Article Preview
TopIntroduction
The author has given a fascinating and deeply subjective account of his experiences as he made his journey through “land of Post Traumatic Amnesia”, which began after he regained consciousness and ended with him regaining his full capacity of attention, concentration, registration -> anterograde memory.
Very often an individual coming out of a coma following a Traumatic Brain Injury (TBI) doesn’t just wake up, but will go through a gradual process of regaining consciousness. This stage of recovery is called Post Traumatic Amnesia (PTA) and may last for hours, days or weeks, depending upon the severity of the trauma.
The term “Posttraumatic Amnesia” (PTA) was first used in 1928 in a paper by Symonds to refer to the period between a TBI and the return of full, continuous memory, including any time during which the patient was unconscious.
There are two types of amnesia: retrograde amnesia (loss of memories that were formed shortly before the injury) and anterograde amnesia (problems with creating new memories after the injury has taken place). Both retrograde and anterograde forms may be referred to as PTA, or the term may be used to refer only to anterograde amnesia.
When fully alert and conscious, the brain, is constantly perceiving, processing, registering and recalling information, but in PTA the injured person’s consciousness is “clouded”, and he is confused and disoriented and unable to remember events that occur after the injury. The person may be unable to state his or her name, where he or she is, and what time it is. (“The first thing that I recall was I didn’t know who I was, where I was, or what I was, I just felt an all encompassing loneliness, a loneliness and emptiness so profound that it surpasses any sort of descriptive words.”) When continuous memory returns, PTA is considered to have resolved, but 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 has patchy recall of events. In others who had more severe head injury, when such ‘islands’ of recall start appearing, it’s considered a sign of recovery.
Behavioural changes can also occur during this phase, where the patient may be quiet and passive, or aggressive, abusive and agitated. (“I was restrained with Velcro straps to my bed. The restraints were there for my own good. I couldn’t understand why I couldn’t get up, take the tube out of my nose and piss standing up. I apparently would use any ploy to get this gastric nasal feeding tube out of my nose”.) Some individuals during this stage may make inappropriate comments and engage in challenging behaviours. (“Hi its Jamie do you remember me?” To which I replied, so full of joy that I wanted to share with him, “Jamie Jamie, I just had an erection!” I shouted excitedly, my understanding of social etiquette had not re-established itself”). Patients usually have little or no awareness of these cognitive and behavioural impairments and will usually remember nothing of what happened during PTA, even though they appear fully awake.
The term ‘delirium’ is not commonly used in TBI literature although there is a growing appreciation that the confusional state seen in PTA includes more than just memory and orientation deficits (Sandel et al., 1995). In psychiatric nosology delirium and amnesia are not the same. The former being made up of impairment of attention, memory, orientation and visuo-constructional ability in addition to many other noncognitive symptoms such as perceptual abnormalities, behavioural disturbance and emotional changes, whereas the latter involves only memory impairment. Definitions of PTA found in most of the TBI literature overlap significantly with what psychiatrists would call delirium followed by amnesic disorder.
PTA was defined as the time elapsed from injury until recovery of full consciousness and the return of ongoing memory (Grant & Alves, 1987). Subclinical delirium describes a phase before or during the resolution of an episode of diagnosable delirium that is less severe and detectable only by more subtle examination of the patient. This is an important concept in TBI because of the need to distinguish lingering amnesic deficits after resolved delirium from a subclinical delirium that involves more diffuse cognitive deficits accompanied by other behavioural symptoms. Additionally delirium can have hyperactive, hypoactive or mixed motoric presentations that may be subtypes of delirium (Meagher & Trzepacz, 2000). These differing motor presentations are often accompanied by other behavioural symptoms such as yelling, punching and mood lability.