What follows is a footnote from Brad whose comments were posted on my most recent entry,
Robert Rodgers, Ph.D.
Robert, I apologize for not including this footnote. Not being a professional researcher and being academically lazy, I failed to reference my source, so I see why you had to say I “speculate”. The date of this paper is 2006. Of course, further research would be entailed to corroborate the statement, but my point was that traditional doctors and neurologists don’t do their research either, or they just don’t care to share it with laypersons and/or patients. The relationship is paternalistic.
Unless you go to public research symposiums (such as those occasionally offered by the MJFF) your fifteen minute office visit is not going to get into a detailed analysis of your symptoms or their etiology. When I asked questions regarding my toe curling (which is only triggered by bicycling) of my family doctor, a sports medicine doctor, and a neurologist, all three merely shrugged and offered no explanations or further interest in the matter. Even after PD fully emerged, it was considered a secondary symptom and in any event it is controlled by L-dopa, so the course of treatment is the same.
An abstract of the article Brad refers above follows:
Eduardo Tolosa1 and Yaroslau Compta1 (2006), Neurology Service, Institut de Neurociències, Hospital Clínic i Universitari de Barcelona, c./ Villarroel 170, 08036 Barcelona, Catalonia, Spain
Dystonia can occasionally be found in idiopathic Parkinson’s disease. It is very uncommon in untreated patients and is more frequently seen as a complication of its treatment. In this review, the various types of dystonia occurring in PD, the differential diagnosis with other parkinsonian syndromes associated with dystonia and treatments available are revised.
Dystonia unrelated to treatment can be typical (blepharospasm, torticollis), atypical (parkinsonian writer’s cramp, camptocormia, anismus), or occurring in early-onset Parkinson disease (the so-called kinesigenic foot dystonia, considered a hallmark of earlyonset Parkinson’s disease). Early and prominent dystonia in untreated patients with parkinsonism should raise the suspicion of other entities other than Parkinson’s disease, such as progressive supranuclear palsy, multiple system atrophy or corticobasal degeneration.
In patients on chronic dopaminergic treatment, peak-dose dystonia, diphasic dystonia and off-dystonia can be seen. The later constitutes the major dystonic feature of chronic levodopa therapy, and a wide variety of strategies are available to manage this complication. Among them, deep brain stimulation of the subthalamic nucleus has proved to be the most effective one.
Dystonic reactions (mainly involving oculomotor cranial nerves and limbs) in operated patients (especially carriers of deep brain stimulation (DBS) devices) are increasingly being reported, constituting a new type of dystonia in patients with Parkinson’s disease: dystonia linked to surgical treatment.