Electrophysiological studies are useful in identify hyperkinetic movement disorders, particularly tremors, myoclonus and differentiate functional from organic disorders. They can provide objective and quantifiable assessments of movement disorders. The most commonly used methods are surface electromyography, electroencephalography, accelerometry and transcranial magnetic stimulation (TMS). In doctoral thesis, we focused on the clinical and electrophysiological characteristics of tremor and myoclonus in various diseases that have not been studied so far.
In the first study, we examined the characteristics of functional tremor (FT) that could serve as predictive factors for response to treatment with repetitive TMS (rTMS). We demonstrated that FT patients, who manifested more cognitive and motor distractibility responded better to rTMS treatmen. The likely explanation is the between-subjects differences on the reliance of FTr generation on explicit vs. implicit motor network. Based on our results, neurologists could more easily decide which FT patients are suitable candidates for treatment.
In the second study, we examined the frequency of myoclonus and tremor of the upper limbs following an epileptic seizure and defined their pathophysiology. Tremor occurred in 33% of patients. Based on electrophysiological results, we found that 30% of patients had a mechanical-reflex type of tremor, which could be a consequence of muscle fatigue after the epileptic seizure. 70% of patients had a central-type tremor, which is likely independent of the seizure itself. Myoclonus occurred in 16% of patients. It was not a result of elevated ammonia levels in the blood. So it was not caused by a metabolic disorder. Patients with myoclonus had associated Todd's paresis more frequently. Electrophysiological studies revealed that myoclonus was of cortical origin which reflects hyperexcitability of the motor cortex. Our study indicate that, in the postictal period, both excitatory and inhibitory processes are simultaneously present in the motor cortex, with inhibition predominating. Excessive excitability after the seizure manifests as cortical myoclonus. The predominance of inhibitory processes is evident from the negative myoclonus and from the occurrence of Todd's paresis.
In the third study, we investigated the clinical and neurophysiological characteristics of myoclonus in toxic-metabolic encephalopathies (TME). Electrophysiological studies revealed that the negative myoclonus in these patients had a subcortical origin. Using TMS measurements, we found that TME is associated with: 1) reduced corticospinal excitability, with a shift in the balance between inhibition and facilitation towards enhanced inhibition; 2) an imbalance between GABA-A and GABA-B intracortical inhibition, with increased GABA-B and reduced GABA-A inhibition; 3) reduced cholinergic inhibition. Changes in cortical excitability correlate with a decline in cognitive functions.
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