What does it feel like to have Parkinson’s? 3. Motor and non-Motor Symptoms

Motor symptoms affect movement in a variety of ways.  In his first book, “Lucky Me” Michael J Fox gives a very good description of the onset of the commonest and signature symptom of PD – the tremor.   He goes on to describe the dyskinesia (large involuntary movements) that usually follows.  I can’t vouch for the accuracy of his description because my onset was completely different.  I have neither tremor nor dyskinesia .

Motor symptoms are caused by a lack of the neurotransmitter, dopamine, that is made in the region of the brain called the substantia nigra (black stuff).  The tremor cannot be treated directly with dopamine because dopamine does not pass the blood brain barrier (BBB) but it does respond to l-dopa (laevo-dihydroxyphenylalanine), the amino acid that is the natural precursor of dopamine in the brain.  L-dopa is usually administered as Sinemet or Madopar, which is l-dopa together  with carbidopa, a substance that slows down the conversion of l-dopa to dopamine in the body but which cannot pass the BBB.  Carbidopa thus preserves the l-dopa so that it lasts longer in the body and more of it is available to the brain, and for longer, than would l-dopa be if administered alone.

Dyskinesia is a symptom not of PD but of long term (>5 years) treatment with l-dopa.  From talking to PD patients and reading about it people seem to find tremor probably the most disabling symptom of PD.  In the second volume of his autobiography, “Always Looking Up” Michael J Fox gives a graphic description of the effects of tremor and dyskinesia which illustrates the gap between the clinician’s and the patient’s assessment of PD.   The clinician says that the outlook for early onset patients is better than for late onset patients.  It is true that late onset without motor symptoms carries a larger risk of cognitive impairment but carries a smaller impact on life expectancy. I do not shake but I do have bradykinesia (slow movement) and I do not envy Michael J Fox his version of PD!.

My consultant tells me that about 30% of patients diagnosed with PD don’t have the tremor. But the peak age for PD diagnosis is 70+ and, if there is no tremor, the other symptoms can easily be attributed to old age.

A team based at University College reported some statistics on 433 individuals from the Queen Square Brain Bank for Neurological Diseases, all pathologically proven to have PD (post mortem!) of which 342 presented with motor symptoms, of whom just over two thirds were initially diagnosed with PD.  Ninety one had only non-motor symptoms, of whom only 16% were initially diagnosed with PD.  GPs are presented with a case of PD to diagnose only a few times in their career and one without motor symptoms only rarely, although 91/433 certainly understates what must be the real proportion of undiagnosed PD cases.

Parkinson’s UK estimated the prevalence of PD (the total number of cases diagnosed per 10000 population) in 2009.  The results were presented as a histogram from which I estimated the numerical values shown in the Table 1 below.  If the prevalence is less than 1% you can calculate the approximate incidence by simply subtracting the previous year’s prevalence form the prevalence in the current year as I have done.

Table 1                 Actual prevalence and incidence of PD in the UK in  2009  (Parkinson’s UK)

Age	35-39	40-44	45-49	50-54	55-59	60-64	65-69	70-74	75-79	80-84	85+
Prev.	0	0.1	1.5	5	11.5	24	46	83	130	172	171
Incid.	0	0.1	1.5	3.5	6.5	12.5	22	37	47	42	0

As the prevalence rises in older age groups this will increasingly understate the true incidence because you cannot get PD twice and the increase in PD diagnoses needed to fit the prevalence data will require a higher incidence applied to the progressively smaller number still susceptible.  A further complication, but one that at least partly offsets this, is the fact that PD patients have a reduced life expectancy, which results in more PD patients dying than those who do not have it, which in turn means that the proportion of susceptible people increases relative to what it would be if PD had no effect on life expectancy.  These two factors do not exactly cancel each other out because PD patients would all have to die before their PD-free contemporaries and we know that this does not happen.  I’m working on a model that will do the calculations properly but this is complex (I have to interpolate data from each age band into separate age-in-years in each year and then   make assumptions about the distribution of year of death for each about the mean life expectancy when the standard deviation is large…..). I could go on but you get the picture!  I am not sure all these estimates and assumptions will produce a more reliable answer than a cruder approach and so I will claim an amateur statistician’s privilege to ignore two factors, each mostly small, whose effects are in opposite directions and rend to cancel each other out.  For my present purposes I wish only to remark that, although it is understandable that diagnoses  of PD might decline in people who are over 80 years old it seems very unlikely that the disease actually disappears abruptly when we reach the age of 80 after the incidence has increased by an average of 1.9 times every 5 years between the ages of 50 and 74.  If we assume that the occurrence of PD continues to increase at the same rate after the age of 74,  but the new cases are simply not diagnosed, we get the results shown in Table 2.

Table 2               Hypothetical prevalence and incidence of PD in the UK if the pattern of increase between 50 and 79 continues to age 100

Age	35-39	40-44	45-49	50-54	55-59	60-64	65-69	70-74	75-79	80-84	85-89	90-94	95-99
Hypo. Incid.	0	0.1	1.5	3.5	6.5	12.4	23.5	44.6	84.71	160.9	305.8	581	1104
Hypo. Prev.	0	0.1	1.5	5	11.5	23.9	47.4	92	177	338	643	1224	2328

OF course this is likely to be an extreme estimate and most probably a proportion of individuals will never contract PD but from these figures we can show (Figure 1 below) the number of undiagnosed cases of PD in older age groups that this implies just to illustrate the potential scale of the problem if life expectancy continues to increase and diagnostic methods improve.

By the age of 100 23% of us would have PD.  But then an even higher proportion of us, and even more of the new PD cases would also have some form of dementia that would mask or dominate PD symptoms anyway.

This may feel like a digression.  If so, I apologise but I’m afraid I’m prone to digress and I think the statistics  support the argument that non-tremulous PD has a higher true incidence than 30% of total PD but is under-diagnosed because PD was defined originally as The Shaking Palsy and this has, quite understandably, led generations of clinicians to see the tremor as the defining symptom of PD – to the neglect of its other, typically less distressing, symptoms.  It has also, until relatively recently, biased research toward the motor symptoms although, to be fair the availability of advanced investigative techniques may have been a more important obstacle to a broader approach to developing an understanding of what goes wrong in PD.

That’s enough for this post –  I’ll carry on shortly in the next post.

Meanwhile … I’m sorry that some of you may find some of the facts about PD that we have to accept are uncomfortable but facts are the only safe basis for understanding and improving our lives.

Best wishes to PD sufferers all over the world – let me know if you find any of this helpful and ask what questions worry/interest/concern you that we can try and address.

What does it feel like to have Parkinson’s? 2. First symptoms

I remember 4  years ago, when I was living in Kiev managing a large multi-country project funded by the EU, wondering why  I was walking toward the kitchen so slowly and deliberately.  I wasn’t tired but there seemed no need to hurry  and I thought that, at 71, it was just old age.

Winters are cold and snowy in Kiev and the pavements are often covered with a thick, uneven layer of ice and Kyril, my ever-solicitous administrator, had made sure that my apartment was just across the road from our office.  I only ever had to walk short distances and hadn’t noticed slowing down.  My colleagues were all friends and, if they noticed, they said nothing, probably also assuming that it was old age.   In April 2010 the project was winding down, spring arrived and I could take an hour in the morning for a brisk walk to Kreshchatiik Park, climb the hill, walk around the top and return.   I felt as if I was walking briskly but I knew that I wasn’t moving as fast as most of the other pedestrians – even old ladies!  Impossible to ignore too was the strange feeling that I was having to learn how to walk again.  I tried to convince myself that I hadn’t walked recreationally for a year or more and it wasn’t surprising that I was out of practice but I also felt as if I was stooping although my reflection in the shop windows told me that I wasn’t.  I noticed occasionally a tightening of my chest when I was walking – the sort of rawness you sometimes experience when you run in very cold weather.  I thought this was a probably some kind of mild chest infection and Kyril brought me some tablets that he assured me would fix it.

Every month I had to sign (in order to authorise) about 100  payments and at the start of 2010 I noticed that my signature was shrinking.  I could write a ‘normal’ signature if I concentrated and wrote slowly but it was tedious enough to sign quickly.  On the other hand if I did it quickly there was a real risk that the signature would vanish before I got to the end.  The shrinking signature didn’t worry me but I was puzzled as to why it was happening.

Towards the end of 2009 I had begun to bite my tongue with alarming frequency.

Others had commented on my slowness.

Margaret and I went on a tour of China in April 2009 and I was notorious for being the slowest walker, to the extent that I was called the tortoise.  In April 2008 I attended the kick-off meeting of the project that I was managing and which had just started.  The meeting took place in Brussels and I was the only English participant and the only native English speaker.  The others (Dutch, German, Swedish, Spanish etc.) all spoke fluent English and I was used to this and normally adjusted how I spoke – slowing down and using short sentences.  We knew each other quite well and the meeting was friendly and informal but at the end the German and the Swedish lady (my Brussels Task Manager) took me on one side and said, with friendly concern, that they had had great difficulty in understanding me because I spoke so fast and so quietly.  Of course I apologised and promised to do better in future but I knew I’d always spoken too fast and in the heat of discussion I had probably got carried away.

There was nothing to connect these symptoms and I assumed they were just manifestations of the deterioration that is an inevitable concomitant of getting old.

My attitude was not one of denial – I didn’t feel ill in any way, I just had no idea why I was slow and felt awkward.  I returned home to Marlow on Thursday 6 June and on the afternoon of Sunday 10  June, relaxing in the sun in the garden after lunch, I felt the chest tightness again , this time spreading to the left arm which ached in the pins and needles way it does when the circulation has been cut off for a short time.  Margaret (who trained as a nurse at the Radcliffe), and I discussed it and decided to call an ambulance.  At Wycombe Hospital I was given tests and assured that I had not had a heart attack and the heart was undamaged but I had probably had an attack of unstable angina.   On Thursday I had an angiogram and was told that one branch of the aorta was blocked and another 90% blocked but this had been cleared and a stent fitted.  The blood supply to the heart was 85% and a by-pass was not justified.  On Friday I returned home none the worse,  thinking that this explained my symptoms during the previous 18 months.

Of course I was wrong …….. The chest discomfort never reappeared but the other symptoms never went away.

None of them was in any way disabling but Margaret insisted that I see a specialist about persistent hoarseness that I’d had on and off for several years but which was becoming worse and permanent.  Having lived abroad for most of the previous eight and a half years and not been able to use the NHS, I had health insurance and I saw a specialist a week or two later.  He pushed a camera down my throat and told me that my vocal chords were fine and I could see a neurologist or a speech therapist if I wanted to.  He probably recognised the “Parkinson’s face” (expressionless, mask-like) but knew the diagnosis would have to come from a neurologist.    A few weeks later I duly saw one who gave me an MRI scan, blood test and a lot of other tests and said, almost muttered, something about extra pyramidal symptoms and Parkinsonism.  When I asked what could be done he was a evasive and spoke about new drugs like rasagiline.  His parting advice was to “do as much as you can”, spoken, it seemed to me, in a tone that was intended to sound encouraging but which sounded quite the opposite. After this I entered a period of denial based on the absence of tremor. Nevertheless  what I read on the internet about PD and only tended to confirm his diagnosis.

Private health insurance is good for conditions that can be fixed but not for chronic, recurrent or long term conditions. In any case I was unlikely to be able to earn enough in future to cover the £7000/year that full health insurance for the two of us was  costing so I asked my GP for a referral to a Speech Therapist.  When she came to our house in April 2011 I was ready to accept the diagnosis and when I told her half way through the interview that the neurologist had mentioned Parkinsonism she said “That’s a relief. I was afraid you didn’t know!”  She was so matter-of-fact about it that at that moment I completely accepted that I had PD (not Parkinsonism) and that I’d had it for at least three years and probably longer.

Our dogs (plus 1 visitor)

What does it feel like to have Parkinson’s? 1. Speaking too fast.

This is equivalent to asking what the symptoms feel like.  I can only speak for myself and I was diagnosed in 2010-11, although with hindsight I may have noticed the first symptoms as early as 2007, none of them were the PDF “early symptoms” – loss of sense of smell, REM behaviour (sleep) disorder, mood disorder, orthostatic hypotension – listed in my 29 May post.  I do have fairly low blood pressure (105/65) but I take small doses of ACE-inhibitor and β-blocker after a stent insertion in June2010, which lower BP anyway.  I still have a good sense of smell – with five dogs (the paler animal at the back on the right is the brother of the bitch wire haired pointer beside him and hr is staying with us for a few days) you know if you’ve lost it!

In 2007 I discovered urinary urgency but this may have been no more than an enlarged prostate.  It hasn’t got much worse since then.  I had suffered from chronic but variable hoarseness for some time when, at a meeting in Brussels, I was advised that I should speak louder and slower but I’ve always spoken too fast.  At the age of 18 it was my turn to read the lesson in Chapel and I delivered 5 verses in 7 seconds and was banned thereafter.

“Speech problems” are really a (fairly disastrous in my case) composite of three separate symptoms:  hoarseness/softness (inaudibility); slurring, as a result of poor coordination of tongue and jaw; festination (speaking too fast).  All three have got worse since 2008.  I had the LSVT (Lee SIlverman Voice Technique/Training) in 2011 and I can shout if I need to (ask the dogs!) but I can sustain a loud note for only about 15 sec now instead of 20-25 sec 18 months ago.  Slurring I don’t seem to be able to do much about but it’s still fairly unobtrusive.  Festination frustrates me a well as Margaret and other friends who, unlike M,  are too polite to say so. I can speak at normal speed if I concentrate hard but not for long.

Festination seems to be the result of an irresistible need to convey meaning too fast.  Below is a paragraph (1) from an account I wrote a long time ago of a trip to Turkey with two friends after our second year at Oxford.  I cannot read it at normal speed. In paragraph (2) the words have been reversed and it must be read from the bottom.  I have no problem reading this at normal speed.  In para (3) I have inserted a  distraction between each word and this too I can read at normal speed.

(1)  On Sunday 14 August we assembled at David‘s parents’ house in Croydon for last minute preparations and packing. On the Monday evening David had characteristically arranged for us to go to a Promenade Concert, deriving as much satisfaction from the fact that the principal item was Sheherezade as if he had personally selected the programme to be an appropriate prelude to a sojourn in Turkey.

(2)  Turkey.  in   sojourn   a   to   prelude   appropriate   an   be   to   programme   the   selected   personally   had   he   if   as   Scheherazade   was   item   principal   the   that   fact   the   from   satisfaction   much   as   deriving   Concert,   Promenade   a   to   go   to   us   for   arranged   characteristically   had   David   evening   Monday   the   On   packing.   and   preparations   minute   last   for   Croydon   in   house   parents’   David’s   at   assembled   we  1960  August  14  Sunday  On

(3)  On ** Sunday ** L4 ** August ** 1960 ** we ** assembled ** at ** David’s ** parents’ ** house ** in ** Croydon ** for ** last ** minute ** preparations ** and ** packing. ** On ** the ** Monday ** evening ** David ** had ** characteristically ** arranged ** for ** us ** to ** go ** to ** a ** Promenade ** Concert, ** deriving ** as ** much ** satisfaction ** from ** the ** fact ** that ** the ** principal ** item ** was ** Scheherazade ** as ** if ** he ** had ** personally ** selected ** the ** programme ** to ** be ** an ** appropriate ** prelude ** to ** a ** sojourn ** in ** Turkey.

Of course you can’t use method (2) when you’re in conversation and I’m not sure whether you can imagine the interrupts between words (method (3)).  I  can speak French or Italian (I’m not fluent but not bad) at a normal speed because I have to check each word before I speak it.  I think (I haven’t really tried it yet) that if I speak English with a French accent I will be able to speak slowly because I will have to check pronunciation of each word.

Before PD set in I was able to adjust the pace of delivery of words but since then I cannot without artificial aids.  It feels as if PD has impaired my ability to choose how fast or how slow I speak.  The only other PD patient I know who speaks as I do also tells me he has always spoken too fast.  Does anyone else have an opinion?

I think festination also affects eating.  I’ve always eaten too fast (yes, as well as speaking too fast) but it is easier to distract yourself from eating.  This, combined with a drop in coordination, I suspect, was responsible for me biting my tongue, sometimes two or three times a day in 2009/11.  I’m not talking about an occasional nip but full scale bites with blood. Since then the pain has helped to teach me not to chomp and resulted in slower and more careful chewing.

I’m not convinced, therefore, that festination is a direct symptom of PD, although it may well be induced by PD.

Symptoms defne Parkinson’s Disease

 

 

It is possible to have a serious illness without symptoms but, for doctors and patients, PD is defined by its symptoms.  The tremor attracts attention but  other symptoms are so varied that their definition has in places become rather woolly.  This is not a trivial issue because we do not yet have a model of the disease process that (1) accounts for what patients experience and (2) would allow doctors to make a reliable prognosis of the probable future course of the illness.  Indeed the outcome varies so much between patients that few neurologists are willing to give more than a vague indication of what an individual can look forward to or over what timescale.

Since doctors cannot explore the brain in the way they can explore other organs they can only use the indirect information provided by the patient about symptoms to infer their cause.  If patients can only describe in vague or general terms what they feel in relation to each symptom then it will be hard to determine, for example, the severity of each symptom, the frequency with which they occur, whether some symptoms occur in a consistent sequence over time, whether some symptoms typically occur together or whether some only rarely, if ever, occur together in the same patient.

Doctors cannot be blamed for this.   A typical GP has around 2000-2500 patients of which 5 or 6, mostly over 75, will have PD, and usually be badly affected.  Tremor is the least ambiguous marker but few GPs will ever have to diagnose more than one or two cases of PD.  A neurological consultant will have more PD patients but for every PD patient (s)he will have 10 patients with dementia, of which 6 or 7 will have AD.  Add to these the patients with other NDDs, stroke. tumours and brain injury and it is easy to see why PD patients may only see a consultant for 5 minutes once a year.

Any statistical analysis of symptoms would ideally need to be done on at least 1000 PD patients, which implies a total  population of around 500 000  if most of those with PD participate.  In practice a population of up to 5 million would probably be necessary to provide enough patients willing and able to participate in a study.  Such  a large population would be scattered over a large area and be difficult to manage.

The web is a better source of subjects since it removes geographical constraints and allows for discussion between subjects to reach a consensus on a symptom, if necessary.  The American organisation 23andMe has a constituency of over 10 000 PD sufferers and controls, about whom it holds a great deal of information,  but it is focussed on genetics.

Below I  have listed my own symptoms, not because they are in any way special but to provide a starting point for discussion – to see if others agree or can refine the description or if they have a different experience.  Others will have a different suite of symptoms, and may experience some symptoms differently.

Symptom	Pres (+) Abs (-)	Motor component	Coordination component	Non-motor component	Response to l-DOPA (Sinemet)
Primary motor
Resting tremor	–		Loss of control of fine movement
Bradykinesia	+	Slow Voluntary movement			None
Rigidity	–
Postural instability	+	Impaired movement in response to loss of balance	?	Failure to detect movement of C of G outside of stable perimeter	None
Impaired gait	+		Impaired muscular coordination		None
Dyskinesia, Dystonia	–	Involuntary movement	Loss of control of fine movement
Secondary motor
Cramping	+	Involuntary muscle contraction			None
Slurred speech	+		Impaired coordination  of jaw/tongue		None
Biting cheek, tongue, lip	+		Impaired coordination  of jaw/tongue	Eating too fast (festination)	None
Swallowing difficulties	+/-				None
Drooling	+		Impaired swallowing reflex	Excess saliva	None
Rapid speech	+	None ?	None ?	Festination	None
Micrographia	+		Impaired coordination?	Festination?	None
Double vision	+		Impaired coordination of optical muscles		None
Akathesia	–
Stoop	+	?	?
Back pain	+	?	?
Masked face expression	+				None
Non-motor
Social withdrawal	+			Mood, sociability	Strong
Depression	–			Mood
Loss of sense of smell	–
REM behaviour (sleep) disorder	–
Mood disorder	+/-				Strong
(Orthostatic) hypotension	+/-				None
Disturbed sleep	–
Constipation	–	Poor muscle tone?
Bladder problems (urgency, incontinence)	+	Impaired control of muscles?			None
Fatigue, lack of energy	+				None
Weight loss or gain	–
Sexual problems (loss of or excessive libido)	–
Fear and anxiety	–
Skin problems	–
Cognitive impairment (slow thinking, dementia)	–
Narcolepsy (tendency to fall asleep)	+				None

 

My motor symptoms do not respond to l-DOPA in the form of Sinemet Plus and, of the non-motor symptoms, only my mood and sociability are improved.   If I reduce the dose from 1½ tablets 3 times a day to 1 tablet 4 times a day there is no change but if I reduce it to 1 tab 3 times  or twice a day I notice a deterioration within 2-3 days, which improves within 20 minutes of restoring the original dose.

When you know you have PD you can recognise every symptom but if you don’t know then it’s easy to dismiss most of them as the inevitable result of the aging process, as indeed they may well be …….

In the next post I will try and describe what the symptoms feel like to me.

Parkinson’s symptoms

James Parkinson described “the Shaking Palsy“ in 1817 and the characteristic tremor, with a frequency of 4-6 Hz and a typical amplitude of about 5 mm has defined the condition ever since.  Very many symptoms have now been described as associated with Parkinson’s and as many as one in three of patients diagnosed with PD have, like me, no tremor.  We are diagnosed instead on the basis of having a number of other characteristic symptoms.

The Parkinson’s Disease Foundation (http://www.pdf.org) divides symptoms  into three categories:

primary motor		secondary motor		non-motor
Resting tremor		Freezing		Early symptoms
Bradykinesia (slow movement)		Rapid speech, sudden acceleration		Loss of sense of smell
Rigidity		Micrographia (small writing)		REM behaviour (sleep) disorder
Postural instability		Mask-like expression		Mood disorder
		Stooped posture		Orthostatic hypotension
		Awkward walking*		Other symptoms
		Dystonia (involuntary muscle contraction)		Disturbed sleep
		Impaired dexterity and coordination		Constipation
		Limited movement		Bladder problems (urgency, incontinence)
		Impaired motor coordination		Fatigue, lack of energy
		Akathisia (inner restlessness)		Depression
		Difficulties in speaking (quiet, slurred)		Loss of sociability*
		Swallowing difficulties		Weight loss or gain
		Drooling		Excessive saliva
		Biting tongue and inside of mouth*		Dental problems
		Sexual dysfunction		Sexual problems (loss of or excessive libido)
		Muscular cramping		Fear and anxiety
		Double vision*		Vision problems
		Stooped posture		Skin problems
		Back pain		Cognitive impairment (slow thinking, dementia)
		Difficulty turning in bed*		Tendency to fall asleep*

*I have added these to the PDF list.

This list is not exhaustive but covers most of those that are usually mentioned, although, I suspect not those that sufferers experience but do not bother to mention.

There is no doubt that the left hand column contains motor symptoms but there is obviously some confusion about some of the other symptoms.  For example:

Are’ drooling’ and ‘excessive saliva production’ the same?

Is ‘double vision’ an example of ‘vision problems’ or of impaired motor function leading to the inability to move both eyes to focus on the same point?

Is biting your tongue a ‘dental problem’ or is it simply another manifestation of the poor coordination of tongue and jaw muscles that affect speech ?

Is ‘constipation’ a non-motor symptom or is it caused by weakness of the muscles responsible for the peristaltic pumping of food and waste material down the bowel?

Are ‘bladder problems’ non-motor or are they caused by weakness of the muscles controlling the urethra?

I would include ‘rapid speech’ in the non-motor column because in my case it happens when there is meaning in the words.  If I say or read a list of unrelated words I can do it fast or slow without difficulty.  This haste is also evident in writing and typing and may be the cause of micrographia.

For esnapel hre is an uncorrected seentence written without spekk check benefit.(!)

(This is actually not too bad ……)

What surprised me when I first began studying he condition was the absence of any advice on what symptoms tend to occur together and which do not and what symptoms tend to show early and which manifest themselves later.  The only information I was given was a gloomy forecast about the high probability of contracting dementia at some point in the future.

I realise now that there is a good reason for this and it isn’t just down to a lack of interest.  But I want to talk more about symptoms in my next post.

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Parkinson’s Disease, science and belief

Evolutionary psychologists have suggested that there is an  evolutionary advantage in a belief in a God because it makes us behave better than we otherwise would.  It has also been argued, though I can’t find the reference, that in earlier stages of evolution there was an advantage in using simple rules based on experience (folklore) as the basis for decision making because it was quicker and produced, on average, more reliable results than trying to work out an answer for ourselves.  If true, these ideas may explain the widespread distrust of, or indifference to, scientific argument.

Scientists are just as susceptible as anyone else to believing in something and rejecting the offer of counter arguments, however logical.  Belief is easier to maintain in areas where the evidence is statistical or judgmental and cannot easily be objectively proved or disproved.

The environment, which depends almost entirely on the analysis and interpretation of large amounts of data, is notoriously such an area, and the issues are muddied, as they often are, by vested interests.  For example most scientists whose interests are strictly technical now accept the reality of climate change.  They mistrust the views of both believers, whose research funds may depend on continuing concern about global warming, and deniers, who resent the costs being imposed on society by attempts to reduce emissions of greenhouse gases, and prefer to evaluate raw data for themselves.

Medicine is another subject where views can be held with religious conviction and cannot be challenged , especially  by anyone who is not medically qualified.

When I first accepted that I had Parkinson’s Disease in spring 2011, being a scientist I naturally set out to try and understand the mechanism and causes of a condition with such a gloomy prognosis.

The first thing that strikes you is the staggeringly vast amount of material published on PD and the second thing is the lack of connectedness between different areas of research.  It’s as if scientific (as opposed to clinical) research takes place in a series of bubbles not connected to each other or even acknowledging parallel activities.

Two years on from then and after about 500 hours of wading through large numbers of documents on the web it is clear that there are apparent inconsistencies and contradictions in the results of  research in Parkinson’s Disease, as well as the lack of connectedness between different topics

Clinical research is admittedly very difficult because: (a) Few PD patients have identical symptoms; (b) The condition develops over a period of 20 years or more;  (c)  The prevalence of PD is only 2.7 cases per 1000 (Alzheimer’s is 17 cases/10000, Dementia [all types] 27/10000); (d)  There is no definitive test for PD, which can be misdiagnosed;  (e)  It is therefore hard to assemble sufficient cases for a statistically significant study and even harder to find a group marched for type, stage and age. Furthermore it is now believed hat PD starts some years before symptoms are noticeable so it is also likely that studies only ever include individuals in which the condition is already well established.

I couldn’t find an overview of recent research on PD and so I set out to write one myself.  I’m not a doctor but I do know what it’s like to have the condition – or at least my personal version of it.

There isn’t enough material o construct a coherent narrative and the best I can do will be to review the information that I consider to be proven for all practical purposes and identify important gaps.  Then I will look at the extent to which the facts support current theories and beliefs regarding the possible origins and causes of PD.  One of the problems is that charities attract funds for research to “Find a Cure for Parkinson’s”.   In the first place I personally doubt whether a “cure”, in the sense of a treatment that will restore any PD  patient to the condition he enjoyed before the disease gripped him or her, will ever be remotely possible.  On the other hand it seems possible that we shall be able to find at least one way to halt the progress of the disease in those who already have it and prevent it from starting in those that do not.

Logically we should start with the science and use it to explain the disease but, even if we could do this it would make very dull reading (and writing!) so, before I get ahead of myself, I want to  talk first about the symptoms and what it feels like to have PD.

Autobiographical background

The next posts will be about Parkinson’s Disease, with which I was diagnosed in 2010,  but I’m starting with a little autobiographical information partly to say something about  who I am but mainly to establish my scientific credentials (such as they are) for writing about the state of scientific knowledge relating to a condition in which I now have a vested interest.

When I was at school in the ’50s only about 10% of us went to University and almost all of us came either from Grammar Schools or, like me, from a Public School.  When he eventually returned from Burma  after the defeat of Japan in 1945 my father took over from his father a small printing business, which provided then a gross income of about £2000/year.  In 1953 my school fees were about £300/year or about  15% of his gross income. Tax levels were high as governments  struggled to pay off the debts of WW II and the school fees were probably more like 25% of his net income. Most parents in his position did the same, making some sacrifices to pay the fees but short of destitution.  Nowadays boarding school fees  are around 100% or more of the national average income before tax and out of reach of anyone earning much less than about £100 000 a year.

For those whose parents couldn’t or wouldn’t pay the fees every  child could take the 11+ exam and the top 25%  or so were allocated to the free Grammar Schools where the teaching was at least as good as in the Public Schools.  In fact most Public Schools needed pupils and took many who had failed the 11+., which made them comprehensive long before Grammar schools merged with Secondary Modern  schools in the ’70s.

A very good review  of the development of education in the UK over the last century, its social aspirations and the reasons for its failures, can be found at http://www.earlhamsociologypages.co.uk/tripcomp.html#begin.

It takes between 11 and 17 years  to educate a child, which is longer than two parliaments and longer than most parties ever hold power so it isn’t surprising that every child’s education is subject to at least one, and sometimes three or four, upheavals as politicians meddle incessantly with exams, discipline, school structure, funding, rights and responsibilities without regard to the need  for continuity and consistency of education.

In truth there is no educational system that will satisfy everyone and few that will please more than a few single interest groups.

One of the late Margaret Thatcher’s more unhelpful contributions was to promote and encourage, albeit perhaps unintentionally, the idea that the (only) purpose of education is to prepare children for work (rather than for life, although in her view they were probably the same thing).  This view seems to be still prevalent and one of the attractions of the Public Schools is that they have always managed to do both very well.

I was always interested in science and to everyone’s surprise, including mine, I ended up at Oxford.  Most Oxford entrants had spent  a second year in sixth form and taken ‘S’ (for Scholarship) level papers.  These were similar to the first year University exams, which we all sat in the summer before we arrived at Oxford, and which were roughly equivalent to the then pass degree standard.  So we all started with a reasonably high standard of maths, physics and chemistry before we began the honours course in physics or, in my case, chemistry.  We were not cleverer than students in the 21st  Century but the selective system, although it had drawbacks, allowed the more intensive teaching and learning that entrance to Higher Education then required.  I suspect, however, that there was little advantage in knowing all the facts that we laboriously acoquired about physics and chemistry because at University we learned the theories that gave the facts an understandable and predictable framework.

Maths, on the other hand, was different.  The techniques of mathematical analysis have to be learned and there is no alternative to a lot of hard work.  Even many of those with an aptitude for maths find it  difficult and there is now even less taste now than there used to be for hard, intellectually challenging work.  It isn’t just the UK, if this is any comfort.  China has the same problem and so does Italy. The top mathematicians are as good as ever but the gap between these and the average has widened considerably.  The consequence is a generally lower standard of mathematical ability even among scientists and engineers.  Employers complain but their expectations and demands of recruits have probably increased as they have cut back apprenticeships and day release schemes.

The first seven years of my life after graduation were spent in academic research, first a D.Phil. in the Sir William Dunn School of Pathology at Oxford, then at the National Institute for Medical Research at Mill Hill and then back to Oxford to the Dept. of Biochemistry.    The next 12 years I passed in industrial R & D in the food industry before I became Director of the Environmental Laboratory for the water industry until it was privatised.  From 1992 until 2010 I was an environmental consultant working in Italy, eastern Europe and China.  In the late 1990s donors began shifting their funding away from small short term projects to much larger multidisciplinary projects and In 2002 I agreed to manage a two-year, seven-country project based in Rostov-on-Don in the north Caucasus.  This was immediately followed by 18 months in Cluj-Napoca (no I didn’t support the football team) in Romania, then two years in Odessa and finally two years n Kiev running a six-country project covering Ukraine, Belarus, Moldova, Georgia, Azerbaijan and Armenia.  In June 2010, at the age of 71, I came back to the UK and three days later suffered a mild attack of unstable angina which necessitated the insertion of a single aortic stent. 

In July I was bullied by Margaret into seeing an ENT specialist about persistent hoarseness.  This led a few weeks later to my being told that I probably had Parkinson’s Disease.  A period of denial lasted about 6 months until a matter-of-fact speech therapist assured me that I definitely had PD.

Naturally I then set out to get to grips with the science underlying PD.  This, it turned out, was easy to say but impossible to accomplish.   There is no shortage of information!  Indeed there must be thousands of terabytes on the web and forests must have been torn down to make the paper on which reports have been written and patient-friendly pamphlets produced.  But nowhere have I found any coherent and/or convincing account of the origins of the disease and its cause(s).  I was told that 80% of the neurones in the substantia nigra of my brain had died and it no longer produced sufficient dopamine to control my muscles but I am pretty confident from what I have learned over the last two years that this is incorrect.  The problem is that but of the research papers on PD do not seem to connect with each other, or lead to conclusions that are implausible or not mutually compatible.

Over the next few weeks I will try to provide an objective review of  the scientific evidence that leads to a hypothesis about the origin of the condition  that can account, at least in principle, for the large diversity of symptoms that may accompany a diagnosis of PD.  The hypothesis is not my own but an assembly of related  elements from different areas of research on which I will welcome comments and criticisms.

SCW