• Journal of Yeungnam Medical Science
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• v.22 no.1
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• pp.96-103
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• 2005

The motor recovery mechanism of a 21-year-old male monoparetic patient with cerebral palsy, who had complained of a mild weakness on his right hand since infancy, was examined using functional Magnetic Resonance Imaging (fMRI) and Transcranial Magnetic Stimulation (TMS). The patient showed mild motor impairment on the right hand. MRI located the main lesion on the left precentral knob of the brain. fMRI was performed on this patient as well as 8 control subjects using the Blood Oxygen Level Dependent technique at 1.5 T with a standard head coil. The motor activation task consisted of finger flexionextension exercises at 1 Hz cycles. TMS was carried out using a round coil. The anterior portion of the coil was applied tangentially to the scalp at a 1.0 cm separation. Magnetic stimulation was carried out with the maximal output. The Motor Evoked Potentials (MEPs) from both Abductor Pollicis Brevis muscles (APB) were obtained simultaneously. fMRI revealed that the unaffected (right) primary sensori-motor cortex (SM1), which was centered on precentral knob, was activated by the hand movements of the control subjects as well as by the unaffected (left) hand movements of the patient. However, the affected(right) hand movements of the patient activated the medial portion of the injured precentral knob of the left SM1. The optimal scalp site for the affected (right) APB was located at 1 cm medial to that of the unaffected (left) APB. When the optimal scalp site was stimulated, the MEP characteristics from the affected (right) APB showed a delayed latency, lower amplitude, and a distorted figure compared with that of the unaffected (left) APB. Therefore, the motor function of the affected (right) hand was shown to be reorganized in the medial portion of the injured precentral knob.

• Sleep Medicine and Psychophysiology
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• v.27 no.1
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• pp.24-31
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• 2020

Objectives: Subjective-objective discrepancy of sleep (SODS) is a common symptom and one of the major phenotypes of insomnia. A distorted perception of sleep deficit might be related to abnormal brain reactivity to insomnia-related stimuli. We aimed to investigate differences in brain activation to insomnia-related stimuli vs. general anxiety-inducing stimuli among insomnia patients with SODS, insomnia patients without SODS, and healthy controls (HCs). Methods: All participants were evaluated for subjective sleep status using a sleep diary and questionnaires; occult sleep disorders and objective sleep status were assessed using polysomnography and actigraphy. Task functional magnetic resonance imaging was performed during insomnia-related stimuli (Ins) and general anxiety-inducing stimuli (Gen). Brain reactivity to Ins versus Gen was compared among insomnia with SODS, insomnia without SODS, and HC groups, and a combined insomnia disorder group (ID, insomnia with and without SODS) was also compared with HCs. Results: In the insomnia with SODS group compared to the insomnia without SODS group, the right precuneus and right supplementary motor areas showed significantly increased BOLD signals in response to Ins versus Gen. In the ID group compared to the HC group, the left anterior cingulate cortex showed significantly increased BOLD signals in response to Ins versus Gen. Conclusion: The insomnia with SODS and ID groups showed higher brain activity in response to Ins versus Gen, while this was not observed in the insomnia without SODS and HC groups, respectively. These results suggest that insomnia patients with sleep misperception are more sensitive to sleep-related threats than general anxiety-inducing threats.