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  • Title: Motor evoked potentials (MEP) and evoked pressure curves (EPC) from the urethral compressive musculature (UCM) by functional magnetic stimulation in healthy volunteers and patients with neurogenic incontinence.
    Author: Schmid DM, Curt A, Hauri D, Schurch B.
    Journal: Neurourol Urodyn; 2005; 24(2):117-27. PubMed ID: 15616965.
    Abstract:
    AIMS: The aim of this study is to assess neurogenic lesions of the somatomotor efferent nervous pathway to the urethral compressive musculature (UCM) by means of motor evoked potentials (MEP) and simultaneously recorded evoked pressure curves (EPC). METHODS: Nine healthy subjects and 33 patients (15 spinal cord injury, 14 cauda equina lesion, and 4 multiple sclerosis (MS)) with neurogenic urinary incontinence were prospectively examined by means of urodynamics and electrophysiology. MEP responses from the UCM were evoked after transcranial (tc) and lumbosacral (ls) single pulse magnetic stimulation. A ratio out of tx/ls latencies was calculated to distinguish between central (i.e., spinal) and peripheral lesions. The mechanical UCM pressure responses (=EPC) were recorded simultaneously with electromyographic (EMG) recordings using a microtip pressure transducer catheter with integrated bipolar surface electrodes. RESULTS: In nine healthy subjects the central latency was 19.0 msec, the peripheral latency was 4.25 msec, and the ratio was 4.4. In patients with incomplete spinal cord lesion the central latency was significantly delayed (22.7 msec), whereas the peripheral responses were normal. The ratio (5.5) was increased. Thirteen of these 15 patients suffered from neurogenic incontinence. Patients with a complete spinal lesion showed no UCM reaction after tc stimulation, whereas peripheral responses were normal. Patients with MS showed significantly prolonged central latencies (25.5 msec). The increased ratio of 6.0 indicated a spinal lesion. Ten patients with incomplete cauda equina lesions and urinary incontinence had normal central latencies but prolonged peripheral latencies of 6.7 msec. The ratio of 3.4 indicated a lesion of the sacral caudal roots. In patients with complete cauda injury neither central nor peripheral responses could be evoked. Tc evoked mechanical pressure responses (i.e., contractions) from the UCM could only be recorded in intact or incompletely injured spinal and peripheral motor nervous pathways, whereas they could be evoked after ls stimulation only in cases with partially preserved sacral caudal roots independent of a spinal lesion. CONCLUSIONS: MEP and EPC from the UCM proved to be a well tolerated disgnostic tool in patients with neurogenic incontinence that distinguished central and peripheral lesions of the motor efferent pathways to the UCM.
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