. Although this behavior may seem less threatening because of its lack of aggressiveness, it may be equally worrisome.
PTA patients are often unaware of their surroundings and will ask questions repeatedly. Patients may also have a tendency to wander off, which can be a major concern in those who have sustained additional injuries at the time of trauma, such as injured limbs, as it may lead to the worsening of these secondary injuries.
Attention
is a cognitive resource that contributes to many mental functions. The ability to engage attention requires a certain level of conscious awareness, arousal and concentration, all mechanisms that are generally impaired by traumatic brain injury. The involvement of attention in such a vast array of cognitive processes has led to the suggestion that attentional deficit may act as an underlying factor in the range of cognitive deficits observed in patients experiencing post-traumatic amnesia.Attention has been regarded as an important factor in the healthy functioning of encoding, verbal comprehension and new learning. Automatic attention processes are recovered before simple memory skills in individuals with mild to moderate brain injury. This implies that the recovery of attentional ability precedes the progression of memory recovery after injury, helping to pave the way to regain ability for new learning. In terms of more severe brain injuries, this automatic attention task performance recovers before disorientation completely resolves.
One of the weaknesses of the method most often used in assessing PTA, the Galveston Orientation and Amnesia Test, is that it does not include any assessment of attention, which could help give a better indication of potential for recovery. By omitting attention, the test is omitting some crucial aspects of a person's cognitive capabilities.
In addition, assessing attention during the period of PTA may help determine whether the patient is still in a state of PTA or if they are experiencing a more permanent form of memory deficit. In patients with mild TBI, the damage consists primarily of diffuse axonal injury without any focal damage. Sometimes, injury of the brainstem was also observed. In these cases, there is likely the presence of an attentional deficit without a true amnesiac state. In more severely brain-damaged individuals, the damage to the temporal lobes and the frontal lobes serves as good indication that amnesia will result. Patients with more chronic forms of memory impairment showed poor performance when tested with PTA scales, making differentiation between the two types of memory impairment very difficult. PTA patients exhibit poor simple reaction time, reduced information processing speed and reduced verbal fluency, which are all attentional deficits that could be used to distinguish these patients from those with more severe and permanent memory problems.
Communication skills
The effects of PTA on communication skills were studied using the Revised Edinburgh Functional Communication Profile, which measures both linguistic elements and pragmatic elements. PTA has effects on memory, perception and attention, which are all important for communication. Patients showed mild deficits in verbal communication skills, and moderate to severe deficits in nonverbal communication skills such as maintaining eye contact, initiating greetings, and responding appropriately. Also, a negative correlation was found between the duration of a patient's episode of PTA and his REFCP score; the longer the PTA episode, the more severe the deficit in non-linguistic pragmatic skills. However, the small sample size of this study means that the results must be interpreted with caution, as they may not generalize to larger samples or to the population at large.Pathophysiology
Currently, the pathophysiological mechanisms which produce post-traumatic amnesia are not completely known. The most common research strategy to clarify these mechanisms is the examination of the impaired functional capabilities of people with post-traumatic amnesia after a traumatic brain injury.Neurological mechanisms
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 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
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 PTA, more particularly in the declarative memory impairments observed in patients experiencing an episode of PTA. The loss of function observed after traumatic 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 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 PTA. In long-term recovery, acetylcholine levels associated with diaschisis may continue to play a role in maintaining memory deficits.
Brain-imaging studies
techniques are useful for examining the changes in the brain that occur as a result of damage. Metting et al. used CT scans to examine the pathophyiological damage in patients currently experiencing an episode of PTA, patients with resolved PTA, and a control group that had not experienced PTA. 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 PTA. No differences were seen between patients with resolved PTA and the control group. This encouraging finding points to the positive long term prognosis of PTA; 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 PTA.Working memory deficits are a common symptom in patients with PTA. The duration of an episode of PTA 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 PTA. Researchers noted that the damage was related to vascularization and neural functionality, but not to structural injury, suggesting that the resolution of PTA 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 experience damage as a result of TBI. Frontal lobe lesions may also play a role in PTA, 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 PTA patients.