Your browser doesn't support javascript.
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 209
Filtrar
2.
BMJ Case Rep ; 12(6)2019 Jun 11.
Artigo em Inglês | MEDLINE | ID: mdl-31189542

RESUMO

Spinal cord injury (SCI) is associated with a range of secondary health issues. Altered neurological function can complicate diagnosis, which may have serious consequences. Here we present the case of a tetraplegic person presenting with confusion and bradycardia. Initial testing revealed severe hyponatraemia (sodium 96 mmol/L) and ST elevation associated with labile blood pressure. Delayed further investigation identified sigmoid volvulus-endoscopic decompression led to resolution of haemodynamic lability and a diagnosis of autonomic dysreflexia. Low mood and poor documentation in the community were found to contribute to poor compliance with an established bowel management plan. Inpatient care involved electrolyte correction and establishment of regular bowel motions. The patient was discharged at baseline neurology with psychological support. This case highlights poor awareness of the secondary health issues affecting those with SCI and the complex relationship between mental and physical health.


Assuntos
Disreflexia Autonômica/fisiopatologia , Hiponatremia/fisiopatologia , Quadriplegia/fisiopatologia , Traumatismos da Medula Espinal/fisiopatologia , Adulto , Disreflexia Autonômica/etiologia , Humanos , Hiponatremia/etiologia , Quadriplegia/etiologia , Traumatismos da Medula Espinal/complicações
3.
Int J Mol Sci ; 20(10)2019 May 18.
Artigo em Inglês | MEDLINE | ID: mdl-31109053

RESUMO

Cognitive impairment following spinal cord injury (SCI) has received considerable attention in recent years. Among the various systemic effects of SCI that contribute towards cognitive decline in this population, cardiovascular dysfunction is arguably one of the most significant. The majority of individuals with a cervical or upper-thoracic SCI commonly experience conditions called orthostatic hypotension and autonomic dysreflexia, which are characterized by dangerous fluctuations in systemic blood pressure (BP). Herein, we review the potential impact of extreme BP lability on vascular cognitive impairment (VCI) in individuals with SCI. Albeit preliminary in the SCI population, there is convincing evidence that chronic hypotension and hypertension in able-bodied individuals results in devastating impairments in cerebrovascular health, leading to VCI. We discuss the pertinent literature, and while drawing mechanistic comparisons between able-bodied cohorts and individuals with SCI, we emphasize the need for additional research to elucidate the mechanisms of cognitive impairment specific to the SCI population. Lastly, we highlight the current and potential future therapies to manage and treat BP instability, thereby possibly mitigating VCI in the SCI population.


Assuntos
Pressão Sanguínea , Vasos Sanguíneos/fisiopatologia , Reflexo Anormal , Traumatismos da Medula Espinal/fisiopatologia , Animais , Disreflexia Autonômica/etiologia , Disreflexia Autonômica/fisiopatologia , Disreflexia Autonômica/terapia , Humanos , Hipotensão Ortostática/fisiopatologia , Hipotensão Ortostática/terapia , Traumatismos da Medula Espinal/etiologia , Traumatismos da Medula Espinal/terapia
4.
Exp Neurol ; 311: 173-181, 2019 01.
Artigo em Inglês | MEDLINE | ID: mdl-30315807

RESUMO

Autonomic dysreflexia (AD), a syndrome caused by loss of supraspinal control over sympathetic activity and amplified vascular reflex upon sensory stimuli below injury level, is a major health problem in high-level spinal cord injury (SCI). After supraspinal sympathetic control of the vasculature below the lesion is lost, the renin-angiotensin system (RAS) is thought to be involved in AD by regulating blood pressure and vascular reactivity. In this study, we aimed to assess the role of different RAS receptors during AD following SCI. Therefore, we induced AD by colorectal distention (CRD) in wild-type mice and mice deficient in the RAS components angiotensin (Ang) II type 1a receptor (AT1a) (Agtr1a-/-) and Ang-(1-7) receptor Mas (Mas-/-) four weeks after complete transection of spinal cord at thoracic level 4 (T4). Systemic blood pressure measurements and wire myography technique were performed to assess hemodynamics and the reactivity of peripheral arteries, respectively. CRD increased mean arterial blood pressure (MAP) and decreased heart rate (HR) in all three animal groups. However, we found less increases in MAP in Mas-/- mice compared to control mice after CRD, whereas AT1a deficiency did not affect the hemodynamic response. We found that the reactivity of wild-type and Mas-/- mesenteric arteries, which are innervated from ganglia distal but close to thoracic level T4, was diminished in response to Ang II in AD after T4-SCI, but this difference was not observed in the absence of AT1a receptors. CRD did not influence the reactivity of femoral arteries which are innervated from ganglia more distal to thoracic level T4, in response to Ang II in AD. In conclusion, we identified a specific role of the Ang-(1-7) receptor Mas in regulating the systemic blood pressure increase in AD in T4-SCI mice. Furthermore, AT1a signaling is not involved in this hemodynamic response, but underlies increased vascular reactivity in mesenteric arteries in response to Ang II, where it may contribute to adaptive changes in regional blood flow.


Assuntos
Disreflexia Autonômica/metabolismo , Disreflexia Autonômica/fisiopatologia , Receptores de Angiotensina/fisiologia , Traumatismos da Medula Espinal/metabolismo , Traumatismos da Medula Espinal/fisiopatologia , Angiotensina II/toxicidade , Animais , Disreflexia Autonômica/etiologia , Pressão Sanguínea/efeitos dos fármacos , Pressão Sanguínea/fisiologia , Frequência Cardíaca/efeitos dos fármacos , Frequência Cardíaca/fisiologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Traumatismos da Medula Espinal/complicações , Vértebras Torácicas
5.
J Med Eng Technol ; 42(5): 381-388, 2018 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-30324856

RESUMO

Patients with a spinal cord injury above the 6th thoracic vertebrae may be prone to autonomic dysreflexia (AD) in response to bladder stimulus associated with a urodynamics investigation. It is essential that these patients are managed carefully in the urodynamics clinic in order to prevent life-threatening hypertension and bradycardia. Part of this management is the measurement and manual recording of pulse rate (PR) and non-invasive blood pressure (NIBP), alongside the standard urodynamics data set. The purpose of recording these additional data is to identify the characteristic drop in PR and rise in NIBP that indicates the onset of AD. This technical note describes the development of a novel, in-house constructed interface that allows PR and NIBP to be recorded alongside the standard urodynamics data set, using a commonly available vital signs monitor and urodynamics workstation.


Assuntos
Pressão Sanguínea , Frequência Cardíaca , Monitorização Fisiológica/instrumentação , Urodinâmica , Disreflexia Autonômica/diagnóstico , Disreflexia Autonômica/fisiopatologia , Humanos
6.
J Neurotrauma ; 35(24): 2861-2871, 2018 12 15.
Artigo em Inglês | MEDLINE | ID: mdl-30113266

RESUMO

Spinal cord injury (SCI) is a devastating neurological condition for which there is no effective treatment to restore neurological function. The development of new treatments for those with SCI may be hampered by the insensitivity of clinical tools to assess motor function in humans. Treatments aimed at preserving neuronal function through anti-inflammatory pathways (i.e., neuroprotection) have been a mainstay of pre-clinical SCI research for decades. Minocycline, a clinically available antibiotic agent with anti-inflammatory properties, has demonstrated promising neuroprotective effects in a variety of animal models and improved motor recovery in a Phase-2 human trial. Here, we leveraged our recently developed T3 severe contusion model in the rat to determine the ability of minocycline to preserve descending sympathoexcitatory axons and improve cardiovascular control after SCI. Forty-one male Wistar rats were randomized to either a treatment group (minocycline; n = 20) or a control group (vehicle; n = 21). All rats received a severe T3 contusion. Minocycline (or vehicle) was administered intraperitoneally at one hour post-injury (90 mg/kg), then every 12 h for two weeks (45 mg/kg). Neuroanatomical correlates (lesion area, descending sympathoexcitatory axons) were assessed, in addition to an assessment of cardiovascular control (hemodynamics, autonomic dysreflexia) and motor behavior. Here, we show that minocycline reduces lesion area, increases the number of descending sympathoexctitatory axons traversing the injury site, and ultimately reduces the severity of autonomic dysreflexia. Finally, we show that autonomic dysreflexia is a more sensitive marker of treatment stratification than motor function.


Assuntos
Disreflexia Autonômica/etiologia , Minociclina/farmacologia , Fármacos Neuroprotetores/farmacologia , Traumatismos da Medula Espinal/complicações , Medula Espinal/efeitos dos fármacos , Animais , Anti-Inflamatórios/farmacologia , Disreflexia Autonômica/patologia , Disreflexia Autonômica/fisiopatologia , Modelos Animais de Doenças , Masculino , Distribuição Aleatória , Ratos , Ratos Wistar , Traumatismos da Medula Espinal/patologia , Traumatismos da Medula Espinal/fisiopatologia
7.
Med Sci Sports Exerc ; 50(12): 2398-2400, 2018 12.
Artigo em Inglês | MEDLINE | ID: mdl-30102676

RESUMO

Boosting is the induction of autonomic dysreflexia (AD) to reflexively activate otherwise dormant thoracolumbar sympathetic circuitry to "boost" the capacity of the cardiovascular system and enhance exercise performance. AD is a life-threatening condition unique to individuals with spinal cord injury (SCI) characterized by a sudden increase in sympathetic activity below the level of the SCI. Here we report on the temporal HR response to an episode of unintentional boosting during a validated field-based exercise performance test in an athlete with tetraplegia.An athlete with SCI (C6 motor-complete, sensory-incomplete) completed a 20 ×20 m repeated sprint field test on two consecutive days. During the 13th sprint on day 2, the athlete unintentionally boosted via bladder overdistension. Average HR when boosted (i.e., sprints 14-20) was considerably higher than before boosting (141 ± 4 vs 116 ± 7 bpm) and compared with corresponding sprints on day 1 (141 ± 4 bpm vs 120 ± 1 bpm). Average time to complete 20 m sprints when boosted was also faster than the corresponding sprints on day 1 (6.70 ± 0.05 s vs 6.87 ± 0.05 s).This case report highlights the immediate effect of boosting on HR and field-based exercise performance and supports the suggestion that exercise performance in athletes with SCI is limited by cardiovascular capacity.


Assuntos
Desempenho Atlético , Disreflexia Autonômica/fisiopatologia , Quadriplegia , Traumatismos da Medula Espinal/fisiopatologia , Atletas , Pressão Sanguínea , Sistema Cardiovascular/fisiopatologia , Teste de Esforço , Frequência Cardíaca , Humanos , Masculino , Bexiga Urinária
8.
Neurourol Urodyn ; 37(8): 2625-2631, 2018 11.
Artigo em Inglês | MEDLINE | ID: mdl-29717510

RESUMO

AIMS: External sphincterotomy (ES) is a therapeutic option for male spinal cord injury patients with detrusor sphincter dyssynergia. However, some patients need to change their voiding management after ES. One of the potential causes of failure is reportedly detrusor dysfunction, but long-term urodynamic follow-up data after ES is limited. In the present study, we reviewed the urodynamic data before and after ES and analyzed it for possible causes of ES failure. METHODS: A total of 37 patients who were followed up at our center for at least 5 years after ES were included. Mean follow-up period was 16.5 years. Urodynamic assessment was routinely performed every 2 or 3 years after ES, and the data were reviewed and analyzed. RESULTS: Of the 37 patients, 27 are still managed with reflex voiding to a condom catheter (success group), while 10 needed to change their bladder management. Mean maximum bladder pressure (MBP) was preserved at a low level after ES. However, after ES, there was a gradual increase over time in both the mean bladder volume at first neurogenic detrusor overactivity (NDO) and the percentage of patients without NDO. The mean preoperative MBP in the success group was significantly higher than that in the failure group. CONCLUSIONS: MBP is maintained at a low level over 20 years after ES. However, NDO gradually decreases over time, which might be one of the reasons for failure after ES. In addition, low preoperative MBP would be a poor prognostic factor for ES.


Assuntos
Esfincterotomia , Uretra/cirurgia , Bexiga Urinaria Neurogênica/cirurgia , Bexiga Urinária Hiperativa/cirurgia , Urodinâmica , Adulto , Disreflexia Autonômica/fisiopatologia , Seguimentos , Humanos , Masculino , Pressão , Reflexo , Estudos Retrospectivos , Traumatismos da Medula Espinal/complicações , Falha de Tratamento , Bexiga Urinaria Neurogênica/etiologia , Bexiga Urinaria Neurogênica/fisiopatologia , Bexiga Urinária Hiperativa/etiologia , Bexiga Urinária Hiperativa/fisiopatologia , Cateterismo Urinário
9.
J Neurosci ; 38(17): 4146-4162, 2018 04 25.
Artigo em Inglês | MEDLINE | ID: mdl-29610439

RESUMO

Cardiovascular disease and susceptibility to infection are leading causes of morbidity and mortality for individuals with spinal cord injury (SCI). A major contributor to these is autonomic dysreflexia (AD), an amplified reaction of the autonomic nervous system (hallmarked by severe hypertension) in response to sensory stimuli below the injury. Maladaptive plasticity of the spinal sympathetic reflex circuit below the SCI results in AD intensification over time. Mechanisms underlying this maladaptive plasticity are poorly understood, restricting the identification of treatments. Thus, no preventative treatments are currently available. Neuroinflammation has been implicated in other pathologies associated with hyperexcitable neural circuits. Specifically, the soluble form of TNFα (sTNFα) is known to play a role in neuroplasticity. We hypothesize that persistent expression of sTNFα in spinal cord underlies AD exacerbation. To test this, we intrathecally administered XPro1595, a biologic that renders sTNFα nonfunctional, after complete, high-level SCI in female rats. This dramatically attenuated the intensification of colorectal distension-induced and naturally occurring AD events. This improvement is mediated via decreased sprouting of nociceptive primary afferents and activation of the spinal sympathetic reflex circuit. We also examined peripheral vascular function using ex vivo pressurized arterial preparations and immune function via flow cytometric analysis of splenocytes. Diminishing AD via pharmacological inhibition of sTNFα mitigated ensuing vascular hypersensitivity and immune dysfunction. This is the first demonstration that neuroinflammation-induced sTNFα is critical for altering the spinal sympathetic reflex circuit, elucidating a novel mechanism for AD. Importantly, we identify the first potential pharmacological, prophylactic treatment for this life-threatening syndrome.SIGNIFICANCE STATEMENT Autonomic dysreflexia (AD), a disorder that develops after spinal cord injury (SCI) and is hallmarked by sudden, extreme hypertension, contributes to cardiovascular disease and susceptibility to infection, respectively, two leading causes of mortality and morbidity in SCI patients. We demonstrate that neuroinflammation-induced expression of soluble TNFα plays a critical role in AD, elucidating a novel underlying mechanism. We found that intrathecal administration after SCI of a biologic that inhibits soluble TNFα signaling dramatically attenuates AD and significantly reduces AD-associated peripheral vascular and immune dysfunction. We identified mechanisms behind diminished plasticity of neuronal populations within the spinal sympathetic reflex circuit. This study is the first to pinpoint a potential pharmacological, prophylactic strategy to attenuate AD and ensuing cardiovascular and immune dysfunction.


Assuntos
Disreflexia Autonômica/metabolismo , Transdução de Sinais , Fator de Necrose Tumoral alfa/metabolismo , Animais , Disreflexia Autonômica/fisiopatologia , Células Cultivadas , Feminino , Artérias Mesentéricas/fisiopatologia , Ratos , Ratos Wistar , Medula Espinal/efeitos dos fármacos , Medula Espinal/metabolismo , Medula Espinal/fisiopatologia , Baço/imunologia , Baço/fisiopatologia , Fator de Necrose Tumoral alfa/antagonistas & inibidores , Fator de Necrose Tumoral alfa/farmacologia
10.
Auton Neurosci ; 209: 100-104, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-28457670

RESUMO

It is well known that athletes with spinal cord injury (SCI) may experience altered autonomic physiology that impacts their exercise capacity and sports performance. This is particularly relevant given the ever-increasing number of individuals with SCI who are actively engaged in sports at all levels, from community-based adaptive sports to elite Paralympic competitions. As such, the purpose of this article is to review the present literature regarding the implications of altered autonomic control on the safety and performance of athletes with SCI. A particular emphasis will be placed on the autonomic aspects of cardiovascular and thermoregulatory control in the athlete population, as well as the implications of autonomic dysreflexia in enhancing sports performance. Further research is needed to understand the autonomic factors that influence athletes with SCI in order to ensure optimal and safe sports competition. Additionally, this information is crucially relevant to the coaches, sports administrators, and team medical staff who work closely with athletes with SCI.


Assuntos
Desempenho Atlético/fisiologia , Disreflexia Autonômica/fisiopatologia , Exercício/fisiologia , Traumatismos da Medula Espinal/fisiopatologia , Animais , Sistema Nervoso Autônomo/fisiopatologia , Pressão Sanguínea/fisiologia , Humanos
11.
Auton Neurosci ; 209: 59-70, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-28506502

RESUMO

Traumatic spinal cord injury (SCI) has widespread physiological effects beyond the disruption of sensory and motor function, notably the loss of normal autonomic and cardiovascular control. Injury at or above the sixth thoracic spinal cord segment segregates critical spinal sympathetic neurons from supraspinal modulation which can result in a syndrome known as autonomic dysreflexia (AD). AD is defined as episodic hypertension and concomitant baroreflex-mediated bradycardia initiated by unmodulated sympathetic reflexes in the decentralized cord. This condition is often triggered by noxious yet unperceived visceral or somatic stimuli below the injury level and if severe enough can require immediate medical attention. Herein, we review the pathophysiological mechanisms germane to the development of AD, including maladaptive plasticity of neural circuits mediating abnormal sympathetic reflexes and hypersensitization of peripheral vasculature that collectively contribute to abnormal hemodynamics after SCI. Further, we discuss the systemic effects of recurrent AD and pharmacological treatments used to manage such episodes. Contemporary research avenues are then presented to better understand the relative contributions of underlying mechanisms and to elucidate the effects of recurring AD on cardiovascular and immune functions for developing more targeted and effective treatments to attenuate the development of this insidious syndrome following high-level SCI.


Assuntos
Disreflexia Autonômica/fisiopatologia , Sistema Nervoso Autônomo/fisiopatologia , Hipertensão/fisiopatologia , Traumatismos da Medula Espinal/fisiopatologia , Animais , Pressão Sanguínea/fisiologia , Peptídeo Relacionado com Gene de Calcitonina/metabolismo , Humanos , Hipertensão/complicações
13.
J Spinal Cord Med ; 41(5): 549-555, 2018 09.
Artigo em Inglês | MEDLINE | ID: mdl-28784041

RESUMO

OBJECTIVES: Identify clinical and pathophysiologic insights into autonomic dysreflexia (AD) in patients with spinal cord injury (SCI). STUDY DESIGN: Analysis of prospectively gathered AD dataset. SETTING: Inpatient Veterans Affairs SCI unit. PARTICIPANTS: 78 male patients with SCI who experienced AD. METHODS: Statistical methods were utilized to identify the frequency of relative bradycardia vs. tachycardia during AD, the effectiveness of supplemental opioids in managing suspected nociceptive pain mediated AD, the effect of chronicity of SCI on response to pharmacological management of AD, and the response to nitroglycerin ointment in suspected bladder related AD. RESULTS: 445 episodes of AD were analyzed. The frequency of relative bradycardia and tachycardia with AD were 0.3% and 68.0% respectively. The addition of opioids to an antihypertensive medication protocol did not significantly decrease AD episode duration or magnitude of systolic blood pressure (SBP) change. A strongly matched positive linear correlation was identified between the duration of pharmacologically treated AD episodes and chronicity of SCI (R2=0.83). Bladder related AD episodes treated with nitroglycerin ointment had a faster onset of action (10.8 minutes vs. 15.9 minutes), faster time to reach a safe target blood pressure (16.5 minutes vs 20.9 minutes), and greater decrease in SBP (84.3mmHg vs. 68.6mmHg) than non-bladder related episodes (P=0.19, 0.23, and 0.02 respectively). CONCLUSIONS: AD may commonly occur with relative tachycardia. While further investigation is needed on the effects of chronicity of SCI and pharmacologic management, this study raises multiple directions for future research to understand clinical signs and treatment variables of AD following SCI.


Assuntos
Disreflexia Autonômica/fisiopatologia , Pressão Sanguínea , Traumatismos da Medula Espinal/fisiopatologia , Anti-Hipertensivos/uso terapêutico , Disreflexia Autonômica/tratamento farmacológico , Disreflexia Autonômica/etiologia , Humanos , Masculino , Pessoa de Meia-Idade , Nitroglicerina/uso terapêutico , Traumatismos da Medula Espinal/complicações
14.
Auton Neurosci ; 209: 71-78, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-28728939

RESUMO

Autonomic dysreflexia is a dangerous elevation in blood pressure in people with spinal cord injury (SCI), produced by a spinally-mediated reflex activation of sympathetic vasoconstrictor neurones supplying skeletal muscle and the gut. Current dogma states that, apart from visceral inputs - such as those originating from a distended bladder or impacted colon - autonomic dysreflexia is triggered by noxious inputs below the lesion. However, while selective stimulation of small-diameter afferents in muscle or skin evokes a sustained increase in muscle sympathetic nerve activity and blood pressure, and a transient increase in skin sympathetic nerve activity and decrease in skin blood flow in able-bodied subjects, such noxious inputs have no effects on blood pressure and skin blood flow in SCI individuals. Conversely, weak electrical stimulation over the abdominal wall, which in able-bodied subjects is not painful and activates large-diameter cutaneous afferents, causes a marked increase in blood pressure in SCI but not in able-bodied subjects. Moreover, vibration of the penis in spinal-injured men, which is not noxious, caused marked vasoconstriction and increases in blood pressure, similar to those produced by non-noxious distension of the bladder during urodynamics procedures. This suggests that activation of large-diameter somatic afferents, not small-diameter afferents, triggers the increases in vasoconstrictor drive that lead to autonomic dysreflexia, arguing against current dogma on the importance of noxious inputs in triggering autonomic dysreflexia.


Assuntos
Disreflexia Autonômica/fisiopatologia , Estimulação Elétrica , Traumatismos da Medula Espinal/fisiopatologia , Sistema Nervoso Simpático/fisiopatologia , Animais , Pressão Sanguínea/fisiologia , Humanos , Medula Espinal/fisiopatologia , Traumatismos da Medula Espinal/terapia
15.
Auton Neurosci ; 209: 25-36, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-28209424

RESUMO

The effects of spinal cord injury (SCI) on sympathetic neurovascular transmission have generally been ignored. This review describes changes in sympathetic nerve-mediated activation of arterial vessels to which ongoing sympathetic activity has been reduced or silenced following spinal cord transection in rats. In all vessels studied in rats, SCI markedly enhanced their contractile responses to nerve activity. However, the mechanisms that augment neurovascular transmission differ between the rat tail artery and mesenteric artery. In tail artery, the enhancement of neurovascular transmission cannot be attributed to changes in sensitivity of the vascular muscle to α1- or α2-adrenoceptor agonists. Instead the contribution of L-type Ca2+ channels to activation of the smooth muscle by nerve-released noradrenaline is greatly increased following SCI. By contrast, mesenteric arteries from SCI rats had increased sensitivity to phenylephrine but not to methoxamine. While both phenylephrine and methoxamine are α1-adrenoceptor agonists, only phenylephrine is a substrate for the neuronal noradrenaline transporter. Therefore the selective increase in sensitivity to phenylephrine suggests that the activity of the neuronal noradrenaline transporter is reduced. While present evidence suggests that sympathetic vasoconstrictor neurons do not contribute to the normal regulation of peripheral resistance below a complete SCI in humans, the available evidence does indicate that these experimental findings in animals are likely to apply after SCI in humans and contribute to autonomic dysreflexia.


Assuntos
Disreflexia Autonômica/fisiopatologia , Vias Autônomas/efeitos dos fármacos , Traumatismos da Medula Espinal/fisiopatologia , Sistema Nervoso Simpático/fisiopatologia , Animais , Artérias/inervação , Disreflexia Autonômica/tratamento farmacológico , Vias Autônomas/fisiopatologia , Humanos , Traumatismos da Medula Espinal/tratamento farmacológico , Sistema Nervoso Simpático/efeitos dos fármacos , Vasoconstritores/farmacologia
16.
Auton Neurosci ; 209: 4-18, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-28228335

RESUMO

A spinal cord injury (SCI) interferes with the autonomic nervous system (ANS). The effect on the cardiovascular system will depend on the extent of damage to the spinal/central component of ANS. The cardiac changes are caused by loss of supraspinal sympathetic control and relatively increased parasympathetic cardiac control. Decreases in sympathetic activity result in heart rate and the arterial blood pressure changes, and may cause arrhythmias, in particular bradycardia, with the risk of cardiac arrest in those with cervical or high thoracic injuries. The objective of this review is to give an update of the current knowledge related to the alterations in cardiac autonomic control following SCI. With this purpose the review includes the following subheadings: 2. Neuro-anatomical plasticity and cardiac control 2.1 Autonomic nervous system and the heart 2.2 Alteration in autonomic control of the heart following spinal cord injury 3. Spinal shock and neurogenic shock 3.1 Pathophysiology of spinal shock 3.2 Pathophysiology of neurogenic shock 4. Autonomic dysreflexia 4.1 Pathophysiology of autonomic dysreflexia 4.2 Diagnosis of autonomic dysreflexia 5. Heart rate/electrocardiography following spinal cord injury 5.1 Acute phase 5.2 Chronic phase 6. Heart rate variability 6.1 Time domain analysis 6.2 Frequency domain analysis 6.3 QT-variability index 6.4 Nonlinear (fractal) indexes 7. Echocardiography 7.1 Changes in cardiac structure following spinal cord injury 7.2 Changes in cardiac function following spinal cord injury 8. International spinal cord injury cardiovascular basic data set and international standards to document the remaining autonomic function in spinal cord injury.


Assuntos
Disreflexia Autonômica/fisiopatologia , Sistema Nervoso Autônomo/fisiopatologia , Sistema Cardiovascular/fisiopatologia , Traumatismos da Medula Espinal/fisiopatologia , Animais , Coração/fisiopatologia , Humanos , Medula Espinal/fisiopatologia
17.
Auton Neurosci ; 209: 79-89, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-28161248

RESUMO

Autonomic dysreflexia (AD) and neuropathic pain occur after severe injury to higher levels of the spinal cord. Mechanisms underlying these problems have rarely been integrated in proposed models of spinal cord injury (SCI). Several parallels suggest significant overlap of these mechanisms, although the relationships between sympathetic function (dysregulated in AD) and nociceptive function (dysregulated in neuropathic pain) are complex. One general mechanism likely to be shared is central sensitization - enhanced responsiveness and synaptic reorganization of spinal circuits that mediate sympathetic reflexes or that process and relay pain-related information to the brain. Another is enhanced sensory input to spinal circuits caused by extensive alterations in primary sensory neurons. Both AD and SCI-induced neuropathic pain are associated with spinal sprouting of peptidergic nociceptors that might increase synaptic input to the circuits involved in AD and SCI pain. In addition, numerous nociceptors become hyperexcitable, hypersensitive to chemicals associated with injury and inflammation, and spontaneously active, greatly amplifying sensory input to sensitized spinal circuits. As discussed with the aid of a preliminary functional model, these effects are likely to have mutually reinforcing relationships with each other, and with consequences of SCI-induced interruption of descending excitatory and inhibitory influences on spinal circuits, with SCI-induced inflammation in the spinal cord and in DRGs, and with activity in sympathetic fibers within DRGs that promotes local inflammation and spontaneous activity in sensory neurons. This model suggests that interventions selectively targeting hyperactivity in C-nociceptors might be useful for treating chronic pain and AD after high SCI.


Assuntos
Disreflexia Autonômica/fisiopatologia , Dor Crônica/fisiopatologia , Neuralgia/fisiopatologia , Traumatismos da Medula Espinal/fisiopatologia , Medula Espinal/fisiopatologia , Animais , Humanos , Células Receptoras Sensoriais/fisiologia
18.
J Neurotrauma ; 35(3): 573-581, 2018 02 01.
Artigo em Inglês | MEDLINE | ID: mdl-29141501

RESUMO

We aimed to create a clinically relevant pre-clinical model of transient hypertension, and then evaluate the pathophysiological cerebrovascular processes resulting from this novel stimulus, which has recently been epidemiologically linked to cerebrovascular disease. We first developed a clinically relevant model of transient hypertension, secondary to induced autonomic dysreflexia after spinal cord injury and demonstrated that in both patients and rats, this stimulus leads to drastic acute cerebral hyperperfusion. For this, iatrogenic urodynamic filling/penile vibrostimulation was completed while measuring beat-by-beat blood pressure and cerebral blood flow (CBF) in patients. We then developed a rodent model mimicking the clinical reality by performing colorectal distention (to induce autonomic dysreflexia) using pre-clinical beat-by-beat blood pressure and CBF assessments. We then performed colorectal distension in rats for four weeks (6x/day) to evaluate the long-term cerebrovascular consequences of transient hypertension. Outcome measures included middle cerebral artery endothelial function, remodeling, profibrosis and perivascular innervation; measured via pressure myography, immunohistochemistry, molecular biology, and magnetic resonance imaging. Our model demonstrates that chronic repetitive cerebral hyperperfusion secondary to transient hypertension because of autonomic dysreflexia: (1) impairs cerebrovascular endothelial function; (2) leads to profibrotic cerebrovascular stiffening characterized by reduced distensibility and increased collagen deposition; and (3) reduces perivascular sympathetic cerebrovascular innervation. These changes did not occur concurrent to hallmark cerebrovascular changes from chronic steady-state hypertension, such as hypertrophic inward remodeling, or reduced CBF. Chronic exposure to repetitive transient hypertension after spinal cord injury leads to diverse cerebrovascular impairment that appears to be unique pathophysiology compared with steady-state hypertension in non-spinal cord injured models.


Assuntos
Disreflexia Autonômica/fisiopatologia , Encéfalo/fisiopatologia , Circulação Cerebrovascular/fisiologia , Hipertensão/fisiopatologia , Traumatismos da Medula Espinal/fisiopatologia , Adulto , Animais , Encéfalo/patologia , Endotélio Vascular/fisiopatologia , Fibrose/patologia , Humanos , Masculino , Ratos , Traumatismos da Medula Espinal/patologia
19.
J Neurotrauma ; 35(3): 560-572, 2018 02 01.
Artigo em Inglês | MEDLINE | ID: mdl-29160143

RESUMO

Prolonged electrical stimulation of the hindbrain's nucleus raphe magnus (NRM) or of its major midbrain input region, the periaqueductal gray (PAG), was previously found in rats to promote recovery from sensory-motor and histological deficits of acute thoracic spinal cord injury (SCI). Here, some visceral deficits of acute and chronic midline cervical (C5) contusion are similarly examined. Cranially implanted wireless stimulators delivered intermittent 8 Hz, 30-70 µA cathodal pulse trains to a brainstem microelectrode. Injured controls were given inactive stimulators; rats without injuries or implants were also compared. Rectal distension or squeezing of the forepaws caused an exaggerated rise in mean arterial pressure in injured, untreated rats under anesthesia on post-injury week 6, probably reflecting autonomic dysreflexia (AD). These pressor responses became normal when 7 days of unilateral PAG stimulation was started on the injury day. Older untreated injuries (weeks 18-19) showed normal pressor responses, but unexpectedly had significant resting and nociceptive bradycardia, which was reversed by 3 weeks of PAG stimulation started on weeks 7 or 12. Subsequent chronic studies examined gastric emptying (GE), as indicated by intestinal transit of gavaged dye, and serum chemistry. GE and fasting serum insulin were reduced on injury weeks 14-15, and were both normalized by ∼5 weeks of PAG stimulation begun in weeks 7-8. Increases in calcitonin gene-related peptide, a prominent visceral afferent neurotransmitter, measured near untreated injuries (first thoracic segment) in superficial dorsal laminae were reversed by acutely or chronically initiated PAG stimulation. The NRM, given 2-3 weeks of stimulation beginning 2 days after SCI, prevented abnormalities in both pressor responses and GE on post-injury week 9, consistent with its relaying of repair commands from the PAG. The descending PAG-NRM axis thus exhibits broadly restorative influences on visceral as well as sensory-motor deficits, improving chronic as well as acute signs of injury.


Assuntos
Disreflexia Autonômica/fisiopatologia , Tronco Encefálico/fisiologia , Estimulação Elétrica , Traumatismos da Medula Espinal/fisiopatologia , Animais , Disreflexia Autonômica/etiologia , Medula Cervical/fisiopatologia , Feminino , Ratos , Ratos Sprague-Dawley , Traumatismos da Medula Espinal/complicações
20.
Am J Phys Med Rehabil ; 97(1): 1-6, 2018 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-29252405

RESUMO

OBJECTIVE: The aims of the study were to observe cardiovascular responses during video urodynamic studies and to identify correlations between autonomic dysreflexia events and video urodynamic study findings in spinal cord injuries. DESIGN: Thirty-four persons with spinal cord injury were enrolled and investigated using continuous cardiovascular monitoring during video urodynamic studies. Associations between cardiovascular responses and video study variables were analyzed. RESULTS: Bladder type-specific cardiovascular responses occurred during the study. The incidence of overactive detrusor during urodynamic study and bladder trabeculation on voiding cystourethrogram was significantly higher in autonomic dysreflexia persons with spinal cord injury (P < 0.05). Systolic blood pressure changes showed moderate negative correlation (r = -0.402, P = 0.020) with bladder compliance and high positive correlation (r = 0.810, P = 0.000) with maximum detrusor pressure. However, no significant differences in neurological level of injury, injury completeness, autonomic dysreflexia symptoms, and voiding type were found. Spinal cord injury increase at each section was significantly higher in overactive detrusor group (P < 0.05). Significant bradycardia or tachycardia correlating with autonomic dysreflexia during urodynamic studies was not observed. CONCLUSIONS: Unpredictable cardiovascular reactions during urodynamic study should be considered carefully in persons with a spinal cord injury above T6. TO CLAIM CME CREDITS: Complete the self-assessment activity and evaluation online at http://www.physiatry.org/JournalCME CME OBJECTIVES: Upon completion of this article, the reader should be able to: (1) Describe limitations of previous cardiovascular monitoring during urodynamic study to observe changes in cardiovascular responses; (2) Identify factors contributing to autonomic dysreflexia during urodynamic testing; and (3) Discuss the effect of morphologic features in voiding cystourethrogram including trabeculation and vesicourethral reflux on autonomic dysreflexia. LEVEL: Advanced ACCREDITATION: The Association of Academic Physiatrists is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.The Association of Academic Physiatrists designates this Journal-based CME activity for a maximum of 0.5 AMA PRA Category 1 Credit(s)™. Physicians should only claim credit commensurate with the extent of their participation in the activity.


Assuntos
Disreflexia Autonômica/fisiopatologia , Doenças da Bexiga Urinária/etiologia , Urodinâmica , Gravação em Vídeo , Sistema Cardiovascular , Humanos , Traumatismos da Medula Espinal/fisiopatologia , Doenças da Bexiga Urinária/fisiopatologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA