Blindness pretending to see

We were all thrown into the world in a specific state; out of all possible ways to exist, the process of thrownness sculpted me and discarded, in my case, all other ways to cut the stone to end up with my unique instance of existence. The end point of thrownness isn’t static, it allows possibilities in life and the ability to choose; its as if thrownness built a house of limited size for you to live in but you are free to wander from room to room. The specificity of your “house” imposes limits to what can be experienced; how we view the world (e.g. through the limitations of our senses) limits what we see.

One of the most important achievements of our thrownness (we went through similar processes of being thrown into the world) is the ability to have a self-aware point of view. A point of view is grounded in thought and therefore must operate within the limits of how we think; for instance we think in successive thoughts (i.e. one after another) and are therefore limited to thinking from moment to moment. Also, our thinking is not perfect because we suppress all other possible thoughts to think our current thought; perfect thought would involve simultaneously thinking all possible thoughts successively and all at once in all possible contexts and times. Because we have a specific point of view this is impossible. We can think of the concept of perfect thought but we can never experience its perfection; this is because words do not carry the experience of something. Perfection is thought of as “not imperfect” and imperfection is something we can experience and not just a word.

Our point of view, whose dimensions and limitations were determined by thrownness, enables us to see but also makes us blind. For example, experiencing the future of my Parkinson’s is impossible because we think only in the present, moment by moment; even predicting the future is done by thinking in the present. Leaping into the future or into the past is impossible because of the thrown limitation of thinking successive thoughts. Similarly, experiencing God as the perfect being or trying to respond perfectly to Parkinson’s is impossible because we can only think in limited contexts; to know a perfect thing requires us to view the perfect thing perfectly.

We are all blind when we see. Those of us who claim to know the future or God are pretending to see despite being as blind as the rest of us.

Disconnect

I was sitting on a chair in front of a full length gym mirror doing Pilates (yes, I go to a Parkinson’s Pilates class!) when I noticed something strange: my reflection was leaning to one side but I felt like I was sitting straight. When I corrected my reflection so it was straight I then felt like I was leaning to one side. It was very strange.

It seems my Parkinson’s is affecting how I sense my body; Parkinson’s is trying to shove me out of the way.

Gretchen Amphlet Parkinson's UK lecture 2013 - Part 4

For Part 1: http://dialoguewithdisability.blogspot.co.uk/2013/04/gretchen-amphlet-parkinsons-uk-lecture.html

For Part 2: http://dialoguewithdisability.blogspot.co.uk/2013/04/gretchen-amphlet-parkinsons-uk-lecture_24.html

For Part 3 - http://dialoguewithdisability.blogspot.co.uk/2013/04/gretchen-amphlet-parkinsons-uk-lecture_25.html


Conclusion – prospects for treatment

Identifying mutations is a crucial first step toward new treatments for Parkinson’s. Understanding which genes are mutated in sufferers and how the protein is affected leads to understanding how the function of the cell is disrupted. Once this is known, drugs can be potentially designed to counteract the affect of the mutant protein and prevent nerve cells dieing. This could introduce the idea of “personalized medicine”; a specific mutation is treated with a specific drug. Another possibility is that a group of related diseases (e.g. neurodegenerative), although caused by mutations in different genes, affect the same function of nerve cells. Therefore, drugs can be designed to affect the specific cellular process more generally and not the mutated protein itself.

These approaches are dependent on understanding the genetics of Parkinson’s; it is crucial that such research is supported.

Gretchen Amphlet Parkinson's UK lecture 2013 - Part 3

For Part 1: http://dialoguewithdisability.blogspot.co.uk/2013/04/gretchen-amphlet-parkinsons-uk-lecture.html

For Part 2: http://dialoguewithdisability.blogspot.co.uk/2013/04/gretchen-amphlet-parkinsons-uk-lecture_24.html

Understanding why nerve cells die in Parkinson’s - Case Studies

What are the faulty proteins doing to cause nerve cells to die? Two studies were presented that examined the role of two genes.

1. a-synuclein

When proteins are made the string of amino acids fold around each other to form a 3D shape: the shape determines a protein's function. Mutations have been found in the a-synuclein gene that cause misfolding of a-synuclein protein. Misfolded protein sticks together to form large cellular structures called Lewy bodies, leading to cell death and Parkinson's.

The same process of DNA encoding proteins via RNA that occurs in humans also occurs in flies (indeed in all living things). This makes it possible to transplant a mutant form of the human a-synuclein gene into flies to trick fly cells into making mutant a-synuclein protein. This causes the formation of Lewy bodies, loss of nerve cells and Parkinson-like motor impairment in flies. Interestingly, also producing normal human Rab11 protein (involved in moving proteins to the cell surface) in these Parkinson's flies dismantles the Lewy bodies, prevents nerve cell death and reverses some Parkinson’s symptoms.

2. dj1

Mitochondria are structures within cells. They are the power plants that produce all the energy needed by the cell. A toxic by-product of energy manufacture is "reactive oxidative species" (ROS), a chemical that can harm the cell. Nerve cells of the substantia nigra, which are lost in Parkinson's, require lots of energy; therefore they produce lots of ROS and are under "stress" to get rid of them before they damage the cell. Damaged cells trigger apoptosis (or “programmed cell death” where cells sacrifice themselves for the greater good) and die. A gene, dj1, helps the cell to clean up ROS. Perhaps unsurprisingly, mutations in dj1 have been found in Parkinson's sufferers; loss of dj1 function results in excessive ROS-induced cell damage, apoptosis and cell death. 

Why I stammer

An important part of being in the world is we react to things; other people, objects, even our own thoughts, emotions and memories. A reaction always involves thought and often elicits an emotional response that diverts you from the course of action you were on.

When I’m talking or about to talk I react to the perceived importance of what I am about to say and to whom I’m saying it with fear and negative memories and I try not to stammer. Of course by getting in the way of myself like this, I stammer. Fear of not being understood makes me think I have to get my speech right first time and therefore I pressurise my underlying susceptibility to blocks; thus, turning my previously fluid speech into fearful treacle.

When the social pressure to perform is removed, I am comfortable with my listener and the importance of what I’m saying is kept under control there is no reaction; therefore no fear, no pressure and no stammer. A way to achieve this non-reaction is to believe you don’t have to get it right first time.

Gretchen Amphlet Parkinson's UK lecture 2013 - Part 2

For Part 1: http://dialoguewithdisability.blogspot.co.uk/2013/04/gretchen-amphlet-parkinsons-uk-lecture.html

Inheritance

Genes, and their mutations, are passed from generation to generation. The classic example of inheritance is eye colour. Eye colour is determined by two different mutant versions of the same gene: a dominant brown eye version (B) and a recessive blue eye version (b). Since we inherit two copies of each gene the combinations BB and Bb will result in brown eyes and only bb will give blue eyes (the B gene is dominant over b). Bb individuals are said to “carry” the b gene even though its affect is masked by the dominant B gene. The way to tell if a trait is dominant is to see if it is present in each generation; if recessive it tends to skip a generation.

Inheriting mutations in Parkinson’s genes

Parkinson’s disease has been observed in multiple members of the same family. When sufferers’ DNA was compared to DNA from non-suffering family members (the sequence of DNA subunits can be read) mutations that only occurred in sufferers were found. These mutations will, via mutant RNA, result in the manufacture of faulty protein that disrupts the normal function of the cell.

By studying such families about 19 “Parkinson’s genes” have been found (both dominant and recessive) and these genes so far account for about 10% of all cases of the disease in the general population.

What about the other 90% of sufferers? Do you carry mutations in these or other Parkinson’s genes? We are all mutants; we carry many mutations in our DNA. However, these changes can have a range of affects, from no impact on protein function to subtle or devastating affects that impact the function on the cell. In one study, sufferers without affected relatives showed more subtle changes in their Parkinson’s genes, causing less obvious changes in protein function. If you inherit two recessive mutations or one dominant mutation you are likely (~100%) to develop Parkinson's whereas these subtle mutations increase the risk only by about 3%.

The genetics of Parkinson’s is likely to be complex, involving many subtle mutations interacting with environmental factors to cause loss of nerve cells; we have only just begun to understand how Parkinson’s is inherited. It is crucial we succeed; understanding the underlying genetics is the only hope we have of developing new treatment to counteract the faulty proteins and prevent the loss of nerve cells.

I’m 1 year old today

It’s my birthday today; not my birth birthday, I have two birthdays now, like the Queen. It is 1 year since I was diagnosed with Parkinson’s disease. What a year its been; I’ve moved house twice, given up driving, started a blog, appeared in the Times newspaper, acquired a walking stick, had a go in a mobility scooter…

I’ve also tried hard to set my thoughts and emotions in order; a diagnosis picks you up and shakes you until you are all jumbled up. It takes patience to fit the pieces together again. Some pieces don’t fit anymore so you have to grieve and learn to live with the gaps. This has been the challenge of the first year living with the awareness of my Parkinson’s and will continue to be in the years ahead.

Gretchen Amphlet Parkinson's UK lecture 2013 - Part 1

The annual Gretchen Amphlet Parkinson's UK lecture was held at Fitzwilliam College in Cambridge on the 17th April 2013. Dr Patrick Lewis (UCL) and Dr Flavio Giorgini (University of Leicester) presented work on the genetics of Parkinson's. The following is a summary of the lecture for the general reader; I will attempt to describe:

1. The underlying physical cause of Parkinson’s
2. Essential genetic knowledge needed to understand genetic disease
3. How Parkinson’s is inherited
4. The ways mutated genes cause Parkinson’s.

The cause of Parkinson’s disease

In 1817 Dr James Parkinson published the first formal description of the motor symptoms of what was then known as the “shaking palsy”. It wasn’t until the 1950s that the primary cause of Parkinson’s was discovered; sufferers have reduced numbers of nerve cells in a structure of the brain called the substantia nigra. Normally, these nerve cells release dopamine, which activates the motor cortex of the brain to initiate and control movement. Therefore, the loss of nerve cells causes a reduction in dopamine levels leading to impaired movement (and other symptoms).

Since the 1950s the main question in Parkinson’s research has been, why do substantia nigra nerve cells die?

Genes, DNA and Mutations

Nerve cells can die from external causes (such as environmental toxins) and internal causes (something going wrong inside nerve cells). Genes control the function of cells so an obvious place to start looking for the internal cause is in genes. Genes are made of the famous double helix molecule DNA, which comprises four different chemical subunits (A, T, C and G) arranged into two strands. In nearly every human cell there are 3 billion subunits of DNA encoding about 30,000 genes.

DNA is the key information-carrying molecule in all living things. DNA “expresses” this information by being transcribed into RNA and RNA is then translated into Protein (RNA is similar to DNA, but it is single stranded and Proteins are made up of amino acid subunits). An analogy might help to illustrate this process: DNA is like a set of handwritten instructions and specific paragraphs are typed up to form an RNA copy. RNA is the template for arranging amino acids in a specific order to make specific Proteins (a bit like a jelly mould to “set” the protein). Proteins form the structure, and control all the functions, of a cell.

Genes can malfunction when they become mutated. For example, gene TTATTCCGG becomes mutated at the third subunit; TTTTTCCGG. This mutation will get copied into RNA and the mutant RNA will fail to arrange the amino acids in the correct order; therefore making the protein faulty and unable to do its job properly.

Disability and Onlyness

Tennyson wrote, "tis better to have loved and lost, than never to have loved at all". At least to lose love means you found it in the first place; you know the joy of that discovery, you've found yourself worthy of its possession, you have been the entire focus of another person and you know the feeling of returning their loving gaze.

Spare a thought for those who are closed off from love; whose life-long and now emerging disabilities have crowded out the capacity to generate such joy. This is the heaviest burden of disability: the greater potential for physical and emotional isolation and having the disability as your only daily companion. It gets in the way, causing you to trip over yourself as you set off on the journey towards someone. 

This is an important, yet mostly hidden away, part of the dialogue with disability...

We make room for ourselves

Throughout our lives we have a consistent sense of self-identity; I identify with the child I was as me, despite the changes in body and mind that have taken place since then. All thoughts are accompanied by the reinforcement of our consistent identity (I think…). Heidegger says in our self-identity we stretch ourselves along. The following image occurs to me:

When we are born we peg one end of a long piece of elastic material into the ground. As we grow up and move through life we pull and stretch this material as we go. When we die we peg the other end of the material into the ground and that is our life, stretched from peg to peg.

As we stretch ourselves along, and before we take the next step, we clear the path in front of us by choosing what to do next. It is this ability to choose that enables us to make room for ourselves.

Instead of a disability (e.g. Parkinson’s or stammering) confining us, it is a misunderstanding of the choices we have within our disability (we have the expectations of someone without our disability) that causes us to make insufficient room for ourselves. There is always something left to do, a piece of elastic to stretch along, and it is an honest and open appraisal of who we are that clears the most space in front of us.

Genetic Testing: advantages and disadvantages

Genetic testing involves sequencing (i.e. reading the letters in) DNA to reveal any mutations that could cause disease. Being tested seems to be an easy thing to agree to. However, knowledge of our genetic inheritance raises a number of difficult ethical issues that complicates the decision.

Once you know you have a mutation in a disease causing gene such awareness cannot be unlearnt. Knowing a mutation is present doesn’t make the mutation worse; it does however change the relationship you have with yourself. The presence of the mutation could come to dominate and divert you from the life you were living. Sometimes ignorance gives us freedom not to prejudge situations or narrow ourselves to only a few choices. For example, knowing from an early age I was susceptible to early-onset Parkinson’s probably would had stopped me pursuing the long term goal of a career in Science. I think the issue of whether you want to know you have a genetic susceptibility to a disease comes down to the question: would you like to hear the clock counting down to the disease or not?

Of course, being armed with knowledge of a mutation may enable us to choose a series of actions to save our lives (e.g. individuals with mutations in breast cancer genes may choose to remove their breast tissue as a precaution). But this depends on the type of mutation you have; not all mutations are made equal. Some will have a profound affect, meaning inheriting such a mutation confers a high likelihood of disease; others will increase the chances of disease only a small amount; and some mutations won’t have any affect. The extent of the reaction to knowledge of a mutation must be related to the severity of the mutation.

The amount of DNA we share with others is dependent on how related we are to them (e.g. parents share 50% with their children). It follows that we potentially have the same mutations as our close relatives. Therefore, knowledge of my mutation may be knowledge of my relative’s mutation and their susceptibility to disease. If I was to get tested, is it right to expose this knowledge through my actions when my relative hasn’t chosen to be tested? Should I keep quiet about my results when it may help them? Does my right to know outweigh their right to not know? This also applies to any children I plan to have. What right to information do we have when it impinges on the right of others to not know? These are difficult questions.

From my point of view, if it will cause greater harm withholding information then the information should be known. For example, it is morally wrong to not tell a young child an oven is hot. In this case the harm is known whereas in genetic testing there is a problem; the test itself needs to be done to assess harm. Nonetheless, I would advocate genetic testing if the results were clearly explained because the emotional difficulty of knowing can be mitigated, whereas the potential physical harm of a mutation is properly dealt with only after it is discovered; discovery is probably worth the risk of emotional difficulty.

"Good evening Mr Hobble-along..."

Someone on a bike has just said these "profound" words to me as we passed each other on the street. I ignored him; what is he and his observational skills (he noticed my symptoms, give him a Nobel prize!) to me? Nothing; just another person who happens to be in the world.

Then it got me thinking. Why did the person on the bike behave like that? I think he was trying to boast his own fragile ego by bringing others down. Such behaviour reveals how uncomfortable he is in his own skin; why else attempt to put scaffolding around your ego if it was robust and strong? He exposes his weakness by saying such things. Why can't he boast his ego by helping others? It is sad that it takes less effort to be nasty; being kind requires considered effort to move aside your selfish needs and let empathy take over; apparently it is beyond some people. Who is the one truly hobbling along?

“I’ve got Parkinson’s”

Telling the world I've got Parkinson's is like taking my clothes off in front of a scrutinizing doctor. I become an object, a thing of the public-self and confined within a narrow spotlight. I feel like I'm naked standing next to myself; I'm exposed but people see me through their own expectations.

But I'm more than a disease and more than what people expect me to be; I am myself as well. When I tell others about my disease I mustn’t allow, “Yes, I’ve got Parkinson’s” to mutate into “I can only be Parkinson’s”. Otherwise, I will get locked in the public arena and lose the other things I am.

I think it is important to be open about Parkinson’s both with yourself and other people because the disease tries to close you down. Nevertheless, people are so varied and as such will have varied reactions to your disclosure; there is nothing you can do about this. What you can control is your reaction to their reaction.

Losing my rhythm

Before the emergence of my Parkinson's, I had a certain rhythm, whose beat structured and eased the interaction between my mind and my body to such an extent that I didn't notice it. My body was like an orchestra fully responding to my instructions as conductor. My life responded to the music and I danced the best I could to the rhythm of work and play.

Now Parkinson's has taken away my rhythm. It has disbanded the orchestra until I'm left waving my baton to empty chairs. My mind and body are out of sync and dance to different music. Without this foundation it is difficult to keep up with the rhythm of life or find someone who dances like you. A Parkinson’s life is an arrhythmic life.

In transit on the Parkinson’s train

Whenever I travel on a train I feel on departure that I’ve been lifted off my foundations and I become reattached only when I arrive at my destination. During the journey I am groundless, displaced, in transition from place to place, never in one place for more than a split second as the train speeds along the track. I am nowhere, faced with the apparent contradiction of sitting in one place and moving at the same time; at least when I’m walking under my own power there is equality between sensing the movement and actually moving my body; on the train I sense the movement but I don’t actually move.

When I was diagnosed with Parkinson’s it felt like I was lifted off my foundations and placed on the Parkinson’s train; I was handed a one-way, non-stop ticket to a destination I am only vaguely aware of. I don’t know how long the journey will last. I am in transition to a future likely dominated by disability yet I seem to be standing still; I am groundless and nowhere.

Fellow sufferers accompany me on the train; we are sat in our seats and we feel the movement of the train but are unable to move or stand up ourselves. Family and friends, as well as doctors and nurses, walk up and down the aisle pushing different refreshment trolleys and handing out dopamine sandwiches and supportive tea.

I am living in transition, moving while standing still and there is no emergency stop button on the train I am on.

Contentedness as a goal

My Parkinson’s symptoms have worsened recently and I found myself entangled in a mass of frustrations, fears and a despairing feeling of, “I’ve still got so much to do in my life but a declining ability to do anything about it”. This is clearly unhelpful to me in the task of coping with my disease. What is the underlying logic that nourishes and sustains these negative feelings?

In the absence of any sense of control over what is happening to you, it is very easy and understandable to crave control. One way to remedy a lack of control is to try to manage your own expectations since you can wish anything you like; expectations seem to control the future. This is facilitated by seeing what other people have in their lives and expecting such a template to be applicable to your life too. But any comparison tends to be unfavourable to the one making the comparison. The eagerness to compare is compounded by the societal pressure of living the perfect life and the peddling of goods and services purporting to give you such a life.

There is a problem with control based on expectations of a the perfect life; life is messy and imperfect. Therefore, expecting unreasonable outcomes to your actions (perfection!) is unfair and empty; it only sets you up to fail.

Comparisons and expectations also miss one crucial factor: the difference between our thrownness and the thrownness of other people. We are all individuals because we were thrown into the world by separate acts of thrownness. We have the same anatomy as other people but the exact configuration is different due to the unique process of being thrown in each case and the experiences derived from a separate point of view within the world. These factors make a comparison shallow and partial.

Any future possibilities are made possible by our thrownness so expectations must take into account the state in which we, as individuals, exist. It should be noted that nobody is responsible for thrownness (it just is) since responsibility as a possibility arises only after we are thrown into the world.

An assessment of expectation must also be fair because a crucial possibility of thrownness is a not-yet: we were thrown into a world where there is always something left to do. Thrownness is limiting but not limited, it gives us many tools we can use in many ways, even if Parkinson’s makes some tools harder to use. Therefore, thrownness must be seen in all aspects of its not-yet.

Instead of society creating a template for us to compare ourselves, Heidegger believed we create our own space in the world. Because we have a specific point of view, when we focus on an object (including ourselves) it becomes located in relation to us and therefore within our space. If we know more about an object and its interconnectedness with other things in the world our space becomes bigger and incorporates more detail.

Therefore, knowing about thrownness and its many possibilities gives us the chance to widen the space occupied by “I’ve still got so much to do…” and find room for “I’ve done so much already…” This allows us to find contentment in what we are already and use that as a foundation to build upon.

What are the priorities within Parkinson’s?

The chronic, progressive and incurable nature of Parkinson’s raises a number of issues. I think the most prominent being how best to cope and live a good life within the confines of the disease.

Parkinson’s symptoms place a burden on your ability to carry out every day tasks most people take for granted (e.g. getting dressed in the morning). This increased demand on your ability to look after yourself causes a reduction in your capacity to do other things. A way to manage this reduced capacity and get the most out of it is to prioritise. It’s like having £100 and working out how much to spend on the essentials (e.g. maintaining a level of care for yourself), regular items (e.g. seeing family and friends) and what are now expensive luxuries (e.g. travelling, being in a relationship or looking after children). This involves determining what is important and how much it costs so you can apportion your reduced capacity in the best way possible.

Related to this is finding the best way to use the limited treatment options available in the face of a progressively debilitating disease. The root cause of Parkinson’s (loss of nerve cells) is not currently treated. The treatment that is available becomes less effective the more nerve cells are lost. What are the priorities in treatment? I have early-onset Parkinson’s so I have potentially another 50 years to live with my disease. Should I be aggressively treated now to improve my quality of life but use up my options in the short term or save most of my options to improve my life when my disability becomes significant in the future? It is a choice between short-term gain and then a sudden decline or a steadier disability. That is the dilemma offered by Parkinson’s.

Coping with Fear and Anxiety

How do we cope with fear and anxiety of Parkinson’s? Fear causes a narrowing of perspective and a shortsighted focus on the thing we are fearful of. We can become addicted to our fear of Parkinson’s and the subsequent wish that we were different. However, this misses our thrownness and the multitude of possibilities thrownness gives us; for example, we don’t have to be led by the nose by fear. We have the ability to think a different emotion and replace our fear; states of mind are changeable. We can’t change the fact of Parkinson’s but remaining open to alternatives gives us the opportunity to choose to think, feel and react differently to the disease.

Anxiety is anxious about possibilities and therefore it is anxious about “nothing”. Possibilities need us to act upon them to make them “something” more; they need free will (within the limits of thrownness) to actualise them. Since anxiety concerns only possibilities we are less anxious when we do something. We may become anxious about the consequences of our actions but we are again concerned only with possibilities.

Therefore, remaining open to alternatives (e.g. “I’m scared I might fall but maybe I can go to the shops today”) reduces fear and doing something (e.g. “I went to the shops today”) makes us less anxious.

Fear and Anxiety

Heidegger defines fear as fearing something within the world that threatens us. Fear causes us to await this something’s arrival, which leads to giving up our possibilities and retreating into bewilderment. In contrast, anxiety is anxious about our possibilities and brings us back to ourselves.

We are both fearful and anxious of Parkinson’s. The disease is seen as something threatening our physical control and in bewilderment we await its arrival. But, Parkinson’s is part of our thrownness and as such is a possibility we are anxious of. Therefore, we threaten ourselves with Parkinson’s, causing us to try and retreat from ourselves in fear. But while waiting for the loss of control to arrive we confront the thrown possibility of Parkinson’s as our own in anxiety. We try and tear our problems away in fear but end up gluing them back to ourselves with anxiety. The oscillation between fear and anxiety can be very painful and disorientating.

What is a prognosis?

The prognosis is one of the hardest things to come to terms with when diagnosed with Parkinson’s: the seemingly inevitable physical disintegration rushing towards me from my future. We rely so much on our physical control that its loss feels like a loss of ourselves. The prognosis of Parkinson’s triggered mourning for myself, not necessarily for what I’ve lost but more for what I might have had. However, there is a problem with mourning this “might”; I try to hold onto something I never held in the first place.

“What I might have had” is grounded in what I expect of my future. Usually, I measure my expectations in comparison to other people but, as Heidegger pointed out, this causes me to become lost to the crowd (or the “They”). Other people are separate to me and as such have unique experiences and instances of thrownness, including their prognoses. Therefore, mourning expectations founded in comparison to other people essentially unlike me is empty. The only entity that I can intelligibly be compared to would be a person with the same experiences and thrownness as myself; I am that person! I must be compared to myself in my current possibilities; my past possibilities have already been used up and possibilities in my future have yet to be discovered.

My current possibilities have to surrender to the limits of my thrownness, which includes Parkinson’s. Therefore, mourning what I might have had ignores my thrownness completely. Further, applying to myself a prognosis based on other people tries to cover up the blindness I have of my future possibilities. I can only compare myself to my current possibilities and judge what possibilities I am currently choosing. 

Therefore, my prognosis is not part of my “now” since it is something unknown in the future.

Variations

Until recently I’ve been travelling with my Parkinson’s on fairly steady, flat ground. My symptoms were predictable and I was learning to negotiate around them. But the negotiations have broken down and the terrain has shifted. I am now travelling on an incline and it has made it more difficult. My symptoms and my limitations are no longer predictable. I need to learn to navigate around this new terrain…

It seems that my Parkinson’s will be a repeating series of negotiation breakdowns, shifts in terrain and learning the new map of my limitations.

It is all too easy to see this shift in symptoms as a decline. But a decline implies you, in your specific case, know the end point of the decline. I know in general where I’m travelling to with my Parkinson’s but I don’t know how I will get there or what I will pass on the way; I know I’m travelling North to South but I go from place to place. Defining every shift in symptoms as a decline turns your colour TV into black and white; you may miss the symptoms that correct themselves (my walking has started to oscillate from good to bad to good again) or improve with medication. If you set yourself up with only decline in mind that is all you will see.