Motherhood after Spinal Cord Injury: Breastfeeding, Autonomic Dysreflexia, and Psychosocial Health: Clinical Practice Guidelines.

The World Health Organization (WHO) recommends that children be breastfed exclusively for the first 6 months of age. This recommendation may prove challenging for women with spinal cord injury (SCI) who face unique challenges and barriers to breastfeeding due to the impact of SCI on mobility and physiology. Tailored provision of care from health care professionals (HCPs) is important in helping women navigate these potential barriers. Yet, HCPs often lack the confidence and SCI-specific knowledge to meet the needs of mothers with SCI. An international panel of clinicians, researchers, consultants, and women with lived experience was formed to create an accessible resource that can address this gap. A comprehensive survey on breastfeeding complications, challenges, resources, and quality of life of mothers with SCI was conducted, along with an environmental scan to evaluate existing postpartum guidelines and assess their relevance and usability as recommendations for breastfeeding after SCI. Building on this work, this article provides evidence-based recommendations for HCPs, including but not limited to general practitioners, obstetricians, pediatricians, physiatrists, lactation consultants, nurses, midwives, occupational therapists, and physiotherapists who work with prospective and current mothers with SCI.

Heart Rate Variability-Based Prediction of Autonomic Dysreflexia After Spinal Cord Injury.

Autonomic dysreflexia (AD) is a common autonomic complication of spinal cord injury (SCI) characterized by a sudden increase is blood pressure triggered by peripheral stimulation, such as bladder distention. Iatrogenic AD events often occur during various medical procedures including urodynamic assessments (UDSs) used to evaluate lower urinary tract (LUT) function in individuals with SCI. To date, there are no established clinical practices that would allow early detection of the development of episodes of AD. Heart rate variability (HRV) is a reliable and non-invasive metric for evaluating autonomic regulation of the cardiovascular system, with demonstrated utility in people with SCI during UDSs. We aim to provide a comprehensive evaluation of cardiovascular function during UDS-induced AD using ultra-short-term HRV analysis and identify changes in cardiovascular dynamics to predict the onset of AD. We assessed cardiovascular data in a total of 24 participants with sensorimotor complete SCI above T6 (17 males, 7 females, median age = 43 [36-50] years) who experienced AD during UDS. We used continuous electrocardiographic recordings to evaluate HRV in 60 sec overlapping windows during filling cystometry. The mean of "normal-to-normal" heartbeats (meanNN), its standard deviation (SDNN), and the root mean square of successive differences (RMSSD) were calculated and used in all subsequent analyses. We found that SDNN and RMSSD diminished during the early phase of bladder filling and sharply increased during AD. Using the lowest point of statistical variability in heart rate (i.e., SDNN), we were able to predict AD events within 240 sec (percentile 25-percentile 75: 172-339 sec) before the first systolic blood pressure peak after AD onset (sensitivity = 0.667; specificity = 0.875). Our results indicated a temporary increase in sympathetic activity during the early phase of bladder filling, which is followed by an increase in parasympathetic outflow to the heart when AD occurs. These findings have significant clinical implications that extend beyond the context of UDS and demonstrate the importance of identifying early changes in HRV in order to accurately predict AD episodes in people living with SCI.

Autonomic dysreflexia associated with cervical spinal cord gliofibroma: case report.

BACKGROUND: Autonomic dysreflexia (AD) is an abnormal reflex of the autonomic nervous system normally observed in patients with spinal cord injury from the sixth thoracic vertebra and above. AD causes various symptoms including paroxysmal hypertension due to stimulus. Here, we report a case of recurrent AD associated with cervical spinal cord tumor. CASE PRESENTATION: The patient was a 57-year-old man. Magnetic resonance imaging revealed an intramedullary lesion in the C2, C6, and high Th12 levels. During the course of treatment, sudden loss of consciousness occurred together with abnormal paroxysmal hypertension, marked facial sweating, left upward conjugate gaze deviation, ankylosis of both upper and lower extremities, and mydriasis. Seizures repeatedly occurred, with symptoms disappearing after approximately 30 min. AD associated with cervical spinal cord tumor was diagnosed. Histological examination by tumor biopsy confirmed the diagnosis of gliofibroma. Radiotherapy was performed targeting the entire brain and spinal cord. The patient died approximately 3 months after treatment was started. CONCLUSIONS: AD is rarely associated with spinal cord tumor, and this is the first case associated with cervical spinal cord gliofibroma. AD is important to recognize, since immediate and appropriate response is required.

Noninvasive Neuroprosthesis Promotes Cardiovascular Recovery After Spinal Cord Injury.

Spinal cord injury (SCI) leads to severe impairment in cardiovascular control, commonly manifested as a rapid, uncontrolled rise in blood pressure triggered by peripheral stimuli-a condition called autonomic dysreflexia. The objective was to demonstrate the translational potential of noninvasive transcutaneous stimulation (TCS) in mitigating autonomic dysreflexia following SCI, using pre-clinical evidence and a clinical case report. In rats with SCI, we show that TCS not only prevents the instigation of autonomic dysreflexia, but also mitigates its severity when delivered during an already-triggered episode. Furthermore, when TCS was delivered as a multisession therapy for 6 weeks post-SCI, the severity of autonomic dysreflexia was significantly reduced when tested in the absence of concurrent TCS. This treatment effect persisted for at least 1 week after the end of therapy. More importantly, we demonstrate the clinical applicability of TCS in treatment of autonomic dysreflexia in an individual with cervical, motor-complete, chronic SCI. We anticipate that TCS will offer significant therapeutic advantages, such as obviating the need for surgery resulting in reduced risk and medical expenses. Furthermore, this study provides a framework for testing the potential of TCS in improving recovery of other autonomic functions such lower urinary tract, bowel, and sexual dysfunction following SCI.

Autonomic dysreflexia in a case of radiation myelopathy and cisplatin-induced polyneuropathy.

INTRODUCTION: While autonomic dysreflexia caused by severe spinal cord lesions can be life-threatening, relevant reports on non-traumatic spinal lesions are rare. Furthermore, modes of innervation of the supraspinal inhibitory pathways at each spinal sympathetic segment remain unknown. Herein, I report the case of a patient with autonomic dysreflexia and radiation myelopathy. The laterality of autonomic dysreflexia was investigated with special reference to the sudomotor function. CASE PRESENTATION: A 51-year-old man with a history of epipharynx carcinoma, radiotherapy, and cisplatin chemotherapy was referred for the evaluation of autonomic function. He was ambulant but displayed spastic tetraparesis, areflexia of the extremities, sensory disturbance below C4 dermatome, dysuria, and impotence. Spinal magnetic resonance imaging demonstrated a cervical lesion involving the lateral portion of C2-C5, bilaterally. The thermal sweating test showed that sweating was lower on the left side of the face and neck, left shoulder, and arm than the corresponding parts on the right side. The rest of the body was anhidrotic. Sweating due to autonomic dysreflexia was symmetric, but more abundant on the left side of the face. Acetylcholine-induced sweating was markedly reduced on the left leg. DISCUSSION: This might be the first documentation of autonomic dysreflexia observed in a patient with radiation myelopathy. The present observations suggested that the supraspinal inhibitory pathway to spinal preganglionic neurons may descend on the same side as thermal sudomotor facilitatory pathways at the cervical level. Furthermore, autonomic dysreflexia was more prominent in the standing position suggesting that the pressure stimulus might enhance autonomic dysreflexia.

Autonomic Hyperactivity.

PURPOSE OF REVIEW: Autonomic hyperactivity is a relatively common consequence of severe acute brain injury and can also be seen with spinal cord and peripheral nerve disorders. This article reviews basic pathophysiologic concepts regarding autonomic hyperactivity, its various forms of clinical presentation, and practical management considerations. RECENT FINDINGS: Paroxysmal sympathetic hyperactivity is most common after traumatic brain injury but can also occur after other forms of severe acute diffuse or multifocal brain injury. Formal criteria for the diagnosis and severity grading of paroxysmal sympathetic hyperactivity have now been proposed. A growing body of literature is beginning to elucidate the mechanisms underlying this disorder, but treatment remains based on observational data. Our mechanistic understanding of other distinct forms of autonomic hyperactivity, such as autonomic dysreflexia after traumatic spinal cord injury and dysautonomia after Guillain-Barré syndrome, remains rudimentary, yet clinical experience shows that their appropriate management can minimize the risk of serious complications. SUMMARY: Syndromes of autonomic hyperactivity can result from injury at all levels of the neuraxis. Much more research is needed to refine our understanding of these disorders and guide optimal management decisions.

Grafting Embryonic Raphe Neurons Reestablishes Serotonergic Regulation of Sympathetic Activity to Improve Cardiovascular Function after Spinal Cord Injury.

Cardiovascular dysfunction often occurs after high-level spinal cord injury. Disrupting supraspinal vasomotor pathways affects basal hemodynamics and contributes to the development of autonomic dysreflexia (AD). Transplantation of early-stage neurons to the injured cord may reconstruct the descending projections to enhance cardiovascular performance. To determine the specific role of reestablishing serotonergic regulation of hemodynamics, we implanted serotonergic (5-HT+) neuron-enriched embryonic raphe nucleus-derived neural stem cells/progenitors (RN-NSCs) into a complete spinal cord transection lesion site in adult female rats. Grafting embryonic spinal cord-derived NSCs or injury alone served as 2 controls. Ten weeks after injury/grafting, histological analysis revealed well-survived grafts and partial integration with host tissues in the lesion site. Numerous graft-derived serotonergic axons topographically projected to the caudal autonomic regions. Neuronal tracing showed that host supraspinal vasomotor pathways regenerated into the graft, and 5-HT+ neurons within graft and host brainstem neurons were transsynaptically labeled by injecting pseudorabies virus (PRV-614) into the kidney, indicating reconnected serotonergic circuits regulating autonomic activity. Using an implanted telemeter to record cardiovascular parameters, grafting RN-NSCs restored resting mean arterial pressure to normal levels and remarkably alleviated naturally occurring and colorectal distension-induced AD. Subsequent pharmacological blockade of 5-HT2A receptors with ketanserin in RN-NSC-grafted rats reduced resting mean arterial pressure and increased heart rate in all but 2 controls. Furthermore, spinal cord retransection below RN-NSC grafts partially eliminated the recovery in AD. Collectively, these data indicate that RN-NSCs grafted into a spinal cord injury site relay supraspinal control of serotonergic regulation for sympathetic activity to improve cardiovascular function.SIGNIFICANCE STATEMENT Disruption of supraspinal vasomotor pathways results in cardiovascular dysfunction following high-level spinal cord injury. To reestablish the descending regulation of autonomic function, we transplanted serotonergic neuron enriched embryonic raphe nucleus-derived neural stem cells/progenitors into the lesion site of completely transected rat spinal cord. Consequently, grafted raphe nucleus-derived neural stem cells/progenitors acted as a neuronal relay to reconnect supraspinal center and spinal sympathetic neurons below the injury. The reconstituted serotonergic regulation of sympathetic activity led to the improvement of hemodynamic parameters and mitigated autonomic dysreflexia. Based on morphological and physiological results, this study validates the effectiveness of transplanting early-stage serotonergic neurons into the spinal cord for cardiovascular functional recovery after spinal cord injury.

Paradoxical effects of continuous high dose gabapentin treatment on autonomic dysreflexia after complete spinal cord injury.

Spinal cord injury (SCI) can have profound effects on the autonomic and cardiovascular systems, notably with injuries above high-thoracic levels that result in the development of autonomic dysreflexia (AD) characterized by volatile hypertension in response to exaggerated sympathetic reflexes triggered by afferent stimulation below the injury level. Pathophysiological changes associated with the development of AD include sprouting of both nociceptive afferents and ascending propriospinal 'relay' neurons below the injury, as well as dynamic changes in synaptic inputs onto sympathetic preganglionic neurons. However, it remains uncertain whether synapse formation between sprouted c-fibers and propriospinal neurons contributes to the development of exaggerated sympathetic reflexes produced during AD. We previously reported that once daily treatment with the anti-epileptic and neuropathic pain medication, gabapentin (GBP), at low dosage (50 mg/kg) mitigates experimentally induced AD soon after injections, likely by impeding glutamatergic signaling. Since much higher doses of GBP are reported to block the formation of excitatory synapses, we hypothesized that continuous, high dosage GBP treatment after SCI might prevent the formation of aforementioned aberrant synapses and, accordingly, reduce the incidence and severity of AD. Adult female rats implanted with aortic telemetry probes for hemodynamic monitoring underwent T4-transection SCI and immediately received 100 mg/kg (i.p.) of GBP and then every six hours (400 mg/kg/day) for 4-weeks after injury. We assessed daily body weight, mean arterial pressure, heart rate, frequency of spontaneous AD, and hemodynamic changes during colorectal distension (CRD) to establish whether high dose GBP treatment prophylactically mitigates both AD and associated aberrant synaptic plasticity. This regimen significantly reduced both the absolute blood pressure reached during experimentally induced AD and the time required to return to baseline afterwards. Conversely, GBP prevented return to pre-injury body weights and paradoxically increased the frequency of spontaneously occurring AD. While there were significant decreases in the densities of excitatory and inhibitory pre-synaptic markers in the lumbosacral dorsal horn following injury alone, they were unaltered by continuous GBP treatment. This indicates distinct mechanisms of action for acute GBP to mitigate induced AD whereas chronic GBP increases non-induced AD frequencies. While high dose prophylactic GBP is not recommended to treat AD, acute low dose GBP may hold therapeutic value to mitigate evoked AD, notably during iatrogenic procedures under controlled clinical conditions.

Onset of the action of intravesical lidocaine after spinal cord injury.

AIMS: To obtain objective evidence for the time to onset of action for intravesical lidocaine utilizing exaggerated sympathetic blood-pressure responsiveness in patients with spinal cord injuries (SCI). METHODS: This prospective observational cohort study analyzed blood pressure responses in individuals with SCI at or above T6 who did (lidocaine-instillation group) or did not (control group) receive 10 ml of 2% lidocaine gel instilled through their catheters before routine suprapubic catheter change. Care was taken to minimize any potentially confounding position change or catheter manipulation. Given the potential for C-fiber mediated systolic blood pressure (SBP) increases after SCI, the time to lidocaine's onset of action for blocking these C-fibers (as seen by the decrease in SBP more than and equal to 10 mm Hg) was assessed with serial blood pressures for 4 to 6 minutes. RESULTS: Blood pressures were evaluated in 32 individuals with SCI (lidocaine-instillation group n = 22, control group n = 10). In the lidocaine-instillation group, 45% individuals demonstrated a sustained decrease in SBP more than and equal to 10 mm Hg, which occurred at a mean of 98.1 seconds (SD 59 seconds) after lidocaine instillation. Despite up to 6 minutes of serial monitoring, the remainder of the lidocaine-instillation group and the entire control group had SBP fluctuations less than 10 mm Hg. The serial mean SBPs of those who responded to lidocaine were significantly less than the remaining groups (P < .001 for both comparisons). CONCLUSION: Utilizing lidocaine's properties to decrease sympathetic-inducing afferents after SCI, the time to onset of action for intravesical lidocaine was found to be approximately 90 seconds. This relatively rapid initial onset on action is especially pertinent when managing autonomic dysreflexia.

Headache Attributed to Autonomic Dysreflexia: Clinical Presentation, Pathophysiology, and Treatment.

A patient presenting with marked elevation in blood pressure and concurrent headache often presents a diagnostic challenge for even the most seasoned clinician. When marked hypertension and headache occur in a patient with a history of upper spinal cord injury, the patient should be presumed to have autonomic dysreflexia until proven otherwise. Autonomic dysreflexia can at times trigger headaches, hypertension, and variations in pulse, as well other autonomic signs and symptoms. Autonomic dysreflexia is a medical emergency for which appropriate treatment may be life-saving. In this review, we address the historical origins, risk factors, pathophysiology, diagnostic criteria, clinical presentation, differential diagnosis, and treatment of headache attributed to autonomic dysreflexia. Included are two case presentations from the authors' clinic, which illustrate the diagnosis and treatment of headache attributed to autonomic dysreflexia.

Severe hyponatraemia and autonomic dysreflexia in a quadriplegic person.

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.

The Blood Pressure Pendulum following Spinal Cord Injury: Implications for Vascular Cognitive Impairment.

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.

Development of a decerebrate model for investigating mechanisms mediating viscero-sympathetic reflexes in the spinalized rat.

Autonomic dysreflexia (AD) often occurs in individuals living with spinal cord injury (SCI) and is characterized by uncontrolled hypertension in response to otherwise innocuous stimuli originating below the level of the spinal lesion. Visceral stimulation is a predominant cause of AD in humans and effectively replicates the phenotype in rodent models of SCI. Direct assessment of sympathetic responses to viscerosensory stimulation in spinalized animals is challenging and requires invasive surgical procedures necessitating the use of anesthesia. However, administration of anesthesia markedly affects viscerosensory reactivity, and the effects are exacerbated following spinal cord injury (SCI). Therefore, the major goal of the present study was to develop a decerebrate rodent preparation to facilitate quantification of sympathetic responses to visceral stimulation in the spinalized rat. Such a preparation enables the confounding effect of anesthesia to be eliminated. Sprague-Dawley rats were subjected to SCI at the fourth thoracic segment. Four weeks later, renal sympathetic nerve activity (RSNA) responses to visceral stimuli were quantified in urethane/chloralose-anesthetized and decerebrate preparations. Visceral stimulation was elicited via colorectal distension (CRD) for 1 min. In the decerebrate preparation, CRD produced dose-dependent increases in mean arterial pressure (MAP) and RSNA and dose-dependent decreases in heart rate (HR). These responses were significantly greater in magnitude among decerebrate animals when compared with urethane/chloralose-anesthetized controls and were markedly attenuated by the administration of urethane/chloralose anesthesia after decerebration. We conclude that the decerebrate preparation enables high-fidelity quantification of neuronal reactivity to visceral stimulation in spinalized rats. NEW & NOTEWORTHY In animal models commonly used to study spinal cord injury, quantification of sympathetic responses is particularly challenging due to the increased susceptibility of spinal reflex circuits to the anesthetic agents generally required for experimentation. This constitutes a major limitation to understanding the mechanisms mediating regionally specific neuronal responses to visceral activation in chronically spinalized animals. In the present study, we describe a spinalized, decerebrate rodent preparation that facilitates quantification of sympathetic reactivity in response to visceral stimuli following spinal cord injury. This preparation enables reliable and reproducible quantification of viscero-sympathetic reflex responses resembling those elicited in conscious animals and may provide added utility for preclinical evaluation of neuropharmacological agents for the management of autonomic dysreflexia.

Distinct roles of angiotensin receptors in autonomic dysreflexia following high-level spinal cord injury in mice.

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.

Development of Cardiovascular Dysfunction in a Rat Spinal Cord Crush Model and Responses to Serotonergic Interventions.

Selection of a proper spinal cord injury (SCI) rat model to study therapeutic effects of cell transplantation is imperative for research in cardiovascular functional recovery, due to the local harsh milieu inhibiting cell growth. We recently found that a crushed spinal cord lesion can minimize fibrotic scarring and grafted cell death compared with open-dura injuries. To determine if this SCI model is applicable for studying cardiovascular recovery, we examined hemodynamic consequences following crushed SCI and tested cardiovascular responses to serotonin (5-HT) or dopamine (DA) receptor agonists. Using a radio-telemetric system, multiple cardiovascular parameters were recorded prior to, 2, and 4 weeks after SCI, including resting mean arterial pressure (MAP) and heart rate (HR), as well as spontaneous or colorectal distension (CRD)-induced autonomic dysreflexia (AD). The results showed that this injury caused tachycardia at rest as well as the occurrence of spontaneous or artificially induced dysreflexic events. Four weeks post-injury, specific activation of 5-HT2A receptors by subcutaneous (s.c.) or intrathecal (i.t.) delivery of Dimethoxy-4-iodoamphetamine (DOI) remarkably increased resting MAP levels in a dose-dependent fashion. During CRD-induced autonomic dysreflexia, systemic administration of DOI alleviated the severity of bradycardia responsive to episodic hypertension. In contrast, selective stimulation of 5-HT1A receptors with 8-OH-DPAT or non-selective activation of DA receptors with apomorphine did not affect cardiovascular performance. Thus, crush injuries induce cardiovascular abnormalities in rats that are sensitive to 5-HT2A receptor stimulation, indicating a reliable SCI model to study how cell-based approaches impact the severity of autonomic dysreflexia and identify a possible target for pharmacological interventions.

A custom made interface to integrate recording of pulse rate and blood pressure during urodynamics investigations.

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.

Minocycline Reduces the Severity of Autonomic Dysreflexia after Experimental Spinal Cord Injury.

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.