Journal of Prenatal and Perinatal Psychology and Health 23(4), Summer 2009
Prenatal Aspects in Alzheimer’s Disease
Rien Verdult, Master’s in Psychology, Private Practice
ABSTRACT: Alzheimer’s disease (AD) is a degenerative brain disorder characterized bya global mental deterioration. Although the etiology is not yet clear, more evidenceshows that a prenatal link is possible. Memory disturbances are central in AD andeventually lead to a loss of autonomy and identity. Anxiety becomes the basic feeling ofAD patients, as well as experiences of mourning, loss of control, and loss of contact. Inthe manifest stage retrogenesis is triggered, that is, patients reverse develop and startto re-live their past. In emotional retrogenesis prenatal and perinatal themes can be re-experienced. In prenatal emotion-oriented care sensorimotor relaxation (‘snoezelen’) isbeing used to reduce anxiety. The patient is given an environment that reflects thecharacteristics of a womb, and the nursing staff ’s approach should be to symbolize the‘good-enough’ mother.
KEY WORDS: Alzheimer’s disease, etiology, retrogenesis, prenatal themes, emotion-oriented care
Dementia is a clinical syndrome characterized by a global
deterioration of mental functioning, afflicting daily life seriously.
Alzheimer’ disease (AD) is the most common cause of dementia. Inabout 60% of patients Alzheimer’s is the main cause of the mentaldecline. As people increasingly get older, more of them developAlzheimer’s disease. Prevalence rates go up sharply with age,doubling about every 5 years, at least until the age of 85, when therise begins to slow. It is estimated that 2-5% of people over 65 yearsof age and up to 20-25% of those over 85 years endure the disease.
Worldwide more than 25 million people suffered various forms ofdementia in 2000. Some speak of the Alzheimer epidemic. By 2030 itis expected that there will be 63 million patients, and 65% of thesewill reside in less developed countries (Swedish Council, 2008).
Rien Verdult, a developmental psychologist and psychotherapist, hasworked with Alzheimer patients for 20 years. He also has a privatepractice as a prenatal psychotherapist for adults and babies. Directcorrespondence to: Opleeuwstraat 59, B 3840 Gors-Opleeuw, Belgium.[email protected]
2009 Association for Pre-and Perinatal Psychology and Health
Journal of Prenatal and Perinatal Psychology and Health
In 1995 1.9 million Americans 64 years or older had AD. By the
year 2015, 2.9 million Americans will have this disease, and of these,more than 1.7 million would need active assistance in personal care. Inmy country of Belgium (10 million inhabitants) 9.3% of people over 65years of age suffer from AD. The number of AD patients is expected torise from 160,000 in the year 2001 to 251,000 in the year 2030.
Alzheimer’s disease is a progressive, degenerative and irreversible
brain disorder that causes intellectual impairment, disorientation andeventually death. AD has a gradual onset and progressive decline. AGerman doctor, Alöis Alzheimer, described the disease in 1905. Thepatient he detailed was Johann Feigl, a man in his early fifties andwho had severe memory problems, challenges in performing everydaytasks, and language difficulties. He was also disoriented as to time andspace. And like Mr. Feigl, most Alzheimer patients have problems withabstract thinking, loss of initiative and decreased judgment. There arechanges in their personalities, as well as their moods and behaviors.
There are other types of dementia, like dementia with Lewy bodies,
which gets its name from tiny structures that develop inside nervecells, and which trigger the degeneration of brain tissue. Anothercommon cause of dementia, which is responsible for about 20% of thedementias is a vascular disease by which the blood supply to the brainis diminished. Other causes of dementia include: Creutzfeld-Jacobdisease, Binswanger’s disease, the frontal lobe dementia or Korsakoff ’ssyndrome. This article is limited to Alzheimer’ disease (AD) becausethis group includes the majority of patients and the other diseases leadto minor variations in their experiential world.
At this moment no cure is available for Alzheimer’s. A variety of
drug treatments claim to show beneficial effects for patients, such as,cholinesterase inhibitors. However, most drugs have minor and short-term positive effects in the early stages of Alzheimer’s disease, and donot cure the patient. A definitive cure for this degenerative disease isnot to be expected within the next two decades.
The causes of Alzheimer’s are not yet fully understood. The etiology
is a complex interaction of many genetic, environmental and life-stylerisk factors, with age and genetics most probably playing the largestpart. The hallmark of AD is the extracellular accumulation anddeposition of insoluble amyloid protein, to be found in the form of
amyloid plaques. Equally conspicuous is the intraneuronal occurrenceof neurofibrillary tangles, consisting mainly of tau-protein. Theseamyloid plaques and neurofibrillary tangles are characteristic, but notspecific to AD. Similar changes can be found in healthy aging processesand in various other neurodegenerative diseases.
Although there seems to be a large heterogeneity in the causes of
AD, the amyloid-cascade-hypothesis has taken a central position as amodel for the general etiology. This hypothesis was first formulated in1992 and points to the cytotoxicity of mature aggregated amyloidfibrils, which are believed to be the toxic form of the proteinresponsible for disrupting the cell’s calcium ion homeostasis and thusinducing apotosis (Hardy & Selkoe, 2002). The amyloid plaques andtangles are considered not to be the key symptoms of AD but ratherthe cause of the disease. The regulation of amyloid plaques underliesa diversity of cellular and molecular factors. Disturbances in thecerebral glucose metabolism, especially in the hippocampal regions,are a further factor in the pathogenesis of AD. The widespread loss ofcortical cholinergic neurotransmission associated with the cognitivedeficits is another important factor. The question remains unansweredwhether these factors are causing AD or are correlated with AD.
Biomedical and genetic research on AD is dominant in the field.
This implies that psychological factors are infrequently included in theetiological research on AD, although it can be speculated that prenatalstress and/or depression can play a crucial role in triggeringbiochemical brain disturbances. In 1985 I myself did a small-scaleresearch on the influence of early loss experiences in the etiology ofAD. When elderly people, born between 1910-1920, had lost one or bothof their parents before the age of 10 years, they had a significantlyhigher risk of becoming demented (Verdult & Miesen, 1986). Althoughthis research had many methodological limitations there was a strongindication that loss experiences could be a risk factor in AD. Early lossexperiences can lead to depression in later life. A possible confirmationon the role of loss experiences in AD could be found in theaccumulating evidence that suggests that a history of depressionconstitutes a significant risk factor for developing AD. A Dutchepidemiologic research effort showed that people with a history ofdepression, particularly with early onset before the age of 60 years,have a three times higher risk of having AD, compared to people whohave never been depressed (Geerlings, den Heijer, Koudstaal &Breteler, 2008). Depression can be seen as a major risk factor in AD(Lu, Edland, Teng, Petersen & Cummings, 2009).
Greater activity of the hypothalamic-pituitary-adrenal (HPA) axis
Journal of Prenatal and Perinatal Psychology and Health
is associated with specific neurological and psychiatric disorders,including Alzheimer’s disease and depression. Hyperactivation ofparaventricular corticotrophin-releasing hormone (CRH) neurons mayform the basis of this increased activity of the HPA axis. Thishyperactivation contributes to the etiology of these disorders(Raadsheer, Van Heerikhuize, Lucassen, Hoogdijk, Tilders & Swaab,1995). Exposure to excessive prenatal stress can alter the level ofactivity of the HPA axis, and this prenatal setting of stress levels canbe consistent into adult life. Research shows that prenatal maternalstress has its effects on the stress of the fetus and newborn (Robles deMedina, 2004), and on the later adult (Nathaliensz, 1999). The HPAaxis is prenatally programmed. From this reasoning it can behypothesized that prenatal stress can be linked to the hyperactivationof CRH-releasing neurons in Alzheimer’s disease.
Recently, a link was discovered between prenatal developmental
processes and the deterioration processes in Alzheimer’s. Researchersat a U.S. biotechnology company, Genentech Inc., proposed a linkbetween the reactivation in AD to that of a process in fetaldevelopment (Nikolaev, Mclaughin, O’Leary & Tessier-Lavigne, 2009).
This research group suggested that a normal process in which excessnerve cells and nerve fibers are pruned from the developing brainduring prenatal life is somehow reactivated in the adult brain andhijacked to cause the death of such cells in AD. In the prenatal braintwice as many neurons as we need are developed. The process ofapoptosis clears out unneeded cells. Unneeded cells are neurons thathave not succeeded in making new connections. Only neurons thatwire together can survive. This prenatal pruning process may betriggered in Alzheimer’s. It is not the beta amyloid precursor protein (APP) that kills nerve cells in AD; it is what is involved in the prenatalpruning. The prenatal pruning process is sparked by another fragmentof the amyloid precursor protein, namely N-APP, causing a cascade ofevents that results in the death of unneeded neurons. This prenatallink implies that getting Alzheimer’s disease is not just bad luck, butrather is the activation of a pathway that is there for developmentalreasons. If this hypothesis could be validated, it can be an importantstep in understanding the psychopathology of AD. Research on whattriggers the reappearance in the adult brain of a process fundamentalto its early prenatal development can open a variety of curingpossibilities.
Memory Disturbances in Alzheimer’s Disease
Cognitive impairment in AD contains memory disorders and
higher cortical dysfunctions like aphasia, apraxia and agnosia. Theloss of memory is the key symptom of Alzheimer’s disease, oftenappearing first in the deterioration process. It is important to stressthat cognitive impairment does not immediately cause a total loss ofall cognitive skills. A pattern unfolds in which some cognitive abilitiesare relatively well preserved and some are seriously impaired. In ADthe multimodal association cortex is impaired (including thehippocampus complex in the medial temporal cortex, and theassociation fields in the dorsolateral and orbitofrontal cortex and thetemporal and parietal cortex). Functional disorders in these areascause impairment of memory for recent events, and in the long runimpairment of the long-term memory, purposeful action, languageexpression and understanding, and three-dimensional perception(Diesfeldt, 2003). Alzheimer’s does not seem to have a noticeableimpact on some brain functions. Functions of the primary motor andsomatosensory cortex, of the primary sensory cortex (auditory andvisual), the cerebellum and the basal ganglia remain intact for arelatively long period of time. This distribution of selective loss andpreservation is reflected in a specific pattern of lost and preservedmemory skills.
In the prevailing models of the architecture of the human memory
a distinction is made between short-term memory or working memoryon the one hand, and long-term memory on the other hand. In the long-term memory a distinction is made between the procedural, implicit orunconscious processes and the declarative or explicit processes. In thelatter, episodic and semantic memory functions can be described. Forthe purpose of this contribution I shall focus on the long-term memoryand more specific the episodic aspects of the memory system.
According to Tulving, an authoritative expert in the field of memoryresearch, episodic memories are impossible without semantic memory.
There is a strong interdependency between the two processes, meaningthat episodic memories depend on prior semantic processes (Tulving &Markovitsch, 1998). All of our personally acquired knowledge, asstored in our semantic memory, is based on episodic experiences. Ineveryday life we do not have to make an effort to notice thatmeaningful experiences are almost automatically recorded in theepisodic memory. This implies that our episodic memory containsmeaningful experiences that we have acquired during our entire lifespan from the moment we were developing our semantic memory. That
Journal of Prenatal and Perinatal Psychology and Health
is why it is stated that episodic memory starts with the acquisition oflanguage skills, which make it possible to store general knowledge inthe semantic memory and thereby make episodic memory possible.
Normally people can find episodic memories from about two years ofage, when the semantic memory is functioning enough to makeepisodic memories possible. Does this mean that we do not havememories from before two years of age? Human beings are unable toretrieve birth memories or prenatal memories from the episodicmemory system, but prenatal research has shown that we have othermemory systems that make it possible to remember birth and wombexperiences (Chamberlain, 1998). Wade (1998) has offered an overviewof possible memory systems that can explain this human possibility toremember beyond the limitations of the episodic long-term memory.
There is evidence for a physically transcendent memory and a cellularmemory source.
The memory decline in AD normally begins with the working
memory, which makes it difficult for patients to update data essentialfor the successful execution of a task, or to retrieve what they havedone a few moments ago. In everyday life this implies that with theslightest distraction they forget what they are doing, or they getconfused when telling a story, or they forget what they have just beeneating or that they have been eating at all. Later in the process theepisodic memory system begins to fall apart. This will mean thatpatients can’t remember an ever-growing larger part of their personalhistory. ‘Was I married?’ ‘Do I have children?’ ‘What work did I do?’These remain unanswered questions for the patient.
In AD the decline of the declarative episodic memory is not
random, but a pattern can be distinguished. Clinical evidence showsthat recent episodic memories are lost earlier than older ones. Thismeans that it is possible that an Alzheimer patient cannot rememberwhat he experienced 5 years ago, even though he might have gonethrough major life-events, such as, losing a spouse, retiring or havingserious health problems. At the same time, however, he can rememberhis childhood fairly well, and with lively details. Essentially, the partsof their lives that AD patients remember goes further and further backin time. The Dutch gerontologist Huub Buijssen (2001) has called thisprocess the gradual and backwards rolling up of the memory. It is alsocalled retrogenesis (Reisberg & Franssen, 1999).
In my clinical work I made a distinction between remembering and
reliving (Verdult, 1993). In the initial stage AD patients can retrieveinformation from the episodic long-term memory, in the same way andwith the same limitations as non-patients do. In this beginning stage
the short-term memory is declining, but the long-term episodicmemory stays relatively intact. I explicitly use the words ‘toremember’, because in this initial phase of AD the patient knows whenhe is talking about his life-span experiences. In other words he candistinguish between actual and past experiences. There is no confusionin time.
However, from the moderate stage of AD on, patients start to live
in the past and this past goes further and further back. A qualitativeshift takes place in the way an Alzheimer patient deals with memories.
Life span experiences are no longer retrieved from the episodicmemory in the normal way within the right context of the life span, butthey are re-experienced in a regressive way. Alzheimer patientsgradually start living in the past. As a rule it can be seen in clinicalpractice that the more AD patients deteriorate the more they go on re-experiencing the past, and the more they go back in time (Verdult,1993). Essentially, the part of their lives that they relive or re-experience is further and further back. This process is also calledemotional retrogenesis. Mrs. A. was reliving the punishments shereceived from her violent father, as if she was experiencing his violencein present time. Mr. B. who survived the holocaust was in fact living ina nursing home, but he himself is reliving his concentration campexperiences, which were triggered by the closed doors of the ward. Mrs.
C. was re-experiencing her childhood sexual abuse, which made hervery defensive in the bathroom during her daily care. These patientshave lost the ability to place their life span experiences in the rightcontext. To them these past experiences are happening now and theyact according to the feelings that go with these experiences.
When the degenerative process goes on, many Alzheimer’s patients
become dependent on care. This means that their remaining quality oflife mostly depends on how they are taken care of. After the SecondWorld War dementia care showed many of the same characteristics astotal institutionalized care, as described by Goffman (1968). Hiscritical analysis of the position of mental patients caused a major shiftin psychiatric care. Sociotherapy emerged stating that if theenvironment can have a devastating influence on cognitive, emotionaland social functioning of patients in long-term care facilities, then theenvironment should be changed in such a way that positive effects canbe reached. In geriatric care sociotherapy was introduced in Europe inthe late seventies (Verdult & Pelgrims, 1986). As long as there is no
Journal of Prenatal and Perinatal Psychology and Health
cure for AD, improving and maintaining the quality of life of peoplewith AD should be the highest priority in care giving. During the lastdecades several psychosocial treatments have been developed indementia care (APA, 1997). Supportive therapies were generated aswell. Folsom (1968) introduced reality orientation. Psychomotortherapy, music therapy, reminiscence, sensorimotor therapy andoccupational therapies were also introduced (Verdult, 1989). Thetherapeutic nihilism was left behind.
A new culture of dementia care had arisen. This shift in care
stressed the uniqueness of the patient, a respect for his subjectivity inexperiencing events and an answer to his psychological disintegrationof a caring and supportive relationship (Kitwood, 1997). Until then itwas thought that Alzheimer patients did not have any insight in theirdisease, and thus were not experiencing their decline. Feelings andemotional needs of Alzheimer patients were denied because of theemphasis on rational insight into symptoms and behaviors. Notknowing, or not being able to describe what exactly is happening toyou, does not means that one has no feelings and no emotional needs.
Clinical observations and research have proven that Alzheimerpatients respond to their illness, even long after their illness-insighthas disappeared. Emotional awareness by AD patients receivesgreater acknowledgement (Miesen, 1997), yet more responsiveness isneeded, for example, AD patients experience the deterioration processwhereby they lose their autonomy and identity. This awareness-context brings the patient into a chronic traumatic experience.
Becoming demented is not only a confrontation with cognitiveimpairment, but also with a disintegration of personality. Elderlyhaving AD can be truly called patients in the real sense of the word,namely, they are suffering. In sum, AD is a painful and threateningprocess (Verdult, 2003).
In the eighties Naomi Feil introduced a new method for
communicating with Alzheimer patients. This counseling method wascalled validation therapy (Feil, 1982). Her message was: ‘step into theirshoes’ instead of trying to orient Alzheimer patients to the reality ofthe health care system. It was believed better to enter their innerworld, acquiring insight into the emotional and associative way inwhich Alzheimer patients respond to their perceptions andexperiences, and communicate with empathy to their feelings andemotional needs. Her method meant a new direction in the care fordementing elderly, namely, emotion-oriented care (Verdult, 1993).
Surprisingly, historic research showed that Aloïs Alzheimer himselfalready pleaded for a ‘non-restraint’ method in the care of psychiatric
patients, including the patients who suffered from the disease thatlater became to carry his name (Jürgs, 1999). Research on emotion-oriented care showed that demented nursing home residents weremore balanced emotionally. They also had a smaller increase indissatisfaction with the current situation (preservation of positive self-image) (Finnema, 2000). Emotion-oriented care does not have positiveeffects on cognitive and social adaptation but does improve thefunctioning of Alzheimer patients, although there is limited evidencefor the effectiveness (Finnema, Droës, Ribbe &Van Tilburg, 2000).
Problem behavior, such as apathy, depression and aggression, does notseem
(Schrijnemaeker, et al., 2002). Most of the mentioned research is donein the Netherlands where there is a high level of institutional care.
Research on the effect of validation therapy on American nursinghome residents showed a slightly positive effect on problem behavior,especially depression and verbal aggression (Toseland, et al., 1997).
These studies can be criticized. The number of studies are limited; thestudied populations have a high degree of heterogeneity; the researchis mostly done on validation therapy and not on other emotion-oriented models; although the goals seem comparable, namelyimproving the well-being of patients, the methods to achieve thesegoals can be totally different; and finally, nursing staff only receivedshort introductions to, and training in, the used approach. In myopinion a valuable research study would be one where the attitudes orviewpoints of nursing staff could be changed in the direction of aperson-centered emotion-oriented care with the hypothesis that theeffects on the emotional functioning of AD patients would improve.
The Experiential World of Alzheimer’s Patients: Loss of Autonomy
Continuing with this theme, a new perspective in dementia care
was introduced with more empathy for the suffering of AD patients.
However, most new models lack a comprehensive view on theexperiential world of AD patients. That is why I introduced a newmodel for describing the inner experiential world of AD patients. Icalled this model a person-centered experiential approach
(Verdult,1993, 1997, 2003). A crucial assumption in this model is that anxietyis the basic feeling of Alzheimer patients. The loss of cognitive abilitiesand consequently the loss of autonomy and identity make Alzheimerpatient suffer painfully. Their growing insecurity and despairundermine their inner strength. In my model the inner world ofAlzheimer patients can be described by four main factors: the loss of
Journal of Prenatal and Perinatal Psychology and Health
autonomy, the process of retrogenesis, hospitalization and its long-term effects, and personality changes. In this article I shall onlydiscuss the loss of autonomy and retrogenesis.
The threatened self.
The loss of autonomy makes it difficult for
patients to produce decisions and judgments, to fill their lives withpurpose, and certainly, to take care of themselves. AD patients becomemore and more depended on their caregivers. In the initial stage of thedisease the environment can conceal first manifestations because theymostly don’t interfere significantly with daily activities. The patients,however, are often aware of, and attempting to understand and dealwith, the functional decline. Cortical information processing is stillpossible, although problems arise more and more. Becoming moreforgetful, misplacing things, minor speech difficulties like not findingthe right word, or orienting problems, can be denied or minimized bythe patient. The mental changes associated with AD are in this earlystage rather non-specific and mainly experienced by the patienthimself.
This initial stage I call the stage of ‘the threatened self ’. As the
patients are experiencing the ever-growing loss of capabilities, thefuture is under threat: ‘What’s going on?’ ’What can I do about it?’ or‘Where will this end?’ The patients can feel insecure and uncertain.
The more they are confronted with their losses, the more they start togrieve. General grief responses, such as denial, sadness and despair,can be commonly seen in AD patients. Alzheimer patients have aperiod of denial, in which they try to minimize their dysfunctions. Theytry to prove to themselves that they are still in control and nothingserious is happening. After this period of denial more grief responsesbecomes apparent. AD patients can be very sad, sometimes depressed;despair can lead to outbursts of intense crying; unable to accept theirdecline patients can become angry. As the AD process is a fight one cannever win, the ongoing decline can make the patient desperate.
The lost self.
In this manifest stage the progress of the mental
deterioration is dominated by dysmnesia, dysphasia, dyspraxia anddysgnosia. These symptoms lead to further loss of autonomy, daily lifegets more confused and taking care of oneself becomes more difficult.
Disorientation in time, place and persons make patients more anxious.
The AD patients behave somewhat out of control and organizing theirlives is difficult. Their coping strategies start to fail more and moreand this makes it difficult to handle daily life situations. Emotionalinformation processing is dominant in this stage.
I call this manifest stage of the Alzheimer’s process the ‘the lost
self ’. In this stage the loss of control is producing a lot of anxiety in
patients. If one does not know where one is, or what is expected in asituation, or what is being said to you, then life becomes out of control.
Patients are more and more looking for containment. By creatingcontrollable situations, by collecting items, by sticking more to ritualsand habits, by making their world smaller, or by claiming contact,these patients try to establish safer environments. By using the‘strange situation’ as research model, Miesen (1992, 1993) showed thatAlzheimer patients have attachment patterns just like children do.
The classical Bowlbian attachment patterns can be seen in Alzheimerpatients. These findings show that AD patients feel more and moreinsecure and look for attachment figures that can offer more securityand containment. In this stage the process of retrogenesis gets startedand identity loss generates feelings of being lost.
The vanishing self.
In the final or terminal stage AD patients
become fully depended on their caregivers. The mental deteriorationcontinues, involving most cognitive functions. Declarative memorydisorders are complete, verbal communication becomes sporadic andunreliable, endless repetition of movements can become apparent, thepatients become apathetic. More and more the patients seem to belocked up in an inner world that loses contact with the outer world.
The anxiety results from the bodily-felt isolation, which is a not-human condition. Mental functioning is reduced to sensorimotorinformation processing.
I call this terminal stage the stage of the ‘vanishing self ’. Their
experiential world can be described as a prototaxic way of being. By aprototaxic experience Harry Stack Sullivan meant a way of being inwhich there is no sense of time and place, and one experiences oneselfas separated from the environment (Chapman & Chapman, 1980). Inthe final stage of Alzheimer’s disease, other people no longer seem toexist and an interpersonal world changes more and more into anintrapersonal world. Said another way, the AD patient closes himselfoff from the outside world and seems to vanish into a difficult innerworld in which body sensations and elementary sensorimotor inputseem to dominate. It is in this final stage that prenatal themes start toreappear. The body’s posture and movements become more and morefetal.
Barry Reisberg, professor of psychiatry at the New York University
School of Medicine created the theory of retrogenesis in AD, statingthat the decline in AD mimics regression toward infancy. Clearly AD
Journal of Prenatal and Perinatal Psychology and Health
patients are unable to function as adults (i.e., the inability to hold ajob, handle finances, or solve abstract problems). They lose social andmoral functioning, the ability to make choices about clothing, theability to take care of themselves, speech, and lose control over bladderand bowels. Thus, Reisberg’s research gives us a better understandingof the process of Alzheimer’s disease. Retrogenesis brings moredefinition to the AD process. I myself have described this process as areturn to childhood, as a process of losing identity (Verdult, 1993).
When AD patients start to live in the past they have lost the largestpart of their history. For example, if an AD patient starts living in hisadolescent period, reliving his boarding school experiences, he thenhas lost his identity as an adult, a middle-aged and old-aged person.
Patients with Alzheimer’s reverse develop
. Clinical and neurological
studies have compared the mental and physical stages of infant andchild development to the reverse process of AD. This is also called aprocess of degenerative developmental recapitulation. Retrogenesis isdefined as the process by which degenerative mechanisms reverse theorder of acquisition in normal development (Reisberg & Franssen,1999; Reisberg, Franssen, et al., 1999; Reisberg, Franssen, Souren, etal., 2002). A distinction can be made between neuropathologic,neurologic, functional and cognitive retrogenesis (Rogers & Arango,2006). According to the theory of neuropathologic retrogenesis parts ofthe brain that undergo late myelination in child development are firstto undergo demyelination and develop pathologic intra- and extracellular changes in AD. From Paul McLean’s triune brain evolutiontheory (MacLean, 1990) it can be deduced that AD patients degeneratefrom cortical functioning, to limbic system functioning, to brain stemfunctioning. The brain deterioration in AD patients reflects the reverseof brain evolution in mankind. Neurologic retrogenetic research hasshown that the so-called developmental reflexes, like sucking, handand foot grasp reflexes, the rooting reflex and the Babinski plantarextension reflex re-appear in patients with advanced stage AD. TwoDutch researchers of Reisberg’s team have shown that the motordecline in AD is mirroring the psychomotor development of the child(Souren & Franssen, 1993). Infantile reflexes, which mark theemergence from infancy in normal development, are indicators for theterminal stage of AD.
As there is a link between neuropathological declines in AD and
progressively worsening cognitive and functional abilities, it can beexpected that the deterioration of the brain can be linked to clinicalmanifestations in different stages of the AD process. The stages in ADcan be translated into corresponding developmental ages. Functions
learned in childhood, like clothing and self care are being lost in AD.
In cognitive retrogenesis the cognitive performance mirrors thepattern of cognitive development in children as described by Piaget(McGregor, 1991; Verdult, 1993). Patients in the initial stage still havecortical functioning and Piagetian formal operational functioning.
Mildly demented patients return to concrete operational andpreoperational functioning, while severe or terminal patients return toa sensorimotor level of cognitive functioning.
I myself described the emotional retrogenesis in AD as a crucial
part of the loss of identity (Verdult, 1993). In the decline of AD threeaspects of emotional retrogenesis can be distinguished. These are there-living of emotions that belong 1) to social roles, 2) to traumaticlifespan experiences, 3) and to unfulfilled basic needs from childhoodand infancy. Mrs. D. can be called a schoolbook example of emotionalretrogenesis. In the stage of the lost self, she started to look after hersmall children and became very upset when she could not do so,thinking they might get lost after school. About a year later sheexperienced herself as a young girl, needed to go home, because herparents were waiting for her. About another year later she regressedto become a toddler playing with her feces when she was angry aboutsomething. When I left the nursing home she was in fetal position,lying in bed all day.
In emotional retrogenesis Alzheimer patients normally start to re-
experience former social roles that they fulfilled in their early adultlives. Usually they return to age of about 25 to 30 years old. Mrs. E. isan eighty-year-old woman who was a secretary in a big company. Everymorning she was looking for the way out to go to work, and becamefrustrated and angry at not being allowed to go, fearing that she mightget fired. Dr. F. was a retired physician who did his consultations onthe ward, not only giving advice to his fellow patients, but also tryingto examine them. Mr. G. was a fisherman and in the nursing home hewould still bring baskets full of fish to the fish market, where he triedto sell his product.
This period of re-experiencing former social roles is followed by a
period of re-experiencing personal traumatic experiences. I agree withFeil that Alzheimer patients re-live old conflicts and traumaticexperiences (Feil, 1982). I don’t agree that they do this in order toresolve these conflicts and traumas, and thereby restore their dignity.
Not only have I never seen this in my clinical work, but also there arepsychotherapeutic and theoretical considerations that underline mythesis and suggest that this is not possible in Alzheimer’s disease(Verdult & Visser, 1990; Verdult, 1991). Their re-living can be seen as
Journal of Prenatal and Perinatal Psychology and Health
a way of trying to resolve trauma on an unconscious level, but nohealing, in the strict sense, takes place on this level. This is visibly apainful reality for AD patients. Mrs. H. was a 75-years-old AD patientwho could be in full panic because she was delivering a baby and themidwife (it was in a Dutch nursing home!) was not there yet. Mr. J. wasa prisoner of war during World War II and during his emotionalretrogenesis he anxiously re-lived his war experiences, fifty years afterthe ending of the World War II. Mrs. K. was 82-years-old and every dayshe sat for hours at the window waiting for her parents to come andget her. It is a well-known fact that Alzheimer patients can look fortheir parents as if they are still alive. Miesen (1992) called this processin Alzheimer patients parent fixation. Mrs. L. was a 73-year-oldwoman who almost daily escaped from the nursing home where Iworked. We usually found her back at her childhood house where shelived with her parents in the first fifteen years of her life, sitting in thefront of the house waiting for her parents to come home.
The process of retrogenesis has been questioned. First,
behaviorally-oriented practitioners don’t believe in a “secondchildhood” for Alzheimer’s patients. This is because in general theydeny the influences of past experiences on actual functioning. Second,and the more fundamental question is: How far can Alzheimerpatients regress? Scientific psychologists state, if they accept thehypothesis of retrogenesis, specifically, that AD patients can regress tothe beginning of memory, do they mean the declarative, episodicmemory? Episodic memory requires a certain level of languageacquisition, so this usually is at the age of two or three years old. Butin my clinical practice I have seen patients sucking on everything theycan get in their hands, just like babies do. I have also fed patients,unable to feed themselves or to be fed with a spoon, with milk bottles.
I have seen terminal stage patients in a fetal position showing birthmovements. Reisberg’s model of retrogenesis is based on the premisethat development starts at birth. He spoke of a mild AD patient withmental abilities and habits of a 12-year-old child regressing to levels ofsuccessively younger children and even infants (Reisberg, 1999).
Prenatal psychology has shown the scenario differently: prenatal andpostnatal development demonstrates continuity. Postnatal life is acontinuation of prenatal life. Human development does not start atbirth but at conception. Why then should the process of retrogenesisstop at birth? In my view the process of deterioration in AD stopswhere development has begun, and that is at conception. Or statedotherwise: where life or consciousness began, Alzheimer’s disease willend (Verdult, 1997).
Emerson (1998b) stated that recapitulation is the
most important concept in understanding the impacts of birth,prenatal life and obstetrical interventions. He defined recapitulationas the process whereby people unconsciously recreate past events andtraumatic experiences in their lives. They do so in an attempt toexternalize traumas from the unconscious so that they might be dealtwith in here-and-now-reality, and cathartically released from theirsystems. Recapitulation and retrogenesis differ on the aspect of adultfunctioning. In recapitulation the person still keeps his adultfunctioning, or can come back into adult functioning. It might be thathis unconscious takes over control, but regardless, there alwaysremains a part of a functioning adult. In retrogenesis no return toadult functioning is possible; the here-and-now has become the there-and-then. Present and past fall together. In this contribution I don’t gointo recapitulation, although I don’t deny that this process is alsoactive in AD patients, as it is in all adults. What I want to describe hereis what Alzheimer patients do when they are re-living birth andprenatal life.
The process of retrogenesis gradually brings Alzheimer patients
further and further back into childhood, infancy and finally into birthand prenatal life. Let it be clear that not all AD patients re-liveprenatal life, only very severe terminal patients can re-experienceprenatal themes. Most patients have died before they even enter thisfinal stage of dementia.
As perinatal experiences and possible trauma can be stored
in the body, birth movements can be seen in terminal patients. If theystill can change lie-positions, to my experience, terminal Alzheimerpatients prefer to lie on their birth lie-side, when they have returnedto fetal position. The birth lie-side is the position of the baby duringthe birth process. It is the side of the baby that lies on the mother’sspinal cord, and this can be seen in postural body signals (Emerson,1996a). These postural signals of birth can also be observed in ADpatients. When AD patients are turned on their non lie-side, in thecontext of a decubitus (bed sore) preventive strategy or because nursesdon’t respect the preferred lie-side, they try to turn back to their birthlie-side. If they are unable to turn themselves, restlessness occurs.
Emerson (ibid.) also described the birth process in four stages, basedon movements of the baby’s head and torso in relation to the mother’spelvis. Stage 1 is the stage of the transverse or descending cranium inwhich feelings of being stuck can be dominant. Mrs. M. was an 81-year-old patient in the severe final stage of dementia. She was lying in bedalmost all day, and mostly in the fetal position, in flexion (chin to the
Journal of Prenatal and Perinatal Psychology and Health
chest). Her legs were pulled to the abdomen. In this position she wasoften seen head-banging against the frame of the bed, which can beinterpreted as a retrogenetic re-living of Stage 1 birth trauma. Movingher from her chair into bed, a transition, could activate a sympatheticshock pattern in her; she could be shouting intensively, trying to bitethe nurses. Transition and cooperation are also Stage 1 themes. InStage 2, the rotational cranium, the head turns towards the sacrum.
This rotational movement can be observed when a terminal ADpatient turns in his bed not on his back, but with his head down, as ifthe mattress was the pelvis. I have seen AD patients saying “No” forhours, a well-known symptom of Stage 2 trauma. In Stage 3 the headis going to be born and it has moved to extension. One can see thetypical Stage 3 posture, head in the neck, in severe patients. Thepushing of the legs is typical in this stage. Mr. N. was put in his wheelchair to go to the bathroom for a shower. He was a 77-years-oldterminal and severely demented man. When he was set up he put hishead in his neck and started to push with his legs, trying to get out ofhis fetal position into an extension position. If cord complications haveoccurred during birth, it can be observed that patients have a tendencyto move backwards and they can be extremely activated if they arecovered with blankets.
As I mostly worked in Dutch nursing homes, and with patients
from the cohort of 1910-1930 of whom 99% were born at home, no birthtrauma due to obstetrical interventions were observed by me. I canimagine that Alzheimer patients born cesarean can show the themesthat perinatal psychology associates with this traumatic birth. Tactiledefensiveness, difficulties with being interrupted, experiencing loss ofcontrol easily, feeling invaded quickly, or showing shock patternsrelated to the cesarean surgery as can be seen in babies and adultsborn by this method (Emerson, 1998; Verdult, 2009a). I presume thatthese manifestations can be observed in Alzheimer patients who relivetheir traumatic birth experiences.
All early experiences leave imprints in our bodies and
shock experiences leave the most intense imprints. The earlier in lifeshock takes place the more intense the bodily imprint will be. Prenatalshock will program those brain systems that are in a critical stage ofdevelopment, especially the brain stem and the oldest parts of thelimbic system, and their connections to the autonomic nervous system.
Shock can program the autonomic nervous system permanently.
Prenatal shock is stored in the body as patterns of tone and tension, aspostures or movements (Emerson, 1996b). The hypothesis ofretrogenesis would deduce that the earlier the imprint has taken place
in prenatal life, the longer it can be activated in AD. Or said otherwise,the earlier programmed, the later activated in AD. In sum, prenatalshock activations can be seen in AD patients in body symptoms andbody movements associated with shock.
In the terminal stage (the ‘vanishing self ’ stage) a distinction is
made between the locomotory and sensory sub-stages. Repetitivemotions and sounds characterize the locomotory sub-stage of theterminal stage of AD. The symptoms in this sub-stage can beassociated with sympathetic shock activation. A terminal AD patientcan demonstrate feeling endangered when he is actually responding topast associative links from his prenatal traumas. As the vulnerabilityincreases in AD, even minor interventions can lead to activation. Hissympathetic nervous system can be ‘turned on’ causing a higherarousal, greater hyperactivity, accelerated and deeper respiration inresponse to the need for more oxygen, an increase of blood flow to themuscles and decreased blood flow to the cortex, increased vigilance tothe environment, and suppression of all physical system not essentialfor defense. His sympathetic activation is a defense against threat. Ifthe sensory sub-stage movements vanish, an increasing loss of self-awareness can be observed; patients don’t respond unless through acombination of close contact, nurturing touches, soft speech and eyecontact. This sensory sub-stage can be seen as parasympathetic shockactivation. As relational isolation and lack of self-awareness increase,anxiety intensifies too. If the sympathetic defense systems (fight-or-flight) are unsuccessful in assuring safety, the parasympatheticnervous system (or freeze) becomes the next line of defense (Porges,2001). The parasympathetic reaction can be described as follows: manyfunctions of the body begin to slow down, leading to a decrease in heartrate and respiration, a sense of numbness, shutting down within themind, and separation from the sense of self. This could be an exactdescription of the sensory sub-stage of the ‘vanishing self stage’ in AD.
Of course these interpretations are speculative. The first problem
is that body functions, like breathing, cardiovascular circulation,thermoregulation, digestion, secretion, motion, and neurologicalfunctioning, decline in AD, especially in the terminal stage of thedisease. The autonomic nervous system declines along with the centralnervous system. This makes it difficult to distinguish between thesymptoms related to the deterioration of the body functions and shockactivation. The second problem is that little or nothing is known aboutthe prenatal life of patients. Most patients don’t, nor do their familiesknow anything about their prenatal life, but clinical hypotheses can beconfirmed by the results of the treatments that are based on these
Journal of Prenatal and Perinatal Psychology and Health
hypotheses. An example can illustrate my position on this subject. Mrs.
O. was lying in bed in fetal position for almost one year when I firstmet her. It was not possible to communicate verbally with her. Thenursing staff found out that she became more open for contact whenthey used vibroacoustic stimulation. I became involved with Mrs. O.
because the nurses observed that she could get “aggressive”, as theycalled it, in certain situations. For me Mrs. O. was a vulnerableprenate, who felt invaded by too much sensory input and by nurseswho asked too much of her. My hypothesis was that she hadexperienced a strong umbilical affective shock, a prenatal defensiveagainst people who gave too little love and attention. When the caregiving of Mrs. O. became less invasive, and changed into more ‘giving’instead of ‘asking’, her ‘aggressiveness’ was reduced. I considered thisas a confirmation of my hypotheses, knowing of course that otherinterpretations are possible.
To discuss all possible traumatic experiences and their re-
appearance in retrogenesis in AD would be lengthy. However, I haveseen severe AD patients showing ‘naval radiation’, as described byHartley (1995). Prenatal psychomotor development is organizedaround the navel center, from which it radiates through the wholebody. Navel radiation is associated with umbilical affect. Frank Lakedefined umbilical affect as the feeling state of the fetus as broughtabout by blood reaching him through the umbilical vein. Thismaternal-fetal ‘affect flow’ transmits the emotional state of the motherto the fetus by way of the umbilical cord (Maret, 1997). This affect flowforms the blueprint for later attachment relations and every prenataltrauma will affect this first relationship negatively. Personally, I thinkthat Frank Lake’s ‘ideal stress/trauma’ index can be associated withsafe attachment; his ‘coping’ level of prenatal stress with ambivalentattachment; ‘oppositional stress’ can be linked to avoidant attachmentand ‘trans marginal stress’ to disorganized attachment patterns(Verdult, 2009b). As demented patients show attachment behaviors(Miesen, 1992, 1993), I myself am looking for attachment signals, evenin severely demented patients, like in the ‘vanishing’ stage.
Disturbances in the prenatal attachment relation can manifest in athreat to dissolve/ disintegrate, a threat of being destroyed, of beingexpelled, or of being invaded (Krens, 2001). In the process of prenatalemotional retrogenesis the threat to dissolve can be seen in strong self-attachment behaviors (i.e., sitting with arms strongly crossed over thechest, or repetitively caressing one’s own hands/arms); the threat ofbeing destroyed can lead to strong defensive behaviors (i.e., pushingaway people, or overstretching/arching). And the threat of being
expelled can lead to reaching out for contact and showing sucking andclamping behaviors. The threat to be invaded can be seen in defensiveand aggressive behaviors or in extreme flexed body positions.
Umbilical movements can be observed in patients in the terminalstage of AD.
I can imagine that cellular movements, as described by Farrant
and Larimore (1995), can be observed in prenatal AD patients. When Iworked with Alzheimer patients, I myself was not yet trained enoughin these early stages of prenatal development to be able to observethese egg and sperm movements in patients. But I would not rule itout that preconception and conception imprints can be retrogeneticallyactivated in AD.
The Symbolic Womb: Prenatal Emotion-Oriented Care for AlzheimerPatients
As a developer and strong supporter of emotion-oriented care
(Verdult, 1993), I try to promote an extension to prenatal care in AD(Verdult, 1997). Three major components of PRenatal EMotion-oriented cARE (PREMARE) can be identified, namely: ‘snoezelen’(sensorimotor relaxation), the adapted ‘womb’-environment, and theattitude of the nursing staff.‘
Snoezelen’ (sensorimotor relaxation).
In severe AD patients the
senses are the gateways to contact. ‘Snoezelen’ is a psychosocialmethod, developed in the Netherlands, which employs active sensorystimulation to share and enter into the experience of the dementedpatient in an attempt to increase and maintain his/her well-being(Achterberg, Kok & Salentijn, 1997). ‘Snoezelen’ was originallydeveloped in the field of mentally disabled persons. It was introducedin geriatric care in the late eighties. ‘Snoezelen’ refers to primaryactivation by selective input of sensory stimulation for deeplyregressed or withdrawn patients. The word is a combination of theDutch words ‘snuffelen’ (to sniff) and ‘doezelen’ (to doze). It is alsoreferred to as multi-sensory stimulation. It can be defined as anapproach which actively stimulates the senses of hearing, touch,vision, taste and smell in a resident-oriented, non-threateningenvironment. It is intended to provide individualized, gentle sensorystimulation without the need for higher cognitive processes, such asmemory and learning, in order to achieve or maintain a state of well-being. It can be applied in a special room with an array of equipment,offering multiple stimulations, and covering all sensory channels (VanWeert, 2004).
Journal of Prenatal and Perinatal Psychology and Health
I prefer to call it sensorimotor relaxation, as the goal should be
reducing anxiety by relaxation in a safe environment. In my approachof ‘snoezelen’ three aspects are important: first ‘snoezelen’ is a way ofmaking affective body contact, secondly the goal should not bestimulation but relaxation, and thirdly the kind a sensory inputoffered to severe terminal patients should reflect the retrogenesis ofthe sensory development in prenatal life (Verdult, 1997).
First, I presume that human contact remains essential in AD. This
contact is not rational using cognitive processing through theneocortex, but emotional and sensorimotor, using emotional processingof the limbic system and sensorimotor processing of the brain stem. By‘snoezelen’ a sensorimotor atmosphere of safety, bonding andcontainment can be created. It can be said that a couple that creates aromantic atmosphere to get closer, is using ‘snoezelen’ to get intodeeper contact. The same is true for terminal AD patients. Thisatmosphere can open the AD patient, can break through the isolation,and can make emotional body contact possible. A relationship can bere-established with severe AD patients who have a strong tendency towithdraw in a closed world. I wish to stress that this kind of bodycontact must respect the patient’s boundaries, for several reasons.
Touch is an emotional stimulus that originates from the earliestprenatal periods and thus remains intact until the last moments of theAlzheimer process. Gentle touching helps severe AD patients to orientto the outside world, and makes contact on an emotional level possible.
As anxiety is the basic feeling of AD patients, every contact shouldattempt to reduce this anxiety.
Second, originally the aim of ‘snoezelen’ with the mentally disabled
was to provide an opportunity for intellectual and social development.
That’s why stimulation was stressed. But in AD patients the goal of‘snoezelen’ should not be stimulation but relaxation within theboundaries of a bonding relationship. Stimulation (or enrichment) hasthe risk of overstimulation, and this risk increases sharply as the moresevere patients lose more neural connections. Sensory input should befine-tuned to the AD patient’s rest-capability to make sense out ofsensory input. I have seen too many special ‘snoezel’ rooms thatresemble disco techs, overloading patients with highly intense anddiverse sensory inputs. This brings no relaxation, no opening, nocontact, no safety, but more activation or withdrawal.
Third, in the prenatal development of the senses a more or less
fixed pattern can be seen. The first tactile senses and the initialelements of the proprioceptive system develop. The auditory sensesstarts to develop from 16 weeks of gestation; then taste and smell. The
visual sense is last to develop. If one accepts the thesis of retrogenesis,this would imply that Alzheimer patients keep responding to sensoryinput in the reverse way. The visual sense disappears before taste andsmell. The auditory sense would start to decline thereafter. If vision,taste, smell and sound have disappeared, vibro-acoustic hearing,elements of proprioceptive sense and touch remain relatively intact.
Touch is the last sense to remain. To disappear in the context of thedeterioration in AD means that the senses remain relatively intact,but the brain connections have been lost, making sensory informationno longer able to be processed. ‘Snoezelen’ with fetal terminal ADpatients should take this reverse prenatal development of the sensesinto account. Visual stimulation can be offered in the beginning of the‘vanishing stage’. This can be done with spotlights, colorful materials,bubble units, flashlights linked to music, or video projections. Whenpatients no longer respond to visual stimuli, aromatherapy can beused to stimulate smell sensations. Through aroma streamers,aromatic oils that reduce stress and anxiety can open up the patient.
Taste sensation can be given if patients are extremely orally oriented.
Sweet is preferred. When severe patients start to close their eyes moreand more and seldom open them, auditory stimuli can be given. Musictherapy is very suitable. Rhythm is important and the closer thisrhythm is to the heartbeat the better. As we know from the researchby Tomatis (1991) prenates, and thereby severe terminal Alzheimerpatients, prefer Mozart to Beethoven, and Vivaldi to Bach. Prenatalhearing is actually more like vibro-acoustic stimulation. Soundvibrations reach the fetus through the uterine wall and stimulate thewhole body, not just the ears. Vibrations can be very relaxing. ABelgian company developed a special chair through which vibrationscan be given to the whole body. Research showed that this vibratingchair could achieve deep relaxation. Also waterbeds are used,sometimes in combination with vibrations. Hydro sound baths can bevery relaxing. The bath is like a womb and the vibrations, which canbe modulated in intensity, can be experienced as prenatal vibration onthe body. The deeper the patient is vanishing, and the deeper he is inhis prenatal life, the developmentally youngest gateways to contactshould be used. As Montague (1971) showed, touch is the mostimportant sense. It starts to develop as early as 6 weeks aftergestation. As it develops that early it remains intact a very long timein AD. So the most important way of communicating with vanishingpatients is by touching. Words no longer reach them and don’t makesense to them, but through affective body contact primitive bondingcan occur.
Journal of Prenatal and Perinatal Psychology and Health
The adapted ‘womb’ environment.
In the context of ‘snoezelen’ or
multi-sensory stimulation for AD patients the questions are whetherthe environment should be enriched and in what ways it should beenriched. Research on sensory stimulation showed that a sensoryenriched environment has positive effects on mood and socialfunctioning of AD patients (Baker, Dowling, Wareing, Dawson & Assey1997; Spaull & Leach, 1998). How severely demented the researchedpatients were is unclear. In the beginning of my experimental workwith ‘snoezelen’, I worked with Mrs. P. She was 79-years-old andseverely demented. She had not spoken for many months, lying in bedmost of the day, being fed with a straw. I brought her to the special‘snoezel’-room, where we had all kinds of materials with which wecould stimulate sensory input, like the feel-bag
filled with rice andother products, light and sound effects, mirrors, dolls and teddy bears,bubble units and so on. After 20 minutes working with Mrs. P, tryingdifferent inputs, all the sudden she said, loud and clear: ‘When is thisgoing to be finished?’ She dropped into her isolated state again andwithdrew completely from the situation, which in my opinion was toooverloading for her. I learned from Mrs. P. that overstimulation insevere AD patients can have reverse effects; too much multimodalsensory input creates anxiety and the only defense she had was towithdraw. My conclusion was that an enriched environment should betuned in with the emotional, communicative and cognitive disabilitiesof the patient.
PREMARE should be provided in a special environment that has
the qualifications of a ‘good-enough’ womb. According to me, a ‘good-enough’ womb should have the following characteristics: (a) it is acocoon in which one can feel safe and secure; (b) the boundaries of thecocoon provide protection; (c) there is a continuous supply of nutrientsnecessary for well-being; (d) the umbilical dialogues are enriching andfacilitating, and not burdening or demanding; (e) there is no overloadof sensory input and uni-modal information processing is possible; and(f) there is no stress nor anxiety. These characteristics can betranslated to the good-enough womb in PREMARE. The patient’s bedor room, and the nursing home ward, or the special ‘snoezel’-room inthe nursing home should all have these characteristics. Severe terminal Alzheimer patients remain most of the day in bed andthis area can be turned into a womb easily, so that a cocoon is created.
With pillows a womb can be constructed that fits to the prenatalposture of the fetal AD patient. With a mosquito net the womb can beclosed. A dimmed red and blue light can create the visual surroundingsof a womb.
Boundaries of the symbolic womb are to facilitate protection and
this implies that they should be respected. Nurses are not allowed toenter the womb surroundings without permission. This is of course notverbal permission, but through body signals patients can communicateopenness and willingness for contact, or withdrawing, rejection andclosing. Invasive interventions are avoided. No pressure or stress isput upon the patients.
Scheduled routines are no longer suitable. As these patients have
less aware moments, personal care is carried out in the more awareperiods, not according to planned schedules. Feeding is also done in themore aware moments and can be done by the bottle, as sucking is thebest way to feed severely terminal patients. It is better to feed patientsmore times a day in small portions, than twice or three times a day onfixed moments. Liquid food is preferred as sucking remains the lastway of food-intake. If AD patients start to suck more, a straw can alsobe used to feed them.
The ‘umbilical dialogues’ with fetal AD patients will be reflected in
the nursing staff attitude of person-centered and emotion-orientedcare. As we have already seen, sensory input is reduced and selectivelyoffered to the patients, depending on his/her level of prenatal sensoryfunctioning. Multimodal stimulation is avoided, as overstimulationproduces more anxiety. The good enough womb offers uni-modalstimuli.
The attitude of the nursing staff.
In PREMARE the attitude of the
nursing staff is crucial for the well-being of the patients in the‘vanishing stage’ of the deterioration process. According to me, thisattitude should have the characteristics of prenatal bondingrelationship, as severe terminal AD patients relive prenatal life. Ipresume that the need to bond and to receive adequate resonanceremains intact. The prenatal bonding and resonance basic emotionalneeds of the fetal AD patient are: (a) the need to be contained and notlose boundaries or be overwhelmed; (b) the need to feel safe and notfeel threatened by unexpected harming interventions; (c) the need tofeel connected and not be isolated or rejected; and (d) the need forspace and not to be invaded or violated (Stroecken, 2000; Krens, 2001;Verdult, 2004; Verny, 1996).
The nursing staff needs to have the qualities of the ‘good-enough’
mother, as described by Winnicott, offering containment, holding andaffective body contact (Verdult, 1994). Mothering qualities are crucialin this final stage of dementia. As Perls stated, contact is an ego-function, but terminal AD patients have lost contact with reality, lostcontact with their inner feelings and needs, and lost the possibility of
Journal of Prenatal and Perinatal Psychology and Health
verbal communication. The pre-expressive self (Prouty, 1998) stillremains. This means that although the terminal AD patient isvanishing more and more, there is still a very reduced but noticeabletendency to express themselves, to convey body sensations andprimary emotions, even if these sensations and emotions can no longerbe integrated. As severe terminal AD patients function more on a brainstem level, nurses have to be aware of sensorimotor informationprocessing; they have to slow down, adjust the pacing to the patient,and avoid disruptions in contact. The nursing staff has to empathicallyrespond and accommodate to these rudimentary expressions of theself. Prouty’s contact reflections (1976) have proven to be verysuccessful in communicating with terminal AD patients. The ultimategoal remains to keep in touch with the vanishing patient, to avoid himgliding into complete isolation.
Prenatal factors play a role in the etiology of Alzheimer’s disease,
although the mechanisms and consequences are not yet clear. In recentyears more research has shown that many diseases have adevelopmental origin. Epigenetic research is becoming a hot item. Inthe long run it will appear that AD is a complex interaction betweengenetic, environmental and developmental factors, including triggersthat originate from prenatal life. As Alzheimer’s is a very complexdisease, there is still a long way to go before this dramatic illness canbe stopped or prevented.
In the meantime the best possible care should be provided to AD
patients who suffer intensely from this devastating disease.
PREMARE is based on clinical observations, interpretations andsometimes speculations. More theory building and research should bedone. I hope that this article can contribute to an improvement of carefor severe AD patients, in respect of their pain.
From my clinical experience, emotion-oriented care is the best way
to provide for Alzheimer sufferers. Patients need support, containmentand affective contact to deal with the loss of autonomy and identity.
The more they re-live childhood, infancy and prenatal life, the morethey need an empathetic ‘good enough’ mother, who is emotionallyavailable, sensitive and responsive to expressed emotions, bodysensations and body postures dating from prenatal life. This ‘goodenough’ nurse is not afraid of what is going on in the deepestexperiential world of the fetal terminal AD patient. Ideally he or shehas experienced his or her own prenatal life and birth, so that severe
terminal patients are met easily in their prenatal needs. To be seenand to be heard, as Winnicott stated, is the most crucial aspect in life,in prenatal life, in infancy, in childhood, in adulthood, in old age, andalso in dementia. Emotion-oriented care giving should meet the‘vanishing patient’ on this level of functioning, in this re-living ofhis/her past. By recognizing his prenatal experiential world, anxietycan be reduced. Essentially, emotion-oriented care means: staying withthe pain!
Achterberg, I., Kok, W. & Salentijn, C. (1997). ‘Snoezelen’: A new way of communicating
with severely demented elderly. In B. Miesen, & G. Jones (Eds.), Care-giving indementia: Research and applications
(Volume 2). New York: Routledge.
American Psychiatric Association (1997). Practice guideline for the treatment of patients
with Alzheimer’s disease and other dementias of late life. American Journal ofPsychiatry, 154
(5 suppl), 1-39.
Baker, R., Dowling, Z., Wareing, L-A., Dawson, J. & Assey, J. (1997). Snoezelen: Its long-
term and short-term effects on older people with dementia. British Journal ofOccupational Therapy, 60
Buijssen, H. (2001). Dementie (Dementia). In: Buijssen, H., Psychologische hulpverlening
aan ouderen (deel 2) (Psychological counseling to the elderly
(part 2). Baarn(Netherlands): HB Uitgevers.
Chamberlain, D. B. (1998). The mind of your newborn baby.
Berkeley, CA: North Atlantic Books.
Chapman, A. H., & Chapman, M. C. (1980). Harry Stack Sullivan’s concepts of personality
development and psychiatric illness
. New York: Brunner/Mazel.
Diesfeldt, H. (2003). Neuropsychology of memory disorders in dementia. In P. De Deyn, E.
Thiery, & R. D’Hooge. (Eds.), Memory, basic concepts, disorders and treatment
Leuven, Belgium: ACCO.
Emerson, W. R. (1996a). Somatic birth simulation
. Petaluma CA: Emerson Training Seminars.
Emerson, W. R. (1996b). The vulnerable prenate. Journal of Prenatal and Perinatal
Psychology and Health, 10
Emerson W. R. (1998). Birth trauma: The psychological effects of obstetrical interventions.
Journal of Prenatal and Perinatal Psychology and Health, 13
Farrant, G. & Larimore, T. (1995). Six universal body movements expressed in cellular
consciousness and their meaning. Primal Renaissance: the Journal of PrimalPsychology, 1
Feil, N. (1982). Validation therapy: How to help disoriented old-old
. Cleveland: Edward
Finnema, E. J. (2000). Emotion-oriented care in dementia: A psychosocial approach
Groningen, Netherlands: De Regenboog.
Journal of Prenatal and Perinatal Psychology and Health
Finnema, E. J., Droës, R. M., Ribbe, M. W. & Van Tilburg, W. (2000). The effects of emotion-
oriented approaches in the care for persons suffering from dementia: a review of theliterature. Journal of Geriatric Psychiatry, 15
Folsom, J. C. (1968). Reality orientation for the elderly mental patient. Journal of
Geriatric Psychiatry, 1
Geerlings, M. I., den Heijer, T., Koudstaal, P. J. & Breteler, M. M. (2008). History of
depression, depressive symptoms, and medical temporal lobe atrophy and the risk ofAlzheimer’s disease. Neurology, 70
Goffman, E. (1968). Asylums: Essay on the social situation of mental patients.
Hardy, J. & Selkoe, D. J. (2002). The amyloid hypothesis of Alzheimer’s disease: Progress
and problems on the road to therapeutics. Science, 297
Hartley, L. (1995). Wisdom of the body moving: An introduction to body-mind centering.
Jürgs, M. (1999). Alzheimer: Spurensuche in Niemandsland
. (Alzheimer: Tracking
symptoms in Nobody’s land
). Munchen, Germany: Econ Ullstein List Verlag
Kitwood, T. (1997). The concept of personhood and its relevance for a new culture of
dementia care. In B. Miesen, & G. Jones (Eds.), Care-giving in dementia; researchand applications
(volume 2). New York: Routledge.
Krens, I. (2001). The first relationship. Journal of Prenatal and Perinatal Psychology and
Lu, P. H., Edland, S. D., Teng, E., Petersen, R. C., & Cummings, J. L. (2009). Donepezil delays
progression to AD in MCI subjects with depressive symptoms. Neurology, 72
MacLean, P. D. (1990). The triune brain in evolution
. New York: Plenum Press.
Maret, S. (1997). The prenatal person: Frank Lake’s maternal-fetal distress syndrome.
McGregor, J. (1991). Cognitive performance on Piagetian tasks by Alzheimer’s Disease
patients. Research in Nursing & Health, 15
Miesen, B. (1992). Attachment theory and dementia. In B. Miesen, & G. Jones (Eds.),
Care-giving in dementia; research and applications
. New York: Routledge.
Miesen, B. (1993). Gehechtheid en dementia
(Attachment and dementia
Miesen, B. (1997). Awareness in dementia patients and family grieving: A practical
perspective. In B. Miesen, & G. Jones (Eds.), Care-giving in dementia; research andapplications
(volume 2). New York: Routledge.
Montagu, A. (1971). Touching: The human significance of the skin. New York: Harper & Row.
Nathalienz, P. (1999). Life in the womb: The origin of health and disease.
Nikolaev, A., Mclaughin, T., O’Leary, D. & Tessier-Lavigne, M. (2009). APP binds DR6 to
trigger axon pruning and neuron death via distinct caspases. Nature, 457
Porges, S. W. (2001). The Polyvagal Theory: Phylogenetic substrates of a social nervous
system. International Journal of Psychophysiology, 42
Prouty, G. (1976). Pre-therapy: A method of treating pre-expressive psychotic and
retarded patients. Psychotherapy: Theory, Research and Practice, 13
Prouty, G. (1998). Pre-therapy and the pre-expressive self. Person-centered Practise, 6
Raadsheer, F. C., Van Heerikhuize, J. J., Lucassen, P. J., Hoogendijk, W. J., Tilders, F. J. &
Swaab, D. F. (1995). Corticotropin-releasing hormone mRNA levels in theparaventricular nucleus of patients with Alzheimer’s disease and depression.American Journal of Psychiatry, 152
Reisberg, B. (1999). Retrogenesis: Landmark Alzheimer’s research adds scientific
precision to the phrase. Presidential Address, International Psychogeriatric Society.
Reisberg, B. & Franssen, E. H. (1999). Clinical stages of Alzheimer’s disease. In M. J. de
Leon (Ed.), An atlas of Alzheimer’s disease
. Carnforth (UK): Parthenon.
Reisberg, B., Franssen, E. H., Hasan, S. M., Monteiro, I., Boksay, I., Souren, L. E.,
Kenowsky, S., Auer, S. R., Elahi, S. & Kluger, A. (1999). Retrogenesis: clinical,physiologic and pathologic mechanisms in brain aging. European Archives ofPsychiatry and Clinical Neuroscience, 249
(suppl 3), 28-36.
Reisberg, B., Franssen, E. H., Souren, L. E. Auer, S. R., Akram, I. & Kenowsky, S. (2002).
Evidence and mechanisms of retrogenesis in Alzheimer’s and other dementias:Management and treatment import. American Journal of Alzheimer’s Disease andOther Dementias, 17
Robles de Medina, P. G. (2004). Prenatal maternal stress and its effects on fetal
. Utrecht: University Press.
Rogers, H. & Arango J. C. (2006). Retrogenesis theory in Alzheimer’s disease: Evidence
and clinical implications. Anales de Psychologia, 22
Schrijnemaeker, V., Van Rossum, E., Candel, M., Frederiks, C. M., Derix, M. M., Sielhorst,
H. & Van den Brandt, P. A. (2002). The effectiveness of emotion-oriented care onelderly people with cognitive impairment and behavioural problems. InternationalJournal of Geriatric Psychiatry, 17
Souren, L. E. & Franssen, E. H. (1993). Verbroken verbindingen
Netherlands: Swets & Zeitlinger.
Spaull, D. & Leach, C. (1998). An evaluation of the effects of sensory stimulation with
people who have dementia. Behavioural and Cognitive Psychotherapy, 26
Stroecken, G. (2000). De stem van het jonge kind
(The voice of the baby
Swedish Council on Technology Assessment in Health Care (2008). Dementia: Etiology
. Stockholm, Sweden, SDU.
Tomatis, A. (1991). Pourquoi Mozart?
). Paris, France: Fixot.
Toseland, R. W., Diehl, M., Freeman, K., Manzanares, T., Naleppa, M. & McCallion, P.
(1997). The impact of validation group therapy on nursing home residents withdementia. Journal of Applied Gerontology, 16
Tulving, E. & Markowitsch, H. J. (1998). Episodic and declarative memory: Role of the
hippocampus. Hippocampus, 8
Van Weert, J. C. (2004). Multi-sensory stimulation in 24-hours dementia care.
Verdult, R. (1989). De beleving van dementie; de rol van de activiteiten begeleiding
(Experiencing dementia; the role of occupational therapy). AS, maandblad voorActiviteitenbegeleiding (AS, journal of occupational therapy), 12
Verdult, R. (1991). Vraagtekens blijven bij validation therapie (Remaining questions on
validation therapy). Tijdschrift voor ziekenverzorging (Journal of Nursing), 3
Journal of Prenatal and Perinatal Psychology and Health
Verdult, R. (1993). Dement worden: een kindertijd in beeld (Dementia: A childhood in
. Baarn, Netherlands, HB uitgevers
Verdult, R. (1994). Belevingsgericht begeleiding bij dementie (Emotion-oriented care in
dementia). Hospitalia, 3
Verdult, R. (1997). Contact in nabijheid; snoezelen met ernstig demente ouderen (Close
contact: sensory stimulation of dementing elderly)
. Leuven, Belgium: ACCO.
Verdult, R. (2003). De pijn van dement zijn; problem gedrag bij dementerende ouderen
(The pain of dementing; problem behaviour of dementing elderly).
Baarn,Netherlands: HB uitgevers.
Verdult, R. (2004). De competente foetus: op weg naar hechting (the competent fetus: on
its way to attachment). Tijdschrift voor Vroedvrouwen (Journal for Midwives), 10
Verdult, R. (2009a). Ceasarean birth in adults. The International Journal of Prenatal and
Perinatal Psychology and Medicine
Verdult, R. (2009b). Die Neuverdrahtung des Gerhirns; Entwicklung des Gerhirns,
pränatale Bindung und die Konsequenzen für Psychotherapie (Rewiring the brain;brain development, prenatal attachment and its consequences for psychotherapy).
In P. Schindler (Ed.), Am Anfangs des Lebens (In the beginning of life)
. Basel (CH):Schabe Verlag (in press).
Verdult, R. & Miesen, B. (1986). Old pain? Loss experiences and dementia
presented at the 3rd Conference on Advances in Preventive Geriatrics, Bratislava.
Verdult, R. & Pelgrims, J. (1986). Bijzondere ouderenzorg in verzorgingshuis ‘De Bijster’;
een sociotherapeutische aanpak (Special care for the elderly in nursing home ‘DeBijster’; a sociotherapeutic approach). Tijdschrift voor Ziekenverzorgenden (Journalof Assisting Nurses), 14
Verdult, R. & Visser, R. (1990). Ervaringen met validationtherapie (Experiences with
validation therapy), Tijdschrift voor ziekenverzorging (Journal of Nursing), 15, 474-478.
Verny, T. R. (1996). Isolation, rejection and communication in the womb. Journal of
Prenatal and Perinatal Psychology and Health, 8
Wade, J. (1998). Two voices from the womb: evidence for physically transcendent and a
cellular source of fetal consciousness. Journal of Prenatal and Perinatal Psychologyand Health, 13
Multi-direction Guidance Motion Tracking for Real-timeUltrasound Strain ImagingAmplitude Modulation Strain Noise Reduction byDisplacement Field CorectionFrequency Compounding for Ultrasound FreesoundElastographyDiscussion On Security For Campus Scientific ResearchResearch On Security Of The WLAN Campus NetworkOperating System Curriculum Teaching Reform andExplorationDiscussion On Database Pr
ALLERGY INFORMATION MEDICATION AND IMPLICATIONS Nitric oxide is a biomarker for inflammatory mediators that reflect activity of the eosinophils, which are the main marker for severity of inflammation in asthma. The definitive test is a BAL (bronchialalveolar lavage) of eosinophils, which correlates with effectiveness of inhaled steroids. FeNO (fractional exhaled nitric oxide) can n