Background: The relationship between traumatic emotional stress, hippocampal injury, memory loss, and traumatic ("dissociative") amnesia was examined.

Method: A survey of the research on emotional trauma, learning, memory loss, glucocosteroid stress hormones, and the hippocampus was conducted, and animal and human studies were reviewed.

Results: It is well documented and has been experimentally demonstrated in animals and humans that prolonged and high levels of stress, fear, and arousal commonly induce learning deficits and memory loss ranging from the minimal to the profound. As stress and arousal levels dramatically increase, learning and memory deteriorate in accordance with the classic inverse U-shaped curve. These memory deficits are due to disturbances in hippocampal activation and arousal, and corticosteroid secretion which can suppress neural activity associated with learning and memory and induce hippocampal atrophy. Risk and predisposing factors include a history of previous emotional trauma or neurological injury involving the temporal lobe and hippocampus, the repetitive and prolonged nature of the trauma, and age and individual differences in baseline arousal and level of cortisol.

Conclusions: Amnesia or partial memory loss is not uncommon following severe stress and emotional trauma. Even well publicized national traumas may induce significant forgetting. Memory loss is a consequence of glucocosteroids and stress-induced disturbances involving the hippocampus, a structure which normally plays an important role in the storage of various events in long-term memory.

A number of scientists have challenged the validity of traumatic "dissociative" amnesia while simultaneously ignoring, excluding, or dismissing the fact that amnesia or memory loss is not at all uncommon following high levels of stress and arousal, or other physical, chemical, or severe emotional insults to the brain. For example, in concluding that there is no evidence for "dissociative" amnesia, Pope and colleagues (1998) made it a point to "rule out the confounding effects of amnesia due to biological... and other neurological factors."

Memory, however, is a biological process, and memory loss, including stress-induced traumatic, dissociative amnesia, can probably best be understood from a biological and neurological perspective. To rule out neurology and biology in order to claim that amnesia does not exist, is disingenuous.

MEMORY LOSS AND HIPPOCAMPAL INJURY DUE TO TRAUMATIC STRESS

It is well established that the hippocampus plays a significant role in consolidating, and storing in long-term memory, various aspects of experience, such as words, places, conversations, written material, contextual details, and positional and spatial relationships (Eichenbaum, Otto, & Cohen, 1994; Frisk & Milner, 1990; Lynch, 1986; Nadel, 1991; Rolls, 1988; Victor & Agamanolis, 1990). Conversely, injury to the hippocampus and overlying temporal lobe is associated with significant memory loss and amnesia (Eichenbaum et al., 1994; Joseph, 1992, 1996a,b; Milner, 1970; Reed & Squire, 1997; Scoville & Milner, 1957; Squire 1992). With bilateral hippocampal ablation patients suffer from profound anterograde as well as retrograde amnesia which may extend backwards several years in time (Milner, 1970; Scoville & Milner, 1957).

Consider, the famous case of H.M. who can recall almost nothing following bilateral hippocampal amputation (Milner, 1970). Dr. Brenda Milner has worked with H.M. for over 25 years and yet she is an utter stranger to him. Every time he discovers his favorite uncle died he suffers the same grief as if he had just been informed for the first time. Nevertheless, H. M. is aware of his deficit and frequently apologizes for his loss of memory. "Right now, I'm wondering" he once said, "Have I done or said anything amiss? You see, at this moment everything looks clear to me, but what happened just before? It's like waking from a dream. I just don't remember...Every day is alone in itself, whatever enjoyment I've had, and whatever sorrow I've had...I just don't remember."

The hippocampus need not be surgically or physically impacted in order to suffer significant injury, for dendritic death and atrophy and significant memory loss can be induced by severe emotional trauma and the stress-induced secretion of enkephalins, norepinephrine, and especially corticosteroids (reviewed in Joseph, 1996a,b; Lupien & McEwen, 1997; Sapolsky, 1996). Although these substances are normally released as part of the "fight or flight" response, repeated or prolonged stress-induced secretory episodes of corticosteroids and enkephalins can injure the dentate gyrus and Ammon's horn (Joseph, 1998; Lupien & McEwen, 1997) and hyperactivate or kill hippocampal (as well as amygdala) pyramidal neurons (Gahwiler, 1983; Henriksen, Bloom, & McCoy, 1978; Packan & Sapolsky, 1990) --structures which normally display synaptic growth and dendritic proliferation in response to new learning (Clugnet & LeDoux, 1990; Rolls, 1987, 1988; Squire 1992).

In reaction to prolonged, or repetitive bouts of stress and arousal the hippocampus may be injured and atrophy (Lupien & McEwen, 1997; Pfaff, Silva, & Weiss, 1971; Sapolsky, 1996; Uno, Tarara, Else, & Sapolsky, 1989), and develop epileptiform and seizure activity including high voltage EEG paroxysmal waves (Gahwiler, 1983; Henriksen, Bloom, & McCoy,1978), thus disrupting learning and memory (Brazier, 1966; Chapman, Markham, Rand, & Crandall, 1967).

Hippocampal atrophy and memory disturbances have been documented among those sexually abused as children (Bremmer, Randall, & Scott, 1995; Stein, Hannah, Koverloa, & McClarty, 1995), and adults traumatized in front line combat (Bremmer, Randall, Southwick, Krystal, Innis, & Charney, 1995; Gurvitz, Shenton, Hikama, Ohta, Lasko, & Gilbterson, 1996).

Hippocampal dendritic death or atrophy has also been induced by social deprivation and impoverished rearing conditions (Diamond, 1985, 1991; Greenough, West, & Devoogd, 1978; Walsh, Budtz-Olsen, Penny, & Cummins, 1969). Be it animal or human, neglect, abuse, and emotional trauma are extremely stressful and negatively impacts the hippocampus, the limbic system, as well as learning and memory (Bremner, Randall & Scott, 1995; Bremmer, Southwick, et al., 1995; Gurvitz et al., 1996; Joseph, 1979, 1996a,b, 1998,1999a,b; Joseph & Gallagher, 1980; Stein et al.,1995).

Under conditions of excessive and prolonged stress and emotional arousal, or following direct activation, the hippocampus may become excessively and activated (Chapman, et al., 1967; Grastyan, Lissak, Madarasz, & Donhoffer, 1959; Green & Arduini, 1954; Joseph, 1992, 1996a,b) and patients may suffer a profound amnesia that extends backwards in time for minutes, hours, days and weeks, after which the amnesia may begin to shrink (Brazier, 1966; Chapman et al., 1967); i.e. shrinking retrograde amnesia (Joseph, 1996b). Indeed, it is well established that although intermediate levels of arousal may promote learning, as arousal and stress levels dramatically increase, memory deteriorates such that an inverted-U shaped learning curve is produced (Christianson, 1992; Conrad, Galea, Kuroda, & McEwen, 1996; Diamond, Bennett, Fleshner, & Rose, 1992; Diamond, Fleshner, & Rose,1994; Joseph, Forrest, Fiducia, Como, & Siegel, 1981; Kirchbaum, Wolff, May, Wippich & Hellhammer, 1996; Newcomber, Craft, Hershey, Askins, Bardgett, 1994; Yerkes & Dodson, 1908).

High levels of stress and arousal interfere with memory, in part by inducing abnormal hippocampal activity (Brazier, 1966; Chapman et al., 1967; Gahwiler 1983; Grastyan et al., 1959; Green & Arduini, 1954; Joseph, 1992, 1996a,b, 1998; Shors, Seib, Levine, & Rose, 1989), and through the elimination of hippocampal long term potention (LTP) which is associated with learning and the storage of long term memories (Diamond et al., 1992; Shors et al., 1989; Spoont, 1992). In fact, high levels of corticosterone and enkephalins directly disrupt learning (Diamond et al., 1992, 1994; Kovacs, Telegdy, & Lissak, 1976; Lupien & McEwen, 1997; Warembourg, 1975), memory retrieval (de Quevain, Roozendall, & McGaugh, 1998) and recognition memory (Wolkowitz, Reus, Weingartner, Thompson, Breier, & Doran, 1990; Wolkowitz, Weignartner, Rubinow, Jimerson, Kling, & Berretini, 1993) including the ability to discriminate between relevant and irrelevant stimuli (Lupien & McEwen, 1997). Even brief (albeit high levels of) stress-induced enkephalin and corticosteroid secretion can exert deleterious influences on long (but not short) term memory and eliminate hippocampal LTP (Diamond et al., 1992, 1994; Shors et al., 1989; Spoont, 1992).

LTP is believed to represent a prolonged form of synaptic activity which binds together those neurons responsible for transferring information from short-term, to long term memory (Lynch, 1986; Lynch, Larson, Muller, & Granger, 1990). That is, through LTP the hippocampus presumably acts to bind various divergent neocortical sites so as to form a circuit of experience and create specific neural networks which supports or maintains specific memories (reviewed in Joseph, 1996b). In fact, hippocampal LTP tends to build up within the first 30 minutes after learning and during memory acquisition (Lynch, 1986; Lynch et al., 1990). Once this information has been consolidated and placed in long-term storage, LTP ceases to be a factor in memory maintenance.

However, during this consolidation phase, hippocampal LTP may be suppressed by high levels of arousal, fear, and the stress induced secretion of corticosteroids (Diamond, Fleshner, & Rose, 1994; Shors, et al., 1989; Spoont, 1992).

In consequence, although immediate retention may remain intact for a few seconds or minutes following severe stress, the buildup of LTP and thus long term memory may be significantly disrupted, resulting in a profound amnesia.

Moreover the hippocampus is implicated not only in long-term (but not immediate or short-term) memory storage, but in memory retrieval (Joseph, 1996b, 1998) and thus storage as well as retrieval can be disrupted. For example, rats given a painful footshock 30 minutes before memory testing demonstrated elevated levels of corticosterone and profound retention deficits. Those shocked two minutes before testing were unimpaired and had normal corticosterone levels (de Quevain, Roozendall, & McGaugh, 1998). As the buildup of glucocorticoids begins several minutes after severe stress, although immediate, short-term memory was unaffected, long term memory and retrieval were disrupted once glucocorticoid levels significantly increased. Indeed, de Quevain et al., (1998) injected a drug that reduced corticosteroid synthesis (metyrapone), and found that those shocked (and injected) 30 minutes before testing demonstrated normal memory retention.

The hippocampus is especially vulnerable to the deleterious effects of stress and high levels of corticosteroids due the abundance of Type II adrenal steroid receptors which abound within this structure (Lupien & McEwen, 1997; Pugh, Fleshner, & Rudy, 1997). For example, when corticosteroids are secreted at high levels they can exert a suppressive influences on membrane receptor proteins, thereby altering excitability and information transmission between neurons (Hua & Chen, 1989; Majewska, Harrison, Schwartz, Barker, & Paul, 1986). Corticosteroids can detach the cellular receptor from its attached protein (Beaulieu, 1987); a condition which interferes with messenger RNA protein transcription and thus the genetics of memory.

Incoming messages cannot be acted on, learning cannot take place, and injured or damage cells cannot be repaired due to RNA/DNA interference. Thus, memory dysfunction (Kirchbaum, et al., 1996; Newcomber, et al., 1994) and hippocampal atrophy results (Joseph, 1998; Lupien & McEwen, 1997; Sapolsky, 1996).

Moreover, in addition to cortisol secretion, severe emotional distress can alter the secretion of norepinephrine, serotonin, and dopamine (Rosenblum, Coplan, & Friedman, 1994; Southwick, Krystal, Morgan, Johnson, Nagy, Nicolaou, Hininger, & Charney, 1993; Spoont,1992; Witvliet, 1997). These neurotransmitter fluctuations not only negatively impact the hippocampus but amygdala neurons (Cain, 1992; Goelet & Kandel, 1986; Kraemer, 1992; Krystal, 1990).

In fact, under conditions of repetitive traumatic stress not just the hippocampus, but the adjacent amygdaloid nucleus may develop epileptiform and seizure activity including high voltage EEG paroxysmal waves (Cain, 1992; Gahwiler, 1983; Henriksen et al., 1978). As the amygdala is associated with all aspects of emotion including emotional memory (Gloor, 1992, Halgren, 1992; Joseph, 1992, 1996a,b), prolonged and repetitive stress can disrupt all aspects of affective functioning including emotional memory. Indeed, hyperactivation of the amygdala (as well as the hippocampus) can induce a profound amnesia (Chapman, 1958, 1960; Chapman et al., 1967; Jasper & Rasmussen, 1958).

TRAUMATIC STRESS, MEMORY LOSS AND TRAUMATIC AMNESIA

It is likely that the deleterious effects of excessive and prolonged stress and high levels of arousal on hippocampal (as well as amygdala) functioning, coupled with other predisposing factors (Bremner, Southwick, Johnson, Yehuda, & Charney, 1993; Joseph, 1996a,b, 1998, 1999a,b), may well explain the post traumatic stress disorders, flashbacks, disturbances of memory or repressed memory syndrome which afflicts some victims of sexual abuse (Briere & Elliott, 1994; Briere and Conte, 1995; Courtois, 1995; Duggal & Sroufe, 1998; Elliot, 1997; Joseph, 1996a; Polusny & Follette, 1995; Williams, 1994), rape (Burnam, Stein, Golding, Siegel, Sorenson, Forsythe, & Telles, 1988; Christianson & Nilsson, 1984; Donaldson & Gardner, 1985), physical assault (Kolko, 1996; Kuehn, 1974; Loughrey, Curran, & Bell, 1993; Peterson & Bell, 1996; Resnick, Kilpatrick, Dansky, Saunders, & Best, 1993), front line combat (Blake, Cook, & Keane, 1992; Grinker & Spiegel, 1945; Kulka, Schlenger, Fairbank, Hough, Jordan, Marmar, & Weiss, 1990; Parson, 1988; Southard, 1919), and natural disasters and related trauma (Escobar, Canino, Bubio-Stipec, & Bravo, 1992; Fisher, 1982; Leopold & Dillon, 1963; Terr, 1994; Wagennar & Groenenweg, 1990).

However, some authors, such as Pope et al., (1998), purposefully exclude "biology," "neurology," "studies of combat in war," "case reports," "subjects who had been interviewed," "ancectodal reports," and so on, in order to falsely claim that there is as yet no "persuasive evidence of the possibility of dissociative amnesia" and that "dissociative amnesia remains unproven" (Pope et al., 1998, p. 214). Of course, with this exclusionary criterion, these authors have in fact tossed out the brain with the bath water, and have excluded almost all reports of dissociative amnesia in order to claim that it does not exist.

It is true that not all individuals who are traumatized suffer from traumatic, dissociative amnesia (repressed memory syndrome), and some victims may experience intrusive imagery (Foa, Riggs, & Gershuny, 1995; Witvliet, 1997)--a function, perhaps of kindling activity in the amygdala (Joseph, 1996a, 1998). On the other hand, some degree of memory loss or distortion is not uncommon (Joseph, 1996a,b; van der Kolk & Fisler, 1995) particularly if the stress is prolonged, repetitive and severe. As noted, when stress and arousal levels dramatically increase, learning and memory functioning deteriorates and may be completely eclipsed. Although Pope and colleagues cite the work of Goodman in order to falsely claim that painful experience, and high levels of arousal promote memory functioning, Goodman and colleagues (Goodman, Bottoms, Schwartz-Kenney, & Rudy, 1991; Saywitz, Goodman, Nicholas, & Moan, 1991) actually found "suppressed memory," and that children up to age 7 required cues and specific questions before they were able to recall the details, even following vaginal and anal touching. "In free recall and demonstration... 78% and 83% failed to report it, respectively" (Saywitz et al., 1991, p. 686).

In fact, children as well as adults demonstrate significant forgetting for even well publicized national traumas such as the assassination of President Kennedy or the Challanger space craft explosion (Neisser & Harsch, 1992; Warren & Swartwood, 1992; Winograd & Killinger, 1983). Private or public, traumatic experiences do not promote learning and memory, and even so called "flash bulb" memories are subject to considerable decay. For example, in evaluating long term memory for the Challenger space craft explosion, Neisser and Harsch (1992) had subjects fill out a questionnaire regarding where they were and how they heard about the Challenger accident and so on. When questioned 32-34 months later, many had forgotten considerable detail, and 75% could not recall filling out the questionnaire; leading Neisser and Harsch (1992) to conclude that "as far as we can tell, the original memories are just gone."

PREDISPOSING FACTORS: AGE, CORTISOL, CORPUS CALLOSUM, PREVIOUS TRAUMAS

Stress-induced memory loss may be fragmentary, circumscribed, or quite mild (van der Kolk & Fisler 1995). Not all people (or animals) respond the same when stressed as there are a number of interacting predisposing factors which differentially contribute to the likelihood of amnesia, reduced information acquisition, and thus the stress reaction. Be it animal or human these risk factors include base line cortisol and arousal level, previous trauma, situational, environmental, genetic, age, gender, and thus individual differences (Bremner et al., 1993; Breslau, Kessler, Chilcoat, Schulz, Davis & Andreski, 1998; Como, Joseph, Fiducia, & Siegel, 1979; Joseph, 1996a, 1998; Joseph & Gallagher, 1980; Joseph et al., 1981; Joseph, Hess & Birecree, 1978; Terr, 1994; Torras-Garcia, Portell-Cortes, Costa-Miserachs, & Morgado-Bernal, 1997).

For example, intermediate levels of glucocorticoids can potentiate those corticosteroids hippocampal receptors normally involved in memory consolidation (Lupien & McEwen, 1997). In consequence, exceedingly low, or exceedingly high corticosteroid levels not only disrupt memory, but produce the classic inverted U-shaped learning curve (Conrad, et al. 1996; Kirchbaum, et al. 1996; Newcomber, et al. 1994). However, because of individual differences in baseline cortisol levels (Kagan, Reznick, & Snidman, 1987, Kalin, Shelton, Rickman, Davidson, 1998) the same stresses experienced by two different individuals can differentially effect memory due to individual differences in overall cortisol secretion and buildup.

In addition, younger subjects appear to be more at risk for memory loss than adults (Spear, 1979; Warren & Swartwood, 1992; Winograd & Killinger, 1983). In part this is may be due to the immaturity of the hippocampus (Joseph, 1996a) which remains exceedingly plastic and does not complete its cycle of myelination until well after the third decade (Benes, Turtle, Khan, & Farol, 1994). The immature hippocampus (and limbic system) is more vulnerable and thus more likely to suffer stress induced injury or abnormal neuroplastic alterations in associated neural pathways (Joseph, 1998, 1999ab).

Memory loss for early childhood is also a function of corpus callosum and neocortical immaturity which limits the ability to share cognitions or to transfer information and memories between the right and left hemisphere until after age 5 (Gallagher & Joseph, 1982; Joseph, 1982; Joseph & Gallagher, 1985; Joseph, Gallagher, Holloway, & Kahn, 1984). That is, emotional experiences processed and stored in the immature memory centers of the right cerebrum, may be stored unilaterally in this hemisphere as the left (speaking) hemisphere is not as adept at processing or storing affective information (Joseph, 1988a); and in children the left cerebrum cannot gain full access to right hemisphere memories and cognitions due to corpus callosal immaturity (Gallagher & Joseph, 1982; Joseph, 1982; Joseph & Gallagher, 1985; Joseph et al., 1984).

In fact, amnesia has been experimentally induced among adults when corpus callosum interhemispheric information exchange has been prevented such as following corpus callosotomy (Joseph, 1986, 1988a,b) or unilateral hemispheric anesthetization, coupled with unilateral information presentation. For example, Risse and Gazzaniga (1979) injected sodium amytal into the left carotid arteries of intact patients so as to anesthetize the left cerebral hemisphere. After the left cerebrum was inactivated, the awake right hemisphere, although unable to speak, was still able to follow and behaviorally respond to commands, e.g., palpating an object with the left hand.

Once the left hemisphere had recovered and interhemispheric information exchange was reestablished, none of the eight patients studied were able to verbally recall what objects they had handled and touched, "even after considerable probing." Rather these patients insisted that they could remember absolutely nothing and many refused to even guess. However, when offered multiple choices in full field, most patients immediately raised the left hand and pointed to the correct object! According to Risse and Gazzaniga (1979), although the memory of touching and palpating the object was not accessible to the verbal (left hemisphere) memory system, which in all regards was completely amnesic, this data was encoded in a nonverbal form within the right hemisphere and was unavailable to the left hemisphere when normal function returned.

The left (speaking) hemisphere was unable to gain access to the information and memories stored in the right hemisphere even after transfer capabilities were reestablished. Hence, when patients were extensively questioned they demonstrated a profound (verbal) amnesia--even though this data was in fact stored within the right hemisphere.

However, as the amytal procedure does not anesthetize the posterior temporal-occipital areas (which process visual stimuli), right- or left-hemisphere anesthetized patients may not demonstrate visual transfer deficits after the unilateral injection wears off (Perrine, Donofrio, Devinsky, Gershengorn, Luciano, & Nelson, 1998). By contrast, due to corpus callosum immaturity, children display significant loss of information and memory when required to transfer complex visual, or tactile information from the right to left hemisphere (Joseph et al., 1984).

As significant interhemispheric information transfer does not reach adult levels until after age 7 due to corpus callosum immaturity (Joseph et al., 1984) and as the right hemisphere is clearly dominant in the processing and storage of emotional experience (Joseph, 1982, 1988a,b), and as the hippocampus does not complete its cycle of myelination until after age 30 (Benes et al., 1994) adults typically have difficulty recalling early childhood events ("childhood amnesia") even though the callosum has matured and transfer abilities have significantly improved (Joseph, 1996a).

However, whereas adults may demonstrate an amnesia for childhood, because of callosal, neocortical, and hippocampal immaturity, children may be more at risk for experiencing loss of memory or a dissociative amnesia if severely stressed. In fact, in a recent study, it was found that the average age of first recallable memory among women from the general population, is 3.3, and for men, 3.7 years of age, whereas among women with a childhood history of severe and chronic sexual, physical, or emotional abuse, the average age of first memory is 6.5, and for men, 5.7 (Joseph, 1999c). Hence, the length of childhood amnesia is more prolonged for those severely abused. Indeed, the younger the victim and the more stressful and prolonged the trauma, the more pronounced might be the memory loss (Joseph, 1996a,b, 1998; Terr, 1994) including loss of memory for early childhood.

For example, consider the well publicized trauma of "Baby Jessica" McClure who at age 18-months, was trapped 22 feet deep below the Earth's surface in a narrow hole for 58 terrifying and painful hours. Although this incident was internationally televised and subject to intense media attention in the United States, as well as one television movie and several books, and despite the amputation of one toe and skin grafts, 10-year old Jessica cannot remember anything of her ordeal (Babineck, 1997).

Similarly, Tara Burke was kidnapped three months shy of her 3rd birthday, held captive in a van for 10 months, and repeatedly sexually assaulted by two men; an ordeal photographed and filmed by her tormentors.

According to her parents, these men kidnapped Tara when she had been left in her parents's vehicle with her 9-year old brother. Both parents had dashed inside a store, and then moments later, a 17-year old man (A.C.) tapped on the van window and told the boy that his mother wanted him. When the boy opened the door, the kidnapper snatched Tara and flung her over his shoulder, and then raced to a waiting car. The kidnapers transferred her to a van where she was confined, stripped naked, and repeatedly sexually assaulted by Luis "Tree Frog" Johnson, age 33, and his 17-year old accomplice (A.C.--it is noteworthy that A.C. had also been a victim of Johnson for almost 8 years). ). She was later sexually assaulted by some of his friends. Johnson and his 17-year old accomplice later abducted an 11-year old boy, "Mac" who was repeatedly raped and beaten with a rubber hose. According to Mac, Tara was also repeatedly beaten. He also observed her being sexually assaulted and molested several times a day by A.C. and Johnson who wanted to have a child by her, but by friend's of Johnson who also liked sex with children.

And then "Mac" escaped, by slipping through the van's roof ventillator. Mac found his way to the police, whom he led back to the van. There they found Tar lying naked in a bed with Johnson's 17-year-old accomplice, "A.C.". According to the police, Tara was so traumatized she didn't know her name, she couldn't tell them anything, she couldn't remember anything, and she didn't even know she was a girl. She was so traumatized that she in fact could never recall what had happened to her.

Despite intense media scrutiny and a subsequent court trial, 18-year old Tara reports that the "memory has been erased" from her mind. "It's like a story that has happened to someone else" (Joseph, 1998b). Indeed, she states that her only memories are "being set up on a bench and them doing things to me. I don't remember what." Rather, it was "Mac" who laid out the sordid details.

ADDENDUM:

THE FRANKLIN CASE:
MURDER, MOLESTATION & RECOVERED MEMORY

In 1990 retired California fireman, George Franklin Sr, received a life sentence for the 1969 murder of an 8 year old girl, Susan Nason--she had been sexually assaulted and killed five days before her 9th birthday. Mr. Franklin was convicted in San Mateo Superior Court on the testimony of his daughter, Eileen Franklin-Lipsker, who reported to police in 1989, that she had recalled memories that had been repressed and forgotten for 20 years.

Specifically Eileen recalled watching her father rape and then kill the victim, her girlfriend, by smashing her skull with a large rock. She claimed that after almost twenty years the memory had come to her when certain actions and facial expressions of her own daughter triggered their recollection. The conviction was later over turned. Mr. Franklin has subsequently threatened to file a lawsuit against those involved, and stated he was going to seek financial compensation for what he has suffered and the harm done to his reputation.

Eileen Franklin was born in San Francisco but raised in Foster City, California, by her mom and dad. According to Eileen, her parents were very violent, with lots of screaming, yelling, and beatings, including an instance where her mother broke her sister's two front teeth. "Mom was a drunk. She drank everyday. When we came home from school she would be in her room, alone. She was extremely neglectful. My father beat everyone. He'd drag us out of bed at night. He'd be drunk and would beat, kick and hit everyone." Eileen admitted, however, "that there are a lot of blanks in my memory. Most of my childhood, up to the 12th grade is mostly blank."

In response to my questions about her earliest memories, Eileen reports that her first memory was from age 3 when she was jumping up and down in her crib next to a window when she somehow broke her nose. Her next memory was a year later, at age 4, when she got out of bed, went into the kitchen in her flannel nightgown, where her father, George Franklin Sr. was making coffee. Her very next memory was a year later, in kindergarten, followed by memories of first grade and going to her grandma's house for Christmas, and a single memory of her teacher from second grade. And then, according to Eileen, the next three years are a "blank." Her memories resume in the 5th maybe the 6th grade" "I'm going to school... the other kids don't like me. I was dirty... I didn't have any social skills....something about... all Hell breaking loose... yelling.... screaming... we're moving to a new home... I've got these terrible feelings... more violence, more screaming.... and then everything until 12th grade is mostly a blank."

As detailed elsewhere (Joseph, 1996, 2000), women with a history of severe childhood sexual abuse (CSA) may become promiscuous, engage in prostitution, and abuse drugs and alcohol (Alexander and Lupfer, 1987; Becker, et al., 1986; Fromuth, 1986; Meiselman, 1978; Simons and Whitbeck, 1991; Stein, Golding, Siegel, Burnam and Sorenson, 1988; Tsai, Feldman-Summers and Edgard, 1979; Wind & Silvern, 1992). It has been found that between 40% to 60% of prostitutes report a childhood history of sex abuse (Silbert & Pines, 1981; see also James & Meyerding, 1977; Miller 1986; Weisberg, 1985). Promiscuity, even among those who dislike sex, is not uncommon (Alexander and Lupfer, 1987; Fromuth, 1986; Tsai, et al., 1979; Wind and Silvern, 1992).

A significant minority also tend to associate with men who will beat or sexually exploit them, and/or they engage in behaviors which increase the risk and which result in a higher incidence of being sexually assaulted and raped (Brown & Finkelhor, 1986; Gorcey et al., 1986; Russell, 1986). Sexual as well as emotional disturbances such as excessive and chronic fear, depression, and anxiety, coupled with feelings of isolation, anger, and worthlessness are common (Herman & Schatzow, 1987; Murphy et al., 1988; Stein et al., 1988).

Likewise, Eileen reports that she led a "dysfunctional life... abusing alcohol, cocaine, pot... almost every day. I was extremely promiscuous.... had sex with hundreds of men. I even worked as a prostitute, doing out calls for a massage parlor. And then I got arrested. It scared me straight. I quit drugs, prostitution, everything... and then married an extremely verbally abusive man-- abusive just like my father. It was 11 years of hell and then he died of a heart attack. And then I met and married Jace Schmitz. For almost four years, it was a wonderful relationship."

"One day I drove by our old house. My parents house. Just driving made me feel terrible. Like a nightmare coming back. I was scared of that house. And then I visited with them and all these memories came back. Horrible memories. My father, molesting me. Forcing me to have sex, and not just with him, but with another man... my father was holding me down letting him fuck me."

"I have a couple of wonderful children. And one day, I was sitting in the family room, holding my son, my daughter was playing on the floor with some girlfriends, when she turned and looked at me and said: 'Isn't that right mommy?' I felt this sudden terror and then I saw in my mind, my father with a rock in his hand. And I saw Suzy. He was walking towards her. I cried out: 'No' and said 'no' inside me, inside my mind. And then the picture, the memory stopped. Over the next few weeks more memories came back in a random, disorganized, hap hazard and non-chronical order. I was remembering my father rape and kill Suzy, my girlfriend. He smashed her head with a big rock. He raped her and then he killed her..."

[-INSERT FIGURE 8 ABOUT HERE-]

Although George Franklin's conviction for murder has been overturned, the question still remains, did Eileen Franklin lie and make up stories about sexual molestation, falsely claiming memory loss, and then recovered memory, and in so doing, falsely accuse a wholly innocent man?

Upon evaluating Ms. Eileen Franklin, I was provided investigative records and other Court and legal documents, including transcripts and summaries of interviews with his wife, daughters, and five of his "girlfriends."

In addition to Eileen, two of Mr. Franklin's other daughters also allege he repeatedly sexually abused them orally, vaginally, and anally, and provided investigators with details. For example, according to Eileen's older sister, the molests began when she was 8 or 9. She claimed that he would order her to spread her legs and pull her labia apart, and that he would make her sit on his lap while he would fondle her.

According to this older sister, on one occasion he ordered her to lay naked with legs spread on her bed, and that after he inserted his penis in her vagina and sexually assaulted her, he demanded oral sex and ejaculated in her mouth.

Franklin's 17-year old sister-in-law claims that on one occasion when she was baby sitting, he returned home, grabbed both of her arms by the wrists and held them over her head with one hand while he fondled her breasts with the other. Another 13-year old sister-in-law made almost identical claims.

Five different women, his "girlfriends" allege he repeatedly expressed sexual interest in girls, and several reported that he even bragged of rape and orgies with 13- year old girls, including instances in which he shared these girls with another man .

He allegedly expressed sexual interest in the daughter of one of her girlfriends, and later he allegedly told two other women (his "girlfriends") that he had repeatedly sexually assaulted a girlfriend's daughter. He allegedly urged, cajoled and repeatedly requested that one woman share her daughter with him, and she claims that he requested that he procure other little girls for him. These five women claimed that he insisted on being called "daddy" during sex and that he used terms of endearments such as his "incestuous little girl."

One of these women reported that Franklin was violent and unpredictable and that he admitted to her that he had "had sexual relations with his daughters." Another of these women reported that she had confided in Franklin and told him she had been molested as a child by her father.

Thereafter, she claims, Franklin "constantly questioned her about it, pressing her for specific details, and insisted that she talk about it while she was having sexual relations with him." According to this woman, he also requested that she take photographs of of her 7 year old daughter with her legs spread apart, exposing her vaginal areas.

She claims he repeatedly asked if he could have sex with her daughter, and told her that he belonged to an organization whose motto was "sex before eight, before its too late," and that she would be depriving her daughter of a wonderful sexual experience. Another of these women stated that during sex he demanded that she "act like a child" and that when he would ask her "how old are you," she was to reply "eight years old." She stated he would also grab her by the wrists and hold her hands over her head while he had sex with her.

A young woman he had met in a restaurant reported that he told her that he had taken a "girl for a ride... and that the girl wanted it but wouldn't ask for it so I took her in the back of the truck and raped her." A business associate of Mr. Franklin reported that on occasions when they drove to San Mateo from Sacramento, that Franklin "often suggested picking up young female hitchhikers and raping them." According to this associate Franklin often expressed a sexual desire for young girls and stated: "The younger they are, the sweeter the meat." According to investigative reports, his reading material included incest stories such as "Little Squeals of Desire," and "Please Dad, Do It For Me."

Susan Nason was sexually assaulted and murdered on or about September 22, 1969. After it has been reported that Susan Nason had been sexually assaulted and killed, George Franklin's wife accused him of the murder. Yet another daughter came to the same exact conclusion and reported him to police.

Twenty years later, after a visit to her parents home, Eileen began to remember her nightmarish childhood during which she was repeatedly sexually assaulted, including, on one occasion by her father and another man. Some time later, when her own daughter turned and asked her a question--a daughter who could be the twin of Susan Nason-- Eileen began to remember the rape and murder of her best friend; a memory that came to her over several days and in a random, nonchronological order.

According to Eileen, and as best as she can remember, she was riding with her father in his van when they came upon Susan Nason walking down the street. Her father stopped, offered Susan a ride, and they headed out towards Half Moon Bay. At some point, according to Eileen, her father stopped the van along a turnout along the hideway.

According to Eileen, her father got into the back of the van and began sexually assaulting Susan on a mattress he kept back there. She says she remembers him holding Susan down on the bed, and that he had grabbed the little girl's wrists which he held, with one hand, over her head. Eileen states she remembers him pulling the little girl's dress up and that he was between her legs thrusting, while Susan whimpered and cried and begged him to stop.

After he ejaculated, he and the little girl exited the van, and they proceeded a short distance down the hillside, where Susan then sat down, huddling and crying. According to Eileen, her father then picked up a big rock and struck Susan twice in the back of the head, killing her.

[END ADDENDUM]

ADULTS ALSO SUFFER TRAUMATIC DISSOCIATIVE AMNESIA

Traumatic dissociative amnesia, however, is not limited to children, but includes "hardened soldiers" (Grinker & Spiegel, 1945; Southard, 1919), as well as, presumably, normal adults (Fisher, 1982; Joseph, 1996a). For example, Fisher (1982) describes a woman who became amnesic for 18 hours after seeing her husband die right before her eyes. In another case, a druggist who was terrorized, handcuffed and robbed by two thieves, subsequently became amnesic and lost all memories of what occurred.

Moreover, some individuals appear to be predisposed to becoming profoundly stressed (Bremner et al. 1993), or suffering severe memory loss, especially if they have experienced a previous emotional trauma or prior injury to the hippocampus or inferior temporal lobe (Joseph, 1996a, 1998). In these latter instances, an emotional shock may induce an amnesia so profound that even personal identity may be forgotten. For example, Schacter and colleagues (1982) described a 21-year-old man (PN) who was discovered wondering the streets of Toronto and who had no idea as to his name or any other personal information. Presumably this amnesia was triggered by an exceedingly traumatic experience: the recent death of his beloved grandfather. However, PN may well have been predisposed to become temporarily amnesic if provided sufficient emotional shock, for a CT scan revealed a right temporal lobe injury suggestive of gliosis.

Similarly, Christianson and Nilsson (1984) described a 23-year-old female who was accosted while jogging, and beaten and then raped. Subsequently, all memory of her identity, her past life, or that of her relatives, boyfriend, or place of work, including all aspects of the rape, were completely forgotten. However, once her memory returned, it was determined she had been sexually abused as a child. Presumably, this childhood sexual trauma predisposed this young woman to suffering amnesia and/or further neurological injury in response to the severe emotional stress of being raped. A CT scan or MRI may have in fact revealed a hippocampal injury as has been reported in other cases of childhood sexual abuse (Bremner, Randall & Scott, 1995; Stein, et al., 1995) or adult trauma (Bremner, Southwick, et al., 1995; Gurvitz et al., 1996).

In fact, although not all those who are abused or assaulted may suffer profound memory loss, a clear relationship has been established between early childhood abuse, and the development of severe social emotional disturbances and limbic system injury (Joseph, 1998, 1999a,b), including child and adult onset psychopathology and dissociative abnormalities (Breitchman, Zucker, Hood, daCosta, Arkman, & Cassavia, 1992; Chu & Dill, 1990; Kolko, Moser, & Weldy, 1988; Putnam, Guroff, Silberman, Barban, & Post, 1986) and posttrauamatic stress disorder (Bremner et al., 1993; Breslau et al., 1998; Deblinger, McLeer, Atkin, Ralphe, & Foa, 1989).

For example, Bremner and colleagues (1993), have shown that at least 26% of Viet Nam veterans with PTSD admit to a history of childhood abuse whereas only 7% of those without PTSD had a similar history. However, Bremner et al. (1993) also speculate that many of those with PTSD probably denied a history of abuse for fear of losing disability benefits and that the percentage is in fact much higher.

DISSOCIATION, THE HIPPOCAMPUS, AND AMNESIA

Under conditions of terror, excessive stress and emotional abuse, not only might learning and memory be disrupted, but children and adults may experience dissociative phenomena such that they feel disconnected and split-off from their body and literally above or "beside themselves" with fear (Courtois, 1995; Grinker & Spiegel, 1945; Joseph, 1996a; Noyes & Kletti, 1977; Southard, 1919; Summit, 1983; van der Kolk & Fisler, 1995). Hence, some victims may later acknowledge or recall some of the details of their ordeal (a function, perhaps of "shrinking retrograde amnesia"), yet simultaneously feel disconnected from what transpired. As stated by Tara Burke who had been kidnaped and repeatedly raped: "it's like a story that has happened to someone else."

It has been determined based on clinical case studies involving head injury, seizures, and neurosurgical stimulation, that dissociative experiences are related to abnormal activation of the hippocampus and overlying temporal lobe (Joseph, 1996a). For example, if direct electical stimulation is applied to the hippocampus (or the hippocampus- amygdala- temporal lobe) patients may involuntarily visualize and remember their own actions as if gazing at a snapshot or from afar (Penfield & Perot, 1963; Gloor, 1992, Halgren, 1992). In fact, it has been repeatedly reported that neurosurgical and seizure patients will claim they have left their bodies and are hovering upon the ceiling staring down (Daly, 1958; Penfield, 1952; Penfield & Perot 1963; Williams, 1956). That is, during the course of hippocampal-temporal lobe activation, they claim to have split off from their body, as if they are two different people, one watching from above, the other being observed down below.

As stated by one neurosurgical patient: "it was though I were two persons, one watching, and the other having this happen to me" (Penfield & Perot, 1963). According to Penfield (1952), "it was as though the patient were attending a familiar play and was both the actor and audience." One patient reported that upon leaving her body she not only saw herself down below, but was taken to a special place "of vast proportions, and I felt as if I was in another world" (Williams, 1956) --descriptions similar to reports of "near death" experience and alien abduction.

It has been theorized (Joseph, 1996a) that since the hippocampus contains "place" neurons which cognitively map and encode one's location and movements within the environment (Nadel, 1991; O'Keefe, 1976; Wilson & McNaughton, 1993), this enablea an individual to not only remember, but to actively visualize themselves and their surroundings, and their previous and current activities (Gloor, 1992, Halgren, 1992; Joseph, 1996a). However, if abnormally activated, they may involuntarily dissociate and visualize themselves as if from afar.

However, these patients might not only experience dissociative out-of-body phenomenon during hippocampal or hippocampal-temporal lobe activation, but subsequently become completely amnesic for all that transpired (Brazier, 1966; Chapman, 1958, 1960; Chapman et al. 1967; Jasper & Rasmussen, 1958); i.e. dissociative amnesia. Likewise, when secondary to traumatic stress and excessive emotional arousal, they may develop a dissociative amnesia.

CONCLUSIONS Although there is considerable controversy regarding the issue, as has been demonstrated experimentally with animals and humans, high levels of arousal and traumatic stress exert deleterious effects on the functional integrity of the brain and the hippocampus. Depending on individual differences and the degree or repetitive nature of the trauma, memory loss may range from the minimal to a profound dissociative amnesia; a consequence of the secretion and buildup of a variety of stress-related neurochemicals including glucocosteroids which can injure and induce hippocampal atrophy.

Hence, to argue otherwise, or to dismiss biology and neurology, as Pope and colleagues have done in order to falsely claim that there is no convincing evidence for abuse- or stress-induced memory loss or dissociative amnesia, is disingenuous, unscientific, and uninformed.