129. Heart rate variability in patients with spinal cord injuries

129. Heart rate variability in patients with spinal cord injuries

e218 Society Proceedings / Clinical Neurophysiology 124 (2013) e189–e223 129. Heart rate variability in patients with spinal cord injuries— L.G. Bon...

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e218

Society Proceedings / Clinical Neurophysiology 124 (2013) e189–e223

129. Heart rate variability in patients with spinal cord injuries— L.G. Bongiovanni, F. Rossini, F. Barbieri, S. Dalla Riva, F. Paluani, L. Fondreschi, F. Brigo, E. De Marchi, S. Monaco (Verona) In spinal cord injury both the level and the extension of the lesions have been related to different response to tilting in Low Frequency (LF) and High Frequency (HF) oscillations of heart rate. To understand the role of sympatho–vagal interaction in such patients, we tried to evaluate, using the LF/HF ratio, the residual possibility in maintaining the cardiovascular homeostasis. 9 subjects with different outcome of traumatic (4) and inflammatory (5) spinal cord involvement, with lesion between C6 and T10, were investigated with power spectral analysis of the blood pressure and heart rate variability in resting condition and during a period of head – up tilt test. The difference between the two conditions was tested using the Wilcoxon signed rank test. In patients with complete ASIA A lesion, the relatively preserved LF activity in resting condition did not increase during tilting, with a parallel decrease of LF/HF ratio. In patients with incomplete lesion (ASIA B, C, D), the LF power of R–R interval showed an inverse relation with the level of the lesion. The LF/HF ratio was partially maintained due to the concomitant adapting HF activity permitting an efficient sympatho–vagal balance. doi:10.1016/j.clinph.2013.06.156

130. Spectral analysis of cardiovascular responses in POTS— L.G. Bongiovanni, F. Barbieri, F. Rossini, A. Demrozi, F. Paluani, L. Fondreschi, G. Cacici, F. Brigo, S. Monaco (Verona) The inability to remain upright without orthostatic hypotension is the typical disabling symptom of Postural Orthostatic Tachycardia Syndrome (POTS), attributed either to the central hyperadrenergic outflow or to the compensatory mechanism after legs and splanchnic blood vessels denervation. To verify this second hypothesis we analyzed the neural autonomic responses to different conditions. 10 patients with POTS and 10 controls were investigated with power spectral analysis of the blood pressure and heart rate variability, in resting condition and during a period of 30 min of head – up tilt test to 60°. The difference between the two conditions was tested using the Wilcoxon signed rank test. No evidence of sympathetic cholinergic and adrenergic failure was found. The most significant and common finding of patients with POTS was a marked increase of the LF/ HF ratio in the power spectrum of the R–R interval in the head – up tilt compared to the reduced values in supine. We did not find an exaggerated pressure response to the Valsalva manoeuvre, but a redistribution of blood flow, due to regional autonomic denervation, was excluded by the preserved increase of blood pressure response during the same test. doi:10.1016/j.clinph.2013.06.157

131. Muscle sympathetic nerve activity during periodic leg movements in sleep in a narcolepsy with cataplexy patient: A microneurographic study—V. Donadio, G. Plazzi, F. Pizza, S. Vandi, V. Leta, R. Liguori (Bologna) Periodic leg movements in sleep (PLMS) are a sleep-related phenomenon with periodic episodes of repetitive stereotypical movements of the lower extremities but the underlying pathogenesis is poorly understood. The aim of this study was to directly record sympathetic outflow by microneurography during PLMS to shed light on the underlying pathogenesis. We recorded muscle sympathetic nerve activity (MSNA) during sleep with and without PLMS in a

woman patient with narcolepsy with cataplexy. The patient underwent nocturnal video-polysomnography with MSNA recording from the peroneal nerve by microneurography. Luckily, MSNA recording site did not change during sleep and it was still preserved also during PLMS. PLMS were evident during early N2 and N3 sleep stages but were absent during subsequently N2 and N3 sleep phases allowing to make a direct comparison of sympathetic activity during the same sleep phase. Sleep phases with PLMS were characterized by a pronounced MSNA increase compared to the same sleep phases without PLMS. Our data demonstrated that sleep phases with PLMS were characterized by a pronounced sympathetic activation. These data suggested that PLMS is not a pure motor phenomenon but it is likely the expression of a generalized increased neuronal excitability during sleep. doi:10.1016/j.clinph.2013.06.158

132. Sympathetic and cardiovascular changes induced by Sodium oxybate treatment in patients with narcolepsy and cataplexy— M.P. Giannoccaro, V. Donadio, G. Plazzi, F. Pizza, S. Vandi, V. Leta, R. Liguori (Bologna) Sodium oxybate (XYREM) is effective on many narcolepsy symptoms but it may also induce a systemic hypertension although the mechanism is unclear. The aim of this study was to elucidate the sympathetic involvement for systemic hypertension induced by Xyrem. We studied 2 hypocretin-deficient narcolepsy with cataplexy patients who underwent microneurographic recording of muscle sympathetic nerve activity (MSNA) from the peroneal nerve with monitoring of blood pressure (BP) and heart rate (HR). The recording was made before and 6 months after Xyrem treatment (6 gr/die). Resting data were 73 bursts/100 heart beats (HB) and 51 b/min for MSNA, 120/85 mmHg for systolic and diastolic BP, 69 beats/min for HR in patient 1; patient 2 showed 79 b/100 HB and 49 b/min for MSNA, 100/65 mmHg for systolic and diastiolic BP and HR 61 beats/min for HR. After 6 months of Xyrem both MSNA and BP increased (patient 1: +15 b/100HB and +12 b/min for MSNA and +40/15 mmHg for BP; patient 2: + 4 b/100HB and +1 b/min for MSNA and +10/10 mmHg for BP) whereas HR showed no significant change. These preliminary data suggested that BP elevation induced by Xyrem could be due to a sympathetic hyperactivity although this conclusion must be supported by additional data. doi:10.1016/j.clinph.2013.06.159

133. Traumatic Bernard–Horner syndrome. Uncoupling of sudomotor and vasoconstrictor activity—A. Ragazzoni, A. Merla, L. Bagnoli (Florence, Chieti) Here we describe a patient with Bernard Horner syndrome who underwent a detailed neurophysiological study with Sympathetic Skin Response and infrared Thermography. One 32-year-old male patient with traumatic complete Bernard Horner syndrome, following neck injury during a motorcycle accident. The patient presented with miosis, ptosis, enophthalmos and anhidrosis of the left hemiface following a trauma of left neck. SSR to electric and acoustic stimuli was absent on the left forehead, but was unremarkable over the right face and the palms. Infrared Thermography revealed hypothermia over the left head and neck. These findings were unchanged 5 months after the trauma. In our patient, traumatic paralysis of sympathetic fibers supplying the head and the neck, led to long-lasting abolition of hemiface sweating associated with increased skin vasoconstriction in the anhidrotic area. The present report points out that sympathetic denervation affects sudomotor cholinergic