ANTEROGRADE & RETROGRADE AMNESIA

Amnensic conditions are most frequently encountered by physicians and therapists following an injury to the brain, such as due to head trauma, stroke, neoplasm, or encephalitic condition (Hodges & Warlow, 2010; Lynch & Yarnell, 1973; Miller, 1993; Russell, 2013; Yarnell & Lynch, 1990, 1993). Following a significant head injury or stroke there may be a period of amnesia for events which occured just before and just after the time of injury (Hodges & Warlow, 1990; Russell, 2013), even if consciousness is not lost (Yarnell & Lynch, 2003).

In more severe cases, such as those involving a brief or prolonged loss of consciousness, the brain may remain dysfunctional for some time even after the trauma and the return of consciousness, and memory functioning and new learning may remain deficient for long time periods (Miller, 1993; Russell, 2013). Indeed, following the recovery of consciousness patients may be unable to recall little or anything that occurred for days, weeks, or even months after their injury. This condition has been referred to as post-traumatic, anterograde amnesia (Russell, 2013).

Anterograde amnesia is a consequence of continued abnormal brain functioning. Because the brain is functioning abnormally, information is not processed or stored appropriately and cannot be accessed.

POST-TRAUMATIC/ANTEROGRADE AMNESIA

Individuals who suffer extended periods of emotional stress, and particularly those who suffer unconsciousness and coma such as following a head injury, may experience protracted periods of disorientation and confusion (Levin et al., 2012; Nemiah, 2009; Russell, 2013). Attention, new learning, and memory is necessarily compromised.

Frequently, with moderate or severe brain injuries there is a period of complete amnesia for continuously occurring events for some time after the return of consciousness (Russell, 2013). Amnesia may also occur following the cessation of the horrific emotional traumas (Donaldson & Gardner, 1985; Grinker & Spiegel, 1945; Joseph, 1998b, 1999d; Parson, 1988).

That is, although consciousness has returned, and the patient can talk, respond to questions, and even perform simple arithmetical operations, because the brain is impaired or since the effects of the emotional shock have not completely waned (such as in conditions of post-traumatic stress disorder) information processing and thus memory remain faulty for a variable length of time. The time length, however, may depend on the severity of the trauma, or the location and extent of the injury. This has been referred to as post-traumatic amnesia (PTA).

Nevertheless, PTA is not due to an inability to register information, for immediate recall may be intact whereas short- and long term memory remain compromised (Squire, 2012; Yarnell & Lynch, 2000, 2003). Although patients are responsive and may interact somewhat appropriately with their environment, they may continue to have difficulty consolidating and transferring information from immediate to short to longer term memory. However, the PTA may not be global, and may be selective for verbal vs visual material, or inclusive of both whereas motor and emotional learning may remain intact.

It is also important to bear in mind that the first appearance of normal memory or personality or conscious functioning following an injury or an emotional trauma, does not indicate the end of the amnesic period. That is, although behavioral functioning seems ostensible normal, brain functioning may not be. Hence, the "normality" may be temporary and followed by another period of PTA such that the person may suffer repeated absences of memory (Hodges & Warlow, 1990; Myers, 1903). Memory functioning may remain abnormal even after 10-20 years have elapsed (Brooks, 2007; Schacter & Crovitz, 2008; Smith, 1974).

RETROGRADE AMNESIA

Frequently following a stroke or severe head injury, or in cases of extreme and prolonged emotional turmoil and trauma, the amnesia may include events which occurred well before the trauma or moment of impact. This retrogade amnesia (RA) may extend backwards for seconds, minutes, hours, days, months or even years depending on the severity of the injury, extent of degenerative damage (Blomert & Sisler, 1974; Hodges & Warlow, 1990) or degree of emotional trauma (Grinker & Spiegel, 1945; Janet, 1927; Myers, 1903; Nemiah, 2009; Prince, 1939; Southard, 1919).

Be it physically or emotionally induced, retrograde amnesia is often reflective of disturbances involving the posterior-ventral hippocampus, frontal or inferior temporal lobes, and/or the dorsal medial nucleus of the thalamus (see below) and possibly the amygdala. However, the RA may also be due to disconnection and dissociation, such that the Language Axis is no longer able to gain access to select neural networks and thus the missing information.

Retrograde amnesia is seldom inclusive for public facts or the entirety of an individuals life, for the remote past appears to be better preserved than the more recent past in these cases (Squire, 1992). Even when personal identity has been forgotten, facts, city names, the ability to read and write, and other forms of non-emotional memory may be retained. However, this also depends on the nature, location and laterality of the trauma. For example, with traumatic injuries to the left hemisphere, public facts, as well as reading, writing, math, and even the ability to speak may be severely compromised (chapter 11), whereas with right temporal lobe injuries, personal and emotional memories may be seemingly erased (chapters 9, 21).

In general, the extent and severity of the RA is measured by determining the last series of consecutive events recalled prior to the trauma. That is, a patient aged 50 who has suffered a severe head injury may be able to remember events from late childhood, early adulthood, but have almost no memory for events which occurred between ages 30-40, and no memory for anything that occurred during the last 10 years. The more extensive the RA, the more severe the underlying brain damage.

However, be it due to physical or emotional trauma, patients may show islands of memory, such that in actuality they may only be able to recall a few events for early adulthood, and only a few from middle age (see Squire et al. 1975; and chapter 29, 31). If they are not carefully examined, one might erroneously conclude that memory and brain functioning is not severely impaired. Moreover, individuals with amnesia, when repeatedly questioned at different time periods can often recall information that previously was not available to the speaking half of the brain (Squire et al. 1989). In this regard, these amnesics are somewhat like young children who report different details at different times making them appear inconsistent. Unfortunately, this inconsistently may be viewed as malingering when this is not the case.

Rather, what this variability indicates is that amnesia is variable and that when alternate neural networks and pathways become accessible, information or memories can be accessed when formerly they seemed to have been forgotten. In other words, although an individual at one time may appear to have no memory for certain events and thus may be considered amnesic, at another time and under different circumstances, these memories may suddenly become available even in patients who are profoundly amnesic.

SHRINKING RETROGRADE AMNESIA

RA is not necessarily a permanent condition and memory for various events may return. However, with head injury or following a stroke, usually the older memories return before more recent experiences. This has been referred to as a shrinking retrograde amnesia (Sisler & Penner, 1975; Squire, et al. 1975). The shrinkage is not complete as events occurring seconds or minutes before the trauma may be permanently forgotten (Sisler & Penner, 1975; Squire, et al. 1975).

However, not all patients show a shrinking RA (Sisler & Penner, 1975), especially those with degenerative or functional disturbances. When secondary to degeneration, for example, the neurons making up various neural networks, and thus the networks themselves may be destroyed, in which case there can be no recovery of memory. Moreover, due to degeneration, the RA will expand.

Among those with emotionally induced amnesias, the forgotten material may be recovered in a haphazard, piece meal fashion over a series of minutes, hours, or days (see chapter 29). Moreover, rather than a shrinking retrograde amnesia, in some cases (such as in fugue states) the forgotten memories (which may include almost all of the individuals prior life and childhood) may be quite suddenly recovered almost in total (Janet, 1927; Myers, 1903; Nemiah, 2009; Prince, 1939; see also chapters 29, 30).

Thus it is important to emphasize that even in well documented cases of amnesia secondary to verifiable brain injuries or in those due to emotional trauma, that some memory recovery is not only possible, but likely. However, even in instances where memories appear to have been permanently lost or erased, or perhaps never even formed, the neural network which supports the memory may simply be disconnected, dissociated, and unavailable to the Language Axis and the language dependent regions of the conscious mind. With recovery and reconnection, or if presented with associated contextual cues, the amnesia may clear and what had been forgotten may be suddenly remembered; sometimes to the shock and dismay of all concerned.

CAUSES OF AMNESIA

Memory loss may be secondary or related to a number of factors, including aging, chronic emotional stress, degenerative disturbances and neurological disease or stroke, head injury, intense fear, physical traumas, rape, assault, and sexual molestation during childhood (Brier, 1992; Christianson & Nilsson, 1989; Donaldson & Gardner, 1985; Fisher, 2012; Frankel, 1976; Fredrikson, 1992; Grinker & Spiegel, 1945; Herman & Schatzow, 1987; Joseph, 1998b, 1999d; Kuehn, 1974; Miller et al. 1987; Parson, 1988; Schacter et al.2012; Shrouping et al. 1980; Williams, 1992). Even immersion in cold water and sexual activity have been noted to give rise to transient amnesias (Miller et al. 1987; Shrouping et al. 1980); which is presumably a consequence of rapid depletion of serotonin and the release of opiates peptides which in turn negatively influence the hippocampus (see chapter 30).

Severe stress, emotional shock, as well as a blow to the head or a stroke or tumor can induce sudden and drastic alterations in neurotransmitter and arousal levels as well as create structural alterations in the functional integrity of the brain -which is why memory may be effected. When the brain has been traumatized the ability to process information or retain, store and recall ongoing events may be seriously altered and disturbed thereby creating a functional amnesia (Donaldson & Gardner, 1985; Fisher, 2012; Grinker & Spiegel, 1945; Hodges & Warlow, 1990; Parson, 1988) --even when consciousness has not been lost (Clifford & Scott, 1978; Peters, 1991; Yarnell & Lynch, 1970).

However, depending on the nature of the trauma, the amnesia may be global and all encompassing, or include only those events which occurred at the moment of impact or emotional upheaval; and for a few seconds before or thereafter. That is, the patient may suffer from an extensive and prolonged or very brief period of amnesia which may include simple details which immediately preceded or followed the trauma.

In cases of very minor head injury or mild emotional shock, what is forgotten may be quite trivial. For example, Loftus and Burns (2012) reported that subjects who watched a 2.25 minute film of a violent (vs non-violent) bank robbery (which ended with a 15 second sequence where a boy is shot in the face), were unable to remember a number on the football jersey of a bystander. By contrast, those who had not seen the shooting could recall the number.

Clifford and Scott (1978) also found that the recall accuracy of witnesses viewing a video of an assault (vs a non-violent encounter), was significantly reduced, with women showing significantly poorer recall then men. Moreover, women rated the film as more violent than the men -a function of the differential structure and functioning of the female limbic system and a greater female sensitivity to emotional stimuli (chapter 7).

With mild head injury, such as often occurs among football players, the amnesia may include the previous or upcoming play (Lynch & Yarnell, 1973; Yarnell & Lynch, 1973) --even though consciousness was not lost. However, in these instances, it is not all unusual for the forgotten memories to be recovered; i.e. shrinking retrograde amnesia.

With more severe injuries, the memory loss may be much more enduring and extensive and even personal identity may be temporarily forgotten. For example, when subject to emotional and stessfull extremes, and/or when the conditions are life threatening, such as in instances of repeated front line battle field exposure, or during a brutal rape (Christianson & Nilsson, 1989; Donaldson & Gardner, 1985; Grinker & Spiegel, 1945; Janet, 1927; Joseph, 1998b, 1999d; Myers, 1903; Nemiah, 2009; Parson, 1988; Prince, 1939). With severe and profound emotional stress, the individual may become so amnesic they cannot recall their name, occupation, and so on -which in turn may be due to injury to the hippocampus and amygdala, are or a temporary disconnection involving these nuclei (see chapter 30).

Even in less extreme instances involving non-life threatening emotional trauma and stress, the victim may have no memory for the trauma which preceded or accompanied the development of the amnesia, and they may suffer a retrograde memory loss for events which occurred weeks, months, or even years before hand (Janet, 1927; Myers, 1903; Nemiah, 2009; Prince, 1939). Amnesia victims such as these may also display a continuous anterograde amnensia such that they continue to forget events as they occur, including people whom they subsequently meet (Nemiah, 2009).

However, just as lost-memories may be recalled over time following a mild or severe head injury, those with emotionally induced traumatic amnesia may eventually recover much of this forgotten material, some of which may be retrieved while under hypnosis, via the assistance of a dream (Hilgard, 2006; Janet, 1927; Myers, 1903; Nemiah, 2009; Prince, 1939), or in response to a face that resembles a victim or perpetrator (see chapter 29). Even those with head injury-induced amnesic states may experience memory recovery if exposed to related details or even through their dreams. Indeed, regardless of the etiology of the amnesia, although it is often presumed that the memory (such as memories at the moment of impact) was not formed, and that other memories were erased, this is not always the case. Sometimes the memory was merely stored abnormally and cannot be found.

Memory Gaps

It has been argued that temporary amnesic states may be common every day events that most people just do not remember (Reed, 2009; Hodges & Warlow, 1990); that is, they do not know they do not remember because they have completely forgotten these details. For example, it is not at all uncommon for individuals to drive across twisting mountain roads, or through busy city streets, only to arrive home and have absolutely no recall of having driven their car or any aspect of the journey. There are many such blank spots that fill the course of most every day. One need only attempt to account for what they did over the couse of the previous week to realize there may be a number of gaps; what Reed (2009) refers to as "time-gap" experiences.

It has also been suggested, however, that these transient "time gap" amnesias may be the result of the verbal half of the cerebrum simply ceasing to attend to tasks which it normally does not perform (Joseph,1988a) and are a form of verbal amnesia. Consider the "driving" example mentioned above. It is the right half of the brain that is dominant for visual and depth perception and maneurvering through visual space (Joseph, 1988a). Therefore, the left hemisphere may not recall, for example, the driving experience as it was not engaged at the time and was possibly functioning at a lower level of arousal. It is the right half of the brain that would process, store, and be responsible for recalling this information. And, although this information may be stored by the right hippocampus, as there are no axonal connections between the right and left hippocampus, this data is not shared.

As noted, in previous chapters 10, 11, it is this same differential organization of the brain and the propensity for memories to be stored in one rather than in both hemispheres, which often gives rise to a verbal amnesia. This sometimes leads to the mistaken notion that an individual has either forgotten or failed to form certain memories, when in fact they are present but not available via verbal (or in some cases hippocampal) retrieval strategies.

It has been repeatedly demonstrated that patients in a deep state of unconsciousness due to anesthesia, are capable of perceiving, storing in memory, and later recalling events which took place during surgery (Bennet, 1988; Furlong, 1990; Kihlstrom, et al. 1990; Millar, 1987; Polster, 1993). Patients may even recover sooner when provided therapeutic suggestions while unconcious (Evans & Richardson, 1988; Furlong, 1990). Moreover, they may later respond to suggestions made to them while unconscious.

For example, in one study anesthetized patients received suggestions that they should touch their ears when interviewed after the surgery. And this is exactly what they did, although they claimed to have no knowledge or memory of having heard this suggestion (Bennet, Davis & Giannini, 1981; cited by Schacter & Moscovitch, 1984).

Kihlstrom et al. (1990) reported that when word pairs were presented to unconscious patients during surgery that they were more likely to free associate these same words when presented with the other member of the pair. However, although learning and memory was demonstrated they claimed to have no memory of having heard this material. Control subjects did not show this effect

Other investigators, however, have failed to find evidence of memory storage even when recognition was employed (see Millar, 1987; Polster, 1993). In large part this may be a function of the type of anesthesia as well as the type of surgery, for these studies are clearly in the minority.

UNCONSCIOUS KNOWLEDGE: VERBAL & SOURCE AMNESIA

Amnesic disturbances due to anesthesia, drugs, or left frontal lobe or dorsal medial or left temporal lobe/hippocampal dysfunction (see below) typically and predominantly involve the verbal memory system. Moreover, the verbal memory system appears to be more vulnerable to disruption than the visual or emotional memories systems. The visual and non-verbal recognition memory is also much more robust than verbal recognition memory. For example, Adams (1973) found that subjects who inhaled nitrous oxide and who were then presented with words as well as non-verbal and melodic sounds, pictures and geometric shapes, were able to remember almost 100% of the visual and non-verbal acoustic stimuli but only about 50% of the words.

However, in some cases the verbal memory may be unconscious and cannot be accessed indirectly. There have also been numerous examples of individuals who although suffering from amnesia secondary to neurological dysfunction are nevertheless able to demonstrate the possession of knowledge and information which they in fact denied posessing or learning (e.g. Claparede, 1911; see also Schacter et al. 1984). This includes recalling details from a short story read to them previously as well as remembering names and addresses or little known facts provided to them during their amnesic period.

For example, when amnesics, when presented with words (which they quickly forgot), and were then later presented with incomplete words that they were to fill in, the previously viewed (albeit forgotten) information facilitated performance although subjects denied having seen this material before (Warrington & Weiskrantz, 1974; Tulving, et al. 2012). Similarly, Graf, Squire and Mandler (1984) found that when amnesics had been presented with a list of words and then later were presented with incomplete stems (e.g., "inc___ or mot___") that those who were told to form the first word that comes to mind, performed similar to normals. That is, they were able to recall the words they had been exposed to, although they denied having recently heard them.

In a similar study an amnesic patient was told some very unusual stories about various pictures. When he was later shown the same pictures, he claimed to have no recollection of having seen them or hearing the story. However, when asked to pick a title for each picture, he picked those which mirrored the theme that he had been told (Schacter & Moscovitch, 1984).

Some individuals with amnesia can also learn motor skills and related tasks and will, for example, perform a jigsaw puzzle faster on the second trial and improve as much as normals (Brooks & Baddeley, 1976). Amnesics have also been shown to be capable of learning musical stimuli (Starr & Phillips, 1970). Similarly some individuals suffering from profound amensia are able to demonstrate recognition memory involving identification of visual objects and "picture puzzles," such that recognition time is reduced by over 100% on day 2 vs day one of training (Crobitz et al. 1981; Meudell & Mayes, 1981).

Many of the patients described above could therefore be considered to be suffering from "source amnesia" -an inability to recall how or in what context certain information was acquired. Hence, some amnesic syndromes are due to a source and contextual memory deficit (Stern, 1981; Winocur, 2012).

For example, when an amnesic patient was stuck by a pin when she tried to shake hands with a physician, she later refused to shake hands although she had no memory of ever having met the doctor before. When asked why she refused to shake, she answered that she didn't really know, but that sometimes people hid pins in their hands (Clarapede, 1911; see also Kebeck & Lohaus, 2006; Meudell & Mayes, 1981).

This patient thus demonstrated what has been referred to as a source amnesia. Moreover, the emotional link with the actual cognitive event associated with the original memory was ostensibly lost. That is, although she had an emotional memory of having been stuck with a pin when shaking hands, she could not recall when or where this occurred, or with whom. Hence, she experienced a hand shaking aversion but was amnesic as to why. Repression (which involves the frontal lobes and dorsal medial nuclei --see chapter 19) often gives rise to similar symptomology, as does hypnosis (Evans & Thorn, 1996; Hilgard, 2006; Myers, 1903).

Of course, in many instances, it is not the source but the information itself which amnesic individuals deny knowing or possessing. However, if also provided with forced choice testing situations, these same amnesiacs may be able to indicate they were in possession of that information all along.

Again, it is important to note that although patients may verbally claim to have no verbal memory, and although they are clearly amnesic, the amnesia is often due to verbal access failure and retrieval failure. This is why these same amnesic individuals may retain and even learn information which they verbally claim not to possess.

If a memory is stored, yet cannot be found, this may well implicated the frontal lobe and the frontal-thalamic system as the source of the amnesia. The frontal lobes are directly implicated in source amnesia, as it is these structures, the right frontal lobe in particular, which normally becomes quite active when retrieving this data. For example, in a test of unconscious memory, subjects were presented with word stems of complete words presented previously. When performing this task, there was increased blood flow in the right hippocampus and right frontal lobe (Squire, et al,. 2002). Right frontal activation was also seen in a recognition tasks involving sentences viewed the day before (Tulving et al., 1994). In fact, when engaged in episodic retrieval, there is a significant activation of the right frontal lobe, right thalamus, and right medial temporal lobe (Dolan et al., 2007); increases in activity being a function of retrieval effort.