NATIONAL QUALIFICATIONS CURRICULUM SUPPORT
Human Biology
Case study on Neurotransmitter
Disorders
Support Materials
[HIGHER]
The Scottish Qualifications Authority regularly reviews
the arrangements for National Qualifications. Users of
all NQ support materials, whether published by
Learning and Teaching Scotland or others, are
reminded that it is their responsibility to check that the
support materials correspond to the requirements of the
current arrangements.
Acknowledgement
Learning and Teaching Scotland gratefully acknowledges this contribution to the National
Qualifications support programme for Human Biology.
The publishers gratefully acknowledges permission to use the following sources: cartoon
showing blood brain barrier, used with permission of Dr Eric H Chudler, Neuroscience for
Kids, http://faculty.washington.edu/chudler/bbb.html; article ‘Stem cell method put to the test
in Parkinson’s study’ by Pallab Ghosh, 14 July 2010 © BBC News website; text on
Alzheimer’s Disease, text from http://en.wikipedia.org/wiki/Alzheimer’s_disease, text from
http://en.wikipedia.org/wiki/Neurotransmitter all © Wikipedia; image of the brain © 2007
Alzheimer’s Association www.alz.org. All rights reserved. Illustrations by Stacy Janis; text
from www.alzheimers-research.org.uk/info/dementia © Alzheimer’s Research Trust; diagram,
developments in the Treatments of Schizophrenia, image reprinted with permission from
Medscape.com, 2011. Available at http://www.medscape.org/viewarticle/550755_15; diagram,
Genetic Loci linked to Schizophrenia © James Publishing; diagram, Lifetime risk of
developing schizophrenia (in percent) © 1994 Irving I Gottesman and used by permission;
diagram, Interaction of Genetic and Environmental Factors, reprinted with permission from
Pickler J Copyright 2005. Psychiatric Times, UBM Medica. All rights reserved.
http://www.psychiatricimes.com; image of Schizophrenia in monozygotic twins © James
Publishing; diagram, risk of developing schizophrenia © 1994 Irving I Gottesman and used by
permission.
Every effort has been made to trace all the copyright holders but if any have been inadvertently
overlooked, the publishers will be pleased to make the necessary arrangements at the first
opportunity.
© Learning and Teaching Scotland 2011
This resource may be reproduced in whole or in part for educational purposes by educational
establishments in Scotland provided that no profit accrues at any stage.
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Contents
Introduction
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Alzheimer’s disease
Article 1: What is Alzheimer’s disease?
Article 2: Causes of Alzheimer’s disease
Article 3: Symptoms of Alzheimer’s disease
Article 4: Diagnosis of Alzheimer’s disease
Article 5: Treatment of Alzheimer’s disease
Assessment
Additional teacher information
Additional resources
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Parkinson’s disease
Article 1: What is Parkinson’s disease?
Article 2: Causes of Parkinson’s disease
Article 3: Symptoms of Parkinson’s disease
Article 4: Diagnosis of Parkinson’s disease
Article 5: Treatment of Parkinson’s disease
Assessment
Additional teacher information
Additional activities
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Schizophrenia
Article 1: What is schizophrenia?
Article 2: Causes of schizophrenia
Article 3: Symptoms of schizophrenia
Article 4: Diagnosis of schizophrenia
Article 5: Treatment of schizophrenia
Assessment
Additional teacher information
Additional activities
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INTRODUCTION
Introduction
The purpose of this case study is to introduce Higher Human Biology students
to some medical disorders associated with neurotransmitters.
It contains both information and activities to permit understanding of the sub topic.
By the end of this case study, not only should the students have gained better
knowledge and understanding of the concepts involved but, through
undertaking the activities and tasks, they should also have developed
additional skills such as evaluation, teamwork and collaborative learning.
Whilst researching and compiling the data for this case study, huge amounts
of information were found – far too much to all be incorporated – and so
substantial amounts had to be edited out in order to produce a doc ument of
manageable size, containing the core concepts. This, inevitably, leaves scope
for further investigation by students and teachers, should they feel it
necessary.
In order to match the timescale for completion of this case study to the
relative proportion of Unit 2 devoted to the concept of neurotransmitter
disorders and their treatment, only three disorders have been addressed,
namely Alzheimer’s disease, Parkinson’s disease and schizophrenia. The
remaining disorders (generalised anxiety disorders and depression) could be
investigated as further activities/research by students if time allows.
To keep things simple, a similar format of materials has been adopted for
each of the three disorders in this case study. This should make classroom
management easier and provide ‘fairer’ workloads for each of the students
involved. Naturally, some articles are larger or more detailed than others, but
efforts have been made to, broadly, provide comparable challenge .
As you will appreciate, there is ongoing res earch into these disorders, and
new theories and discoveries are continuously being made public.
Consequently, whilst compiling this case study we found some schools of
thought which challenge, or clash with, the original premises set out in the
SQA course descriptor for this aspect of the unit. In order to avoid conflict
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and confusion, we have focused only on aspects which agree with and support
the SQA content.
Should additional information be required, original sources of information
(eg web addresses) have been listed where the sources can be found in full.
Furthermore, some teacher information has been supplied to supplement the
contents of the student pages.
Success criteria
At the end of this task, students should have :
 become ‘expert’ in one aspect of a neurotransmitter related disorder
 conveyed their expertise to the other members of their group
 become knowledgeable about the main aspects of all five of their own
group’s articles, and have taken notes regarding the disorders researched
by other groups
 correctly answered questions regarding the content of the articles about
their own group’s allocated disorder
 participated in the construction and delivery of a presentation to the whole
class on their own group’s allocated disorder.
Skills
In order to achieve the above criteria, students should have practi sed and
displayed the following skills, based on SQA documentation:
 Evaluation – by reading and identifying the importance of data within their
article.
 Selecting relevant information from texts – from their own article for
inclusion in their report to their group.
 Thinking independently – by constructing their own synopsis of the article
for delivery to their group.
 Working collaboratively – on returning to their original group to convey
and receive information within the group (also if working with others who
were tackling the same article).
 Demonstrating knowledge – as ‘experts’ briefing their group members.
Also as part of their group, whilst delivering a presentation to the whole
class.
 Demonstrating understanding – through explanation to their group and
class, and when correctly answering questions about the articles.
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INTRODUCTION
 Presenting information – as oral communication when explaining their
article to the group and when answering questions abo ut articles, and
whilst delivering their presentation.
 Skills for learning, life and work – through the use of literacy and
communication to demonstrate their knowledge and understanding of
biology.
Overall skills matrix
Skill
All three disorders
1. Demonstrating knowledge

2. Applying knowledge
3. Demonstrating understanding

4. Selecting information

5. Presenting information

6. Processing information
7. Planning, designing and carrying out
8. Evaluating

9. Drawing conclusions
10. Making predictions and generalisations
11. Skills for learning, life and work
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INTRODUCTION
The task: teacher’s guide
Due to the nature of the sub-topic, practical work on neurotransmitters is not
feasible.
As a result, this case study presents information abo ut three different
neurotransmitter-related disorders in the form of a series of five articles for
each disorder and resources which students will be required to work through.
In order to involve active learning and develop the skills of collaboration,
teamworking, etc, the task is group based, and will require forward planning
on behalf of the class teacher.
Depending on your students’ prior experience of group work, the amount of
time spent explaining the task will vary.
A summary of the main elements is given below.
 The class should be split into groups of five students, with each group
being allocated a disorder to study. In larger classes, more than one group
may study the same disorder.
 Each disorder in the case study has five articles about the condition, and
each member of the group should study one of these articles in order to
become an ‘expert’ on that aspect of the disease. They will then report
back to the rest of their group to teach them the key learning points.
 You may wish to allow members from different groups who may be
studying the same article to work together to collaboratively identify the
key points to be learned.
 Depending on the ability/experience of the class, allocate a suitable period
of time for students to read/discuss the article and become ‘expert’.
Probably, 15–20 minutes should suffice. The students should be
encouraged to take notes for use when reporting back to their own group.
 After the allotted time, the student ‘experts’ should ‘train up’ the other
members of their group on the key points contained within their article.
This should take 20–25 minutes by the time each student has fed back the
information and notes have been taken.
 By the end of the task, all members of each group should be familiar with
the different aspects of their allocated disorder covered by the five
articles.
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INTRODUCTION
 To check their grasp of the content, the teacher should ask questions round
the class about the articles. The best way to assess how well the students
have understood and then trained up their classmates is to ask each of the
five questions for each article but only to the four members of the group
who were not studying that particular article.
 Sample questions are provided for each of the five articles covering each
disorder. You should feel free to choose alternative questions if you wish.
 In order to allow all groups to learn about each disorder, each group
should prepare and present a presentation on their allocated disorder to the
whole class. As well as disseminating information to their classmates, this
offers an opportunity for peer assessment. This could be a homework task
or a collaborative activity in class or in the school ’s library. A period
could be allocated to allow production of the presentation.
 The presentation can take different forms, such as PowerPoint, flipchart,
production of an ‘NHS style’ information pamphlet, etc.
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The task: Becoming an ‘expert’
This is a group task, where each member of the group will be expected to
participate fully and contribute to the overall success of the group.
Each group will be allocated the task of becoming ‘expert’ on a particular
neurotransmitter-related disorder.
Note that questions about all the articles on your group’s allocated disorder
will be asked of any/all group members at the end of the activity.
1.
Your teacher will organise your class into groups.
2.
Within each group each student is given a number.
3.
Each student in the group will be given a different numbered article
about their allocated disorder to study and become an ‘expert’ on.
It is your responsibility to become your group ’s ‘expert’ on the key
information contained in the article that you have been allocated. At the
end of the task, your teacher will question several group members about
the scientific content of all of the articles.
4.
Your teacher will tell you how much time (eg 10 –15 minutes) you will
have to learn the information in your article. You will be expected to
make notes. You may be allowed to discuss which points in the article
you feel are most important with members from different groups if there
are others who are studying the same article.
5.
Now that you are an ‘expert’ on your article, it is your task to teach the
others in your group what you have learned. Concentrate on the
significant core scientific points in your article.
6.
Each member of your group will, in turn, teach the others in the group
about the information in their article. Each group member will be
expected to take notes as questions will be asked to several members
from each group. Once again, your teacher will allocate a time for the
completion of the task. Given that each member of the group will report
back to the others, and notes require to be made, this task will require
more time (eg 20–25 minutes).
7.
By the end of the task, every member of the group should have learned
about the entire set of articles about the disorder and should be able to
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INTRODUCTION
answer questions about it. Your teacher will ask members of each group
questions about any of the articles from thei r own group.
8.
In order to allow every member of the class to become knowledgeable
about all of the disorders, each group should be required to prepare and
deliver a presentation to the whole class on their allocated disorder.
You will be expected to take notes whilst listening to other groups’
presentations so that you become knowledgeable about them.
Note that you may have the opportunity to ask questions of the other
groups after they have made their presentation (remember that they may
also ask you questions).
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Alzheimer’s disease
Article 1: What is Alzheimer’s disease?
This incurable, degenerative and terminal disease was first described by
German psychiatrist and neuropathologist Alois Alzheimer in 1906 and was
named after him. Most often it is diagnosed in people over 65 years of age,
although the less-prevalent early-onset Alzheimer’s can occur much earlier.
In 2006, there were 26.6 million sufferers worldwide. Alzheimer’s is
predicted to affect 1 in 85 people globally by 2050. [1]
As we age, the brain does also and changes
occur. Recent advances in brain-scanning
techniques have revealed some significant
details which help scientists pinpoint the parts of
the brain that function or fail as individuals age.
As a result of these and other changes, some
people suffer from degeneration in brain
function.
The symptoms may include memory loss,
problems with reasoning and communication
skills, and a reduction in a person’s abilities and
skills in carrying out daily activities such as
washing, dressing, cooking and caring for self.
From :Alzheimer’s Association,
http://www.alz.org/brain/09.asp.
This collection of symptoms is described as dementia.
The word dementia is an umbrella term that describes a serious deterioration
in mental functions, such as memory, language, orientation and judgement.
People often ask whether Alzheimer’s disease and dementia are the same
thing. The answer is both yes and no. Alzheimer ’s disease is one cause of
dementia, but several other diseases can cause it too. Alzheimer’s disease is
the most common cause of dementia, accounting for around two-thirds of
cases in the elderly. Other diseases that cause dementia are vascular
dementia, dementia with Lewy Bodies and fronto-temporal dementia.
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In dementia, brain cells stop working properly and production of a
neurotransmitter, acetylcholine, can be reduced. This happens inside specific
areas of the brain, which can affect how a person thinks, remembers and
communicates.
Dementia is a major cause of ill-health, affecting 820,000 people in the UK –
a number that rises daily. Research into dementia is making progress, but is
very under-funded, especially when compared with other diseases. [2]
Being one of the most common causes of dementia, Alzheimer ’s disease
deserves greater understanding and research. Some famous people, such as
former USA president Ronald Reagan, suffered from Alzheimer’s disease.
Terry Pratchett, author of the science fiction/fantasy Discworld series of
books, was diagnosed with early-onset Alzheimer’s disease and made a BBC
documentary ‘Living with Alzheimer’s’, which explains his experiences of
the condition.
References
[1] Wikipedia. http://en.wikipedia.org/wiki/Alzheimer ’s_disease.
[2] Alzheimer’s Research Trust. http://www.alzheimersresearch.org.uk/info/dementia/.
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Article 2: Causes of Alzheimer’s disease
Unfortunately, there is no single cause which has so far been identified for
Alzheimer’s disease.
As part of the group of conditions which together are described as dementia,
Alzheimer’s disease is often associated with elderly people and so age, in
itself, is a contributory factor towards Alzheimer ’s disease. It should be noted
that early-onset Alzheimer’s also occurs.
Alzheimer’s disease is the most common form of dementia. Medical research
has identified four genes that influence disease development. Three of these
genes affect younger people and one affects older people . [1]
Several competing hypotheses exist that try to explain the cause of the
disease. The oldest, on which most currently available drug therapies are
based, is the cholinergic hypothesis, which proposes that Alzheimer’s disease
is caused by reduced synthesis of the neurotransmitter acetylcholine . This is
due to the loss of cholinergic neurons in various parts of the brain. The
cholinergic hypothesis has not maintained widespread support, largely
because medications intended to treat acetylcholine deficiency have not been
very effective. [2]
Acetylcholine is a member of a group of chemicals called neurotransmitters.
Neurotransmitters are endogenous chemicals that transmit signals from a
neuron to a target cell across a synapse. Neurotransmitters are packaged into
synaptic vesicles clustered beneath the membrane on the presynaptic side of a
synapse and are released into the synaptic cleft, where they bind to receptors
in the membrane on the postsynaptic side of the synapse. Release of
neurotransmitters usually follows arrival of an action potential at the synapse,
but may also follow graded electrical potentials. Low -level ‘baseline’ release
also occurs without electrical stimulation. [3]
Neurotransmitters, such as acetylcholine, are released from the presynaptic
membrane and then rapidly diffuse across to receptors on the postsynaptic
membrane. Having ‘passed on’ the impulse to the target cell, the acetylcholine
molecules are then removed by enzyme degradation (breakdown of the
acetylcholine) to free the receptors on the post-synaptic membrane.
The enzymes that degrade the acetylcholine are called cholinesterase
enzymes, and their action is to reduce the level of acetylcholine in the
synapse.
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This works well for people with normal brain function , but the cholinergic
hypothesis, mentioned above, suggests that Alzheimer’s sufferers already
have a reduced synthesis of acetylcholine and that further removal of the
neurotransmitter may contribute to the condition.
References
[1] http://www.alzheimers.org.uk/site/scripts/documents_info.php?documentID=168 .
[2] http://en.wikipedia.org/wiki/Alzheimer ’s_disease.
[3] http://en.wikipedia.org/wiki/Neurotransmitter .
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Article 3: Symptoms of Alzheimer’s disease
Alzheimer’s disease displays numerous symptoms, many of which involve
unusual behaviour.
Common types of unusual behaviour include the following.
Repetitive behaviour
People with dementia often carry out the same activity, make the same
gesture or ask the same question repeatedly. Medical professionals sometimes
call this ‘perseveration’. This repetition may be because the person doesn ’t
remember having done it previously, but it can also be for other reasons, such
as boredom.
Restlessness
Some people with dementia suffer from general restlessness. This can be a
sign of hunger, thirst, constipation or pain, or the person may be ill or
suffering from the side-effects of medication. Other possibilities are
boredom, anger, distress or anxiety, stress due to noisy or busy surroundings,
or lack of exercise. It may also be due to changes that have taken place in the
brain.
Shouting and screaming
The person may continually call out for someone, shout the same word, or
scream or wail over and over again. They could be in pain or ill, experiencing
difficulties with visual perception or hallucinations, or the behaviour could be
a result of brain damage.
Lack of inhibition
The person may behave in a way that other people find embarrassing because
of their failing memory and general confusion. In a few cases, this may be
due to specific damage to the brain.
Night-time waking
Many people with dementia are restless at night and find it difficult to sleep.
Older people often need less sleep than younger people in any case. Dementia
can affect people’s body clocks so that they may get up in the night, get
dressed and even go outside.
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Trailing and checking
Living with dementia makes many people feel extremely insecure and
anxious. This can result in the person constantly following their carers or
loved ones around, or calling out to check where they are. A few moments
may seem like hours to a person with dementia, and they may only feel safe if
other people are nearby.
Hiding and losing things
People with dementia sometimes hide things and then forget where they are −
or forget that they have hidden them at all. The wish to hide things may be
due to feelings of insecurity and a desire to hold on to what little the person
still has.
Suspicion
Some people with dementia can become suspicious. If they have mislaid an
object they may accuse someone of stealing it, or they may imagine that a
friendly neighbour is plotting against them. These ideas may be due to failing
memory, an inability to recognise people and the need to make sense of what
is happening around them.
The preceding article is adapted from the Alzheimer ’s Society (UK) fact
sheet:
http://www.alzheimers.org.uk/factsheet/525?gclid=CKX99s3U8KQCFchH4w
odSzoNvg
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Article 4: Diagnosis of Alzheimer’s disease
This article gives a heavily edited list of diagnostic techniques applied to the
diagnosis of Alzheimer’s disease. Much of the fine detail has been omitted,
but if you require access to the full article, it is avail able at
http://www.alz.org/alzheimers_disease_steps_to_diagnosis.asp .
Finding the right doctor
The first step in following up on symptoms is to find a doctor you feel
comfortable with. Alzheimer’s Association clients report they are most likely
to be satisfied seeing someone who is well informed about Alzheimer ’s
disease. Your local Alzheimer’s Association can help you find the right
doctor.
There is no single type of doctor who specializes in diagnosing and treating
memory loss or Alzheimer’s disease. In some cases, the primary care doctor
may refer a patient to one of the following specialists:
 A neurologist, who specialises in diseases of the brain and nervous system
 A psychiatrist, who specialises in disorders that affect mood or the way
the mind works
 A psychologist, with advanced training in testing memory, concentration,
problem solving, language and other mental funct ions.
Understanding the problem
There is no single test that proves a person has Alzheimer ’s. Experts estimate
a skilled physician can diagnose Alzheimer’s with more than 90% accuracy.
Be prepared for the doctor to ask:




What kind of symptoms have you noticed?
When did they begin?
How often do they happen?
Have they got worse?
Dementia screening tests
An increasing number of test developers, healthcare facilities and others are
marketing dementia screening tests directly to consumers. The Alzheimer ’s
Association believes that home screening tests cannot and should not be used
as a substitute for a thorough examination by a skilled doctor.
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Reviewing medical history
The doctor will interview the person being examined or family members to
gather information about current and past illnesses. The doctor will also
obtain a history of medical conditions affecting other family members,
especially whether they may have had Alzheimer ’s.
Mental status tests
The mini-mental state examination (MMSE) is one of the tests most
commonly used to assess mental function. In the MMSE, a health
professional asks a patient a series of questions designed to test a range of
everyday mental skills.
Examples of questions include:
 Remember and repeat a few minutes later the names of three common
objects (for instance horse, flower, penny) .
 State the year, season, day of the week and date .
 Count backward from 100 by 7s or spell ‘world’ backwards.
The mini-cog
Another popular mental status test is the ‘mini-cog’, which involves two
tasks: (1) remembering and a few minutes later repeating the names of three
common objects, and (2) drawing the face of a clock showing all 12 numbers
in the right places and a time specified by the examiner.
Physical examination
The doctor will ask about diet, nutrition and use of alcohol. Review all
medications. It is helpful to bring a list or the containers of all medicines
currently being taken, including over -the-counter drugs and supplements. The
doctor will also check blood pressure, temperature and pulse. Listen to the
heart and lungs. Collect samples of blood and urine.
Information from these examinations can help identify other disorders that
may cause memory loss, confused thinking, trouble focusing attention or
other symptoms similar to dementia.
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Neurological examination
During the neurological examination, the doctor may test:






reflexes
coordination and balance
muscle tone and strength
eye movement
speech
sensation.
Brain imaging
Structural imaging provides information about the shape, position or volume
of brain tissue. Structural techniques include magnetic resonance imaging
(MRI) and computed tomography (CT).
Functional imaging reveals how well cells in various brain regions are
working by showing how actively the cells use sugar or oxygen. Functional
techniques include positron emission tomography (PET) and functional MRI
(fMRI).
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Article 5: Treatment of Alzheimer’s disease
Drug treatments for Alzheimer’s disease
No drug treatments can provide a cure for Alzheimer’s disease. However,
drug treatments have been developed that can improve symptoms or
temporarily slow down their progression in some people. This article explains
how the main drug treatments for Alzheimer ’s disease work, clarifies their
availability and sets out the most recent guidance from the National Institute
for Health and Clinical Excellence (NICE) on their usage.
What are the main drugs used?
There are two main types of drugs used to treat Alzheimer ’s disease. Aricept,
Exelon and Reminyl all work in a similar way, and are known as
acetylcholinesterase inhibitors. Ebixa works in a different way to the other
three.
Aricept (donepezil hydrochloride), produced by Eisai and co -marketed with
Pfizer, was the first drug to be licensed in the UK s pecifically for
Alzheimer’s disease.
Exelon (rivastigmine), produced by Novartis Pharmaceuticals, was the second
drug licensed in the UK specifically for Alzheimer ’s disease.
Reminyl (galantamine) was co-developed by Shire Pharmaceuticals and the
Janssen Research Foundation. Originally derived from the bulbs of
snowdrops and narcissi, it was the third drug licensed in the UK specifically
for Alzheimer’s disease.
Ebixa (memantine) is produced by Merz and marketed in Europe by
Lundbeck. It is the newest of the Alzheimer’s drugs.
How do the drugs work?
Aricept, Exelon and Reminyl
Research has shown that the brains of people with Alzheimer ’s disease show
a loss of nerve cells that use a chemical called acetylcholine as a chemical
messenger. [1] The loss of these nerve cells is related to the severity of
impairment that people experience.
Aricept, Exelon and Reminyl prevent an enzyme known as
acetylcholinesterase from breaking down acetylcholine in the brain. Increased
concentrations of acetylcholine lead to increased communication between the
nerve cells that use acetylcholine as a chemical messenger, which may in turn
temporarily improve or stabilise the symptoms of Alzheimer ’s disease.
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All three cholinesterase inhibitors work in a similar way, but one mig ht suit
an individual better than another, particularly in terms of side -effects
experienced.
Ebixa
The action of Ebixa is quite different to, and more complex than, that of
Aricept, Exelon and Reminyl. Ebixa blocks a messenger chemical known as
glutamate. Glutamate is released in excessive amounts when brain cells are
damaged by Alzheimer’s disease, and this causes the brain cells to be
damaged further. Ebixa can protect brain cells by blocking this release of
excess glutamate.
The preceding article is adapted from Alzheimer’s Society (UK),
http://www.alzheimers.org.uk/site/scripts/documents_info.php?documentID=
147.
References
[1] Tariot et al. (2004)
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Assessment
The following provides sample questions which may be asked to test
students’ grasp and understanding of the content of the different articles.
Due to the students’ requirement to successfully identify and extract facts
from the articles, these questions are predominantly of a ‘closed’ type. Scope
exists, however, to create a more open -ended approach by asking other
group/class members if they agree/disagree with the original answer given by
their classmate and why they have that opinion.
Article 1: What is Alzheimer’s disease?
1.
2.
3.
4.
5.
Who is the disease named after and when was it first identifie d?
What term describes Alzheimer’s disease when it is diagnosed in people
less than 65 years of age?
Alzheimer’s disease is the most common cause of which larger group of
conditions?
Give three examples of symptoms associated with
Alzheimer’s/dementia.
Approximately how many people in the UK suffer from Alzheimer ’s
disease?
Article 2: Causes of Alzheimer’s disease
1.
2.
3.
4.
5.
How many genes have so far been linked to Alzheimer ’s disease?
Which hypothesis explaining Alzheimer’s do most drugs currently
attempt to treat?
What causes the lack of neurotransmitter associated with Alzheimer ’s
disease?
The concentration of which neurotransmitter is thought to be reduced in
Alzheimer’s?
Having passed on the impulse, what normally happens to this
neurotransmitter and what is the name of the type of enzyme which
carries out this process?
Article 3: Symptoms of Alzheimer’s disease
1.
2.
3.
4.
5.
22
What is meant by perseveration?
Give two possible causes of restlessness in Alzheimer ’s sufferers.
Why might night-time waking not always indicate Alzheimer’s in older
people?
Why might Alzheimer’s sufferers wish to hide things?
Describe examples of behaviour which might be shown by a suspicious
sufferer.
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Article 4: Diagnosis of Alzheimer’s disease
1.
2.
3.
4.
5.
Which three types of specialist might the Alzheimer’s sufferer be
referred to?
With what degree of accuracy might a skilled physician correctly
diagnose Alzheimer’s?
Why is it important to review the patient ’s medical history and that of
their family?
Give two examples of questions that could be asked in the mini mental
state examination.
What do the abbreviations MRI, PET and CT refer to in terms of
imaging techniques?
Article 5: Treatment of Alzheimer’s disease
1.
2.
3.
4.
5.
Which three drugs act as acetylcholinesterase inhibitors?
How might the action of these drugs improve the Alzheimer ’s sufferer’s
condition?
Although the three drugs work in similar ways, why might one suit the
patient better than another?
Which substance is often released by brain cells damaged by
Alzheimer’s disease?
How does treatment with Ebixa work?
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ALZHEIMER’S DISEASE
Additional teacher information
The following pages contain information mainly edited out of the five student
articles plus supplementary information from various sources. This provides
supporting statistics and perspectives which teachers could use to
broaden/deepen teaching and learning.
Alzheimer’s disease
The average human lifespan in 1900 was 47 years; today it is 75 years. [1]
In 1900, the total human population was appr oximately 1.6 billion people; in
2011 it is estimated to be 7 billion. [2] Note: 7 billion = 7,000,000,000 people.
As we live longer, and our population size grows, the total number of elderly
people also increases.
Advances in diagnostic methods include improved technology like higher
resolution magnetic resonance imaging (MRI) and positron emission
tomography (PET) scans. These help scientists pinpoint the parts of the brain
that function or fail as individuals age. The technology has also generated a
wealth of information about the physical changes in the aging brain:
 Brain weight and volume decrease – On average, the brain loses 5–10% of
its weight between the ages of 20 and 90.
 The grooves on the surface of the brain widen, while the swellings on th e
surface become smaller.
 So-called ‘neurofibriallary tangles’, decayed portions of the branch-like
dentricles that extend from the neurons, increase.
 ‘Senile plaques’, which are abnormally hard clusters of damaged or dying
neurons, form. [1]
As a result of these and other changes, some people suffer from degeneration
in brain function. The symptoms of this may include memory loss, problems
with reasoning and communication skills, and a reduction in a person ’s
abilities and skills in carrying out daily activities such as washing, dressing,
cooking and caring for self.
This collection of symptoms is described as dementia.
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Senile dementia is a term that specifically refers to dementia in people over
65. Dementia in people under this age is much rarer and is often referred to as
early-onset dementia.
In dementia, brain cells stop working properly. This happens inside specific
areas of the brain, and can affect how a person thinks, remembers and
communicates.
Dementia is a major cause of ill-health, affecting 820,000 people in the UK, a
number that is rising daily. Research is making progress, but is very under funded, especially when compared with other diseases. [3]
Being one of the most common causes of dementia, Alzheimer ’s disease
deserves greater understanding and research. This incurable, degenerative and
terminal disease was first described by German psychiatrist and
neuropathologist Alois Alzheimer in 1906 and was named after him. Most
often, it is diagnosed in people over 65 years of age, although the lessprevalent early-onset Alzheimer’s can occur much earlier. In 2006, there were
26.6 million sufferers worldwide. Alzheimer ’s is predicted to affect 1 in 85
people globally by 2050. [4]
References
[1] USC Health Magazine. http://www.usc.edu/hsc/info/pr/hmm/01spring/brain.html .
[2] About.com: Geography.
http://geography.about.com/od/obtainpopulationdata/a/worldpopulation.htm.
[3] Alzheimer’s Research Trust. http://www.alzheimersresearch.org.uk/info/dementia/.
[4] Wikipedia. http://en.wikipedia.org/wiki/Alzheimer ’s_disease.
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ALZHEIMER’S DISEASE
The following article is taken from the Alzheimer ’s Society (UK) fact sheet
(http://www.alzheimers.org.uk/site/scripts/documents_info.php?documentID=
100).
Alzheimer’s disease is the most common cause of dementia, affecting around
465,000 people in the UK. The term ‘dementia’ is used to describe the
symptoms that occur when the brain is affected by specific diseases and
conditions. This factsheet outlines the symptoms and risk factors for
Alzheimer’s disease, and describes what treatments are currently available.
Alzheimer’s disease, first described by the German neurologist Alois
Alzheimer, is a physical disease affecting the brain. During the course of the
disease, ‘plaques’ and ‘tangles’ develop in the structure of the brain, leading
to the death of brain cells. People with Alzheimer ’s also have a shortage of
some important chemicals in their brains. These chemicals are involved with
the transmission of messages within the brain.
Alzheimer’s is a progressive disease, which means that gradually, over time,
more parts of the brain are damaged. As this happens, the symptoms become
more severe.
Symptoms
People in the early stages of Alzheimer’s disease may experience lapses of
memory and have problems finding the right words. As the disease
progresses, they may:
 become confused, and frequently forget the names of people and places, or
forget appointments and recent events
 experience mood swings
 feel sad or angry
 feel scared and frustrated by their increasing memory loss
 become more withdrawn, due either to a loss of confidence or to
communication problems.
As the disease progresses, people with Alzheimer’s will need more support
from those who care for them. Eventually, they will need help with all their
daily activities.
While there are some common symptoms of Alzheimer ’s disease, it is
important to remember that everyone is unique. No two people are likely to
experience Alzheimer’s disease in the same way.
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Mild cognitive impairment
Recently, some doctors have begun to use the term ‘mild cognitive
impairment’ (MCI) when an individual has difficulty remembering things or
thinking clearly but the symptoms are not severe enough to warrant the
diagnosis of Alzheimer’s disease. Recent research has shown that a small
number of individuals with MCI have an increased risk of progressing to
Alzheimer’s disease. However, the conversion rate from MCI to Alzheimer’s
is small (about 10–15%), and consequently a diagnosis of MCI does not
always mean that the person will go on to develop Alzheimer ’s.
What causes Alzheimer’s disease?
So far, no one single factor has been identified as a cause for Alzheimer ’s
disease. It is likely that a combination of factors, including age, genetic
inheritance, environmental factors, diet and overall general health, are
responsible. In some people, the disease may develop silently for many years
before symptoms appear and the onset of clinical disease may require a
trigger.
Age
Age is the greatest risk factor for dementia. Dementia affects one in 14
people over the age of 65 and one in six over the age of 80. However,
Alzheimer’s is not restricted to elderly people: in the U K, there are over
16,000 people under the age of 65 with dementia, although this figure is
likely to be an underestimate.
Genetic inheritance
Many people fear that they may inherit Alzheimer ’s disease, and scientists
are currently investigating the genetic background to Alzheimer’s. We do
know that there are a few families where there is a very clear inheritance of
the disease from one generation to the next. This is often in families where
the disease appears relatively early in life.
In the vast majority of cases, however, the effect of inheritance seems to be
small. If a parent or other relative has Alzheimer ’s disease, your own chances
of developing the disease are only a little higher than if there were no cases
of Alzheimer’s in the immediate family.
However, carriers of the ApoE4 gene variant have a much higher chance of
developing Alzheimer’s disease. For more information see Factsheet 405,
Genetics and dementia.
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ALZHEIMER’S DISEASE
Environmental factors
The environmental factors that may contribute to the onset of Alzheimer ’s
disease have yet to be identified. A few years ago, there were concerns that
exposure to aluminium might cause Alzheimer ’s disease. However, these
fears have largely been discounted.
Other factors
Because of the difference in their chromosomal make -up, people with Down’s
syndrome who live into their 50s and 60s may develop Alzheimer ’s disease.
People who have had severe head or whiplash inj uries also appear to be at
increased risk of developing dementia. Boxers who receive continual blows to
the head are at risk too.
Research has also shown that people who smoke, and those who have high
blood pressure or high cholesterol levels, increase th eir risk of developing
Alzheimer’s.
Getting a diagnosis
If you are concerned about your own health, or the health of someone close to
you, it is important to seek help from a GP. An early diagnosis will:
 help you plan for the future
 enable the person with dementia to benefit from the treatments that are
now available
 help you identify sources of advice and support.
There is no straightforward test for Alzheimer ’s disease or for any other
cause of dementia. A diagnosis is usually made by excluding other causes
which present similar symptoms. The GP will need to rule out conditions
such as infections, vitamin deficiency, thyroid problems, brain tumours,
depression and the side-effects of drugs.
Specialists
The GP may ask a specialist for help in making a diagnosis. The specialist
may be an old-age psychiatrist, a neurologist, a physician in geriatric
medicine or a general psychiatrist. Who you see depends on age of the person
being examined, how physically able they are and how well services are
developed in the local area.
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Tests
The person being tested will usually be given a blood test and a full physical
examination to rule out or identify any other medical problems. The person ’s
memory will be assessed, initially with questions about recent events a nd past
memories. Their memory and thinking skills may also be assessed in detail by
a psychologist.
A brain scan may be carried out to give some clues about the changes taking
place in the person’s brain. There are a number of different types of scan,
including computerised tomography (CT) and magnetic resonance imaging
(MRI).
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Additional resources
The following resources provide further information about Alzheimer ’s
disease and its effects.
They include some sources used in the compilation of the arti cles in the case
study that had to be edited down to a more manageable size. These sources
contain the complete information and can be used to supplement and enhance
the five articles provided. The list is by no means exhaustive and there are
many other sources available.
1.
Effects of Alzheimer’s disease video clip
http://video.about.com/alzheimers/Alzheimer -s-Disease.htm
2.
Alzheimer’s Society
http://www.alzheimers.org.uk
3.
Alzheimer’s Association
http://www.alz.org
4.
Wikipedia
http://en.wikipedia.org/wiki/Alzheimer’s_disease
5.
NHS Choices – Alzheimer’s disease
http://www.nhs.uk/Conditions/Alzheimers -disease/Pages/Introduction.aspx
6.
Bupa – Alzheimer’s disease
http://hcd2.bupa.co.uk/fact_sheets/html/alzheimers_disease.html
7.
BBC – Dementia
http://www.bbc.co.uk/health/physical_health/conditions/dementia1.shtml
8.
Alzheimer Scotland
http://www.alzscot.org/
9.
About.com – Alzheimer’s disease
http://alzheimers.about.com/
10.
The Telegraph – TV review, Terry Pratchett living with Alzheimer’s
http://www.telegraph.co.uk/culture/tvandradio/4515763/T V-reviewTerry-Pratchett-Living-with-Alzheimers-BBC2-Minder-Five.html
11.
Alzheimer’s Research Trust
http://www.alzheimers-research.org.uk/info/dementia/
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Parkinson’s disease
Article 1: What is Parkinson’s disease?
Parkinson’s disease is a chronic neurological condition that affects about
120,000 people in the UK. [1] The disease is named after Dr James Parkinson,
who was the first to provide details of the condition in ‘An Essay on the
Shaking Palsy’ in 1817.
Parkinson’s disease affects men and women although men are statistically
more likely to develop it than women. [ 2] Most sufferers are over the age of 50
but younger people can also develop it.
If the symptoms develop when the person is between 21 and 40, it is known
as young-onset Parkinson’s disease. The actor Michael J. Fox was diagnosed
with young-onset Parkinson’s disease and now campaigns to raise awareness
of the disease and raise funds for research.
Of the 10,000 people diagnosed with Parkinson’s disease in the UK each
year, one in 20 is under the age of 40. [2] If a person is diagnosed before they
are 18, this is known as juvenile Parkinson’s disease. This is very rare.
Parkinson’s disease is caused by a loss of nerve cells in a part of the midbrain that produces the chemical dopamine. This chemical acts as a
messenger between the brain and nervous system to coordinate movement. If
there are not enough of these dopamine -producing cells, then dopamine levels
fall and there is less control over movement. This causes movements to
become slow and abnormal.
If the loss of nerve cells is severe enough, the symptoms of Parkinson ’s
disease may appear. These include slower movement, shaking (tremor) and
stiffness of muscles. People who suffer from Parkinson’s disease typically
have a stooped posture and a characteristic position of the arms and legs . [3]
There is no cure for Parkinson’s disease as yet and the reasons for people
getting the disease are not clear, although it is understood to be a
combination of genetic and environmental
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PARKINSON’S DISEASE
factors. [1] Although Parkinson’s disease is not fatal, its symptoms do worsen
over time.
References
[1] www.parkinsons.org.uk.
[2] www.nhs.uk.
[3] Beatty, J. (1995) Principles of Behavioural Neuroscience. Brown and
Benchmark.
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Article 2: Causes of Parkinson’s disease
Parkinson’s disease is caused by a loss of nerve cells in a region of the brain
called the substantia nigra. The nerve cells in this part of the brain produce
the chemical dopamine, which acts as a messenger between the brain and the
nervous system to co-ordinate movement. If there are fewer of the dopamineproducing cells, as is the case in sufferers of Parkinson’s disease, the quantity
of dopamine produced is reduced. This leads to less control over movement,
causing it to become slow and abnormal. However, it is worth noting that
autopsy studies have shown neuronal losses and other signs of P arkinson’s
disease (insoluble clumps of protein known as Lewy bodies) in several other
regions of the brain. [1]
The loss of nerve cells in the substantia nigra and consequent reduction in
dopamine levels usually occurs over a number of years. When 80% of the
nerve cells in this region have been lost, the symptoms of Parkinson’s disease
appear and these become worse with time. [2]
Dopamine is one of the catecholamines. These are a group of biochemically
related compounds that have a range of functions withi n the nervous system.
Dopamine serves as a neurotransmitter. [3[ Catecholamines, including
dopamine, are synthesised from the amino acid tyrosine, which is common in
the human diet. [3] The pathway for the production of dopamine is as follows :
tyrosine
L -dopa
tyrosine hydroxylase
(enzyme)
free dopamine
dopa decarboxylase
(enzyme)
This dopamine is either bound into vesicles and stored for synaptic release or
destroyed by the enzyme monoamine oxidase (MAO). MAO inhibitors are
often used in the treatment of Parkinson’s disease as they block the action of
MAO. [2]
Some studies have shown that Parkinson’s disease tends to run in families
and that there is a link between a number of different genes and the
development of Parkinson’s disease. [4] However, further research is required
in this area and studies are also ongoing into the impact of environmental
factors like toxins on the development of Parkinson ’s disease.
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References
[1] Schnabel, J. (2010) Secrets of the shaking palsy. Nature 466.
[2[ www.parkinsons.org.uk.
[3] Beatty, J. (1995) Principles of Behavioural Neuroscience. Brown and
Benchmark.
[4] www.nhs.uk.
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Article 3: Symptoms of Parkinson’s disease
The symptoms of Parkinson’s disease develop gradually and worsen over
time. Each sufferer of Parkinson’s disease is affected differently, not only in
terms of their symptoms and how severe they are, but also i n how they
respond to treatment.
There are three main symptoms associated with Parkinson ’s disease. When all
three of these symptoms appear together, it is known as parkinsonism. The
main symptoms are slowness of movement (bradykinesia), shaking (tremor)
and stiffness of muscles (rigidity). [1]
Parkinson’s sufferers may find it difficult to move, especially at the start of
the movement, and it may take them longer to perform everyday tasks.
Bradykinesia is the term that describes this slowness of movement. People
who suffer from bradykinesia may have short, shuffling steps . [2] This is
known as festination. This slowness of movement can even affect facial
muscles, lessening the ability of the person to use facial expressions as a
form of communication.
Shaking, or tremor, is an involuntary rhythmical movement that often begins
in one of the hands. [1] Tremor is more likely to occur when the particular part
of the body is at rest and it often becomes worse over time, spreading up the
arm and sometimes the foot on the same side of the body. Although many
people associate Parkinson’s disease with tremor, up to 30% of people who
suffer from Parkinson’s disease do not have tremor as one of their
symptoms. [1[
The third main symptom of Parkinson’s disease is rigidity – when the muscles
are stiff or tense. This causes difficulty when trying to move or turn around,
make finger movements or even facial expressions.
There are a wide range of other symptoms associated with Parkinson ’s
disease. Additional physical symptoms include:





falling and dizziness
bladder weakness and constipation
eye problems
speech and communication problems
difficulty swallowing.
Additional mental symptoms include dementia, depression and anxiety.
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Furthermore, research suggests that up to 90 % of people with Parkinson’s
disease suffer from sleep problems. [2]
References
[1] www.nhs.uk.
[2] www.parkinsons.org.uk.
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Article 4: Diagnosis of Parkinson’s disease
There are no existing tests that can be carried out to conclusively show that a
person has Parkinson’s disease. Instead, GPs base their initial diagnosis on a
combination of a patient’s symptoms, medical history and a clinical
examination. A GP would examine the patient to look for any signs o f
Parkinson’s disease, eg slowness of movement, tremor, stiffness or
difficulties with handwriting or making facial expressions . [1] However, in the
early stages of Parkinson’s the disease can be difficult to diagnose as the
symptoms can be mild.
A GP with an average patient list of 1500 people will only see a patient with
Parkinson’s disease every 3.3 years. [2] This makes it very difficult for GPs to
build up and maintain an expertise on the condition. If a GP suspects
Parkinson’s disease, then the patient should be referred untreated to a
hospital clinician with sufficient expertise in movement disorders to make the
diagnosis. [2]
After being referred to a specialist the patient may be offered a test to look
more closely at the brain. A positron emission tomography (PET) scan can
detect a loss of dopamine from the basal ganglia but there are only about 20
of these scanners in Europe and they are very expensive.
Computed tomography (CT) or magnetic imaging resonance (MRI) scans may
be carried out instead. These may help to identify the presence of a structural
lesion or lesions which may cause or contribute to parkinsonism . [1] They may
also be used (possibly in conjunction with blood tests) to rule out other
disorders that may be responsible for the patient ’s symptoms.
Patients may be offered a single photon emission computed tomography
(SPECT) scan, which can be used when there is uncertainty between
Parkinson’s disease and other non-degenerative parkinsonism. This takes a
series of pictures of the brain to detect if there is any dopamine deficiency,
which is seen in people who suffer from Parkinson ’s disease. [3] . DaTSCANSPECT involves a SPECT scan used in conjunction with a radio pharmaceutical agent (a chemical that contains a radioactive element), which
allows identification of structures within the body. The DaTSCAN uses an
iodine-based compound which passes through the blood –brain barrier and
becomes attached to dopamine transporters in the region of the brain that has
degenerated in Parkinson’s disease. [1] The SPECT scan can measure the
uptake of these isotopes, which can be used as a measure of these dopamine
transporters. [1]
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Studies into other diagnostic tools are ongoing. Researchers in Sydney have
developed a blood test that appears to be able to detect Parkinson’s disease
soon after symptoms appear, [1] but this test is still very experimental.
References
[1] www.parkinsons.org.uk.
[2] www.sign.ac.uk/pdf/qrg113.pdf.
[3] www.nhs.uk.
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Article 5: Treatment of Parkinson’s disease
There is currently no cure for Parkinson’s disease. Drug treatment is the main
method used to control the symptoms. [1] Parkinson’s symptoms occur when
levels of dopamine are too low. However, dopamine cannot be used directly
to relieve these symptoms as it is incapable of crossing the blood –brain
barrier.
The blood–brain barrier is a group of
cells that line the brain’s blood
vessels, protecting vital brain
structures from foreign substances. [2]
This barrier poses a major obstacle
when trying to deliver therapeutic
drugs to the brain to treat a range of
conditions, including Parkinson’s
disease.
From: www.faculty.washington.edu/chudler/bbb.html.
Levodopa (or L -dopa) is an amino acid that can be converted into dopamine
and is often used to replace the dopamine lost in Parkinson ’s disease. It is one
of the main drugs used to treat the symptoms of Parkinson ’s disease and can
be used at all stages of the condition. [1] Unlike dopamine, it can pass through
the blood–brain barrier. There are, however, many side-effects from taking L dopa, including nausea, involuntary movements (called dyskinesia),
confusion, mood swings and sleepiness. [1]
Dopamine agonists are also used in the treatment of Park inson’s disease.
These act like dopamine to stimulate nerve cells and they can be used during
all stages of Parkinson’s disease. [1] They can prevent side-effects like
dyskinesia, and research has shown that they can be effective against the
symptoms of Parkinson’s disease that are unrelated to movement. [1] They do
also, however, have a range of side -effects.
MAO-B inhibitors can be used to block the enzyme monoamine oxidase type
B that breaks down dopamine. These inhibitors are used to make L -dopa last
longer or cut down how much is needed. [1] There is also a range of sideeffects associated with their use. The side-effects of each drug treatment may
be experienced by some but not others – ‘Drug treatment for Parkinson’s is
prescribed to suit the individual. Each person will react to their medication in
different ways’ (Professor Adrian Williams, consultant neurologist). [1]
There are also a number of therapies that can be used to help people manage
their symptoms. These include occupational therapy, physiotherapy and
speech therapy. Surgical procedures such as deep brain stimulation are an
option but are generally only used for those whose symptoms cannot be
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effectively controlled by medication and who have had Parkinson ’s disease
for some time. [1] Research into developing more effective treatments for
Parkinson’s disease is ongoing. Some progress has been made in researching
the use of stem cells and gene therapy but it will be some time before these
techniques can be utilised.
References
[1] www.parkinsons.org.uk.
[2] www.michaeljfox.org.
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Assessment
Article 1: What is Parkinson’s disease?
1.
2.
3.
4.
5.
How many people in the UK suffer from Parkinson ’s disease?
Which gender is more likely to suffer from Parkinson ’s disease?
What is meant by young-onset Parkinson’s disease?
What are the main symptoms of Parkinson’s disease?
What combination of factors is thought to cause Parkinson ’s disease?
Article 2: Causes of Parkinson’s disease
1.
2.
3.
4.
5.
Name the region of the brain where nerve cells are lost , leading to
Parkinson’s disease symptoms.
What impact does this loss of nerve cells have on dopamine levels?
What percentage of nerve cells in this region is lost before Parkinson’s
symptoms appear?
Describe how dopamine is formed within nerve cells.
Name the chemical that destroys dopamine in the nervous system.
Article 3: Symptoms of Parkinson’s disease
1.
2.
3.
4.
5.
Name the three main symptoms of Parkinson’s disease.
Name the term used to describe the occurrence of the main three
symptoms of Parkinson’s disease.
Why might a Parkinson’s sufferer find it difficult to communicate?
What percentage of Parkinson’s sufferers do not suffer from tremor?
Name one other physical and one mental symptom of Parkinson ’s
disease.
Article 4: Diagnosis of Parkinson’s disease
1.
2.
3.
4.
5.
What signs of Parkinson’s disease would a GP look for to make an
initial diagnosis?
Why should a GP refer a patient to a hospital clinician withou t treating
them if they suspect Parkinson’s disease?
Why are PET scans not often used to diagnose Parkinson ’s disease?
What are CT and MRI scans specifically used for in the diagnosis of
Parkinson’s disease?
Describe what is involved in a DaTSCAN-SPECT.
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Article 5: Treatment of Parkinson’s disease
1.
2.
3.
4.
5.
42
Why does the blood–brain-barrier pose a challenge to treating
Parkinson’s disease?
Describe the use of L-dopa in the treatment of Parkinson’s disease.
What do dopamine agnoists do that help rel ieve symptoms?
Describe the use of MAO-B inhibitors in the treatment of Parkinson’s
disease.
Which two techniques are being focused on now for treating
Parkinson’s disease?
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Additional teacher information
Background neurobiology
Parkinson’s disease is a chronic neurological condition that affects about
120,000 people in the UK. [1[ The disease is named after Dr James Parkinson,
who was the first to provide details of the condition in ‘An Essay on the
Shaking Palsy’ in 1817. Most sufferers are over the age of 50 but younger
people can also develop Parkinson’s disease.
Parkinson’s disease is caused by a loss of nerve cells in the region of the mid brain called the substantia nigra (‘black substance’). This is an
‘evolutionarily ancient clump of neurons near the brainstem that normally
synthesizes the neurotransmitter dopamine and pumps it into movement regulating brain regions’. [2]
Dopamine’s full chemical name is 4-(2-aminoethyl) benzene-1,2-diol and its
chemical formula is C 6 H 3 (OH) 2 -CH 2 -CH 2 -NH 2 . It belongs to the
catecholamines, a group of biochemically related compounds that perform a
range of functions in the nervous system. Other catecholamines include
epinephrine and norepinephrine. Dopamine acts as a neurotransmitter in the
brain but also acts as a neurohormone when released by the hypothalamus.
The diagram shows that the production of catecholamine neurotransmitters
depends on the enzyme tyrosine hydroxylase. In the production of dopamine,
L -3,4-dihydroxyphenylalanine ( L -dopa) is formed from tyrosine and
converted to dopamine by the enzyme dopa decarboxylase. The dopamine is
then packaged in vesicles for release into the synapse in response to a pre synaptic action potential or destroyed by the enzyme monoamine oxidase . [3]
On release at a synapse, it activates five types of dopamine receptors , D1–D5
and their variants.
Causes of Parkinson’s disease
If there are fewer of the dopamine-producing cells, as is the case in sufferers
of Parkinson’s disease, the amount of dopamine produced is reduce d. This
means that less dopamine reaches the striatum, which is the co-ordination
centre for various brain circuits. [4] This leads to less control over movement,
causing it to become slow and abnormal. However, it is worth noting that
autopsy studies have shown neuronal losses and other signs of Parkinson ’s
disease (insoluble clumps of protein known as Lewy bodies) in several other
regions of the brain. [2]
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The cause of the loss of nerve cells is still a bit of a mystery but it is thought
to be influenced by the ageing process because in most populations relatively
few diagnoses are made in people younger than 40 . [2] Gender matters too,
possibly related to oestrogen production as women have only two -thirds the
risk of men of developing Parkinson’s disease. [2] However, many causes of
Parkinsons’s are described as ‘idiopathic’ as the ultimate cause is unknown.
Research indicates that the causes may be a combination of genetic and
environmental factors. In the past 10 years researchers have identified a
number of rare examples of where a single genetic mutation appears to have
caused Parkinson’s disease. [5] On the other hand, in the early 1980s, a group
of heroin users in California took drugs contaminated with a chemical called
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). After ingestion of this
substance, the drug users suffered from a form of Parkinson’s disease that
was at least to some extent ‘environmental’ in its origin. [5]
Symptoms of Parkinson’s disease
The symptoms of Parkinson’s disease develop gradually and worsen over
time. Each sufferer of Parkinson’s disease is affected differently, not only in
terms of their symptoms and how severe they are but also in how they
respond to treatment. There are three main symptoms associated with
Parkinson’s disease. When all three of these symptoms appear together, it is
known as parkinsonism. The main symptoms are slowness of movement
(bradykinesia), shaking (tremor) and stiffness of muscles (rigidity) . [1] In
addition to these there are a wide variety of other physical and mental
symptoms associated with Parkinson’s disease. These are described in more
depth in the student articles and on the websites www.nhs.co.uk and
www.parkinsons.org.uk.
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Diagnosis of Parkinson’s disease
There are no existing tests that can be carried out to conclusively show that a
person has Parkinson’s disease. If Parkinson’s disease is suspected by a GP,
then the patient should be referred untreated to a specialist with more
experience. They may then be offered a brain scan.
A positron emission tomography (PET) scan can detect a loss of dopamine
from the basal ganglia but there are only about 20 of these scanners in Europe
and they are very expensive. [1] Computed tomography (CT) or magnetic
imaging resonance (MRI) scans may be carried out instead. These may help
to identify the presence of a structural lesion or lesions which may cause or
contribute to parkinsonism. [1] They may also be used (possibly in conjunction
with blood tests) to rule out other disorders that may b e responsible for the
patient’s symptoms.
A single photon emission computed tomography (SPECT) scan can be used
when there is uncertainty between Parkinson’s disease and other nondegenerative parkinsonism. DaTSCAN-SPECT involves a SPECT scan used
in conjunction with a radio-pharmaceutical agent that allows identification of
structures within the body. The DaTSCAN uses an iodine -based compound
that passes through the blood–brain barrier and becomes attached to
dopamine transporters in the region of the br ain that has degenerated in
Parkinson’s disease. [1] The SPECT scan can measure the uptake of these
isotopes, which can be used as a measure of these dopamine transporters . [1]
Several other diagnostic tools are being researched.
Treatment of Parkinson’s disease
As there is no cure for Parkinson’s disease, the main treatments are drug
treatments used to relieve symptoms. Dopamine cannot be used directly as it
is unable to pass through the blood–brain barrier. The concept of the blood–
brain barrier was first described by Paul Ehrlich over 100 years ago after dyes
that he injected into the bloodstream of animals stained tissues in most organs
except the brain.
The blood–brain barrier has three main functions: to protect the brain from
foreign substances, to protect the brain from hormones and neurotransmitters
in the rest of the body, and to maintain a constant environment for the brain
to function efficiently. In general, it allows some molecules to pass through it
but prevents others from doing so. Large molecules do not pass through
easily. Low-lipid-soluble molecules do not penetrate the barrier. Molecules
that have a high electrical charge are also slowed by the barrier. It is thought
that dopamine is unable to pass through the blood–brain barrier because of its
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charge. The blood–brain barrier can be disrupted in several ways, including
exposure to microwaves, radiation and some forms of infection . [6]
Levodopa ( L -dopa) is one of the main drugs used to treat the symptoms of
Parkinson’s disease as it is a precursor for dopamine and it is able to pass
through the blood–brain barrier. It can be converted into dopamine to replace
the lost dopamine. Although it is the main drug treatment for Parkinson ’s
disease, it has many side-effects. Dopamine agonists are also used in the
treatment of Parkinson’s disease. These act like dopamine to stimulate nerve
cells and they can be used during all stages of Parkinson ’s disease, but they
too have side-effects. [1]
MAO-B inhibitors can be used to block the enzyme monoami ne oxidase type
B that breaks down dopamine. These inhibitors are used to make L -dopa last
longer or cut down how much is needed. [1] There is also a range of sideeffects associated with their use. More information on these types of drugs,
their brand names and their side effects is available at
www.parkinsons.org.uk. Different people react differently to medication but
as symptoms worsen, drug treatment can become less effective and the side effects can become disabling. [1]
There are also a number of therapies that can be used to help people manage
their symptoms. These include occupational therapy, physiotherapy and
speech therapy. Surgical procedures can be used but they are normally only
an option for those who have had Parkinson’s disease for some time and
whose medication is not effectively controlling their symptoms. [1] The range
of surgical procedures available includes deep brain stimulation and lesioning
techniques. Deep brain stimulation involves implanting a wire with four
electrodes at its tip into one of three parts of the brain : the thalamus, the
globus pallidus or the subthalmic region. MRI scans are used to position the
electrodes. Lesioning techniques damage certain cells in specific parts of the
brain by creating a small lesion using an electric current. These lesions can
have a beneficial impact on some of the symptoms of Parkinson ’s disease. [1]
Research into developing more effective treatments for Parkinson ’s disease is
ongoing. Two areas that are being researched are the use of stem cells and
gene therapy. Researchers are looking into replacing the dopamine-making
cells lost in Parkinson’s disease with new healthy dopamine-making cells
derived from stem cells grown in a laboratory. [1] If this is possible, then it
may offer a cure for Parkinson’s disease.
Gene therapy could possibly be used to prevent the dopamine -producing cells
from dying and also promote the regeneration of cells. Scientists are aiming
to deliver various types of gene products directly to the areas of the brain
affected. The main two groups of products being used are neurotrophic
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factors like glial cell line derived neurotrophic factor (GDNF) to promote the
growth and survival of these cells, and proteins that increase dopamine
production. For example, the protein biopterin can make the process of
producing dopamine more efficient. [1[ Gene therapy would hopefully allow
the genes for these proteins to be delivered inside the appropriate cells.
Researchers are currently studying the potential use of altered viruses to
transfer therapeutic genetic material to the brains of Parkinson ’s sufferers
without spreading to other areas or causing infection. More information on
stem cell research and gene therapy can be found at www.parkinsons.org.uk.
References
[1] www.parkinsons.org.uk.
[2] Schnabel, J. (2010) Secrets of the shaking palsy. Nature 466.
[3] Beatty, J. (1995) Principles of Behavioural Neuroscience. Brown and
Benchmark.
[4] www.parkinsonsdiseasesurgery.net.
[5] www.michaeljfox.org.
[6] www.faculty.washington.edu/chudler/bbb.html .
From: www.drugdevelopmenttechnology.com/projects/rasagiline/images/Brain_Cros s_Section.jpg Diagram 2 www.ncbi.nlm.nih.gov/bookshelfbr.fcgi?b...part=A570 .
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Additional activities
1.
Students can carry out their own research on Parkinson ’s disease
instead of using the articles or research aspects of the condition not
covered by the articles.
The following list of websites is particularly useful but there are many
others.
1.
2.
3.
4.
5.
6.
7.
8.
9.
www.parkinsons.org.uk
www.nhs.uk
www.michaeljfox.org
www.parkinsons.org
www.ninds.nih.gov/disorders/parkinsons_disease/parkinsons_dise
ase.htm
www.pdf.org
www.bbc.co.uk/health (publication from Scottish Intercollegiate
Guidelines Network)
www.sign.ac.uk/pdf/qrg113.pdf
www.nice.org.uk/nicemedia/pdf/cg035publicinfo.pdf (publication
from the National Institute for Health and Clinical Excellence –
England and Wales).
2.
Some of these websites have some very useful video clips on
Parkinson’s disease that may be used with students or for more
background information. The NHS and Michael J. Fox websites are
particularly good for video clips.
3.
As an alternative to PowerPoint or poster presentations, students could
work in groups to produce an NHS-style information pamphlet on
Parkinson’s disease.
4.
Students could also read articles about the latest research being carried
out on Parkinson’s disease. There are several articles available either
through the websites of major newspapers or through the Nature or New
Scientist websites (www.nature.com or www.newscientist.com) or
directly from scientific journals. Access to some of the articles requires
subscription but others are free.
The following article may be of particular interest as it discusses the potential
use of stem cell research in the treatment of Parkinson ’s disease. It is taken
from the BBC website. Other recent relevant BBC articles include ‘Low
vitamin D levels linked to Parkinson’s disease’ (July 2010), ‘Immune genes
key in Parkinson’s disease’ (August 2010) and ‘Brain pacemaker surgery
hope’ (April 2010).
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HEALTH
14 July 2010 Last updated at 00:12
Stem cell method put to the test in
Parkinson’s study
By Pallab Ghosh Science correspondent, BBC News
Scientists hope to better understand how Parkinson’s develops
UK researchers are launching a study into the potential of using a
person’s stem cells to treat Parkinson’s disease.
An Oxford University team will use adult stem cells, which have the ability
to become any cell in the human body, to examine the neurological condition.
Skin cells will be used to grow the brain neurons that die in Parkinson ’s, a
conference will hear.
The research will not involve the destruction of human embryos.
Induced pluripotent stem (IPS) cells were developed in 2007.
At the time, scientists said this technology had the potential to offer many of
the advantages of embryonic stem cells without any of the ethical downsides.
Three years on, it seems to be living up to that claim.
Compare and contrast
The team at Oxford University is among the first in the world to use IPS to
carry out a large scale clinical investigation of Parkinson ’s, which is
currently poorly understood.
Kieran Breen from Parkinson’s UK explains how the study works:
Researchers will be taking skin cells from 1,000 patients with early stage
Parkinson’s and turning them into nerve cells carrying the disease to learn
more about the brain disorder, the UK National Stem Cell Network annual
science meeting will hear.
The technique is useful because it is difficult to obtain samples of diseased
nerve tissue from patient biopsies.
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IPS enables the researchers to create limitless quantities of nerve cells to use
in experiments and to test new drugs.
‘Parkinson’s disease is the second most common neurodegenerative disease in
the UK and is set to become increasingly common as we live longer, ’ said Dr
Richard Wade-Martins, head of the Oxford Parkinson’s Disease Centre.
‘Once we have neurons from patients we can compare the functioning of cells
taken from patients with the disease and those without to better understand
why dopamine neurons die in patients with Parkinson ’s.’
The research is being funded by Parkinson’s UK.
The charity’s director of research, Kieran Breen, described it as ‘vital
research that will help us better understand the causes of this devastating
condition and how it develops and progresses.
‘We hope the work will pave the way for new and better treatmen ts for people
with Parkinson’s in the future.’
About 120,000 people in the UK are living with Parkinson ’s.
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Schizophrenia
Article 1: What is schizophrenia?
Schizophrenia is a complex mental disorder. It is considered to be many
illnesses concealed as one. A biochemical imbalance in the brain is believed
to cause symptoms. Recent research suggests that schizophrenia may be a
result of faulty neuronal development in the f oetal brain. This changes the
brain circuits and develops into full-blown illness in late adolescence or early
adulthood.
The causes are thought to be a variety of contributing factors, includ ing:
 genetics – one in ten people with
schizophrenia has a parent with
the condition
 early environment in the womb
or during birth
 neurobiology
 social, such as stress, trauma and
poverty
 use of recreational drugs,
including ecstasy, LSD,
amphetamines (speed), cannabis
and prescription drugs. [3]
There are three main types of
schizophrenia: [1]
1.
2.
3.
Imagehttp://www.psychiatrictimes.com/schizophrenia/con
tent/article/10168/52516
disorganised schizophrenia
(or ‘hebephrenic
schizophrenia’) – no emotion, speech disorganised
catatonic schizophrenia – waxy flexibility, reduced or too much
movement, rigid posture
paranoid schizophrenia – strong delusions or hallucinations.
Although the meaning of the name means ‘split mind’, from its Greek roots, [1]
a schizophrenic does not have a ‘split mind’; this is more common in
dissociative identity disorder (also known as ‘multiple personality disorder’
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or ‘split personality’) It is common for these conditions to be confused with
each other.
Schizophrenia causes distorted and bizarre thoughts, perceptions, emotions,
movement and behaviour. It cannot be defined as a single illness; it is thought
of as a syndrome or disease process that is hugely diverse and displays many
symptoms. It tends not to affect children. The peak incidence of onset occurs
normally between 15 to 25 years of age for men and 25 to 35 years of age for
women. [5]
Schizophrenia affects up to 1% of the population (up to 600,000 people in the
UK). [9]
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Article 2: Causes of schizophrenia
Inheritance
Schizophrenia is caused by a
combination of genes making a
person vulnerable to the
condition. Even if a person has
many of the key components
they may not necessarily
develop the disease. Most
people with schizophrenia have
no family history of the
disorder. Twin studies show
twins separated at birth, with
schizophrenic parents, are at
high risk of developing the
disease. If genetics was the only
factor in developing
From: http://www.schizophrenia.com/research/hereditygen.htm
schizophrenia, then both
monozygotic twins should
always develop this illness. A good environment could delay the onset of the
disorder. Twin studies are no longer considered ethical and twins are now
adopted by the same family. As these studies are rare, data examination is
difficult but gives an insight into genetic factors verses environmental
factors. [8]
Features of the schizophrenic brain that show abnormality
[9]
 Enlarged: ventricles,
basal nuclei.
 Decreased: grey
matter,
hippocampus,
amygdala, metabolic
activity, blood flow
in certain brain
regions.
From:
http://www.jamesdisabilitylaw.com/images/Schizophrenia_MRI_Scans.gif.
 Areas implicated in
schizophrenia:
forebrain, hindbrain (cerebellum) and limbic system ( cingulate gyrus,
amygdala, hippocampus and thalamus).
Developmental neurobiologists have found that schizophrenics have neurons
that have formed incorrect connections during foetal development. Changes
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SCHIZOPHRENIA
during puberty make faulty connections. Not all schizophrenic people have
these abnormalities, nor do they occur only in individuals with this illness. It
appears that many of these differences are there before the person becomes
ill.
Neurotransmitters [15]
The neurotransmitter system is linked as a possible cause of schizophrenia as
the neuroleptic drugs (antipsychotics) that alter these transmitters also relieve
schizophrenia.
High dopamine levels can block the specific pathways of your brain
responsible for functions such as memory, emotion, social behaviour and self awareness, explaining the psychotic symptoms, such as hearing voices.
Receptor sensitivity in the prefrontal cortex or the membrane structures could
be a cause.
It could be that the serotonin system interacts with the dopamine system to
modify the way in which it operates. The serotonin receptors ar e important in
the treatment of schizophrenia. Clozapine, the antipsychotic drug, seems to
work by blocking serotonin sites in the brain.
An underactivity of glutamate supports the dopamine hypothesis, since
dopamine receptors inhibit the release of gluta mate and reduced glutamate
function is linked to poor performance on tests requiring frontal lobe and
hippocampal function. Positive symptoms fail, however, to respond to
glutamatergic medication.
Traces have been found of hallucinogenic chemicals in the cerebro-spinal
fluid (CSF) of schizophrenics. The CSF removes excess chemicals in the
brain. This suggests that schizophrenics are producing more of these
chemicals than normal. [8] Interaction of gamma aminobutyric acid and
acetylcholine may cause an imbalance. One neurotransmitter may affect
others which are not usually involved in the development of disease.
Stressful life events, drug abuse and other causes
Contributing factors to schizophrenia are homelessness, poverty, bereavement
and abuse. Cannabis, cocaine and amphetamines are known to increase the
levels of dopamine in the brain; they trigger similar symptoms of psychosis to
those that are often experienced by somebody with schizophrenia. Drugs
make schizophrenia worse. Brain injury, viruses, hormonal activity
(particularly in women), diet, allergic reaction or an infection may also be
linked to development of the disorder.
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Article 3: Symptoms of schizophrenia
The symptoms of schizophrenia can be separated into two main categories:
positive and negative. It seems that the positive symptoms may be accounted
for by the dopamine hypothesis whereas the negative symptoms are explained
by serotonin or changes in brain structure.
There is no one particular characteristic or symptom that is always present in
a schizophrenic person.
Positive symptoms (in addition to existing behaviours)
 Hallucinations: These can involve any sense, but the most common is
hearing voices. Changes in the speech area are evident (using brainscanning equipment) in the brains of people with schizophrenia when they
hear voices. This research shows that the brain mistakes thoughts for real
voices.
 Delusions: These are false beliefs that are held with complete conviction,
even though they are based on mistaken, strange or unrealistic views.
 Thought disturbances: People experiencing psychosis often have trouble
keeping track of their thoughts and conversations. Some people find it
difficult to concentrate and will move quickly from one idea to another.
Negative symptoms (an impairment of usual behaviours)
 Withdrawn.
 Emotionless and flat.
 Psychomotor disturbances (or catatonic behaviour): The patient may adopt
strange frozen postures for a long period of time (extreme cases are for
several years) or engage in repetitive movements such as pacing or
rocking.
 Lack of volition, apathetic, lack of motivation , for example not wanting to
leave the house and changes in sleeping patterns.
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Article 4: Diagnosis of schizophrenia
A doctor will refer the patient to a psychiatrist.
Psychiatric evaluation
The psychiatrist will ask a series of questions about the patient ’s symptoms,
psychiatric history and family history of mental health problems.
He will be looking for the presence of two or more of the f ollowing
symptoms for at least 30 days: [16]






hallucinations
delusions
disorganised speech
disorganised or catatonic behaviour
negative symptoms (emotional flatness, apathy, lack of speech)
major problems coping with work, relating to other people and maintaining
oneself
 continuous signs of schizophrenia for at least 6 months, with active
symptoms (hallucinations, delusions, etc) for at least 1 month
 no other mental health disorder, medical issue or substance abuse problem
is causing the symptoms.
Medical history and exam
The patient will be asked about their personal and family health history. The
psychiatrist will need to complete a physical examination to check for
medical issues that could be causing or adding to the problem. [16]
Laboratory tests
The psychiatrist needs to eliminate the possibility of something else being the
cause of the symptoms. Laboratory tests cannot diagnose schizophrenia, but
blood and urine tests can rule out other medical causes of symptoms. A n MRI
or CT scan can identify the brain abnormalities associated with
schizophrenia. [16]
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Article 5: Treatment of schizophrenia
Help is more beneficial the earlier it is sought, making the need for hospital
treatment less likely.
Medication
Patients may need to trial different medications to see which best suits their
needs. Medication can provide short-term relief for a patient, and they may
become well enough to come off it and remain well. Other patients may
benefit from long-term treatment. These patients may find staying on th e
lowest effective dose of medication is the best way of dealing with
symptoms. [3[
‘Typical’ antipsychotic/neuroleptic drugs or major tranquillisers
These help to weaken and control (not cure) positive symptoms such as
delusions and hallucinations. They help patients to think more clearly and
look after themselves better. They work well in four out of five patients. The
drug reduces the action of dopamine in the brain. The sedative action makes
it more difficult to cope with side-effects or to benefit from counselling,
particularly in high doses. The side-effects could be:





neuromuscular effects (shaking and stiffness)
feeling slow
restlessness
unwanted movements, mainly of the mouth and tongue
antimuscarinic effects (blurred vision, rapid heart beat, constipation and
dizziness).
Newer, ‘atypical’ antipsychotics/neuroleptics
These more popular drugs (eg risperidone, olanzapine, quetiapine,
amisulpride and zotepine) have fewer side-effects and improve negative
symptoms as they work on different chemical s in the brain and are less likely
to produce unwanted movements. However, they can cause metabolic sideeffects such as: [1]





weight gain
diabetes
tiredness
high cholesterol
high blood pressure.
From: http://www.medscape.org/viewarticle/550755_15.
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Psychological treatments
Therapies that involve talking (psychotherapy, counselling and cognitive
behaviour therapy) can help patients understand and cope with their disorder.
Once they understand what makes them unwell, patients can form new ways
of thinking and behaving. Consequently their health can impro ve and they
function better in everyday life. Family therapy sessions help families learn
about the disorder, ways of supporting someone with schizophrenia and how
to solve some of the practical problems that may arise. [3]
Transcranial magnetic stimulation
Transcranial magnetic stimulation (TMS) is a non-invasive new treatment
used in research studies. This trial technology causes depolarization in the
neurons of the brain. TMS uses electromagnetic induction to induce weak
electric currents using a rapidly changing magnetic field, causing activity in
specific or general parts of the brain. This treatment has helped patients who
have mainly ‘negative’ symptoms, and has had some success in treating
voices. [3]
Rapid tranquillisation
This treatment is risky and traumatic. It is rarely used but may be necessary
to urgently pacify a patient. Subsequently, the patient would receive a full
explanation, support and an opportunity to discuss the incident. [3]
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Assessment
Article 1: What is schizophrenia?
1.
2.
3.
4.
5.
What does recent research suggest as a cause of schizophrenia?
Name three of the factors that contribute to schizophrenia.
Name the three main types of schizophrenia.
Which age groups are more likely to suffer from schizophrenia?
How many people in the UK suffer from schizophrenia?
Article 2: Causes of schizophrenia
1.
2.
3.
4.
5.
Describe how the structure of the brain is different in people suffering
from schizophrenia.
What do scientists suggest happens during foetal development that may
be one cause of schizophrenia?
Explain the impact of high dopamine levels.
Name two neurotransmitters that may be linked to schizophrenia.
Describe two other factors that may contribute to schizophrenia.
Article 3: Symptoms of schizophrenia
1.
2.
3.
4.
5.
Which hypothesis is thought to account for the positive s ymptoms of
schizophrenia?
What is thought to cause the negative symptoms of schizophrenia?
What is the difference between positive and negative symptoms?
Describe two positive symptoms of schizophrenia.
Describe two negative symptoms of schizophrenia.
Article 4: Diagnosis of schizophrenia
1.
2.
3.
4.
5.
If a GP thought a patient was schizophrenic, who would they refer them
to?
Describe the symptoms that may lead to a diagnosis of schizophrenia.
How many days should these symptoms have occurred for b efore a
diagnosis can be made?
What questions may a psychiatrist ask when trying to make a diagnosis?
What scanning methods are used to detect the brain abnormalities
associated with schizophrenia?
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Article 5: Treatment of schizophrenia
1.
2.
3.
4.
5.
What are ‘typical’ antipsychotic/neuroleptic drugs used for?
Describe two side-effects of their use.
Describe two benefits of using ‘atypical’ antipsychotics/neuroleptics.
Describe the benefits of family therapy sessions.
What is TMS and how does it help to treat schizophrenia?
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Additional teacher information
What is schizophrenia?
Schizophrenia is a mental disorder in which the normal processes of thinking
and emotional responsiveness are disrupted. [4 ] The label ‘schizophrenic’ is
commonly misunderstood to mean that the affected person has a ‘split
personality’. Some schizophrenics may hear voices and may experience the
voices as distinct personalities, but a schizophrenic does not have distinct
multiple personalities. In a large representative sample from a 1999 study,
12.8% of Americans believed that individuals with schizophrenia were ‘very
likely’ to do something violent against others and 48.1% said that they were
‘somewhat likely’ to. The perception of individuals with psychosis as violent
has more than doubled in prevalence since the 1950s, according to one meta analysis. [4] The negative social stigma has been identified as preventing
patients from recovering from schizophrenia.
Causes of schizophrenia
The cause of schizophrenia is due to many contributing factors.
 Inheritance
www.jamesdisabilitylaw.com/schizophrenia.htm
Reprinted by permission of the author. From Got tesman, I.I.
(1991) Schizophrenia Genesis: The Origins of Madness . W.H.
Freeman, New York, p.96 (c) 1991 Irving I.
It is thought that about 40% of cases of
schizophrenia are inherited and 60%
occur spontaneously. Recent research
suggests that schizophrenia may result
from a large number of genetic
abnormalities, so there is little chance of
a single cause and cure for it. [17]
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Why does schizophrenia develop at late adolescence?
Adolescence can be stressful. People likely to develop schizophrenia may
find it difficult to reach psychological maturity with regard to bonding with
parents or peers or both. This may lead to crucial self -construction
difficulties, and the psychosis emerges out of such ‘blocked adolescence’.
Also during adolescence, brain connections and signalling mechanisms
selectively change over time to meet the needs of the environment. Overall,
grey matter volume increases at earlier ages, followed by sustained loss and
thinning occurring around puberty, which correlates with advancing cognitive
abilities. Scientists think this process shows a greater organi sation of the
brain as it cuts out old connections and increases in myelin, which enhance
transmission of brain messages. [14]
Abnormal brain development
In addition, schizophrenia has increasingly been recognised as a collection of
neurodevelopmental disorders that involve alterations in brain circuits.
Viral theory [14]
This theory states that some of our genes came from viruses and became
integrated into our DNA. Blomberg hypothesises that about 1% of the human
genome is made up of retroviruses. These remain ‘dormant’ but are activated
by other viruses during foetal development or infancy.
Blood samples were taken from 53,000 pregnant women in the USA during
the 1950s and frozen. Buka (1999) discovered 27 schizophrenics from these
women. Buka found that their mothers’ blood contained more antibodies
(suggesting a viral infection during pregnanc y). The most commonly found
was herpes.
Some of these genes are responsible for making proteins and are detected in
the CSF of the brain. Karlsson found DNA from these viruses in 29% of
recently diagnosed schizophrenics. There was no evidence of this material in
healthy patients. [8[
Types of schizophrenia
There are many ways to categorise schizophrenia. [4]
Schneider’s first-rank symptoms
Psychiatrist Kurt Schneider (1887–1967) distinguished schizophrenia
according to its symptoms. Although they have significantly contributed to
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the current diagnostic criteria, they are no longer considered specific enough
and first-rank symptoms are now being de-emphasised for diagnosis. [4]
DSM-IV-TR (American Psychiatric Association’s Diagnostic and Statistical
Manual of Mental Disorders)
This is the most widely used standardised criteria for diagnosing
schizophrenia in the USA and the rest of the world.
ICD-10 (World Health Organization’s International Statistical Classification
of Diseases and Related Health Problems)
This is used in European countries and puts more emphasis on Schneiderian
first-rank symptoms, although agreement between the DSM-IV-TR and ICD10 is high.
Subtypes
The DSM-IV-TR contains five sub-classifications of schizophrenia, although
classifications may change:





Paranoid type: Presence of delusions and hallucinations. Thought disorder,
disorganised behaviour and affective flattening are absent (DSM code
295.3/ICD code F20.0).
Disorganised type: Thought disorder and flat affect are present together
(DSM code 295.1/ICD code F20.1).
Catatonic type: Patient may be almost immobile or exhibit agitated,
purposeless movement. Symptoms can include catatonic stupor and waxy
flexibility (DSM code 295.2/ICD code F20.2).
Undifferentiated type: Psychotic symptoms are present but the criteria for
paranoid, disorganised or catatonic types have not been met (DSM code
295.9/ICD code F20.3).
Residual type: Positive symptoms are present at a low intensity only (DSM
code 295.6/ICD code F20.5)4.
The ICD-10 defines two additional subtypes:
1.
Post-schizophrenic depression: A depressive episode arising in the
aftermath of a schizophrenic illness where some low -level schizophrenic
symptoms may still be present (ICD code F20.4) .
2.
Simple schizophrenia: Insidious and progressive development of
prominent negative symptoms with no history of psychotic episodes (ICD
code F20.6). [4]
Schizophrenia should be categorised by the negative symptoms, according to
Slater and Roth. [4]
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Additional activities
1.
Students can carry out their own research on schizophrenia instead of
using the articles or research aspects of the condition not covered by the
articles.
The following list of websites is particularly useful but there are many
others:
www.faculty.washington.edu/chudler/schiz.html
www.pitjournal.unc.edu/node/104
www.mind.org.uk/help/diagnoses_and_conditions/schizophrenia
www.nhs.uk/Conditions/Schizophrenia/Pages/Introduction.aspx
www.bbc.co.uk/health/emotional_health/mental_health/disorders_schiz.
shtml
www.pages.drexel.edu/~rm35/
www.psychology4a.com/Psychopathology.htm
www.tolerancelost.com/schizophrenia/
2.
Some of these websites have some very useful video clips on
schizophrenia that may be used with students or for more background
information. The NHS, BBC, tolerance lost and pit journal websites are
particularly good for video clips.
3.
Students could also read articles about the latest research being carried
out on schizophrenia or discuss the nurture verses nature debate. There
are several articles available either through the websites of major
newspapers or through the Nature or New Scientist websites
(www.nature.com or www.newscientist.com) or directly from scientific
journals. Access to some of the articles requires subscription but others
are free.
The following case studies may be useful and there are a few questions
to link back and assess comprehension of the information cards.
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Case history 1
Jane was seen by a consultant on a domiciliary visit to the vicarage of St
Mary’s church. Her father, the vicar, explained that J ane was a sixth-form
student at a local private school. She had always done well at school and had
achieved high grades in her fifth-form exams. She was hoping to go to
university. Over the last few months, however, her behaviour had changed.
She had started refusing to go to school, but had declined to give any reason
why. She spent her days writing in her room and had not eaten for the last
three days. She would not let her parents in to see her and had barricaded the
door. There was no history of drug abuse.
The consultant talked to her through the door and finally persuaded her to
trust him sufficiently to let him in to her room. He found that Jane was a tall,
thin girl with a pale face. The room smelt of urine, and the walls had been
covered in a fine, spidery writing. When the consultant tried to read what it
said, she shouted at him. Jane looked at him suspiciously and at times seemed
to be conferring with an unseen person as to how trustworthy the doctor was.
The doctor could see scratch marks on her neck where Jane had cut herself
with the blade of a pair of scissors. She said that this was ‘to let the bad
blood out’. Jane appeared alert and knew the day and the time. When asked
about her refusal to eat, Jane mumbled about her parents trying to pois on her
because, she said, ‘My mother offered me an Arrowroot Thin biscuit...that
would make me thin...and she offered me some cabbage...that would turn me
into a cabbage.’
The doctor felt that Jane’s health was at risk because she had been harming
and starving herself, and that there was evidence of a mental disorder that
warranted admission to hospital for further assessment.
What evidence is there that Jane is suffering from a psychotic disorder?
What are the diagnostic features of schizophrenia in t his case?
Why does schizophrenia often appear to begin in adolescence?
(http://priory.com/schizo.htm)
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Case history 2
J. Albert Arthur Andrew Churchill Chamberlain was a man who went under
several aliases and had a career as a small time con man. Some days he was
Albert Chamberlain and some days he was Andrew Churchill.
He presented to his GP with feelings of ‘great sadness and loss of sincerity’,
as he put it. His GP found his speech difficult to understand, but his main
concerns seemed to be about his ex-wife. He claimed that his ex-wife was
plotting with the British security forces to remove his ‘sincerity and
personality’. The GP noted down some of his speech verbatim: ‘My divorced
wife has an albigisty of conscience which she has terpolated with the security
forces. They’re debating my existence even now. They’re saying we will
drain his face of emotions, put our emotions into him and alter what the
doctor’s writing on the page to alter the circumstance and the circumcision of
the truth.’
On further questioning the patient seemed wholly convinced that a transmitter
had been inserted into his neck – he said he could actually feel it there – and
that the transmitter was designed to put his wife ’s thoughts into his head. He
could distinctly hear conversations between his wife and agents of the British
security forces commenting on his thoughts and actions.
What positive symptoms does this patient exhibit?
What is the significance of his using words like ‘albigisty’ and ‘terpolated’?
What kind of schizophrenia is this?
(http://priory.com/schizo.htm)
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Case history 3
Shakil, 32, was brought to casualty by his brother , who had found him in a
nearby seaside town, by accident. Shakil had been missing from home for
several years. By chance his brother had seen Shakil walking down the road
and had followed him home. Home had turned out to be ramshackle flat
above an empty sewing machine shop. His brother had been disgusted to find
the remains of Shakil’s last meal, an unplucked, ungutted and uncooked
pigeon. Shakil said he had put the bird in the oven for half -an-hour to cook it,
but since the electricity supply had been long since discontinued, the attempt
had been pointless. Shakil had been unwilling to draw unemployment benefit
because he said the money should be sent to the third world instead. A god,
called Abu-Lafram, living in the bathroom, had told Shakil that he should
deny himself for the benefit of the third world. Shakil had little furniture left
– he had sold most of it to buy bread and alumi nium tin foil. He had used the
tin foil to line the walls of the flat, to protect Abu Lafram from the evils of
Western civilisation that seeped through the walls. His brother had been most
upset when he had told Shakil the bad news that his mother had died whilst
Shakil had been away from home. Shakil had started to laugh.
On interview in casualty Shakil was unkempt and dressed in a grimy boiler
suit, to which adhered blood and feathers. A large pentagram was daubed on
the breast pocket. Shakil giggled at times and appeared to be listening to
some voice that other people could not hear. He was mildly thought
disordered and distractible, pacing about casualty, preaching the gospel of
Abu-Lafram to other patients, using various neologisms. When he was asked
how he felt about the death of his mother, Shakil grinned and said that his
mother was a ‘white cloud in a darkening and prejudiced sky’.
He claimed to be a prophet of Abu-Lafram and that he had been chosen as his
first earthly disciple. Abu-Lafram talked to him throughout the day in a
sonorous male voice, ‘realer than the realest reality’. The thoughts he had had
since knowing Abu-Lafram were ‘the purest of pure’ and were broadcast out
of Shakil’s head by Abu-Lafram for ‘the benefit of all mankind’. Shakil did
not believe that he was ill, but was adamant that he was a ‘chosen one’.
What evidence is there to support a diagnosis of schizophrenia?
What is the relevance of the patient’s lack of insight?
(http://priory.com/schizo.htm)
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References
[1] http://faculty.washington.edu/chudler/schiz.html .
[2] http://pitjournal.unc.edu15/node/104.
[3] www.mind.org.uk/help/diagnoses_and_conditions/schizophrenia .
[4] www.en.wikipedia.org/wiki/Schizophrenia.
[5] www.nhs.uk/Conditions/Schizophrenia/Pages/Introduction.aspx .
[6] www.bbc.co.uk/health/emotional_health/mental_health/dis orders_schiz.shtml.
[7] www.pages.drexel.edu/~rm35/.
[8] www.psychology4a.com/Psychopathology.htm.
[9] www.priory.com/schizo.htm.
[10] www.tolerancelost.com/schizophrenia/.
[11] www.sfn.org/index.aspx?pagename=brainBriefings_Adolescent_brain.
[12] Beatty, J. (1995) Principles of Behavioural Neuroscience. Brown and
Benchmark.
[13] www.sciencedirect.com.
[14]
www.genomenewsnetwork.org/articles/12_00/Schizophrenia_virus_pregnancy.shtm .
[15] http://www.brainexplorer.org/schizophrenia/Sch izophrenia_Aetiology.shtml.
[16] http://www.helpguide.org/mental/schizophrenia_treatment_support.htm .
[17] http://www.jamesdisabilitylaw.com/schizophrenia.htm .
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