=20
ascii version
Early in October 1994, I had to be admitted to hospital because of what was
regarded as an acute confusional episode or episode of delirium which was
caused by Parkinsonian medication.  When I first began taking L-dopa some 7=
 or
8 years ago, I became aware that it had a profound influence on my mood,
causing my mood to swing upwards making me very creative and enthusiastic
about doing things so that I would get up early in the morning feeling that=
 I
wanted to be busy doing things and sit up late at night feeling I wanted to=
 be
busy doing things.  Sometimes there seemed to be so many things that I migh=
t
do, that I had difficulty choosing to do anything.
 
 
I learned to live with this situation and dealt with it by maintaining my
medication at the lowest level possible consistent with good mobility. A lo=
w
dose of tryptanol at night was helpful.  If I noticed my mood becoming
elevated, I would cut down on the medication.  I noticed that caffeine woul=
d
cause my mood to rise over a few days so I gave up caffeine.  During the
winter of 1993, I found myself reluctant to go outdoors and decided I had a
mild attack of agoraphobia-like syndrome.  I was depressed off and on as ar=
e
about 50% of Parkinsonians, so I developed the notion that in the wintertim=
e
there was some reason to suppose that my dopamine levels were low, in a
similar manner to seasonal affective disorder.
 
 
The symptoms recurred during the winter of 1994. After an industrious
literature search, I hit upon the plan of using  bright light therapy to
improve this situation which was quite painful.  When I first tried the bri=
ght
light therapy, I had very intense dreams and regarded these with some favou=
r
and enthusiasm, and  on the second night I could hardly wait to get to bed =
as
the dreams were so vivid and interesting. =20
 
 
I continued taking my anti-Parkinsonian medication in about the same way as=
 I
always had, occasionally trying for more mobility and having established
somewhat of a ceiling above which my mood would become too euphoric and I
would then need to back down. =20
 
I continued at this low level of medication despite encouragement from my
neurologist, at every visit, to increase the medication.  I was in regular
contact with my general practitioner and had in fact discussed my medicatio=
n
with him on my birthday, 28th September, which was during the week prior to=
 my
admission to hospital.
 
 
When during the winter of 1994 I had tried the bright light therapy and
noticed improvement and noticed my mood becoming elevated about two months
prior to my admission to hospital, I ascribed the change in mood to the bri=
ght
light therapy and knowing that hypomanic attacks had been precipitated by
bright light therapy, I stopped the bright light therapy.
 
 
My strategy was unsatisfactory  as my mood continued to rise, probably due =
to
the increasing length of daylight. As springtime came  my mood went higher =
and
higher. =20
 
 
I saw  my general practitioner on 28th September which I believe was Wednes=
day
and at that time was spending my money foolishly and showing other symptoms=
 of
a hypomanic attack.  Nevertheless, I remained oriented in time and place un=
til
the Sunday evening when I had what I thought was a fit and was incontinent,
finding myself lying on the floor in a cold puddle of urine.  I supposed th=
at
no one would take any great notice of these symptoms and, in the eventualit=
y,
was proved right.  I spoke to my family to ask my daughters to  visit me as=
 I
thought I may be developed a serious medical problem, not realising at that
time that an increase in  Levodopa effect has been described as causing fit=
s.=20
I subsequently lost contact with time.  I didn't know where I was and wasn'=
t
quite certain who I was and events appeared to be repeating themselves and =
I
couldn't find the places in my memory that referred to myself in the presen=
t.
I spent some time looking in the mirror to see myself whereupon my mind wou=
ld
clear temporarily.
 
 
Not being in tune with time and having some difficulty locating myself in
place, I found it difficult to take my medication on a regular basis and in
fact had no idea of what medication I took at that time.  My usual medical
adviser, although contacted early in the week, did not attend, nor did he
attend when called when things got somewhat out of hand on the Thursday
morning.=20
 
 Another practitioner on arriving, found my supply of medication and, since=
 he
had no idea what medication I was taking, came to the conclusion that my
condition was a result of self-medication. =20
 
 
The symptoms I experienced were different to those I previously experienced=
.=20
And although I recognised there was something not quite right, I didn't hav=
e a
clear plan to deal with this new situation.  My admission to hospital could
have been prevented entirely:
 
1.   If the medical practitioner whom I consulted on 28.09.94 had been
     familiar with mood disorders and taken a psychiatric history, and coul=
d
     have realised I was having a drug induced problem fulfilling the
     criteria for a hypomanic attack,  similar to the effects of "speed" an=
d
     weight reduction pills.
 
 
2.   If the medical practitioner my daughter rang after the episode of the
     fit on the Sunday evening had attended
 
 
3.   If the earlier episodes of sleep disturbance, loss of appetite,
     euphoria, overspending, vivid dreams, over-valued ideas that were
     recognised for over 3-4 weeks by family members, my psychologist and
     myself had been acted on
 
 
4.   If someone had warned me that vivid dreams precede hallucinations and
     hallucinations precede loss of contact with reality
 
 
5.   If there had been a plan to monitor the side effects and moods and a
     plan to deal with changes before things were out of hand
 
 
6.   If I had realised that the therapeutic window was becoming narrower.
 
 
In Harrison's "Principles of Internal Medicine", 13th edition Part 14
Neurological Disorders, Lewis L. Judd comments on the necessity for general
care physicians to take some note of mood disorders.
 
  He states that" non-psychiatric physicians frequently fail to accurately
recognise or diagnose patients with mood disorders and that 10.2 to 21% or
primary care outpatients are suffering from clinically significant mood
disorders."  And again, "the effective practice of internal medicine now
requires that practitioners be thoroughly familiar with the accurate diagno=
sis
of mood disorders in their patients." St Cyr, Taylor and Lang in Neurology,
1993 p.43 Supplement 6, S47-S52, in an article entitled "Neuropsychological
and Psychiatric Side Effects In the Treatment of Parkinson's Disease" state
the following:
 
 
     "Because the most obvious symptoms of Parkinson's Disease are motor,
     psychological components are seldom taken into account when planning
     pharmacological treatment."
 
 
The abstract for the above article states in part that " all medications
currently used to treat Parkinson's Disease carry some risk of causing
confusion, hallucinations or disruption of such higher order medical
operations such as problem solving and learning."
 
  This article contains guidelines for the management of neuropsychological
and psychiatric side effects.=20
 
 
In "The Journal of the American Geriatric Society", 39;708-716, 1991, in an
article called' Behavioural Complications of the Drug Treatment of Parkinso=
n's
Disease", Jeffrey L. Cummings (MD) states that:
 
 
     "Of patients treated with dopaminergic agents, 30% develope visual
     hallucinations, 10% have delusions, 10% have euphoria, 1% have mania,
     10-15% experience increased anxiety, 15% have confusional periods and =
a
     few exhibit altered sexual behaviour".
 
 
They state that "dosage reduction is the optimum management strategy, thoug=
h
anti-psychotic agents may be necessary in patients with delusions and lithi=
um
may control drug induced mania."
 
 
     "Clozapine, an anti-psychotic agent with few extra-parameteral side
     effects, has been successfully used to treat delusions in Parkinson's
     Disease and may be an alternative to conventional anti-psychotic agent=
s
     for some patients".
 
 
     "Confusion, or delirium, are loosely used words and the exact syndrome=
=20
     described when the word is applied in conjunction with drug therapy in
     Parkinson's Disease has really been carefully described.  Nevertheless
     it is evident that a portion of patients treated with anti-Parkinsonia=
n
     agents, developed delirious states with fluctuating arousal, impaired
     attention and incoherent verbal output.  Frequency ranges from 5-25% i=
n
     most investigations."
 
 
The US Pharmocopia 1995 edition, states of  the side and adverse effects of
Levodopa:
 
     "Incidence more frequent  Mental depression, mood or mental changes su=
ch
     as aggressive behaviour."
 
 
Thus we have complications which are very well documented even appearing in
popular videos such as Awakenings by Sachs,  as well as being in the produc=
t
information.=20
 
 The side effects are very common and resemble very common psychiatric
conditions.  Although I have at times volunteered information to prescriber=
s
concerning side effects of the medication, I cannot recall any prescriber
taking a  psychiatric history to elucidate such problems.=20
 
 Perhaps this failure represents an unfamiliarity with psychiatric problems=
,
perhaps it represents an inability to understand the progression of the
symptoms, ie. the spectrum or continuum that exists in most psychological o=
r
psychiatric states varying from normal to a point where serious action is
required.=20
 
 
Perhaps it represents an inability to keep up with the literature or a
reluctance to conduct Medline searches, or lack of time in which practition=
ers
search for useful information.  One possible solution may be to have a
textbook of medicine complete with pharmacopia on CD Rom and to have Medlin=
e
on line on the practitioner's desk rather than only in a library.
 
 
My own feelings are that many practitioners feel uncomfortable in the area =
of
psychiatry and feel that psychiatry is not related to the practice of real
medicine.  For example, had my daughter complained I had shot my foot off w=
ith
a shotgun, then I would have immediately been hospitalised and appropriate
treatment given.  Complaints that I was not myself and that I was paranoid =
and
totally out of contact with reality however, fell on deaf ears and no actio=
n
was taken until I was almost totally out of touch with reality, walking dow=
n
the street in a state of somewhat dishevelled undress. =20
 
 
The isolation of medicine and psychiatry is like the isolation of any branc=
h
of medicine, doomed to failure since it is clear to see that the brain
functions according to the laws of physics and most certainly in my case my
condition was due entirely to my medication, not to some notional psychiatr=
ic
condition. =20
 
 
A very small intervention, perhaps a few mgs of Valium, or cessation of ant=
i
Parkinsonian medication at any time in the previous month could have avoide=
d
my admission to hospital altogether.  Hospital admission was therefore caus=
ed
by many factors including:  lack of knowledge, lack of a plan, failure by
medical practitioners to recognise and attend to the early symptoms of well
known complications, and lack of interest in psychology, leading to poor
communication.
 
 
ADMISSION TO HOSPITAL
 
My admission to hospital was preceded by some debate as to whether I had a
medical problem or a psychiatric problem.  My admission to hospital was onl=
y
achieved after the police had been called and numerous phone calls made to =
my
usual general practitioner and relatives and others.  Finally, another gene=
ral
practitioner attended who did not know my case but who, after discussions w=
ith
my psychologist and my brother who had by this time arrived from Numurka,
decided that medication was the cause of the problem and had me admitted to
the Wangaratta Hospital.  There had been some suggestion that I be admitted=
 to
Beechworth.  But since I had worked there before and had formed strong beli=
efs
as to the standard of both medical and psychiatric care in this institution=
,
which I was having nightmares about despite being awake, I was fortunately
admitted to a general hospital. =20
 
 
I experienced my admission somewhat in the form of a nightmare where I
believed people were trying to harm me, even kill me.  I recollect challeng=
ing
people to have the courage to die with me since they kept assuring me that =
no
evil would befall me, though I knew quite well that death awaited me. =20
 
 
My next experience was of everything appearing to have stopped, somewhat li=
ke
being under anaesthetic and of a very gradual return to function.  I can
remember being placed in a bed where I had some concern about the name tag
which belonged to someone else, the tag not having been changed, at least t=
hat
is my recollection.  I was also concerned that my identification tag was on=
 my
foot where I presumed it would be difficult for anyone to recognise me.  I
became oriented by watching television by use of a mirror.  This was a
difficult task, requiring the manipulation of drips, catheters and shackles=
.=20
However, looking at my self in the mirror seemed to help with my orientatio=
n
considerably as I wasn't quite certain as to where I was in my life, what w=
as
happening to me and who I was. Seeing a picture of myself in the mirror cau=
sed
things to snap into focus.  Watching my favourite television programs also
helped me to become aware of what was happening in the world.  There was on=
e
time I was quite concerned when I found the television was showing the Gulf
War, which I thought was over, so I thought I was experiencing past events =
as
a prison.  However, it turns out that a new confrontation had arisen and th=
e
television was reflecting real time events. =20
 
 
As soon as I was able, I suggested the hospital contact my general
practitioner to establish that I was taking my usual regime of medication
prior to admission and so that he could liaise with my physicians concernin=
g
my illness.  He did in fact come and visit me but there is no evidence that
consultation with him regarding my medicated occurred.  Thus the myth that =
the
admission was due totally to my own erratic self-medication persisted. =20
 
 
After a couple of days I developed very strong muscular contractions and fo=
und
that I was feeling very hot and had to keep myself cool by spilling my wate=
r
jug on my shirt.  One of the nursing staff noted that I had a bruise on my
buttocks and so I deduced that I was having early signs of incipient
neuroeleptic malignant syndrome.  I concluded I must have been given
Haloperedol and inspection of the chart on my bed proved this to be the cas=
e.=20
And even though I am on record as having written a yin and yan showing that=
 I
was somewhat not quite with it, thinking of the balance of things and thing=
s
being out of balance, I wrote "no more Haloperedol - this contraindicated".=
=20
And of course Haloperedol is well known to be contraindicated in Parkinsons
Disease.  This is because it causes neuroleptic malignant syndrome which ca=
n
also a result of ceasing Parkinsonian medication.
The US Pharmacopeia 1995 states that "a syndrome resembling neuroeleptic
malignant syndrome which includes intermittent dystonia, substantial
agitation, hypothermia and mental changes, has been reported after the abru=
pt
discontinuation of the levodopa therapy."
 
 
Haloperedol, or Serenase as it is also known, also has a reputation for
causing Parkinsonism.  It is a dopamine antagonist and would on theoretical
grounds alone be contraindicated in someone who has 10% or less of the
dopamine receptors that normal people have.  Even MIMS, a copy of which is =
to
be found in every ward, strongly indicated that Haloperedol in Parkinson's
Disease is contraindicated.  Also,the combination of Haloperedol and Levodo=
pa
is contraindicated. =20
 
My own modest experience  in psychiatry left me with the indelible impressi=
on
that treatment of psychiatric conditions with drugs such as phenothiazines =
and
haloperidol regularly create parkinsonian-type problems.
 
 
Since I was experiencing  severe muscle contractions which I had deduced we=
re
likely to be caused by Haloperedol, and since I knew that Haloperedol was w=
ell
known to be contraindicated in Parkinson's Disease, I lost a considerable
amount of confidence in my management and was caused considerable agitation
and concern.=20
 
 Furthermore, no one took any notice of the severe muscular contractions th=
at
I was having, which were unlike anything I had previously experienced in
Parkinson's Disease.  No one seemed to sort the wheat from the chaff althou=
gh
the nursing notes clearly document the rigidity.  I was also concerned that
nobody took any notice of my belief that I had had a convulsion that ascrib=
ed
my incontinence to my mental state.  However, both MIMS and the US
Pharmacopoeia state that convulsions have been reported but that a causal
relationship to the use of Levodopa has not been established. =20
 
It is interesting to note that I had a very mild episode of buildup of L-do=
pa
subsequent to my discharge and at that time I had a similar but mild episod=
e
of what I had previously described as a fit.
 
In hospital my condition apparently resolved with minimal medication, 2=ABm=
gs of
valium being all that was required to quieten me down and this was required
only intermittently. =20
 
 
The main treatment appears to be the reduction or cessation of anti-
Parkinsonian medication and this, combined with very amounts of sedation,
appears to have been very satisfactory in controlling the mental condition
which resolved quickly and was apparently completely resolved at the time o=
f
discharge on 20th October 1994. =20
 
 
COMMENTS ON HOSPITAL ADMISSION
 
1.   Admission to a general hospital is much to be favoured although at a
     general hospital it is quite possible for physical symptoms to be
     ascribed as psychological or psychiatric happenings, ie. the division
     between psychiatry and medicine still remains. =20
 
 
2.   A great deal of anxiety and lack of confidence was experienced because
     of the Haloperidol incident.  One supposes that having on-line
     information could possibly prevent such a problem, although the fact i=
t
     is included in the MIMS suggests that a lack of experience with
     psychiatric conditions and complications may have something to do with
     the problem.  In general, one has the feeling that hospitals such as
     Wangaratta, which have access to a psychiatric hospital, tend to deal
     with psychiatric problems on a rather arbitrary basis, ie. by sedating
     them and sending them to Beechworth.  The solution to this problem mig=
ht
     be continuing education with seminars on psychiatric problems being a
     regular part of hospital educational policy.
 
 
3.   Failing to take seriously one's complaints, eg. the muscular
     contractions and the possibility of early neurologic malignant syndrom=
e
     problems, reflects a failure to regard such symptoms as part of a
     continuum.  The extreme case being neuro-malignant syndrome preceded b=
y
     the series of muscular contractions and also a failure to keep up with
     up to date information.   Having the US Pharmacopia on-line at the
     nurse's desk may have avoided such problems.
 
 
4.   Prescribers should take a detailed history and, to recognise the early
     signs and symptoms of hypomania as a sign of too much levodopa.  I was
     discharged without an ongoing plan to avoid future episodes.
 
 
5.   The involvement of one's psychiatrist with the medical board in other
     considerations of a civil libertarian nature such as driving, proved t=
o
     be a considerable difficulty.  One has to experience this problem in
     order to fully appreciate the difficulties involved. =20
 
 
Finally, the phenomonological nature of psychiatric symptoms and diagnoses
means that a person who exhibits symptoms of psychiatric conditions such as
hypomania, all be it caused entirely by medication, is at risk of being
regarded as having a permanent mental illness.  Again, the failure of adequ=
ate
communication between general practitioner and involvement of general
practitioner at the hospital level, led to the simplistic view that the who=
le
episode was caused by my own self-medication, whereas in actual fact, I had
taken a considerable amount of medical advice and informed myself about
Parkinson's disease and its medication.
 
 
After discharge from Wangaratta Hospital, I was apparently well although fe=
lt
under-medicated but calm in my mind and went to spend 2 weeks with my niece=
 in
the country.  After this, I went to the Royal Melbourne Hospital to the
neuropsychiatric unit.  The aim of this exercise was to have some
investigations done and to stabilise the medication.  I was reluctant to pl=
ace
myself in the hands of the department of psychiatric services, having had
previous experience working in areas of civil liberties.  However, I resolv=
ed
to use the opportunity to observe the process of being a patient as well as=
 to
obtain some useful investigations, such as MRI scans.  I decided to test th=
e
theory that there was a vast division between medicine and psychiatry by
asking for a medical opinion.  I was still of the view that I had had a fit
and thought it most unreasonable that no one had taken any serious steps to
investigate such a possibility. =20
 
 
The experience proved to be more traumatic and difficult than I could possi=
bly
imagine for several reasons.  Firstly, the notion of stabilising the
medication ran along the lines of increasing the dosage until psychiatric
symptoms were observed and then backing off.  This caused, amongst other
things, a very low biolathic, the effects swinging up and down with the
medication, which at that time was quick release for the main part, being
ordinary sinimet being taken 4 hourly and then 3 hourly intervals.  I was
banned from using the library and was unable to have my own television set.=
  I
was unable to express my belief that caffeine elevated my mood and that I w=
as
therefore to be given decaffeinated coffee.  I was unable to use my compute=
r
or to use a portable phone.  My cognitive state was not as good as I had
thought and I was limited to thinking things through in a very slow and
painstaking way, being unable to think of more than one thing at once, ie. =
I
was virtually unable to do any multi-tasking.  I had previously observed th=
is
problem which is subsequently resolved to a considerable extent in people w=
ho
had hypomanic attacks.  I was uncertain as to whether this was due to their
medication or to the effects of the hypomanic attack itself.  However,
discussion with others who had been heavily sedated or who had had
anaesthetics, showed that such a phenomenon is not uncommon and so I decide=
d
finally that it is probably due to the haloperidol, or to be precise, it co=
uld
have been caused by the haloperidol, there being no necessity to regard the
parkinsonian medication as causing that particular problem.=20
 
 
I certainly felt unlistened to, especially with regard to the mood swings a=
nd,
although I was slow to prove it correct in that the mood swings abated once=
 I
changed to slow release sinimet, it was very frightening at the time to be
able to make a prediction to correlate one's mood swings with one's medicat=
ion
and yet to have no one be interested enough to survey the literature or to
make some change to see if the observations were correct. =20
Nissenbaum, H Quinn NP, Brown RG et al, wrote an article entitled "Mood Swi=
ngs
Associated with the On/Off Phenomenon in Parkinson's Disease" in Psychologi=
cal
Medicine 1987, 17 8 99 - 1904.  Because I was unable to use the library's
medical services, I was unable to find any such references as to why I was
unwell, nor does it appear that anyone else searched for such references or
critically evaluated my observation that my mood was swinging up and down i=
n
relationship to the presumed level of medication.  No one took my thought
seriously that one ought to measure people's levels of medication but I was
clearly able to demonstrate, especially when I went home and was by myself,
that my mood was swinging up and down with the levels of medication.  This
stopped when the medication levels were levelled out with slow release
medicine. =20
 
 
Various cognitive function tests were undertaken and various assumptions we=
re
made from them concerning my IQ, based on assumptions that my IQ was
previously high and had changed.  Although that it is known that recent
psychotic episodes, and even anaesthetics, can cause difficulty in cognitiv=
e
function and functions requiring a time element may not adequately reflect =
the
accuracy that parkinsonians are capable of and although parkinsonian
medication is known to interfere with cognitive function, conclusions were
drawn as to my capacity to function intellectually without qualification su=
ch
as one might expect to the effect that various conditions may have interfer=
ed
with the testing procedure and that the test applied to my cognitive functi=
on
at a particulaR time, I subsequently underwent extensive psychological
testing.  The whole question of cognitive function boils down to whether or
not there is selective loss of cognitive function which can be overcome by
various strategies or whether there is a global dementing alzheimer-type
process.
 
 
Sensere and others found that if one allows for processing speed and exclud=
es
the 8% of people with alzheimer's disease, the same as the general populati=
on,
and the 8 or so $ of persons with confusion due to the parkinsonian
medication, one arrives at the 15% of so called dementia said to be associa=
ted
with parkinson's disease, and one finds that the IQ of persons with
parkinson's disease, allowing for processing time, especially for those
individuals who have left handed disease, is the same as the IQ of an age
matched sample of the general population.
 
 
The second psychological opinion arrived at these conclusions independently=
 of
Sainsere.  It is possible to come to these conclusions via the process of
careful testing from personal observation, from the psychological literatur=
e
and from the psychiatric literature via Medline and Saincere.
 
 
The question of the association between parkinson's disease and alzheimer's
disease has in fact caused considerable grief and heartache to me personall=
y
since my first information was that there was a 30% incidence of alzheimer'=
s
disease associated with parkinson's disease.  As I waited for this global
dementia to descend upon me, and noticed only selective difficulties, I bec=
ame
suspicious and was most pleased when I found the articles by Saincere et al
where good controls were used and sound methodology was implemented.
 
 
These examples of IQ testing and confusion regarding dementia, etc, and moo=
d
swings related to the level of medication could have been avoided had my
observations been taken seriously.  The problems consist of: =20
 
     1.   not listening to the patient
     2.   ascribing what the patient says to a psychiatric condition, ie.
          assuming that everything the patient says is nonsense because he
          is in a psychiatric ward
 
     3.   not being familiar with, or having on-line, the appropriate
          literature.
 
 
The difficulties of information retrieval can be overcome, to some extent,
having Medline facilities on the nurses desk, thus obviating the necessity =
for
a separate trip to the library.  However, it seems to me that a specialist
unit functioning as a referral for people with parkinson's disease should b=
e
well aware of the literature referred to.
 
 
RETURN TO THE COMMUNITY
 
On return to the community, my problems, which I thought were over, begun a=
ll
over again. =20
The myth that there is no prodromal stage in drug induced problems or in
bipolar disorder per se, led to difficulties in establishing a monitoring
system.  The problem of mood swing with the quick release sinimet, also
bedevilled me for some time.  Instead of relying on the literature, my
prescribers relied on advice from the neuropsychiatric unit, ignoring my
protestations regarding the swinging of my mood.
 
 
The problem was further compounded by the notion that there is an absolutel=
y
fixed in concrete safe dosage of anti-parkinsonian drugs.  In real life, th=
e
absorption is very variable and other factors such as length of day, obviou=
sly
affect catocoline secretion. =20
 
Even after having had obvious psychological problems relating to my
medication, I found that prescribers still were reluctant or unable and in
fact did not elicit a psychiatric history nor look for early signs of chang=
es
of mood.=20
 
 
ON RETURN FROM HOSPITAL
 
Because my moods were swinging up and down and my moods included being
cantankerous and difficult, and in fact my moods were somewhat like that of
someone with a mood swing disorder, except that there was a clear relations=
hip
between the medication and the mood.  When i went home, I was faced with a
considerable amount of difficulty.  I had to explain my situation to my
neighbours, family and friends and to do this, I hit upon the idea that liv=
ing
with parkinson's was like living on alcohol.  At first it seems a delightfu=
l
and simple exercise and much to be desired.  However, people drinking alcoh=
ol
have difficulties such as feeling cantankerous and feeling happy and trusti=
ng
people and not trusting people, getting into fights easily, and crying for =
no
reasons.  I explained all this to my daughter who explained to me that wome=
n
often have these sorts of problems and they are hormonal and what did I thi=
nk
was so unusual about this situation. =20
 
 
This difficulty had not been resolved in hospital despite my observations w=
ith
continued references to the necessity to measure blood levels and make some
recognition of the changing of mood with blood levels of levodopa. =20
 
 
I had difficulty arranging for someone to monitor these moods.  My attempts=
 at
contacting the department of psychiatric services led to them contacting my
general practitioner and my general practitioner arriving, having in mind t=
o
admit me to hospital, whereupon the whole set of difficulties would have
started again.  I was fortunately able to acquire to services of an
occupational therapist to act as casemanager, who agreed to visit me over t=
he
weekend to make certain my moods were under control.
 
 
The custodial, rather than home care, approach to my difficulties meant tha=
t
the people who should have taken an interest in my condition, ie. those wit=
h
psychiatric training, were not of great assistance in my return to the
community.
 
I now have a psychiatrist who is trying mood stabilisers, a wise neurologis=
t,
a clever psychologist, live on minimal medication and am going easy on brig=
ht
light,, which  is powerful and probably needs a controlled trial.  Do not
stare at quartz lights withoutultraviolet protection.  UV need not be dark,=
 so
use the clearest UV sunglasses, or put UV in your prescription glasses. 200=
0
lux is said to be the go, so use outdoor QI flloodlights   and a timer to
lengthen the daylight, like making the sun rise early and set late. Monitor
all this with someone else, and have a plan of lowering PD medication and l=
ow
dose valium or clonazepam early if mood swings up. Do not try bright light =
if
you have a personal or family history of moodswings or bipolar disorder.=20
 
 
The following is a career related draft that may help people understand
cognition.
 
PARKINSON'S DISEASE  AND MEDICAL PRACTICE
 
 
EARLY DAYS
 
When I first developed Parkinson's disease about 8 years ago, I
noticed that medication affected my mood in the same way that
adrenalin affects people's moods.  I lost my appetite, I became  busy
with all sorts of projects, starting early in the morning and finishing
late at night.  On one occasion,  when I lay down to rest in the
evening, I immediately felt pressure to get up in the morning and be
busy .  My neurologist suggested that a low dose of tryptanol would
be useful in this situation, and indeed  this was correct.
 
EARLY STRATEGIES=20
 
 When I asked medical advice about my condition, people thought I
should take more medication because I was fairly slow, but I tended
to resist this temptation because I knew that the more medication I
took, the more my mood was to swing up.  I also noticed that
caffeine tended to enhance this effect, so I avoided  caffeine.  On
many occasions, perhaps 20 or more, I noticed an increase in
medication or caffeine tended to cause this elevation of mood, and
so, despite encouragement to increase my medication, I would
always back off the medication and maintain a normal mood.=20
 
FINE MOTOR SKILLS LIMIT PRACTICE
 
Fine motor skills rather than psychological considerations limited my
practice of medicine, and by  1994 I was mainly teaching bioscience
to nursing students and amusing myself researching unusual
conditions.
 
During 1994 I found I could not  always examine eyes reliably, so I=20
stopped making appointments, being virtually retired in any case.=20
 
 
WINTER DOLDRUMS
 
During the winters of 1993 and 1994, I suffered anxiety complications
relating to my illness and medication.  This took the form of a mild
agoraphobia which was quite unpleasant and painful.  Since I was
also depressed, as at least 50% of Parkinsonians are, I hit upon the
idea of using bright light therapy, a well recognised treatment for
winter-effective disorder.  I used the bright light therapy as described
in the literature and found that I felt well, and was more active.=20
 
FALLING OFF ON THE HIGH SIDE
 
  I ceased the bright light therapy in order to prevent my mood
swinging too high.  However, possibly due to the increase in the
length of daylight, my mood kept swinging upwards.  Though this
upward swing in mood was recognised by my family, my
psychologist and myself, my general practitioner noticed nothing
amiss when I consulted him during  a classical bipolar high.  Such
episodes are  well described complications of  Parkinson's disease
medication, as well as being immortalised in the Sachs video
"Awakenings"
 
 
The early opportunity for treatment was missed, I became disoriented
in time and place and required admission to hospital where my
condition settled promptly with minimal sedation and withdrawal of
Parkinsonian treatment.
 
GETTING HIGH BOTHERS PEOPLE
 
Getting high on L-Dopa for a few days bothered people in a way that
depression and anxiety could never do, galvanising them into action. =20
 
VERY RAPID MOODSWINGS RELATED TO MEDICATION LEVELS
 
Two weeks after discharge from hospital, I went to a teaching
hospital to have my treatment stabilised with increased dosage of
quick release sinemet as recommended in the literature.   However,
also reported is the problem of moods that swing very rapidly,
corresponding to on/off times and presumably to the medication.=20
Each 3 hours, as the medication level went up, and as it went down
again, I experienced a succession of moods.  I would feel friendly
towards people and then quite unfriendly.  I had feelings of great
warmth towards everyone in the world, and then feelings that  people
were not my friends.  I would cry for no apparent reason. I was
cantankerous and easily irritated.=20
 
Despite the clear relationship of these mood swings to my
medication level, and despite my belief, based on pharmacology and
past experience, that the way to deal with this would be to use a slow
release variety of medication to level out the peaks and troughs, the
classic approach was adhered to.=20
 
 Subsequent to my discharge, and after the changes in mood became
intolerable and affected my relationship with my family, the
medication was changed to slow release.  My moods stabilised=20
instantaneously and remarkably.
 
LOWEST SAFE DOSE
 
Stabilsation should first establish a safe, low, steady level of
medication by gradually reducing medication, using psycological well
being as the yardstick rather than mobility. I am able to manage on
200mg or less per day of Sinemet CR, as distinct from 1000 mg 8
months ago.
 
 
LONG TERM  VARIATIONS  IN MOOD
 
The slower, long term variations in mood appear to depend on the
total amount of medication over a long time, perhaps by emulating
the coming of Spring in seasonal affective disorder.
 
INSIGHT
 
Learning to live with PD medication is like drinking alcohol. One can
learn how much is safe and how much leads to trouble, and to
modify one's behaviour accordingly. Except at the extremes of mood,
we are aware of our moods, and those who know us well can easily
detect when we are not ourseves.  One has to  have a plan to deal
with moods, like Ulysses being bound to the mast and putting wax in
the sailors ears, thus avoiding the siren's trap.
 
 
IS HE CLEVER ENOUGH TO BE A DOCTOR?
 
 Whilst my medicine was being stabilised, cognitive tests were
performed.  At the time the tests were performed, I could not think
clearly.  I could think accurately but quite slowly and I could not
address many issues at the one time, so I put all my effort into
concentrating on one task at a time.  This problem with thinking has
been described after cardiac arrests and anaesthetics.=20
 
Parkinsonians, especially those whose disease involves the left side,
are known to be slow in processing time, but accurate.  Thus my
cognitive functions were tested at a time when I was somewhat at a
disadvantage, without allowance for the difficulties known to exist in
Parkinson's disease.  Even whilst functioning under these difficulties,
my verbal IQ was found to be in the superior range. =20
 
 
Subsequent to my discharge, I noticed that my capacity to think
clearly and to multi-task improved considerably.  Subsequent
psychological testing confirmed that my IQ was in the expected
range for medical practitioners.  Processing speed was down, but
accuracy was maintained.=20
 
ALZHEIMER MYTH EXPLODED BY CONTROLLED STUDY
 
 The relationship between Parkinson's disease and cognitive function
is confusing,  Early estimates suggested that 30% of persons with
Parkinson's disease would develop Alzheimer's disease.  However,
work by St Cyr and others, using matched controls, suggests that the
incidence of Alzheimer's disease in Parkinsonians is the same as that
of the general population in the same age group, ie. about 7-8%.=20
Furthermore, if one allows for the 7-8% of Parkinsonians who suffer
confusion relating to their medication, and uses tests which are not
highly time dependent, one finds that Parkinsonians have the same
IQ and cognitive functions of the general population.
 
  St Cyr and others found that "No global cognitive decline was
observed in the Parkinsonian group, moreover memory and
visiospatial abilities were generally intact".   =20
 
AN OUNCE OF PREVENTION
 
I am more aware of the early symptoms of levodopa excess, eg. vivid
dreams which I at first thought were beneficial, are actually
precursors to hallucinations and loss of contact with reality.  Even
though my prescribers know that I have had difficulty with the
psychological side effects of my medication, they still look at me and
say "you're a bit slow, take a bit more medicine".  I, however, have
become  once bitten, twice shy and have resisted the temptation. =20
 
 
My condition is regularly monitored by:  myself, my family, a nursing
sister, a neurologist, a psychiatrist and general practitioner. I take my
medication with excellent reliability.=20
 
A strategy of monitoring, L-DOPA dose reduction, and early
intervention with benzodiazepines is in place. Clonazepam is helpful
as a mood stabiliser. The use of other  mood stabilizers  and
clozapine is under consideration.
 
A DIFFERENT TYPE OF DOCTOR
 
 People still ask me about medical matters, especially if they have
been to see their doctor and do not feel happy with the explanation
of their illness.  I am using a system with a medical textbook on CD
Rom, where I can look up conditions and also  access the US
Pharmocopea on CD Rom.  I am therefore able to print out useful
information  and help people understand their condition.  I see that
there could be a niche where I could happily function as a medical
practitioner doing this sort of educational consultation. I have just
reviewed the literature on Pompe's disease for a friend My mobility
prevents me  from operating and performing other highly
manipulative procedures, but I do not attempt tasks beyond my
capacity. =20
 
CONCLUSION
 
I feel that  I am able to be a retired medico, with an interest in
counselling and education, and whilst I have responsibly set
restrictions on myself, am not averse to having reasonable conditios
imposed.
 
FURTHER READING
 
"Behavioural complications of drug treatment in Parkinson's disease",
Geoffrey L Cummings MD,  Journal American Geriatric Society 39,
708-716 1991=20
 
 Parkinson's disease and depression require critical evaluation (Anne
E Taylor, Jean Saint Cyr, Anthony E Lang and Frank T Kenny in Brain
1986 109, 279-292).
 
 
"Frontal lobe dysfunction in Parkinson's disease" by Anne E Taylor=20
Jean Saint Cyr Anthony E Lang, Brain 1986 109, 845-883.
 
"Neurolopsychological and psychiatric side effects in the treatment of
Parkinson's disease", Jean Saint Cyr, AE Taylor and AE Lang,
Neurology 1993, 43, supp 6, 47 DS52
 
Enclosed
Copy of psychological report from J. Roodenburg
 
Copy of the side effects printout from the US Pharmacopia on CD
Rom, written clearly in plain language  and suitable for handing to
the patient.
 
Copy of the psychiatrist's notes of my admission to=20
District Hospital,