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Intermittent Autonomic Disorders and Emotion: A Two-way Street?
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Abstracts / Autonomic Neuroscience: Basic and Clinical 192 (2015) 56–141
evaluate whether differential loss of myelinated and unmyelinated fibers occurs in T1D and T2D, we studied 9 patients with T1D, 11 patients with T2D and 10 age-matched control patients with nerve conduction studies, autonomic function tests, skin biopsy of distal and proximal leg (hairy skin) and glabrous skin biopsy of the index finger. T1D and T2D patients had similar HgA1c, neuropathy exam and symptom scores. T1D patients had longer length of diabetes and lower BMI compared to T2D patients. T1D patients had significant loss of myelinated and non-myelinated fibers with lower myelinated fiber densities, intra-epidermal nerve fiber density (IENFD) and composite autonomic system score (CASS). T2D patients had no significant loss of myelinated fibers (20.3 vs. 21.7 myelinated fibers /mm for healthy controls), but had significant decrease in non-myelinated fibers as evidenced by decreased IENFD and abnormal CASS. T1D and T2D patients had similar intraepidermal nerve fiber density at the distal leg, and similar sweat volumes using quantitative sudomotor axon reflex testing. T1D patients had a trend towards worse cardiac autonomic function with CASS score mean of 3 vs 2 for T2D patients. These results suggest that focus on distal, nonmyelinated fiber function and pathology may be more sensitive for T2D patients than traditional myelinated fiber-based measures of diabetic neuropathy. doi:10.1016/j.autneu.2015.07.437
P21.14 Eyeball pressure stimulation causes paradox sympathetic activation in moderate-severe post traumatic brain injury patients R. Wanga, T. Intravootha, S. Moellera, J. Koehna, M. Liua, F. Canavesea, F. Aurnhammerb, H. Marthola, M.J. Hilza a Department of Neurology, University of Erlangen-Nuremberg, Erlangen, Germany b Department of Internal Medicine, Waldkrankenhaus St. Marien GmbH, Erlangen, Germany Background: Long-term mortality is increased in patients with a history of traumatic brain injury (TBI). Pathophysiology is unknown but might be related to central autonomic dysfunction compromising cardiovascular control. In patients with a history of mild TBI, we found compromised cardiovascular responses to parasympathetic challenge by eyeball-pressure-stimulation (EPS). We hypothesize that EPS also yields abnormal responses in patients with a history of moderate-severe TBI. Methods: In 51 patients with a history of moderate-severe-TBI (32.71 ± 10.49 years, 43.12 ± 33.35 months post-injury, GCS 9.29 ± 4.49), and 30 controls (29.13 ± 9.77 years), we recorded respiration, RR-intervals (RRI), systolic and diastolic blood-pressure (BPsys, BPdia), before and during monocular EPS (120 seconds; 30 mmHg), using an ophthalmologic ocular-pressuredevice. We calculated spectral-powers of mainly sympathetic low (LF: 0.04-0.15Hz) and parasympathetic high (HF: 0.15-0.5Hz) frequency RRI-fluctuations, sympathetically mediated LF-powers of BPsys, normalized RRI-LF- (LFnu-RRI-) powers, normalized RRI-HFpowers (HFnu-RRI-powers), and RRI-LF/HF-ratios. We compared parameters between groups before and during EPS by RANOVA with post-hoc analysis (significance: p b 0.05). Results: At rest, LF-BPsyspowers were lower in patients than controls (11.31 ± 13.23 vs. 15.16 ± 9.56, p = 0.011). During EPS, only controls significantly increased RRIs and HFnu-RRI-powers, and decreased LF-RRI-powers, LFnu-RRI-powers, RRI-LF/HF-ratios, and LF-BPsys-powers. In postTBI-patients, EPS only increased BPsys (132.00 ± 13.13 vs. 129.22 ± 14.52 mmHg, p b 0.001) but changed no other parameter. Conclusions: Already at rest, autonomic BP-modulation is compromised in moderate-severe post-TBI-patients. During EPS, moderate-severe post-TBI-patients fail to activate parasympathetic cardiovascular
modulation but mount a paradox sympathetic activation. This central-autonomic dysregulation might contribute to cardiovascular fatalities. Acknowledgement: The study was partially funded by the International-Brain-Research-Foundation, IBRF, Flanders, NJ, USA. doi:10.1016/j.autneu.2015.07.441
P21.15 Intermittent Autonomic Disorders and Emotion: A Two-way Street? Andrew P Owensa,b, David A. Lowc, Hugo D. Critchleyd,e,f, Christopher J. Mathiasa,b,g,h a Institute of Neurology, University College London b National Hospital Neurology and Neurosurgery, UCL NHS Trust, London c School of Sport and Exercise Sciences, Liverpool John Moores University, Liverpool d Psychiatry, Brighton and Sussex Medical School, Brighton e Sussex Partnership NHS Foundation Trust, Brighton f Sackler Centre for Consciousness Science, University of Sussex g The Lindo Wing, Imperial College NHS Healthcare Trust h Hospital of St John & St Elizabeth, London, UK Background: Although psychiatric patients may report physiological symptoms similar to postural tachycardia syndrome (PoTS), autonomically (neurally) mediated syncope (AMS) or essential hyperhidrosis (EH), autonomic diagnostic criteria are rarely met [1, 2]. However, cognitiveaffective symptoms are common in AMS, PoTS, and EH [3, 4]. Aim: To investigate psychological symptoms in EH, PoTS and AMS. Methods: 22 healthy controls, 25 EH, 30 PoTS and 25 AMS patients completed the Anxiety Sensitivity Index, Beck Depression Inventory, Body Vigilance Scale, Cardiac Anxiety Scale, The Self-consciousness Scale, Childhood Traumatic Events Scale and State Anxiety Inventory. Results: Depression was most attributable somatic and cognitive factors, e.g., poor sleep (PoTS p = .008, AMS p = .020, EH p = .002), indecisiveness (PoTS p = .000, AMS p = .003, EH p = .001), concentration difficulty (PoTS p = .000, AMS p = .008, EH p = .005). Anxiety was most attributable to somatic hypervigilance of autonomic symptoms similar to physical manifestations of anxiety, e.g., fear of fainting (PoTS p = .034, AMS p = .022, EH p = .047), sweaty/clammy hands (EH, p = .000; PoTS, p = .014, AMS, p = .021), avoiding physical exertion (EH, p = .002, PoTS, p = .001, AMS=, p = .001). Conclusions: Neither social anxiety nor trauma were common in AMS, EH or PoTS. Rather than being trait-like or neurotic phenomena, cognitive-affective symptoms typically related to the pathophysiology of patients’ respective autonomic conditions. However, PoTS patients reported broader depressive symptoms and were sensitive to multifactorial cardio-thoracic, neuropathic and thermoregulatory symptoms common in PoTS phenotypes, which may elucidate the broader spectrum of cognitive-affective symptomatology in PoTS. These findings support a contributing role of autonomic dysfunction to PoTS, EH and AMS psychological symptoms. 1. Ruchinskas, R.A., et al., The relationship of psychopathology and hyperhidrosis. Br J Dermatol, 2002. 147(4): p. 733-5. 2. Lkhagvasuren, B., et al., Prevalence of postural orthostatic tachycardia syndrome in patients with psychiatric disorders. Psychother Psychosom, 2011. 80(5): p. 308-9. 3. Eccles, J.A., et al., Neurovisceral phenotypes in the expression of psychiatric symptoms. Front Neurosci, 2015. 9: p. 4. Mathias, C.J., et al., Postural tachycardia syndrome–current experience and concepts. Nat Rev Neurol, 2012. 8(1): p. 22-34. doi:10.1016/j.autneu.2015.07.442
Abstracts / Autonomic Neuroscience: Basic and Clinical 192 (2015) 56–141
evaluate whether differential loss of myelinated and unmyelinated fibers occurs in T1D and T2D, we studied 9 patients with T1D, 11 patients with T2D and 10 age-matched control patients with nerve conduction studies, autonomic function tests, skin biopsy of distal and proximal leg (hairy skin) and glabrous skin biopsy of the index finger. T1D and T2D patients had similar HgA1c, neuropathy exam and symptom scores. T1D patients had longer length of diabetes and lower BMI compared to T2D patients. T1D patients had significant loss of myelinated and non-myelinated fibers with lower myelinated fiber densities, intra-epidermal nerve fiber density (IENFD) and composite autonomic system score (CASS). T2D patients had no significant loss of myelinated fibers (20.3 vs. 21.7 myelinated fibers /mm for healthy controls), but had significant decrease in non-myelinated fibers as evidenced by decreased IENFD and abnormal CASS. T1D and T2D patients had similar intraepidermal nerve fiber density at the distal leg, and similar sweat volumes using quantitative sudomotor axon reflex testing. T1D patients had a trend towards worse cardiac autonomic function with CASS score mean of 3 vs 2 for T2D patients. These results suggest that focus on distal, nonmyelinated fiber function and pathology may be more sensitive for T2D patients than traditional myelinated fiber-based measures of diabetic neuropathy. doi:10.1016/j.autneu.2015.07.437
P21.14 Eyeball pressure stimulation causes paradox sympathetic activation in moderate-severe post traumatic brain injury patients R. Wanga, T. Intravootha, S. Moellera, J. Koehna, M. Liua, F. Canavesea, F. Aurnhammerb, H. Marthola, M.J. Hilza a Department of Neurology, University of Erlangen-Nuremberg, Erlangen, Germany b Department of Internal Medicine, Waldkrankenhaus St. Marien GmbH, Erlangen, Germany Background: Long-term mortality is increased in patients with a history of traumatic brain injury (TBI). Pathophysiology is unknown but might be related to central autonomic dysfunction compromising cardiovascular control. In patients with a history of mild TBI, we found compromised cardiovascular responses to parasympathetic challenge by eyeball-pressure-stimulation (EPS). We hypothesize that EPS also yields abnormal responses in patients with a history of moderate-severe TBI. Methods: In 51 patients with a history of moderate-severe-TBI (32.71 ± 10.49 years, 43.12 ± 33.35 months post-injury, GCS 9.29 ± 4.49), and 30 controls (29.13 ± 9.77 years), we recorded respiration, RR-intervals (RRI), systolic and diastolic blood-pressure (BPsys, BPdia), before and during monocular EPS (120 seconds; 30 mmHg), using an ophthalmologic ocular-pressuredevice. We calculated spectral-powers of mainly sympathetic low (LF: 0.04-0.15Hz) and parasympathetic high (HF: 0.15-0.5Hz) frequency RRI-fluctuations, sympathetically mediated LF-powers of BPsys, normalized RRI-LF- (LFnu-RRI-) powers, normalized RRI-HFpowers (HFnu-RRI-powers), and RRI-LF/HF-ratios. We compared parameters between groups before and during EPS by RANOVA with post-hoc analysis (significance: p b 0.05). Results: At rest, LF-BPsyspowers were lower in patients than controls (11.31 ± 13.23 vs. 15.16 ± 9.56, p = 0.011). During EPS, only controls significantly increased RRIs and HFnu-RRI-powers, and decreased LF-RRI-powers, LFnu-RRI-powers, RRI-LF/HF-ratios, and LF-BPsys-powers. In postTBI-patients, EPS only increased BPsys (132.00 ± 13.13 vs. 129.22 ± 14.52 mmHg, p b 0.001) but changed no other parameter. Conclusions: Already at rest, autonomic BP-modulation is compromised in moderate-severe post-TBI-patients. During EPS, moderate-severe post-TBI-patients fail to activate parasympathetic cardiovascular
modulation but mount a paradox sympathetic activation. This central-autonomic dysregulation might contribute to cardiovascular fatalities. Acknowledgement: The study was partially funded by the International-Brain-Research-Foundation, IBRF, Flanders, NJ, USA. doi:10.1016/j.autneu.2015.07.441
P21.15 Intermittent Autonomic Disorders and Emotion: A Two-way Street? Andrew P Owensa,b, David A. Lowc, Hugo D. Critchleyd,e,f, Christopher J. Mathiasa,b,g,h a Institute of Neurology, University College London b National Hospital Neurology and Neurosurgery, UCL NHS Trust, London c School of Sport and Exercise Sciences, Liverpool John Moores University, Liverpool d Psychiatry, Brighton and Sussex Medical School, Brighton e Sussex Partnership NHS Foundation Trust, Brighton f Sackler Centre for Consciousness Science, University of Sussex g The Lindo Wing, Imperial College NHS Healthcare Trust h Hospital of St John & St Elizabeth, London, UK Background: Although psychiatric patients may report physiological symptoms similar to postural tachycardia syndrome (PoTS), autonomically (neurally) mediated syncope (AMS) or essential hyperhidrosis (EH), autonomic diagnostic criteria are rarely met [1, 2]. However, cognitiveaffective symptoms are common in AMS, PoTS, and EH [3, 4]. Aim: To investigate psychological symptoms in EH, PoTS and AMS. Methods: 22 healthy controls, 25 EH, 30 PoTS and 25 AMS patients completed the Anxiety Sensitivity Index, Beck Depression Inventory, Body Vigilance Scale, Cardiac Anxiety Scale, The Self-consciousness Scale, Childhood Traumatic Events Scale and State Anxiety Inventory. Results: Depression was most attributable somatic and cognitive factors, e.g., poor sleep (PoTS p = .008, AMS p = .020, EH p = .002), indecisiveness (PoTS p = .000, AMS p = .003, EH p = .001), concentration difficulty (PoTS p = .000, AMS p = .008, EH p = .005). Anxiety was most attributable to somatic hypervigilance of autonomic symptoms similar to physical manifestations of anxiety, e.g., fear of fainting (PoTS p = .034, AMS p = .022, EH p = .047), sweaty/clammy hands (EH, p = .000; PoTS, p = .014, AMS, p = .021), avoiding physical exertion (EH, p = .002, PoTS, p = .001, AMS=, p = .001). Conclusions: Neither social anxiety nor trauma were common in AMS, EH or PoTS. Rather than being trait-like or neurotic phenomena, cognitive-affective symptoms typically related to the pathophysiology of patients’ respective autonomic conditions. However, PoTS patients reported broader depressive symptoms and were sensitive to multifactorial cardio-thoracic, neuropathic and thermoregulatory symptoms common in PoTS phenotypes, which may elucidate the broader spectrum of cognitive-affective symptomatology in PoTS. These findings support a contributing role of autonomic dysfunction to PoTS, EH and AMS psychological symptoms. 1. Ruchinskas, R.A., et al., The relationship of psychopathology and hyperhidrosis. Br J Dermatol, 2002. 147(4): p. 733-5. 2. Lkhagvasuren, B., et al., Prevalence of postural orthostatic tachycardia syndrome in patients with psychiatric disorders. Psychother Psychosom, 2011. 80(5): p. 308-9. 3. Eccles, J.A., et al., Neurovisceral phenotypes in the expression of psychiatric symptoms. Front Neurosci, 2015. 9: p. 4. Mathias, C.J., et al., Postural tachycardia syndrome–current experience and concepts. Nat Rev Neurol, 2012. 8(1): p. 22-34. doi:10.1016/j.autneu.2015.07.442