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Ataxia
Bradykinesia
Choreoathetosis
Corticobasal Degeneration
Dyskinesias (Paroxysmal)
Dystonia
Essential Tremor
Hereditary Spastic Paraplegia
Huntington's Disease
Multiple System Atrophy
Myoclonus
Parkinson's Disease
Progressive Supranuclear Palsy
Restless Legs Syndrome
Rett Syndrome
Spasticity
Sydenham's Chorea
Tardive Dyskinesia
Tics
Tourette's Syndrome
Tremor
Wilson Disease
 

Electrophysiology (CD and other forms of dystonia)

Electromyography (EMG) is a diagnostic test in which the electrical activity of voluntary (skeletal) muscles is measured at rest and during voluntary action. In patients with dystonia, EMG may reveal little or no activity at rest or prolonged bursts of electrical activity with overflow to muscles that are not normally involved. More specifically, abnormal EMG patterns at rest may include any of the following:

  • Relatively long spasms that result in abnormal, sustained postures
  • Repetitive bursts of electrical activity that are mid-range in length (i.e., approximately 200 to 500 milliseconds). (Note: EMG bursts usually do not last longer than approximately 100 milliseconds.)
  • Irregular bursts or jerks that are short (i.e., less than 100 ms), resembling those associated with myoclonus.

In addition, any of the above EMG patterns may also occur with voluntary movements. Patients with dystonia usually have difficulty selectively initiating movement of appropriate muscles required for certain voluntary actions and experience simultaneous contraction of antagonist muscles. In addition, there is a decrease in or loss of the active inhibition of antagonist muscles that normally occurs with voluntary contraction of agonist muscles. Some researchers suggest that decreased inhibition leading to an "overflow" of movement may result from loss of inhibition at the level of the cerebral cortex, brainstem, and spinal cord via the basal ganglia and its pathways. (The basal ganglia cells of origin of the inhibitory pathways are under the control of the activities of the neurotransmitter dopamine.) Such a theory may potentially explain how dystonia may result from or be triggered by different mechanisms. According to such a theory, significant loss of inhibition potentially leading to dystonia may result from lesions of certain areas of the brain; specific genetic abnormalities; or a genetic predisposition that may be triggered by environmental factors, such as abnormal sensory input resulting from repeated use and/or trauma of the affected body part.

There is some evidence suggesting that certain abnormalities in the brain's ability to process sensory information may also play some role in causing dystonia by altering brain motor control. According to researchers, this possibility is supported by various factors, including the "sensory tricks" observed in many patients with cervical dystonia and the fact that some patients may develop certain sensory symptoms prior to the development of CD. Further research is needed to learn more about the potential causative role of loss of inhibition, sensory dysfunction, peripheral trauma, and/or other mechanisms in dystonia.