Originally Posted by efuller
So, you've got some abnormal muscle firing. You don't mention any abnormal neurological tests. I can't think of any abnormal findings that would correlate with this specific of a dystonia.
Thinking of the neurological wiring on this, It's hard to imagine a neurolgical lesion that would cause just this. It seems that CNS pain avoidance is the best explanation of what your seeing. Did you say that he was able to relax it during the non weight bearing exam?
One could say, "see how well walking like that prevents the pain." It seems very unlikely that walking like that would cause the medial arch to hurt.
Thanks for your thoughts.
I had a chat to the patient's pediatrician yesterday; he agreed to review for further neurological evaluation. My basic tests for muscle strength and sensory changes were normal; I did not go beyond this because I believe he needs a more expert workup than I can provide to rule out my concerns
Yes relaxation occurs non weight-bearing.
Constant tension of FHL, plantar aponeurosis or plantar ligaments caused by EHL contraction might cause mild inner longitudinal arch pain. Although they are plausible mechanisms for potential pain generation I doubt true in this case.
There are a couple of examples in the literature of EHL focal dystonia treated with botox when causing problems - currently that does seem indicated in this case to me, patient has mild very episodic inner longitudinal arch pain which resolves wearing shoes.
About wiring; I find the explanation below from wiki helpful and seems to fit the presentation.
The cause of dystonia is not yet precisely understood. Misfiring of neurons in the sensorimotor cortex, a thin layer of neural tissue covering the brain, is thought to cause contractions. The source of this misfiring may be a result of impaired inhibitory mechanisms during muscle contraction. When the brain tells a given muscle to contract, it simultaneously silences muscles that would oppose the intended movement. In dystonia, it appears that the ability of the brain to inhibit the surrounding muscles is impaired leading to loss of selectivity.
Furthermore, the sensorimotor cortex is organized as discrete "maps" of the human body. Under normal conditions, each body part (such as individual fingers) occupies a distinct area on these cortical maps.
In dystonia, these maps lose their distinct borders and overlap occurs.
Exploration of this initially involved over-training particular finger movements in non-human primates which resulted in the development of focal hand dystonia. Examination of the primary somatosensory cortex in the trained animals showed grossly distorted representations of the maps pertaining to the fingers when compared to the untrained animals. Additionally, these maps in the dystonic animals had lost the distinct borders that were noted in the untrained animals. Imaging studies in humans with focal dystonia have confirmed this finding. Also, synchronous afferent stimulation of peripheral muscles induces organizational changes in motor representations, characterized both by an increase in map size of stimulated muscles and a reduction in map separation, as assessed using transcranial magnetic stimulation.
The cross-connectivity between areas that are normally segregated in the sensory cortex may prevent normal sensorimotor feedback and so contribute to the observed co-contraction of antagonist muscle groups, and inappropriately timed and sequenced movements that underlie the symptoms of focal dystonia.
It is hypothesized that a deficit in inhibition caused by a genetically mediated loss of inhibitory interneurons may be the underlying cause of the deficits observed in dystonia.
While usually painless, in some instances the sustained contraction and abnormal posturing in dystonia may cause pain.
Focal dystonia is generally "task specific," meaning that it is only problematic during certain activities.
So to speculate on this
through swing the extensors are functioning normally
they don't turn off during stance after initial contact as expected - they fire again through swing . .. . . etc
when resting there is no motor impulse - tone diminishes and foot relaxes
this is different from an UMN lesion which causes permanent loss of inhibition such as in CVA.
Does this make diagnosis of Focal dystonia more persuasive now?
I cant see how you could you test to rule out this phenomena - if that is true then diagnosis would be by ruling other explanations . . . including yours . .. which so far I feel reasonably confident about.
Foot and Ankle Clinic
1365 Grant Ave.
Winnipeg Manitoba R3M 1Z8
phone  837 FOOT (3668)
fax  774 9918