This summer I learned to walk. More precisely, I learned to walk normally. My gait had gotten unsteady, and I was dragging my right foot. Work with an excellent physical therapist helped straighten me out. But balance problems, tremors, and hesitations continued.
At the beginning of August I was diagnosed with Parkinson’s. I want to describe the phenomenology of my version of it, and begin thinking through its implications for the philosophy of perception and action. But first the disease itself.
▶ For a first-person account of Parkinson’s by a neurologist, see this recent article in Nature.
What Parkinson’s is
The immediate underlying problem is a deficiency of the neurotransmitter dopamine. Levels at diagnosis are typically 30% to 70% below normal. Dopamine is involved in many neural processes, not only motor activity but decision-making and the regulation of emotion. The symptoms from which Parkinson’s is diagnosed — tremor, bradykinesia, rigidity, and postural instability — will in time be accompanied by others, including loss of smell (mine, however, is rather more sensitive than less), autonomic dysfunction, troubled sleep, and dementia.
Diagnosis typically occurs five to eight years after the conjectured onset of the disease. Before diagnosis, in the so-called “presymptomatic” phase, there may have been nonmotor symptoms, including rigidity, aversion to novelties, and depression. In my case the presymptomatic phase may have begun as early as 2005. With no doubt fallible hindsight I can recall evidence of motor problems at least two years ago.
Dopamine deficiency, once regarded as the cause of Parkinson’s, is now accounted rather as a symptom. (Progress in understanding “causally deep” diseases like Parkinson’s consists in travelling back along the chain of causes; the aim, however, is not to find ultimate causes but to find the most effective points of therapeutic intervention; manipulability is key.) It is now thought that Parkinson’s, like Alzheimer’s, includes the buildup of aggregates of proteins that eventually disable or kill the neurons that contain them. A cascade of further problems ensues. In Parkinson’s the proteins in question are “synucleins”, smallish proteins which, in aberrant forms, tend to stick together. Mitochondrial malfunctions [pdf] are also present that may both cause and be caused by the protein aggregates. As yet there is no cure for either abnormality. Consensus on the chain of causes that issues in Parkinson’s ends here.
What degrades first is the substantia nigra, the “black stuff”, responsible for production and regulation of dopamine. Like other parts of the midbrain, it is very old, and was perhaps already present in the first vertebrates, 500 million years ago. The breakdown of proteins eventually spreads to other areas associated with motor activity and with impulse control, and ultimately to the cortex. Motor symptoms improve upon the administration of levodopa (a dopamine precursor that can pass through the blood-brain barrier, made famous by Oliver Sacks’s Awakenings). But eventually its effects diminish, as the condition of the brain worsens. For nonmotor symptoms there is no established treatment. Nothing is yet known to stop or slow down the progress of the disease, although exercise, especially “forced” exercise, is thought to have some positive effect. I now own a treadmill.
▶For a recent survey on Parkinson’s diagnosis, etiology, and treatment see Nature Outlook (2010) [paylink], and Michael J. Fox’s website.
I will mention two striking perceptual effects of my symptoms. The first is that my perception of spatial relations has changed. Things a block away seem — unsurprisingly — further, no doubt because it requires more effort than it used to to walk five hundred feet. Things within fifty feet or so, on the other hand, feel closer. I say “feel” because I’m referring not to visual perception, not to how things look, but to how close they seem [paylink], and thus how threatening if they are moving toward me or I toward them. The involuntary fear of heights that Hume notes is impervious to reason has become almost overwhelming; the involuntary flinching that occurs if something large looms too quickly now kicks in sooner. Crowds have become more unnerving. Even when I am in the kitchen with only my wife I sometimes stop short three or four feet from her, though I realize even as I stop that there’s no risk of collision.
This is owing, I suspect, to my decreased mobility. It takes effort to turn, effort to bend at the waist, effort to start moving out of the way. My awareness of that — I don’t mean explicit thoughts of being immobile but the feeling of stiffness, of effortful change of posture — seems to have resulted in a recalibration of my “proximity detectors”, and that in turn to altered perceptions of the ambient space and objects within it.
A second effect has again to do with spatial perception. I notice a marked reluctance to reach down. A book on the floor feels farther away. It is as if the perception of something like Gibsonian affordances has been altered, or the locomotive field, the viscosity, of nearby space. The same applies more generally to reaching in general, especially if the thing to be reached is behind me.
A third effect, more cognitive than perceptual, and thankfully infrequent, has occurred when I find myself in a kneeling position on the floor and momentarily unable to rise. The thought that immediately comes to mind is not that I can’t stand up, but that I have forgotten how. Incapacity is refashioned into ignorance.
It would follow, if I had indeed forgotten, that I would now have to learn anew the sequence of acts by which one rises to a standing position. That is indeed what I did this summer as I worked on my gait and balance. One exercise consisted simply in this: from a standing position, lean forward until you start to fall, and (deliberately) take a single step forward to maintain your balance. I was taking several small steps, which is more likely to be ineffective.
Until new habits have worn in, I must plan acts that before were performed “on the fly”, without deliberation. To get off the floor from a kneeling position if I cannot give myself a boost with my arms, I have learned to first set my left foot on the floor in front of me, and then, as I unbend my left left knee, pull up the right leg so that at the end both legs are straight and my feet are flat on the ground. I’ve described the act in Molloy- or Kafka-like detail; in such detail must I construct it. Needless to say doing things thus is slow and inefficient by comparison with the fluent, unreflected doing I was used to. The slowness associated with Parkinson’s has to do not only with the reluctance of the nervous system to respond to one’s intentions, but with the need to substitute plans for long-standing habits.
All this provides further illustration, if any is needed, for the close relation between perception and action argued for by Merleau-Ponty in the 1940s (Phénoménologie de la perception, 1945; see Jean-Luc Petit "La Spatialité originaire du corps propre", Revue de synthèse 124.1 (2003): 139–171) and more recently by Susan Hurley [pdf], Alva Noë, and others. Parkinson’s, in its early stages, has no direct effect on perception (although it may hinder visual perception by affecting the basal ganglia, which control visual saccades). What it does to perception will therefore be by way of its influence on motor control. Early-stage Parkinson’s provides a natural settingf in which to test the so-called ‘enactive hypothesis’. The more general point that loss of motor capacity provides a test has, of course, not gone unnoticed. What I would urge is a more fine-grained analysis of its effects, for example, that the space around one could feel different than before in various ways — with respect to “looming”, for example — that do not consist in its looking different, and that the feel I am trying to articulate — with respect to heights, say — seems to be an amalgam of perceptions, motor inclinations, and emotions.
I see some evidence in my experience also that for certain emotions, notably anxiety, the Jamesian theory may be true, at least in a weak form according to which certain bodily goings-on, though not perhaps necessary, suffice for it to be present. The awkward tension I often feel in my muscles, especially in the abdomen and upper torso, resembles that of anxious anticipation, and it requires concentration not to feel anxious as a result. On the other hand, if the capacity to have emotions depends in part on the capacity to express them, then one can make sense of the impassivity of Parkinson’s patients even without invoking the “dopamine hypothesis” alluded to earlier.
I am sobered by the thought that it was child’s play for my understanding to make intelligible to itself my altered dispositions in terms of more-or-less reasoned preferences. I’ve noticed that to the extent that I’ve become more impulsive (more likely to interrupt, for example), reasons come readily to mind both to explain and to excuse my behavior. The higher capacities seem to operate here in the manner of an overly accommodating servant who manages to make sense of even the most outlandish expressions of his master…