Carrey Everett
Student number: 802043616
August 2009
DECLARATION
I declare that this dissertation is my own, unaided work. It is being submitted for the Degree
of Masters of Technology at the University of Johannesburg. It has not been submitted
before for any degree or examination in any other Technikon or University.
_________________
Signature of Candidate
ii
ABSTRACT
Memory loss refers to the loss of ability to learn new information and the inability to retrieve
information previously learnt (Karlawish & Clark, 2003). It is estimated that more than 40%
of individuals over the age of 60 are affected by memory loss (Jackson, 2004). There are
no recommended treatment options available for mild forms of memory loss (D‟Esposito &
Weksler, 2000).
The aim of the study was to determine the effects of the anthroposophical medicine,
Scleron® in the treatment of memory loss associated with ageing, assessed by digit span;
verbal and visual recall and recognition and a memory questionnaire.
The trial was a double-blind placebo controlled study using matched pairs. Participants
selected to take part in the study were between the ages of 60 and 75 and presented with
subjective symptoms of memory loss. Participants were excluded from the study if they
scored less than 24 out of 30 on the Mini-Mental State Exam; were previously diagnosed
with memory or cognitive disorders; had a previous history of stroke, epilepsy, head injury,
psychiatric disease and drug or alcohol dependence. Participants were divided into two
groups in matched pairs according to age, education level, occupation and Mini-Mental
State Exam scores. At the start of the study, participants completed a memory test and
memory questionnaire. Participants in the experimental group received Scleron®, while
participants in the placebo group received unmedicated tablets. Participants were required
to take 2 tablets in the morning for a period of six weeks. The memory test and memory
questionnaire was once again completed by participants at the end of the study. Thirty six
participants completed the study.
The results of the study were analysed and frequencies and descriptives were calculated
for the sample group. The Wilcoxon test was used to compare the data within groups, while
the Mann-Whitney test was used to compare the results between the two groups.
iii
After analysis of the results of the study, it was concluded that Scleron ® did not appear to
improve the symptoms of memory loss when using tests of digit span, verbal and visual
recall or verbal and visual recognition. Furthermore, it did not appear to improve subjective
symptoms of memory loss assessed by the use of a memory questionnaire.
iv
This work is dedicated to all the wonderful participants that took part in the study.
v
ACKNOWLEDGEMENTS
Thank you to the following people for their assistance and support:
Dr Karen Dümmer and Pharma Natura for assistance and supplying the medication
vi
GLOSSARY
vii
TABLE OF CONTENTS
Declaration ii
Abstract iii
Dedication v
Acknowledgements vi
Glossary vii
Table of Contents viii
List of Appendices xi
List of Tables xii
List of Figures xiii
CHAPTER ONE
INTRODUCTION 1
1.1 Problem Statement 1
1.2 Aim of the study 1
1.3 Hypothesis 1
1.4 Null hypothesis 2
CHAPTER TWO
LITERATURE REVIEW 3
2.1 Memory 3
2.1.1 Introduction 3
2.1.2 Types of memory 3
2.1.2.1 Sensory memory 3
2.1.2.2 Short-term memory 4
2.1.2.3 Long-term memory 4
2.1.3 Storage of memory 5
2.1.4 Memory and the brain 6
2.1.5 Assessment of memory 7
2.1.5.1 Memory tests 7
2.1.5.2 Memory questionnaires 8
viii
2.2 Memory loss and ageing 9
2.2.1 Types of memory loss associated with ageing 9
2.2.1.1 Age-associated memory impairment 9
2.2.1.2 Mild cognitive impairment 10
2.2.1.3 Dementia 10
2.2.1.4 Other factors contributing to memory loss in the
elderly 10
2.2.2 Changes in memory with ageing 11
2.2.3 Brain changes associated with ageing 11
2.2.4 Investigation of memory loss 12
2.2.5 Treatment of memory loss 12
2.2.5.1 Conventional medical treatment 13
2.2.5.2 Herbal and nutritional supplements 13
2.2.5.3 Lifestyle changes 15
2.3 Homoeopathy 16
2.3.1 Introduction 16
2.3.2 Potentization 16
2.3.3 Anthroposophical medicine 17
2.3.4 Scleron® 19
CHAPTER THREE
METHODOLOGY 21
3.1 Sample group 21
3.1.1 Inclusion criteria 21
3.1.2 Exclusion criteria 21
3.2 Research design 22
3.3 Research procedure 22
3.4 Tests utilised 23
3.4.1 Mini-Mental State Exam 23
3.4.2 Memory tests 23
3.4.2.1 Digit span 24
3.4.2.2 Verbal and visual recall 24
ix
3.4.2.3 Visual and verbal recognition 24
3.4.3 Memory questionnaire 25
3.5 Data collection and analysis 25
3.6 Ethical consideration 25
CHAPTER FOUR
RESULTS 27
4.1 Introduction 27
4.2 Memory test scores 30
4.2.1 Verbal recall 30
4.2.2 Digit span 31
4.2.3 Verbal recognition 32
4.2.4 Visual recall 33
4.2.5 Visual recognition 34
4.3 Memory questionnaire 35
CHAPTER FIVE
DISCUSSION 37
5.1 Interpretation of results 37
5.2 Limitations of the study 41
CHAPTER SIX
CONCLUSION AND RECOMMENDATIONS 42
6.1 Conclusion 42
6.2 Recommendations 43
REFERENCES 45
x
LIST OF APPENDICES
xi
LIST OF TABLES
xii
LIST OF FIGURES
xiii
CHAPTER ONE
INTRODUCTION
Memory can be defined as processes involved in the recording, storage and later retrieval
of information (Goldstein, 2005). Memory loss involves the inability to learn new information
and to retain previously learnt information (Karlawish & Clarke, 2003). Concerns about
memory loss and cognitive ability is one of the most common reasons elderly patients visit
their doctors (Devons, 2002) and it is estimated that memory loss affects more than 40% of
individuals over the age of 60 (Jackson, 2004). Although some aspects of memory appear
to remain unaffected by the ageing process, it has been shown that age-associated
memory loss results in a decline in working and episodic memory (Hänninen, 1996). There
is currently no recommended medication for the treatment of age-associated memory loss
(D‟Esposito & Weksler, 2000).
The aim of this study is to determine the efficacy of Scleron ® in the treatment of age-
associated memory loss and to determine its effect when testing everyday memory; digit
span; and verbal and visual recall and recognition.
1.3 Hypothesis
The anthroposophical remedy, Scleron® is more effective than the placebo in improving
symptoms of memory loss in elderly patients, when using tests of digit span; verbal and
visual recall and recognition; and a memory questionnaire.
1
1.4 Null Hypothesis
The anthroposophical remedy, Scleron® is not more effective than the placebo in improving
symptoms of memory loss in elderly patients, when using tests of digit span; verbal and
visual recall and recognition; and a memory questionnaire.
In chapter two, memory and types of memory loss will be discussed. Furthermore, the
diagnosis and possible treatment options for age-related memory loss will be discussed in
greater detail.
2
CHAPTER TWO
LITERATURE REVIEW
2.1 Memory
2.1.1 Introduction
Memory can be defined as “the processes involved in retaining, retrieving, and using
information about stimuli, images, events, ideas, and skills after the original information is
no longer present” (Goldstein, 2005). Memory involves three main processes, namely
encoding, storage and retrieval. Initially information is encoded by converting sensory
information into a neural code that can be processed by the brain. This encoded
information is then stored, so that it can be maintained in memory over a period of time.
Finally, retrieval allows for the later access of this stored information (Weiten, 2001).
In 1968 Richard Atkinson and Richard Shriffrin proposed a model that divides memory into
three structural components, namely sensory memory, short-term memory and long-term
memory. This original model of memory is known as the modal model of memory
(Goldstein, 2005).
Sensory memory is concerned with incoming sensory information (Passer & Smith, 2004).
Information is only stored in sensory memory for less than a quarter of a second, unless it
is can be further processed (Harding & Beech, 1996).
3
2.1.2.2 Short-term memory
Short-term memory represents a limited memory store that temporarily holds a small
amount of information. Sensory memory is retained in short-term memory as memory
codes. These may be mental images stored as visual codes, sound stored as phonological
codes or the meaning of a stimulus may be stored as semantic codes. Patterns of
movement for physical actions are stored as motor codes (Passer & Smith, 2004). On
average, short-term memory only stores between five and nine unrelated items at a time
and without rehearsal information is only kept for about 20 seconds. However, the capacity
of short-term memory can be greatly increased by a process known as chunking. This
involves combining single items into a larger, more meaningful unit (Weiten, 2001). Modern
cognitive scientists however, prefer to classify short-term memory as working memory.
Working memory describes the transient ability to simultaneously store and process a
limited amount of information (Hänninen, 1996). Working memory is critical for
comprehension of language and reasoning (Zarah et al., 2007).
Long-term memory is a vast unlimited memory storage with the ability to store large
amounts of information for long periods of time (Passer & Smith, 2004). Long-term memory
can subdivided into three categories: (Figure 2.1) procedural, semantic and episodic
memory. Procedural memory refers to memories that are not consciously accessible. This
would include motor skills and mental processes. General knowledge for world events is
referred to as semantic memory, while episodic memory is related to memory for personal
events and situations. Together, semantic and episodic memory is referred to as
declarative memory (Parkin, 1999).
4
LONG-TERM
MEMORY
DECLARATIVE PROCEDURAL
MEMORY MEMORY
SEMANTIC EPISODIC
MEMORY MEMORY
It is accepted that permanent changes in the synaptic connections between neurons allows
for the formation of memories (Parkin, 1997). The Canadian psychologist, Donald Hebb
(1948), first introduced the theory that memories may be the result of physiological
changes that occur at the synapse. At the most basic level, electrical impulses are
conducted along neurons. Figure 2.2 indicates how an impulse passes along the pre-
synaptic neuron. This impulse results in the release of a neurotransmitter at the synapse
which then allows for that electrical impulse to continue to the post-synaptic neuron. Hebb
believed that this activity resulted in structural changes at the synapse, with increased
transmitter release and greater firing. Although there are still many unanswered questions
surrounding the creation and storage of memories, modern research has proved this theory
to be true. It is also now understood that acetylcholine is the neurotransmitter primarily
implicated in the formation of memories (Goldstein, 2005).
5
.
Figure 2.2 The transmission of an impulse by the neuron (Weiten, 2001).
There are still many unanswered questions surrounding where memories are stored in the
brain. Figure 2.3 indicate the areas of the brain believed to be responsible for the storage
of memories. Memories appear to primarily be stored in the cortex. Sensory memory
depends on the detection of a stimulus formation by the various sensory organs of the
body. These stimuli are then processed by the sensory areas of the cerebral cortex. The
cerebellum, along with other areas of the brain, is fundamental in the formation of
procedural memories (Passer & Smith, 2004) and working memory appears to be
associated with the frontal lobes (Weiten, 2001).
The study of anterograde amnesia has provided scientists with a unique insight into where
memories are stored in the brain. One of the most well-known cases is of a man referred to
as H.M. This patient underwent surgery to remove his hippocampus in the hope of relieving
the debilitating epileptic seizures he suffered from. Unfortunately, the surgery also
6
destroyed his ability to form long-term memories. Scientists now understand that the
hippocampus and related structures in the medial temporal lobe are responsible for the
development of new declarative memories (Weiten, 2001).
Some researchers believe that new information is temporarily stored in the hippocampus,
until it can be transferred to the cortex; while others support the view that the hippocampus
does not store any information but rather is required by the cortex in the process of
developing new memories. The amygdala appears to be involved in the formation of
emotional memories (Myers, 2006).
.
Figure 2.3 The Brain (Weiten, 2001).
There are many standardised psychometric tests that can be used to test objective
symptoms of memory complaints. Memory questionnaires may assess subjective aspects
of memory.
7
information on verbal memory, visual memory, general memory, attention and delayed
memory. A large amount of normative data is also available for nine different age groups
(Parkin, 1999). The disadvantage of this test is that it takes about fifty minutes to complete,
making it a time-consuming test to administer (Parkin, 1997). Furthermore, there is only
one form available. This may have an influence on the results if retesting is required, as the
practice effect is known to influence the results if the same test is administered twice
(Lezak, 1995).
Self report questionnaires provide the simplest way of investigating everyday memory.
These questionnaires allow the patient to describe their memory complaints according to
scales that usually test the frequency or severity of the problem (Hickox & Sunderland,
1992). Furthermore, memory questionnaires help provide insight into how the patient‟s
8
memory problems affect their everyday life. An example of a commonly used questionnaire
is the Everyday Memory Questionnaire (Parkin, 1997).
Memory loss is the inability to learn new information, while information that was previously
learnt, cannot be retrieved (Karlawish & Clark, 2003). According to studies, it is estimated
that memory loss effects more than 40% of individuals over the age of 60 (Jackson, 2004).
Memory loss in the elderly can be divided into three categories, namely age related
memory loss; mild cognitive impairment and dementia (Small, 2002). In some instances,
memory impairment may be caused by treatable medical conditions, as well as the use of
medication (Jackson, 2004).
The National Institute of Mental Health Work Group on Ageing and Memory in 1986
proposed the following criteria for the diagnosis of age-associated memory impairment
(D‟Esposito & Weksler, 2000):
The patient must be over the age of 50
The patient must present with a subjective complaint of gradual memory loss,
which can be confirmed with objective evidence of impairment of at least one
standard deviation below the mean for young adults on a standardised memory
test
There must be no evidence of dementia or any other medical condition that could
cause memory loss
AAMI often appears to be worse if the person is tired, sick, distracted or under a great
deal of stress (Hopkins, 2008; Nielsen et al., 1998).
9
2.2.1.2 Mild cognitive impairment
Mild cognitive impairment is characterised by changes in cognitive function that are more
severe than of normal ageing, but unlike dementia, no functional impairments are evident.
Studies suggest that patients with mild cognitive impairments have an increased chance of
developing Alzheimer‟s disease (Karlawish & Clark, 2003). It is estimated that each year
10-15% of patients with mild cognitive impairment progress to Alzheimer‟s disease
(Hopkins, 2008).
2.2.1.3 Dementia
Dementia may be defined as progressive changes in two or more cognitive areas that
affect performance of everyday activities (Karlawish & Clark, 2003). The deterioration in
mental capacity is therefore, worse than what is expected to occur as a result of the normal
aging process. The most common causes of dementia include Alzheimer‟s disease,
frontotemporal dementia and Lewy body dementia (Fields, 1998).
2.2.1.4 Other factors contributing to memory loss in the elderly (Jaffe & Kemp, 2007)
10
2.2.2 Changes in memory with ageing
Studies have shown that ageing affects various aspects of memory. Although the
traditional concept of short-term memory is well preserved, ageing affects working memory,
as well as components of long-term memory (Hänninen, 1996).
Evidence indicates that semantic and procedural memory do not appear to be affected by
the ageing process, while episodic memory is greatly affected. Furthermore, it has been
shown that the aspects of episodic memory that are most affected are anterograde
memory or memory for events that recently occurred. Memory for events that occurred
years ago (retrograde memory) remain intact (D‟Esposito & Weksler, 2000). This explains
why subjects often complain of forgetting day-to-day events but easily recall significant
events that happened years before. Free recall ability of elderly subjects appears to decline
significantly, while tests of recognition become more “familiarity-based.” Elderly patients
have more difficulty with recognition tests that require the use of context (Parkin, 1997).
Memory loss associated with ageing is mainly due to neuronal loss. Neurons are lost, in
particular from the two areas of the brain most critical to memory, the frontal lobes and
hippocampus (Parkin, 1997). In addition, ageing causes a decrease in brain weight, gyral
atrophy and ventricular dilation (Hänninen, 1996). Brain size appears to gradually decline
from the early 20‟s, while a rapid rate of shrinkage begins at about the age of 55. This
shrinkage may be due to significant loss of white matter (Lezak, 1995). Memory is further
affected by a reduction in cerebral circulation. It is estimated that blood flow to the brain
decreases by 15-20% between the ages of 30 and 70 (Hopkins, 2008).
Another theory explaining memory loss as people age is the “processing speed”
hypothesis. In other words, memory loss occurs because the brain gets slower at operating
and processing information. Linked to this theory is the concept of fluid intelligence. Fluid
intelligence refers to our ability to think flexibly and to problem-solve. It has been shown
11
that ageing results in a significant decline in fluid intelligence and this is what may underlie
age-related memory loss (Parkin, 1999).
The initial evaluation of memory loss should include a thorough medical history,
investigating the onset and course of symptoms, possible risk factors and family history of
dementia, an inventory of all current medication and a physical examination (Small, 2002).
The Mini-Mental State Examination is an important test in this initial assessment. It consists
of 30 items that test memory, orientation, calculation, language and visual skills. A score of
less than 24 out of 30 indicates that a cognitive impairment is present (Lloyd & Sharpe,
2002) and is therefore, a useful screening for dementia. If Alzheimer‟s disease is present,
scores may also indicate the stage of the disease: mild Alzheimer‟s may fall between the
ranges of 20-24; scores of 12-20 indicates moderate disease, while less than 12 indicate
severe disease (Karlawish & Clark, 2003).
Neuropsychological tests may be used to detect more subtle changes in memory; while
brain imaging, such as positron emission tomography, may be required if a diagnosis of
dementia is suspected. Depression screenings should be performed and if metabolic
causes of memory loss are suspected, laboratory investigations may include thyroid and
liver function tests, as well as tests for anaemia and vitamin B12 deficiencies (Small, 2002).
12
2.2.5.1 Conventional medical treatment
A study performed by Ferris et al., (2007), to test the efficacy of memantine in age-
associated memory impairment (AAMI) found no significant effect on memory. Mematine is
a non-competitive N-methyl-D-aspartate receptor agonist that has been shown in several
trials to be useful in the treatment of moderate to severe Alzheimer‟s disease. The study
was intended to determine whether memantine could be used in patients with AAMI to
improve learning, memory or attention. This randomised, double-blind placebo controlled
study assessed sixty participants between the ages of 50 and 79 complaining of memory
loss and performing at least one standard deviation below the mean for young adults on a
standardised memory test. Subjects were excluded if they scored below 26 on the MMSE;
suffered from depression; or had a medical or neurological condition that could account for
memory loss. Memantine was found to have an effect on attention and processing speed
but no significant effect on memory.
Phosphatidylserine (PS)
This is a phospholipid that is highly concentrated in membranes of the brain cells and is
essential for healthy cell membranes. The production of PS decreases with age and
deficiencies may result. It has been shown to enhance memory and learning abilities and
supplementation is particularly important in the treatment of age-related decline (Holford,
2007; Adderly, 2000). There are no known side-effects. A randomised double-blind,
placebo-controlled trial was conducted by Crook et al. (1991) using PS in the treatment of
age-associated memory loss on 149 participants. Participants experienced a 30%
improvement in memory, recall and learning.
13
Ginkgo biloba
Ginkgo biloba is a herbal remedy that has been used for thousands of years in Eastern
cultures to enhance memory. It contains two phytochemicals, namely Gingko flavone
glycosides and Terpene lactones. It improves blood flow to the brain and is commonly
recommended in the treatment of age-related memory loss and to improve short-term
memory. Holford (2007) recommends using 30 to 50mg three times a day, for at least three
months. A study was conducted at the University of Johannesburg to investigate the use of
homoeopathically and phytotherapeutically prepared Ginkgo biloba on short term memory
loss in the elderly. The results revealed no significant statistical changes from the placebo
(McKechnie, 1999).
Dimethylaminoethanol (DMAE)
DMAE is a precursor to choline which is able to cross the blood-brain barrier, increasing
the brains production of the neurotransmitter acetylcholine. DMAE is said to reduce
symptoms of anxiety, improve concentration and learning. Supplementation of between
100 to 500mg daily is recommended to enhance memory. It is not advisable for patients
with schizophrenia, mania or epilepsy to take DMAE (Holford, 2007).
Vitamin B
B Vitamins are essential for normal brain and nerve function. Most important are vitamins
B6, B12 and folate which are fundamental to neurological and cognitive function (Welland,
1998). Holford (2007) indicates the importance of vitamin B5 (pantothenic acid) in the
production of acetylcholine in the brain.
Acetyl-L-Carnitine (ALC)
Acetyl-L-carnitine is an amino acid that enhances the production and absorption of
acetylcholine by the brain therefore, increasing memory and learning abilities. It is thought
that ALC protects the brain from the damaging effects of high levels of cortisol, caused by
stress (Adderley, 2000). Balch (2000) recommends the use of ALC to reduce the
progression of Alzheimer‟s disease.
14
2.2.5.3 Lifestyle changes
Regular exercise
Regular exercise not only enhances circulation to the brain but may also help to reduce the
risk of conditions such as cardiovascular disease and diabetes, which may increase
memory loss (Jaffe & Kemp, 2007). Studies have shown that physical activity may reduce
the risk of developing Alzheimer‟s disease in later life (Small, 2002).
Healthy diet
Poor eating habits and obesity increase the risk of cardiovascular disease and diabetes
which in turn has a profound effect on memory. Therefore, a memory-healthy diet should
be low in sources of saturated fat, high in “good fats” such as fish and seeds and high in
foods rich in antioxidants such as berries, tomatoes and broccoli (Small, 2002).
Sufficient sleep
Sufficient amount of sleep is vital for memory as consolidation of memories occurs during
sleep. Insufficient sleep may also result in poor concentration (Jaffe & Kemp, 2007).
Stop smoking
It has been shown that smoking not only increases the risk of cardiovascular disease,
which can negatively affect memory, but may also increase the risk of developing
Alzheimer‟s disease (Small, 2002).
Mental “exercise” is crucial for keeping the mind sharp and alert. Activities that may help
include playing bridge or chess, completing crossword puzzles or number games, and
reading books or newspapers (Jaffe & Kemp, 2007). It has been reported that people who
15
remain mentally active have a lower risk of developing Alzheimer‟s disease than those who
do not (Small, 2002).
2.3 Homoeopathy
2.3.1 Introduction
Homoeopathy is a complete medical system that aims to restore health by enhancing the
body‟s own healing ability. Homoeopathy was founded by the German doctor, Samuel
Hahnemann in 1790; and is derived from the Greek words homois meaning “same” and
pathos meaning “suffering.” Hahnemann noticed that the signs and symptoms produced
during an illness were the bodies attempt to heal itself. This observation formed the basis
for his principle that a substance that can produce a similar disease “picture” in a healthy
person can in fact be used to restore the sick to health. Homoeopathy is therefore, based
on the Law of Similars – “Let likes be cured by likes” (Hammond, 1996).
2.3.2 Potentization
Hahnemann discovered that by diluting the remedies, he could increase their curative
abilities and reduce unwanted side-effects. This lead to the development of a process
known as potentization. Remedies are made by a process of successive dilution and
succussion (vigorous shaking). The curative ability of the remedy is increased by each
stage of dilution and succussion (Bellavite & Signorini, 1995).
The most commonly used scales of dilution include the decimal and centesimal scales. The
decimal scale (denoted by X or D) refers to a one in ten dilution, whereby one part of the
original substance is diluted in nine parts of water or alcohol. The first dilution is referred to
as 1X. The centesimal scale (denoted as C) is a one in a hundred dilution. To produce a
remedy using this scale, one part of the original substance in diluted in ninety-nine parts of
alcohol or water and the first dilution is referred to as 1C (Roy, 1999).
16
2.3.3 Anthroposophical Medicine
Anthroposophical medicine was founded in the early 1900‟s by the Austrian scientist and
philosopher, Rudolf Steiner, in collaboration with the Dutch medical doctor, Ita Wegman. It
is derived from the Greek words anthropos meaning “human” and sophia meaning
“wisdom” (Evans & Rodger, 1992). It encompasses the knowledge and experience of
conventional medicine but extends this theory by acknowledging that human beings are
composed of body, mind and spirit (Weleda, 2007). It also acknowledges the direct
relationship between man and the other three kingdoms of nature (Bednarek, 2007).
The anthroposophical model, as seen in Table 2.1, views man as a fourfold organism or
being consisting of four distinct but related parts. The first of these parts is the physical
body. The physical body refers to our material body and is common to all humans, animals,
plants and minerals. The etheric body or life force consists of formative forces which
control the organisation of the physical body and therefore, maintain the physical body. The
etheric body is particularly active during the embryonic stage of development and is
involved in processes such as growth, repair and reproduction. The etheric body is
common to humans, animals and plants. The next aspect of man is the astral body. The
astral body is primarily concerned with consciousness; feelings, thoughts and desires; and
instinctive drives. It is common only to humans and animals. The astral body has a
catabolic effect on the physical body and a constant tendency towards illness. Finally the
ego is what differentiates man from all other kingdoms of nature and is centred on self-
consciousness. The ego refers to the person‟s inner core or sense of identity. The ego has
a dual effect on the physical body, acting with the astral body in “breaking down”
17
processes, while working with the etheric body in “building up” processes (Evans &
Rodger, 1992; Bednarek, 2007).
KINGDOM OF HUMAN
REALM QUALITY
NATURE ELEMENT
Spirit Self- Human Ego
consciousness
Soul Consciousness Animal Astral Body
Life Life Plant Etheric Body
Material Weighable and Mineral Physical
measurable Body
Health relies on the delicate balance between the ego, astral body, etheric body and
physical body and imbalances may result in illness.
The human body can then be divided into three functional systems. The first of these
systems is the nerve-sense system. This system is concentrated in the head and radiates
throughout the rest of the body; it includes all activities of the nerves, brain, spinal cord and
sense organs. The nerve-sense system is associated with consciousness and catabolic
processes and therefore, constantly erodes the life and vitality of the physical body. In
opposition to the nerve-sense system is the metabolic-limb system. This system is centred
around the assimilation of nourishment and the activity of the limbs. This system rebuilds
and replenishes the physical body. Finally, the rhythmic system includes breathing and the
pulse and is concerned with the rhythms of the body. It is centred in the heart and lungs.
The rhythmic system also brings harmony and balance to the opposing systems in the
body (Evans & Rodger, 1992; Bednarek, 2007).
Health depends on equilibrium between the nerve-sense system and the metabolic-limb
system, while the rhythmic system plays a crucial role in maintaining this balance.
18
According to anthroposophical medicine, there are two main groups of disease that stand
in direct opposition to each other. On the one side are the inflammatory diseases; while on
the other side are the degenerative or sclerotic conditions. These two forces constantly
interact and neutralise each other, and in a healthy state, mutually maintain balance in the
body (Wolff, 1988). Excesses in the metabolic-limb system, resulting in increased warmth
and fluid, indicate an inflammatory condition. Degenerative or sclerotic conditions, caused
by an excess in the nerve-sense system may be characterised by loss of fluid, excessive
hardening and a build-up of mineral deposits in the body (Evans & Rodger, 1992).
Treatment therefore, aims to determine where this imbalance lies and then to influence the
activity of the element to regain equilibrium and health (Bednarek, 2007).
Anthroposophical medicine, with the use of natural substances, aims to stimulate the
natural healing ability of the patient. The medicines are chosen (from the mineral, plant or
animal kingdom) for the forces they posses, to oppose the dominant forces resulting in a
particular illness (Bednareck, 2007). The therapeutic properties of the substances used are
accentuated by the preparation process. This system of medicine makes use of potentised
remedies. The raw material is dissolved repeatedly in water or alcohol and then succussed
rhythmically at each stage of the dilution process (Evans & Rodger, 1992).
Today there are many doctors who practice anthroposophy throughout the world,
particularly in Switzerland and Germany (Wolff, 1988) and many other practitioners use the
wide range of over-the-counter remedies that are available.
2.3.4 Scleron®
19
Scleron® is composed of Plumbum metallicum D12, which is processed with honey (Mel
D12) and cane sugar (Saccharose D12) (Husemann & Wolff, 1987). The package insert
recommends the use of Scleron® for mental alertness, premature ageing, weak memory
and concentration and also in the treatment of arteriosclerosis and sclerotic conditions
(Cara, 2007).
Chapter three will discuss the methodology used in this trial, including research design;
research procedure; tests utilised; and data collection and analysis.
20
CHAPTER THREE
METHODOLOGY
The sample group consisted of forty men and women between the ages of 60 and 75 years
presenting with symptoms of memory loss related to ageing. Participants were recruited
through adverts placed at the University of Johannesburg‟s health clinic, and at retirement
villages and health shops in the area. An advert was also placed in three local newspapers,
namely the Fourways Review, Sandton Chronicle and Roodepoort Record. Participants
were selected according to the following inclusion and exclusion criteria:
21
3.2 Research Design
This trial was a double-blind placebo controlled study using matched pairs and was
conducted at the Doornfontein campus of the University of Johannesburg and at retirement
villages over a six week period. Scleron® and the unmedicated tablets were supplied by
Pharma Natura. All tablets were packaged in identical bottles and labelled from 1- 40. The
instructions for taking the medication were also included on the bottle. The participants
were divided into groups in matched pairs and allocated a number. The pairs were
matched according to age, occupation, Mini-Mental State Exam score and highest level of
education. Participants in the experimental group were given Scleron ®, while participants
in the placebo group received unmedicated tablets. Pharma Natura kept a record of which
numbers corresponded to the experimental or placebo group. Neither the researcher nor
participants knew which group they were in and the grouping of participants was only made
known to the researcher after all testing was completed.
Interested volunteers were invited to attend an initial consultation to determine if they were
suitable to participate in the trial. At this consultation, volunteers were provided with a
patient information sheet and required to sign a consent form (Appendix A). A health
questionnaire (McKechnie, 1999) was completed by each participant (Appendix B), which
included an inventory of all current medication. Blood pressure was taken and the Mini-
Mental State Exam was administered to each individual (Appendix C). Participants
matching the above-mentioned criteria were then selected to take part in the study.
22
confirming that the medication had been taken each day (Appendix E). Follow-up dates
were also given to each participant at this consultation. All participants were contacted
telephonically every two weeks to encourage compliance.
At the final consultation, participants were once again required to complete the memory
questionnaire (Appendix D) and memory test (Appendix H and I). The second memory test
was slightly different to the first test, to ensure that results were not due to the practice
effect.
There are many standardised memory tests available however, none are standardised for
South African subjects. It was therefore, decided to create a modified memory test in order
to make allowances for the vast differences in literacy and education levels found in South
Africa (Lowies, 2007). The memory test consisted of five sections and tested verbal recall;
digit span; verbal recognition; visual recall and visual recognition (Appendix F and H).
Participant‟s responses were recorded by the researcher (Appendix G and I).
23
3.4.2.1 Digit Span
Short-term memory (Appendix F and H) can be assessed using tests of digit span which
measure immediate memory (Wilson, 1996). The participants were presented with a
random series of numbers at a rate of one digit per second and asked to repeat back the
digits in the correct order. The series of numbers increased each time the participant was
able to correctly recall the digits (Parkin, 1999). A score for digit span was calculated for
each participant. A typical adult span is 5 – 9 digits (Goldstein, 2005).
Verbal recall (Appendix F and H) was tested by reading out a list of 15 words to each
participant. The participant was required to recall as many of the words as possible
immediately and then again after a 15 minute delay. The number of words correctly
recalled in each trial was recorded by the researcher. A score for immediate and delayed
verbal recall (after 15 minutes) was recorded for each participant.
Visual recall (Appendix F and H) was tested in the same way, but participants were
presented with a page of 15 pictures to study. Participants were required to recall as many
of the pictures as possible immediately and after a 15 minute delay. The response of each
participant was once again recorded and a score for immediate and delayed visual recall
was calculated. Tests of immediate recall assess spontaneous memory retrieval (Passer &
Smith, 2004), while delayed recall tests aspects of long-term memory (Lezak, 1995).
Verbal recognition (Appendix F and H) was tested by presenting each participant with a list
of 15 words to study. After a short delay the participants were presented with a list of 45
words containing the original 15 words, as well as 30 other associated words. Participants
were asked to indicate which words were on the first list. The number of correct words and
the number of associated words recalled was recorded for each participant.
24
Visual recognition (Appendix F and H) was tested by presenting the participant with a
geometric shape or picture. After a short delay, participants were presented with 4 similar
but slightly different shapes and asked to identify which shape was identical to the shape
initially presented. A score for visual recognition was recorded. Recognition tasks require
the patient to indicate if a stimulus is familiar (Passer & Smith, 2004).
The obtained data was analysed and frequencies and descriptives were calculated for the
sample group. Reliabilities for the memory questionnaire were calculated using Cronbach‟s
alpha. The Wilcoxon test was used to compare the data within groups, while the Mann-
Whitney test was used to compare the results between the two groups.
Participation in the research was on a completely voluntary basis and participants had the
right to withdraw at any stage of the research. All participants had the right to privacy and
confidentiality and all participants were assigned a number so that no personal information
was given out in the study. Participants were informed of the benefits of the study. There
were no anticipated risks involved in the participation of this study. Participants were
informed of the results of the study. Permission to conduct this study was granted by the
25
Higher Degrees Committee of the University of Johannesburg on 10 March 2008. Ethical
clearance number 03/08.
26
CHAPTER FOUR
RESULTS
4.1 Introduction
Forty participants between the ages of 60 and 75 were recruited to take part in the study.
The participants were divided into two groups in matched pairs according to Mini-Mental
State Exam score, age, occupation and highest level of education obtained.
The obtained data was analysed and frequencies and descriptives were calculated for the
sample group. Reliabilities for the memory questionnaire were calculated using Cronbach‟s
alpha. The Wilcoxon test was used to compare the data within groups, while the Mann-
Whitney test was used to compare the results between the two groups.
Reliabilities for the memory questionnaire were determined using Cronbach‟s alpha. If
Cronbach‟s alpha is greater or equal to 0.70, then it is determined to be a consistent
measurement. Cronbach‟s alpha was 0.735 at the start of the study and 0.824 at trial
completion.
At the beginning of the trial 40 participants were selected to take part, however, only 36
participants completed the trial (19 from the placebo group and 17 from the experimental
group). Two participants from the experimental group withdrew from the study due to ill
health, while the third participant from that group was diagnosed with depression and put
on anti-depressant medication and was therefore, excluded from the study. The patient in
the placebo group that did not complete the study, withdraw on recommendation from her
doctor. From the 36 participants that completed the study, 11 participants were male
(30,56%) and 25 were female (69,44%).
Participants completed the Mini-Mental State Exam (Appendix C) at the beginning of the
study to exclude any participants suspected of suffering from dementia. Table 4.1 indicates
the scores participants obtained out of 30.
27
Scores Placebo Group Experimental Group
(out of Number of Percentage Number of Percentage
30) participants participants
30 11 55% 8 40%
29 7 35% 8 40%
28 2 10% 3 15%
27 0 0% 1 5%
Participants were between the ages of 60 and 75. The average age of the sample group
was 66.69. Table 4.2 shows the distribution of the ages for the sample group.
16 15
14
Number of Participants
12 11
Professional
10
Managerial
8 7
Clerical
6
Other
4 3
2
0
Participants were asked to indicate their highest level of education. Figure 4.2 indicates
the number of participants in each education category: 16 participants had a tertiary
education (44.44%), 13 had a matric certificate (36,11%) and 7 had not completed high
school (19,44%).
18
16
16
Number of Participants
14 13
12
High School Incomplete
10
Matric
8 7
Tertiary Education
6
4
2
0
29
4.2 Memory Test Scores
The results obtained from both groups were compared using the Mann-Whitney test.
Analysis of the results of testing at the beginning of the study revealed no significant
differences between the experimental and placebo groups. It can therefore, be concluded
that the groups were statistically similar at trial entry. The Wilcoxon test was used to
compare results within each group at trial entry and completion.
Verbal recall (Appendix F and H) was tested at the beginning of the study and again at the
end of the six week period. Verbal recall included a score for immediate recall and delayed
recall.
Figure 4.3 indicates the average pre-test score for immediate verbal recall in the
experimental group was 6.88, while the placebo group scored 7.21. After the six week trial
the experimental group scored 6.76 and the placebo group scored 7.05.
The standard deviation for the experimental group was 2.027 at the start of the study and
2.137 at the end of the six weeks. Standard deviation for the placebo group was 2.347
before the study, and 2.198 at the end of the study.
Evaluation revealed that there was no significant differences in immediate verbal recall
scores, within either the experimental (p= 0.724) or placebo group (p=0.832). Furthermore,
no difference was found when comparing the results between the experimental and
placebo group (p=0.822).
Scores for delayed verbal recall can be seen in figure 4.3. In the placebo group, the scores
increased from 4.68 to 5.53. The experimental group scored an average of 5.18 at the start
of the study and 5.12 after the six week period.
30
The standard deviation for the placebo group before the study was 2.286 and 2.716 after
the study, while the standard deviation for the experimental group was 1.704 before and
1.654 at the end of the study.
Statistical analysis revealed that there was once again no significant differences within the
placebo (p=0.074) or experimental (p=0.746) group from trial entry to completion.
Comparison between the experimental and placebo group revealed no significant
improvements (p=0.701).
Pre-test Post-test
The initial score for digit span (Appendix F and H) in the experimental group was 7.35 and
7.29 at the end of the study, while the placebo group‟s pre-test score was 6.79 and the
post-test score was 6.47. This is indicated in figure 4.4.
The standard deviation for the experimental group prior to the study was 1.272 and 1.724
after the study, while the placebo group was 0.787 initially and 1.467 after the six week
period.
There was no statistically significant difference found within the experimental (p=0.822) or
placebo (p=0.368) group. Furthermore, no differences were found when comparing the
experimental and placebo group (p=0.141).
31
7.6
7.35
7.4 7.29
Verbal recognition (Appendix F and H) was tested at the beginning of the study and again
at the end of the six week period. Participants were given a score for the number of correct
words recognised, as well as a score for the number of wrong (associated) words that the
participant recorded from the given list.
Figure 4.5 indicates that the placebo group remembered an average of 9.79 correct words
at the start of the study, but marked 3.35 words that were not on the list. The score for the
correct words increased to 10.84 at the end of the study, while the score for incorrect
words decreased to 1.84. The initial score for the experimental group was 9.76 and they
marked an average of 3.53 incorrect words. At the end of the six week period, the score for
the experimental group increased to 11, however the score for the number of incorrect
words marked was 3.31.
The standard deviation for the placebo group before the study was 3.360 and 2.713 after
the study, while the experimental group was 2.047 before and 2.716 after the six week
period.
Statistical analysis revealed that there was no significant difference within either the
placebo (p=0.137) or experimental (p=0.115) group for verbal recognition. However, there
was a significant difference in the number of associated words recalled in the placebo
32
group (p=0.021) but no difference in the number of associated words recalled in the
experimental group (p=0.728). Further evaluation between groups however, revealed no
significant differences between the experimental and placebo group (p=0.885).
12 10.84 11
9.79 9.76
10
8
Placebo
6
3.35 3.53 3.31 Experimental
4
1.84
2
0
Incorrect
Incorrect
Correct
Correct
words
words
words
words
Pre-test Post-test
A score of immediate and delayed recall (Appendix G and H) was calculated for each
participant. Figure 4.6 indicates that the experimental group scored 8.24 for immediate
recall but only 6.82 for delayed recall at the start of the study. At the end of the six week
period their score for immediate recall was 8.18, while delayed recall remained unchanged
at 6.82. The placebo group scored 7.58 for immediate recall and 6.42 for delayed recall. At
the end of the study, this group scored 8.37 for immediate recall and 6.74 for delayed
recall.
The standard deviation for immediate recall in the experimental group was 2.682 at the
start of the study and 2.378 at the end. The experimental group also had a standard
deviation of 2.555 for delayed recall at the start of the study and the standard deviation was
2.069 at the end. Prior to the study the standard deviation for immediate recall in the
placebo group was 7.58 and 2.432 at the end, while the standard deviation for delayed
recall in the same group was 2.036 at the start and 2.941 at the end of the six week period.
33
There was no statistically significant difference within the experimental (p=0.543) or
placebo (p=0.218) group for immediate visual recall. Furthermore, evaluation between the
groups revealed no improvement in tests of immediate visual recall (p=0.923). Analysis
also revealed that there was no significant difference within the experimental (p=0.875) or
placebo (p=0.793) group for delayed visual recall. No significant differences were found
between groups for delayed visual recall (p=0.653).
Pre-test Post-test
It can be observed from figure 4.7 that the placebo group scored 4.21 for visual
recognition (Appendix G and H) on the pre-test and 4.16 on the post-test. While the
experimental group scored 3.65 at the initial assessment and increased to 4.53 at the end
of the study.
Prior to the study the standard deviation for the placebo group was 0.918 and the same
group had a standard deviation of 0.688 at the end of the study. The standard deviation for
the experimental group was 0.996 before the study and 0.800 at the end of the six week
period.
On analysis it was found that there was a significant difference in pre- and post-test scores
for visual recognition in the experimental group (p=0.012). There was no significant
34
difference for the placebo group (p=0.816). However, comparison between groups
revealed no statistically significant improvement (p=0.057).
5 4.53
4.5 4.21 4.16
4 3.65
3.5
3
Placebo
2.5
Experimental
2
1.5
1
0.5
0
Pre-test Post-test
Analysis of the results of the memory questionnaire (Appendix D) revealed that participants
in the placebo group rated their symptoms of memory loss as an average of score of 39.95
at the beginning of the study and 38.16 at the end of the six week period. There was little
improvement in the experimental group, with participants scoring an average of 40.82 on
their pre-test questionnaires and 39.24 on their post-test questionnaires. This is indicated
in figure 4.8.
The standard deviation for the placebo group was initially 6.519 and 6.483 at the end of the
six week period, while prior to the study the experimental group had a standard deviation of
6.654 and a standard deviation of 8.012 at the end of the study.
The placebo group showed only a slightly significant difference for the memory
questionnaire scores from the start of the study to the scores at the end of the study
(p=0.049). No significant difference was found in the experimental group (p=0.450).
Comparison between groups however, revealed no significant changes (p=0.849).
35
41.5
40.82
41
40.5 39.95
40
39.5 39.24
Placebo
39
38.16 Experimental
38.5
38
37.5
37
36.5
Pre-test Post-test
The results and outcomes of the study will be discussed in chapter five.
36
CHAPTER FIVE
DISCUSSION
Memory is a difficult and complex subject and there are many factors that may influence
the ability to test memory successfully. Firstly, many patients with symptoms of memory
loss may be experiencing early stages of cognitive decline or dementia. Secondly, there
are many risk factors and associated conditions that may influence a patient‟s memory
(Parkin, 1997). For this reason, a Mini-Mental State Exam was performed on all
participants wanting to participate in this study. Participants who scored less than 24,
indicating possible dementia, were excluded from the study. Participants also had to
complete a questionnaire regarding their current and past medical history. All participants
with conditions known to affect memory, such as previous history of head injury, stroke,
depression and drug or alcohol abuse, were excluded from the trial.
Education levels are also known to be well correlated with memory (Parkin, 1997), for this
reason division of participants into groups was based on matched pairs according to age,
occupation and education level.
Participants in this study were required to perform a memory test and complete a memory
questionnaire at the beginning of the study and after a six week treatment period. The
memory test consisted of five sections and tested digit span; visual and verbal recall and
recognition.
Digit Span was used to assess short-term memory. The average population is able to
remember between 5 and 8 digits in the correct order. It has been shown that ageing does
not significantly affect the results of digit span (Parkin, 1997). This was clearly seen in the
results as participants scored well on this particular test. The placebo group scored an
average of 6.79 at the beginning of the study and 6.47 at the end of the study. The results
in the experimental group were similar, with an average of 7.35 scored at the start of the
37
study and 7.29 at the end. As a whole, most participants in the sample group scored
between the averages of 5 to 8 digits however, one participant in the experimental group
was able to complete a 10-number sequence in the pre-test trial; while on the post-test 3
participants, two from the experimental and one from the placebo group, were able to
complete the 10-number sequence. As can be seen in figure 4.4, statistical analysis
revealed that within both the experimental (p=0.822) and the placebo group (p=0.368)
there was no significant difference between scores obtained at trial entry and completion.
Elderly patients tend to perform more poorly on tests of free recall than they do on tests of
recognition (Parkin, 1997). In this study, participants were required to perform tests of
verbal and visual recall and recognition.
The tests for free recall were divided into immediate and delayed recall, and had both a
verbal and visual component. Recall memory tests assess aspects of short-term memory
and attention, while delayed recall tests longer-term retention and retrieval (Lezak, 1995).
Figure 4.3 indicates the results of the verbal recall test. Participants in the placebo group
scored 7.21 before the study and 7.05 after the study on tests of immediate verbal recall.
Participants in the experimental group had similar results with a score of 6.88 prior to the
study and 6.76 afterwards. Research suggests that elderly patients typically perform worse
on tests of delayed recall (Parkin, 1999) and this was clearly seen in this study. Although
little change is seen in the scores between the placebo and experimental groups, it is
interesting to note the changes to both groups in immediate and delayed recall. The
placebo group immediately recalled 48% of the words pre-test and 47% of the words post-
test. However, on the delayed section of the test, they only recalled 31.2% of the words
pre-test and 36.87% post-test. The experimental group correctly recalled 45.87% of the
words pre-test on immediate recall and 45% post-test but performed worse for delayed
recall, recalling 34.53% pre-test and 34.13% post-test. Tests of verbal recall, therefore,
revealed no significant changes between the experimental and placebo groups in either
immediate or delayed verbal recall.
Evidence suggests that the average score for immediate recall is between 6.3 and 7.8 for
persons under the age of 70 and that performance on the test may be influenced by level
38
of education, verbal abilities and general mental capabilities of each individual (Lezak,
1995). The average scores for each group were therefore, relatively high to start with,
making it difficult for large improvements to be expected in testing after the study.
Another observation that can be made when performing tests of recall is a phenomenon
known as primacy and recency effect. The primacy effect refers to the ability to recall more
words presented at the beginning of a given sequence, while recency favours the recall of
words at the end of a given list (Goldstein, 2005). This was clearly evident during the study
as participants tended to remember the first or last words of a given list, while words in the
middle were more frequently forgotten.
As with verbal recall, there were no significant differences for visual recall in either the
experimental or placebo groups, as is illustrated in figure 4.6. The placebo group scored
7.58 pre-test for immediate visual recall and 8.37 post-test, while the experimental group
scored 8.24 pre-test and 8.18 post-test. On delayed recall, the placebo group scored 6.42
pre-test and 6.74 post-test, while the experimental group remained unchanged at 6.82 pre-
and post-test. Tests of visual recall revealed no significant changes between the
experimental and placebo group in either immediate or delayed visual recall.
Figure 4.7 illustrates the results of the visual recognition test. As can be seen the
experimental group did show a significant improvement (p=0.012), scoring 3.65 pre-test
and 4.53 post-test. The placebo group had no significant change (p=0.816), scoring 4.21
39
pre-test and 4.16 post-test. However, comparison between the placebo and experimental
groups did not reveal statistically significant changes.
Recognition tests may be useful to differentiate problems in storing new information from
problems in retrieving stored information (Lezak, 1995). Therefore, memory loss
associated with ageing may be related to the retrieval of information rather than to the
storage of new information.
Memory testing can be greatly affected by the level of education a patient has obtained. To
avoid significant differences in education levels between the groups, participants were
grouped in matched pairs. However, the sample group as a whole had a relatively high
level of education. As can be seen in figure 4.2, 44.44% of participants had a tertiary
education; 36.11% had at least obtained a matric certificate and only 19.44% did not
complete matric. This factor may have influenced the results of the study, as the scores
were relatively high at the beginning of the study and therefore, a significant change could
not be expected at the end of the study. Although it was decided not to use a standardised
memory test, due to the vast differences in education and literacy levels found in South
Africa, it would have been useful to have normative data for this particular age group to
compare the results to. Future studies may possibly find it useful to select a group with a
minimum level of education and then to use a standardised memory test to assess
participants, therefore removing this variable from the study. The results also indicate that
although the subjects complained of subjective memory loss, their test scores were not
very low. Performing a memory test at the start of the study and only selecting participants
with a certain level of impairment may have also yielded better results.
40
Performance on memory tests may also be related to factors such as fear of failure,
anxiety, medication and illness (Lezak, 1995). Therefore, how each participant was feeling
the particular day that testing was conducted may have affected the results of the study.
Memory can also be affected by cultural attitudes and preconceptions about ageing
(Hopkins, 2008).
There were numerous limitations that may have affected the results of this study. Firstly
memory loss is a slow and progressive process that occurs over many years. Brain
changes begin to occur years before symptoms are even noticed. Therefore, it is difficult
to expect any remedy or treatment to make significant changes in only a six week period.
Increasing the duration of the study to between six months and one year, may prove to
yield more significant results in this area.
Secondly, due to difficulties finding a standardised test for South Africa, participants were
not tested before the trial to determine the level of impairment of each participant.
Participants in general scored well on the memory test at the start of the study, and there
were possibly an insufficient number of participants with a significant amount of memory
impairment. Conducting a standardised test at the beginning of the study would have
ensured that all participants had a significant impairment, therefore allowing more room for
a significant improvement.
Memory is difficult and complex to test. Factors such as the education level of participants
can have an impact on the results of studies. Participants in this study were of a high
educational level, and did not necessarily reflect the education level of the general
population. It has also been shown that people with a high level of intelligence are less
likely to meet the criteria of age-associated memory impairment that people of a lower
intelligence level (Nielsen et al., 1999).
Chapter six will discuss the conclusions and recommendations of the study.
41
CHAPTER SIX
6.1 Conclusion
The purpose of the study was to assess the use of Scleron ® in the treatment of age-related
memory loss measured by digit span; verbal and visual recall and recognition and a
memory questionnaire.
Participants underwent a six week study. The memory test and questionnaire was
administered at the start of the study and again after taking the remedy for six weeks.
After analysis of the results it can be concluded that Scleron® did not appear to improve the
symptoms of memory loss when using tests of digit span, verbal and visual recall or verbal
and visual recognition. Furthermore, it did not appear to improve subjective symptoms of
memory loss assessed by the use of a memory questionnaire.
The hypothesis could therefore, not be accepted. However, the results of the study may
have been improved if the duration of the study was extended. Changes in memory occur
slowly over many years, and six weeks of treatment was an insufficient period of time to
expect a significant improvement to be noted. Furthermore, the lack of a standardised test
impacted the results as the selected participants did not necessarily have a significant level
of impairment. Changes to these aspects of the methodology may improve the outcome of
future studies. With memory loss affecting an estimated 40% of patients over the age of 60,
there is an increasing need to investigate effective treatment options.
In conclusion, the results of the study indicate that Scleron® was not shown to be more
effective than the placebo in improving memory as tested by digit span, verbal recall and
recognition, visual recall and recognition or the memory questionnaire.
42
6.2 Recommendation
Since memory loss in later life affects such a large portion of the population it may be
viable to further investigate the use of homoeopathy to improve symptoms of memory loss.
The following recommendations should be considered:
It may be beneficial to lengthen the duration of the study and possibly test
participants more frequently. Many participants were extremely anxious to be tested
the first time, but seemed to relax significantly at the second testing. Therefore, it
may be beneficial to consider the first memory test as a „practice run‟ and not give
any medication until the second test. Participants would therefore, only be given
medication after the second memory test and the final memory test would be
performed at the end of the study. In this way, the affects of anxiety on the results
may be reduced and a base-line score could be determined for each participant
before treatment is started. Future research should be conducted over a six month
to one year period.
Selecting participants with a minimum level of impairment may allow for more
significant levels of change with the administration of the remedy. A memory test
may be used as a screening method before participants are selected.
The number of participants in each group should be increased to increase the
statistical significance of the study.
Homoeopathy is based on the individualised treatment of the patient; therefore,
Scleron® may not have matched the symptom picture of each participant. Future
studies may wish to select a remedy based more specifically on each patient‟s
symptoms.
It may be interesting to compare the use of homoeopathic remedies with commonly
used supplements, such as Gingko biloba and Phosphatidylserine.
Many factors may influence memory. It may therefore, be beneficial to conduct the
study in a more controlled environment, so that factors such as stress, anxiety, lack
of sleep or illness do not affect the results of the study.
The test was conducted in English. Participants, whose first language was not
English, may have had some trouble in understanding and completing the test in
43
English. Performing the test in their own language or excluding participants who
were not English speaking may improve the results.
Many participants expressed concern and fear at developing conditions, such as
Alzheimer‟s and dementia. Addressing these concerns at the beginning of the study
may help reduce the affect of anxiety and stress on the results of the study
A standardised means of testing with normative data available may have been
beneficial. This would have allowed the results of the sample group to be compared
to a normal population.
Scleron® is recommended as a tonic in the elderly (Cara, 2007). Assessing how the
remedy improved or affected the quality of life of participants, may also be
beneficial.
44
REFERENCES
Adderly, B. (2000). You Must Remember This. Better Nutrition. 62(5) pp 60-55.
Allen, H.C. (1999). Allen’s Keynotes: Rearranged and Classified. 9th edition. New Delhi: B.
Jain Publishers (Pty)Ltd. pp 255-257.
Balch, P.A. (2000). Prescriptions for Nutritional Healing. 3rd edition. New York: Penguin
Putman Inc. pp 77.
Cara, R. (2007). Sales consultant from Pharma Natura (Distributors of Scleron®). E-mail
correspondence on 11 May 2007.
Crawford, J.R., Henry, J.D., Ward, A.L. and Blake, J. (2006). The Prospective and
Retrospective Memory Questionnaire (PRMQ): Latent structure, normative data and
discrepancy analysis for proxy-ratings. British Journal of Clinical Psychology, 45: 83 – 104.
Crook, T.H., Tinlenberg, J., Yesavaga, J. Petrie, W. Numzi, M.G. and Massari, D.C. (1991).
Effects of phosphatidylserine in age-associated memory impairment. Neurology. 41(5):644-
649. Available from http://www.ncbi.nlm.nih.gov/pubmed/2027477. (Accessed on
19/04/2009).
45
Derouesne, C., Lacomblez, L., Thibault, S. and LePoncin, M. (1999). Memory complaints in
young and elderly subjects. International Journal of Geriatric Psychiatry, 14:291 -301.
D‟Esposito, M. and Weksler, M.E. (2000). New Frontiers. Geriatrics, 55(6):55 – 60.
Devons, C.A.J. (2002). Comprehensive geriatric assessment: making the most of the
ageing years. Current Opinion in Clinical Nutrition and Metabolic Care. 5(1):19-24.
Evans, M. and Rodger, I. (1992). Anthroposophical medicine: Healing for the Body, Soul
and Spirit. London: Thorsons. pp 9 – 23.
Ferris, S., Schneider, L., Farmer, M., Kay, G. and Crook, T. (2007). A double-blind,
placebo-controlled trial of memantine in age-associated memory impairment. International
Journal of Geriatric Psychiatry. 22: 448 - 455. (Published online 20/11/2006 in Wiley
InterScience www.interscience.wiley.com).
Fields, R. B. (1998). The Dementias. In: Clinical Neuropsychology – A pocket handbook for
assessment. Edited by: Snyder, P.J. and Nussbaum, P.D. Washington: American
Psychological Association. pp 211.
Folstein, M. F., Folstein, S.E. and McHugh, P. R. (1975). Mini Mental State: A practical
method of grading the cognitive state of patients. Psychiatric Research. 12: 189 – 198.
Goldstein, E.B. (2005). Cognitive Psychology. Belmont: Thomson Wadsworth. pp136 - 221.
Hammond, C. (1996). The Complete Family Guide to Homeopathy. Great Britain: Element
Books Limited. pp 14 – 35.
46
Hänninen, T. (1996). Age-Associated Memory Impairment, A neurological and
epidemiological study. Neurologian klinikan julkaisusarja, No 39. Available from:
http://www.uku.fi/laitokset/neuro/39the.htm (Accessed on 12/05/2007).
Holford, P. (2007). New Optimum Nutrition for the Mind. London: Piatkus Books Ltd. pp
130 – 142.
Karlawish, J.H.T. and Clark, C.M. (2003). Diagnostic Evaluation of Elderly patients with
Mild Memory Problems. Annals of Internal Medicine, 138(5): 411 - 419.
Jackson, C. (2004). Mild memory loss: Assessment and Management. Available from
http://www.patient.co.uk. (Accessed on 20/04/2007).
Jaffe, E. and Kemp, G. (2007). Age-related Memory Loss: Recognising, Reducing and
Preventing symptoms. Available from http://www.helpguide.org/life/prevent_memory_loss
.htm (Accessed on 30/04/2007).
47
Lloyd, G.G. and Sharpe, M.C. (2002). Medical Psychiatry. In: Davidson’s: Principles and
Practice Medicine. 19th Edition. Edited by Haslett, C., Chilvers, E.R., Boon, N.A. and
Colledge, N.R. London: Churchill Livingstone. pp 248-249.
Myers, C.E. (2006). Memory Loss and the Brain. Available from
www.memorylossonline.com (Accessed on 02/04/2009).
Parkin, A.J. (1999). Memory: A Guide for Professionals. New York: John Wiley and Sons
Ltd. pp 6 - 9, 53 – 54.
Parkin, A.J. (1997). Memory and Amnesia: An Introduction. 2nd Edition. USA: Blackwell
Publishers. pp 6 – 7, 30 – 31, 75 – 78, 124 – 145.
Passer, M.W. and Smith, R.E. (2004). Psychology- The Science of Mind and Behaviour.
2nd Edition. New York: McGraw-Hill. p 240.
48
Roy, M. (1999). The Principles of Homoeopathic Philosophy- A self directed learning text.
London: Winter Press. pp1-7.
Small, G.W. (2002). What we need to know about age related memory loss. British Medical
Journal, 324: 1502-1505.
Sunderland, A., Harris, J.E. and Baddeley, A.D. (1984). Assessing everyday memory after
severe head injury. In: Everyday memory, actions and absent-mindedness. Edited by: J.E.
Harris & P.E. Morris. London: Academic Press. pp 193 – 212.
Vermeulen, F. (2001). Concordant Materia Medica. New Delhi: Indian Books and
Periodicals Publishers. pp 779-782.
Wechsler, D. (1945). A standardised memory scale for clinical use. Journal of Psychology,
19: 87 – 95.
Weitin, W. (2001). Human Memory. In: Psychology- Themes and Variations. 5th Ed.
Belmont: Wadsworth. pp 265 – 297.
Wolff, O. (1988). Anthroposophical Medicine and its Remedies. South Africa: The Tobias
Therapeutic Association. pp 42 – 48.
49
Zarahn, E., Rakitin, B., Abela, D.,Flynn, J. and Stern, Y. (2007). Age-related changes in
brain activation during delayed item recognition task. Neurobiology of Ageing. 28:784 –
789. (10.1016/j.neurobiolaging.2006.03.002)
50
APPENDIX A: Patient Information and Consent Form
Memory loss begins at about the age of 60 and presents with symptoms such as difficulty
remembering names, telephone numbers or appointments. People often complain of
misplacing objects or getting confused about the details of recent conversations. If you
experience these sorts of symptoms and are between the ages of 60-75, you are invited to
take part in this study. Participants with the following conditions may, however, not take
part in the study:
A history of stroke, epilepsy, head injury, brain surgery, brain tumours, depression,
drug or alcohol addiction
Alzheimer‟s or Parkinson‟s disease
At the first meeting you will be told all about what will happen during the trial. You will be
asked to sign a consent form; fill out a questionnaire about your medical and medication
history; and complete a short memory test. Your blood pressure will also be taken. The first
consultation will take about 20 minutes. If you meet the criteria, you will be invited to take
part in the study. At the second consultation, you will need to complete a memory
questionnaire and a memory test will be performed. At the end of this consultation, you will
be given your medication. You will be placed into either the experimental or placebo group
but neither you nor I will know which group you belong to until the end of the study. If you
fall into the experimental group, you will be given the medication, while participants in the
placebo group will be given a placebo tablet which contains no medication. You will need to
51
take 2 tablets every morning for 6 weeks and will be given a chart to sign everyday
indicating that you have taken the medication. During this time, I will call you every two
weeks to find out how things are going. I will have a final consultation with you after the 6
weeks. You will once again be requested to complete the memory questionnaire and
memory test. The second and third consultations will take about 45 minutes each. At the
end of the study you will be notified of the results of the study and participants who were on
the placebo will be offered free treatment.
The potential benefits of this study lie in the possible improvement of your memory,
concentration and alertness. There are no anticipated risks in taking part in this study and
there are no known side effects to this remedy. However, if you experience anything
unusual while participating in this study, stop taking the medication and contact me
immediately. All your information will be kept confidential at all times and you will be
assigned a number, so that your name is not linked to any of your private information.
Participation in the study is voluntary and you may withdraw at any stage, if you so wish. I
will be available to answer any questions or deal with any problems that you may have
during the course of the study.
I have been informed as to the procedures that will be followed during the course of this
study. I hereby give my consent to participate in the study and am willing to follow
instructions regarding treatment. Furthermore, I understand that I may ask questions at
anytime and that I have the right to withdraw from the study at any stage.
52
I have explained the aim and procedure of the study to the participant. I have given the
participant the opportunity to ask any questions regarding the study and have answered all
questions to the best of my ability.
53
Appendix B: Patient Details
A. Personal Details
Name:
Address:
Current Medication:
54
Please indicate if you have / have a history of any of the following:
Dementia Yes No Alzheimer‟s Disease Yes No
Parkinson‟s Disease Yes No Stroke Yes No
Epilepsy Yes No Head Injury Yes No
Cerebral Embolism Yes No Brain Surgery Yes No
Episodes of Amnesia Yes No Alcohol Dependence Yes No
Drug Dependence Yes No Depression Yes No
Have you ever received any psychiatric treatment Yes No
If Yes, please specify for what disease:
55
Appendix C: Mini Mental State Exam (Folstein et al, 1975)
Max Patient
Points Score
Orientation:
5 What is the (year), (season), (date), (day), (month)?
5 Where are we (country), (province), (city), (building), (floor)?
Registration:
Name three common objects (e.g. apple, table, tree). Take one
second to say each. Then ask the patient to repeat all three after you
3 have said them. Give 1 point for each correct answer. Then repeat
them until he/she learns all three. Count trials and record.
Trials: ( )
Attention:
Spell „WORLD‟ backwards. The score is the number of letters in the
5 correct order.
(D_L_R_O_W_)
Recall:
Ask for the three objects repeated above. Give 1 point for each
3
correct answer.
Language:
2 Name a „pencil‟ and a „watch‟
1 Repeat the following: „No ifs, ands or buts.‟
Follow a three-stage command: „Take a paper in your right hand, fold
3
it in half, and put it on the floor.‟
Read and obey the following:
1
“CLOSE YOUR EYES”
1 Write a sentence:
56
1 Copy the following design:
30 TOTAL
57
Appendix D: Memory Questionnaire
Adapted from the Everyday Memory Questionnaire (Sunderland et al, 1984) and
Prospective and Retrospective Memory Questionnaire (Crawford et al, 2006).
Participant Number:
Please complete the questionnaire by ticking the box that most accurately describes your
answer to each of the following questions below.
Score: 1 = Seldom
2 = Sometimes
3 = Often
4 = Most of the time
58
23. I ask someone the same thing twice. 1 2 3 4
24. Unless I am reminded, I forget appointments. 1 2 3 4
25. I forget to buy something at the shop that I meant to buy. 1 2 3 4
26. I forget to return phone calls. 1 2 3 4
SCORE:
59
Appendix E
Please record that you have taken the remedy by signing each day on the table below.
If you take any other medication during the treatment period, please record the date and
what medication you used:
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
If you have any other questions please feel free to contact me:
Carrey Everett: 083-300-7425
60
Appendix F: Memory Test 1
Adapted from the Auditory-verbal learning test (Rey, 1964) and Wechsler Memory Scale
(Wechsler, 1945).
61
Section C: Verbal Recognition
Instructions: The patient is presented with a list of 15 words to study for 15
seconds. After a 5 second delay, the patient is given a list of 45 words, which
includes words from the first list. The patient must indicate which words were
from the first list of words. Scores are recorded.
Word List Recognition list:
Boat Tea School Dog Moon Dress
School Mother Ship Computer Cook Hairbrush
Apple Book Stairs Radio Float Teacher
Guitar Toothbrush Milk Skirt Boat Apple
Television Ear Ear Sun Chair Drum
Chair Sun Paper Clothes Tea Book
Dog Dress Flour Son Brother Toothbrush
Flower Television Mother Peach Music
Nose Pool Orange Hear
Flower Plant Guitar
Table Teeth Cat
Frog Father Coffee
62
Section D: Visual Recall
Instructions: The patient is given a page of 15 pictures to study for 20 seconds.
After a 5 second delay, the patient is asked to recall as many of the pictures as
possible. An immediate recall score is recorded. The patient is then asked to
recall as many pictures as possible after a 15 minute delay.
63
Section E: Visual Recognition
Instructions: The patient is shown a picture depicting a shape or geometric figure
for 5 seconds. The patient is then shown 4 different designs, and asked to
indicate which matches the original picture.
Shape A: 1.
2.
3.
4.
Shape B: 1.
2.
3.
4.
64
Shape C: 1.
2.
3.
4.
Shape D: 1.
2.
3.
4.
65
Shape E: 1.
2.
3.
4.
66
Appendix G: Evaluation Sheet – Memory Test 1
Participant Number:
67
Section C: Verbal Recognition
Words on list Words not on list
Apple Orange Peach
Boat Ship Float
Book Paper Cook
Chair Stairs Table
Dog Frog Cat
Dress Skirt Clothes
Ear Nose Hear
Flower Flour Plant
Guitar Drum Music
Mother Father Brother
School Pool Teacher
Sun Son Moon
Tea Milk Coffee
Television Computer Radio
Toothbrush Teeth Hairbrush
Words on list 15
Verbal Recognition
Words not on list 30
68
Section D: Visual Recall
Immediate Recall Delayed Recall (After 15 minutes)
Apple Fish Apple Fish
Bee Hammer Bee Hammer
Bird House Bird House
Boat Jacket Boat Jacket
Candle Rabbit Candle Rabbit
Car Sun Car Sun
Carrots Umbrella Carrots Umbrella
Clock Clock
Score 5
69
Appendix H: Memory Test 2
Adapted from the Auditory-verbal learning test (Rey, 1964) and Wechsler Memory Scale
(Wechsler, 1945).
70
Section C: Verbal Recognition
Instructions: The patient is presented with a list of 15 words to study for 15
seconds. After a 5 second delay, the patient is given a list of 45 words, which
includes words from the first list. The patient must indicate which words were
from the first list of words. Scores are recorded.
Word List Recognition list:
Monkey Water Horse Flower Donkey Bed
Garden Hotel Orange Peach Pen Crane
Pencil Bird Hospital Kitchen Shoes Dog
Kitchen Train Mother House Water Garden
Socks Orange Ape Pony Socks Brother
Brother Bed Warm Doctor Hotel Bedroom
Cold Horse Rock Sister Blue Chilly
Dentist Parrot River Pencil Bird
Cold Sheet Dentist Teeth
Train Fridge Write
Plane Red Eagle
Monkey Tree Swim
71
Section D: Visual Recall
Instructions: The patient is given a page of 15 pictures to study for 20 seconds.
After a 5 second delay, the patient is asked to recall as many of the pictures as
possible. An immediate recall score is recorded. The patient is then asked to
recall as many pictures as possible after a 15 minute delay.
72
Section E: Visual Recognition
Instructions: The patient is shown a picture depicting a shape or geometric figure
for 5 seconds. The patient is then shown 4 different designs, and asked to
indicate which matches the original picture.
Shape A: 1.
2.
3.
4.
Shape B: 1.
2.
3.
73
Shape C: 1.
2.
3.
4.
Shape D: 1.
2.
3.
4.
74
Shape E: 1.
2.
3.
4.
75
Appendix I: Evaluation Sheet – Memory Test 2
Participant number:
76
Section C: Verbal Recognition
Words on list Words not on list
Bed Sheet Red
Bird Parrot Eagle
Brother Mother Sister
Cold Warm Chilly
Dentist Teeth Doctor
Garden Flower Tree
Horse Pony Donkey
Hotel Hospital House
Kitchen Fridge Bedroom
Monkey Dog Ape
Orange Blue Peach
Pencil Pen Write
Socks Shoes Rock
Train Plane Crane
Water River Swim
Words on list 15
Verbal Recognition
Words not on list 30
77
Section D: Visual Recall
Immediate Recall Delayed Recall (After 15 minutes)
Balloons Pumpkin Balloons Pumpkin
Bicycle Scissors Bicycle Scissors
Cake Shoe Cake Shoe
Cow Suitcase Cow Suitcase
Duck Tap Duck Tap
Fork Telephone Fork Telephone
Ladder Tree Ladder Tree
Lamp Lamp
Score 5
78