Simultaneous EMG-fMRI during startle inhibition in monosymptomatic enuresis--an exploratory study
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Updated: May 18, 2026

Reliable Acquisition of Electroencephalography Data during Simultaneous Electroencephalography and Functional MRI
Published on: March 19, 2021
Sebastian Schulz-Juergensen1, David Wunberg, Stephan Wolff
1Department of General Pediatrics, University Hospital Schleswig-Holstein, Campus Kiel, Arnold-Heller-Strasse 3, Haus 9, 24105 Kiel, Germany. schulz-juergensen@pediatrics.uni-kiel.de
Insights
Monosymptomatic enuresis (ME) may stem from impaired cortical control. Healthy children showed stronger prefrontal cortex activation to inhibit startle reflexes than those with ME, suggesting a link to this maturational disorder.
Area of Science:
- Neuroscience
- Pediatric Neurology
- Sleep Medicine
Background:
- Monosymptomatic enuresis (ME) is increasingly viewed as a central nervous system maturational disorder.
- Reduced prepulse inhibition (PPI) of the startle reflex is observed in children with enuresis.
- The precise neural level (brainstem vs. cortical) of abnormal PPI in enuresis remains unclear.
Purpose of the Study:
- To investigate the cortical and brainstem mechanisms underlying abnormal PPI in children with monosymptomatic enuresis.
- To differentiate between brainstem and cortical inhibitory deficits in ME pathogenesis.
- To explore the role of prefrontal cortex activation in the control of startle reflexes in ME.
Main Methods:
- Simultaneous recording of electromyography (EMG) and functional magnetic resonance imaging (fMRI) in nine children with ME and ten healthy controls.
- Experimental paradigm involving acoustic startle stimulation with and without prepulse inhibition.
- fMRI data analysis using multiple regression and parametric modulation with startle amplitudes.
Main Results:
- No measurable PPI was detected in either group within the MRI scanner.
- Hemodynamic changes in response to startle stimuli were similar across acoustic and prefrontal cortical areas in both groups.
- Healthy children exhibited a stronger correlation between startle amplitude and BOLD signal changes in the anterior cingulate cortex during PPI conditions compared to ME patients, indicating greater prefrontal cortex engagement for inhibition.
Conclusions:
- Methodological challenges may affect PPI recordings within MRI scanners.
- Results suggest that impaired high-level cortical control mechanisms in the prefrontal cortex are implicated in the pathogenesis of monosymptomatic enuresis.
- This highlights the potential role of prefrontal cortex dysfunction in the lack of arousal and inhibited micturition reflex seen in ME.
Abstract:
Evidence is growing that monosymptomatic enuresis (ME) is a maturational disorder of the central nervous system with a lack of arousal and lacking inhibition of the micturition reflex. Previous studies have shown a significant reduction of prepulse inhibition (PPI) of startle in children with enuresis. However, it is still unclear whether the abnormal PPI in enuresis is based on an inhibitory deficit at brainstem or cortical level. Nine children with ME and ten healthy children were investigated using simultaneous recording of EMG from the M. orbicularis oculi and functional MRI. The experimental paradigm consisted of acoustic startle stimulation, with startle-alone stimuli and prepulse-startle combinations. Functional MRI data were processed using multiple regression and parametric modulation with startle amplitudes as a parameter. Neither patients with enuresis nor healthy children revealed measurable PPI in the MRI scanner. Startle stimuli caused equal hemodynamic changes in the acoustic cortex, medial prefrontal and orbitofrontal cortex in both groups. The amplitude of startle correlated with more prominent BOLD signal changes in the anterior cingulate cortex in healthy subjects than in patients with ME. This pronounced frontal activation in healthy controls was related to the PPI condition, indicating that the prefrontal cortex of healthy children was activated more strongly to inhibit startle than in patients with ME. In conclusion, apart from the possibility that recordings of PPI inside the MRI scanner may be compromised by methodological problems, the results of this study suggest that high cortical control mechanisms at the prefrontal level are relevant for the pathogenesis of ME.
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