Search tips
Search criteria 


Logo of capmcAbout usÀ propos de nous
Arch Phys Med Rehabil. Author manuscript; available in PMC 2011 June 6.
Published in final edited form as:
PMCID: PMC3108991

A Systematic Review of the Management of Autonomic Dysreflexia Following Spinal Cord Injury

Andrei Krassioukov, MD, PhD, FRCPC,1,2,3 Darren ER Warburton, PhD,1,4 Robert Teasell, MD, FRCPC,5 Janice J Eng, BSc (PT/OT), PhD,1,3,6 and The SCIRE Research Team



To systematically review the clinical evidence on strategies to prevent and manage autonomic dysreflexia (AD).


A key word search of several databases (Medline, CINAHL, EMBASE and PsycInfo), in addition to manual searches of retrieved articles, was undertaken to identify all English-language literature evaluating the efficacy of interventions for AD.


Studies selected for review included randomized controlled trials (RCTs), prospective cohort studies, and cross-sectional studies. Treatments reviewed included pharmacological and non-pharmacological interventions for the management of AD in individuals with spinal cord injury. Studies that failed to assess AD outcomes (e.g. blood pressure) or symptoms (e.g., headaches, sweating) were excluded.


Studies were critically reviewed and assessed for their methodological quality by two independent reviewers.


Thirty-one studies were assessed, including 6 RCTs. Preventative strategies to reduce the episodes of AD caused by common triggers (e.g. urogenital system, surgery) primarily were supported by Level 4 (pre-post studies) and Level 5 (observational studies) evidence. The initial acute non-pharmacological management of an episode of AD (i.e. positioning the patient upright, loosening tight clothing, and eliminating any precipitating stimulus) is supported by clinical consensus and physiological data (Level 5 evidence). The use of antihypertensive drugs in the presence of sustained elevated blood pressure is supported by Level 1 (prazosin) and Level 2 evidence (nifedipine and prostaglandin E2).


A variety of options are available to prevent AD (e.g., surgical, pharmacological) and manage the acute episode (elimination of triggers, pharmacologic); however, these options are predominantly supported by evidence from non-controlled trials and more rigorous trials are required.

Keywords: autonomic dysreflexia, management, pharmacological, spinal cord injury


Autonomic dysreflexia (AD) is a well-known clinical emergency in individuals who have suffered a spinal cord injury (SCI). It especially occurs in individuals with an injury at level T6 or above.13 An episode of AD is characterized by the acute elevation of arterial blood pressure (BP) and bradycardia (slow heart rate), although tachycardia (rapid heart rate) also may occur. Objectively, an increase in systolic BP greater than 20–30 mmHg is considered a dysreflexic episode.2 However, because the usual resting arterial BP in individuals with cervical and high thoracic SCI is approximately 15 to 20 mmHg lower than in able-bodied individuals,3, 4 acute elevation of blood pressure to normal or slightly elevated ranges could indicate AD in this population. AD can present with a variety of symptoms (Table 1) and can vary in intensity from asymptomatic,5, 6 to mild discomfort and headache, to a life threatening emergency, such as when systolic blood pressure climbs to 300 mmHg.3 Untreated episodes of AD may have serious consequences, including intracranial hemorrhage, retinal detachment, seizures and death.711

Table 1
Signs and Symptoms of Autonomic Dysreflexia in Patients with Spinal Cord Injuries

It has been observed that, the higher the injury level, the greater the degree of clinically-manifest cardiovascular dysfunction.1214 Another important factor relating to the severity of AD is the completeness of the spinal injury; only 27% of incomplete tetraplegics present with signs of AD, in comparison with 91% of tetraplegics with complete lesions.13 While AD occurs more often in the chronic stage of SCI at or above the 6th thoracic segment, there also is clinical evidence of episodes of AD in the first days and weeks after injury.14, 15

A variety of non-noxious or noxious stimuli can trigger episodes of AD.2, 3 However, AD most commonly is triggered by irritation of the urinary bladder or colon. Physiologically, AD is caused by a massive sympathetic discharge triggered by either a noxious or non-noxious stimulus originating below the level of the SCI.16 Numerous reports of AD have been described in the literature. Symptoms usually are short-lived, either due to treatment or because the episode itself is self-limiting. However, there have been reports of AD, triggered by a specific stimulus, being sustained for periods ranging from days to weeks.17 Numerous different mechanisms have been proposed as potentially responsible for the development of AD. It is known from animal experiments that autonomic instability following SCI results from changes occurring within the spinal and peripheral autonomic circuits, both in the acute and chronic stages following injury.16, 1820 Destruction of the descending vasomotor pathways results in the loss of inhibitory and excitatory supraspinal input to the sympathetic preganglionic neurons, and is currently considered to be the predominant factor underlying the unstable blood pressure that tends to follow SCI.21 Furthermore, the results of numerous animal and human studies suggest that changes within the spinal cord (specifically spinal sympathetic neurons and primary afferents) underlie the abnormal cardiovascular control and AD following SCI.19, 2225 Altered sensitivity of peripheral alpha-adrenergic receptors (receptors in the sympathetic nervous system) is one mechanism that may contribute.26, 27

The purpose of this systematic review has been to provide an overview of the clinical evidence supporting the efficacy of the various strategies currently used to prevent and manage AD in the SCI population. These findings were part of the Spinal Cord Injury Rehabilitation Evidence project, the details of which are available at


A keyword literature search of original articles, previous practice guidelines and review articles was conducted, so as to identify all English-language literature, published from 1950 to 2007, evaluating the efficacy of any intervention related to AD in the SCI population. Population key words - spinal cord injury, paraplegia, tetraplegia, and quadraplegia - were individually paired with autonomic dysreflexia, autonomic, dysreflexia, blood pressure, nifedipine, phenazopyridine, beta blockers, detrusor hyperreflexia and detrusor dyssynergy. Studies which did not have outcomes evaluating AD (e.g. blood pressure) or AD symptoms (e.g., headaches, sweating) were excluded.

The keyword search yielded 2168 articles related to AD following SCI. A total of 2138 articles were removed from the sample, because they did not have outcomes evaluating AD or AD symptoms, leaving 31 articles from which data could be extracted.

The rigor and quality of each study was scored by two independent reviewers. We used the 11-item Physiotherapy Evidence Database (PEDro) Scale28 to score RCTs, and a modified version of the Downs and Black (D&B) Tool29 to score non-RCTs. Maximum scores for the PEDro and D&B instruments are 10 and 28, respectively, with higher scores indicating better methodological quality.

The description by Sackett et al.30 of levels of evidence was used to draw conclusions about the studies based on the study design. We collapsed Sackett’s30 levels of evidence into 5 categories, where Level 1 evidence was attributed to ‘good’ to ‘excellent’ RCTs with a PEDro score ≥6; and Level 2 evidence corresponded to RCTs with PEDro scores ≤5, non-randomized prospective controlled trials, and cohort studies. Evidence from case control studies was assigned to Level 3. Level 4 corresponded to evidence from pre-post/post-test or case-series; and evidence was categorized as Level 5 if it was derived from observational reports, case reports involving a single subject, or clinical consensus.29 We did not require a minimum sample size per study, due to the relatively limited number of publications in this field. Note that it is possible to have a small RCT (Level 2), but with poor quality (e.g., high drop-out rate, incorrect statistical analyses).


The 31 selected articles were categorized according to (1) preventative strategies to reduce episodes and symptoms of AD from common triggers (e.g., from the urogenital system, gastrointestinal system, general surgery and exercise);3148 and (2) therapeutic management strategies, either acute or chronic, for AD.45, 4961 The management of AD included both non-pharmacological and pharmacological strategies. The pharmacological studies assessed nifedipine (n=5),4953 captopril (n=1),54 terazosin (n=3),5557 prazosin (n=1),58 phenoxybenzamine (n=2),50, 59 prostaglandin E2 (n=1),60 sildanefil (n=1),61 and nitrates (n=1).45 Only 6 of the 31 studies were RCTs.33, 40, 41, 48, 58, 61. The RCTs had PEDro scores ranging from 5 to 10 (good to excellent). The majority of the non-RCT trials had a low Downs and Black score with the majority below 15 out of 28 points.

A. Preventative Strategies

The largest proportion of preventative studies focused on the management of AD triggered by stimuli originating within the urogenital system (n=14). These studies assessed interventions intended to prevent AD during the evaluation of urinary bladder function and during invasive procedures (n=9),3139 anorectal procedures (n=2),40, 41 pregnancy and labour (n=4),4245 general surgery (n=2),46, 47 and functional electrical stimulation (FES) exercise (n=1).48 The characteristics and outcomes of studies assessing preventative strategies for AD are presented in Table 2.

Table 2
Prevention of AD

1. Prevention of AD during bladder procedures

Urinary bladder irritation or distention is the most widely-recognized trigger of AD following SCI.5, 35, 62 The first proposed defense against AD triggered by urinary bladder irritation consists of a bladder management program and continuous urological follow-up.6365 An established bladder management program, with intermittent catheterization or an indwelling Foley catheter, allows individuals with SCI to plan for bladder emptying when convenient or as necessary.66 However, no studies were identified which specifically assessed the effect of bladder management programs on AD symptoms.

Urological follow-up includes annual urodynamic evaluations and cystoscopy, depending upon the bladder management program. During the last decade, these strategies have decreased the frequency of urinary tract infections and the development of renal failure in individuals with SCI.67, 68 However, conservative management is not always successful, and alternative strategies (e.g., Botulinum toxin, capsaicin, anticholinergics, sacral denervation and bladder and urethral sphincter surgery) are required to decrease afferent stimulation from the urinary bladder, thereby to prevent the development of AD. In addition, urodynamic and cystoscopy procedures themselves are associated with significant activation of urinary bladder afferents and have the potential to trigger AD;5, 53, 69, 70 consequently, strategies to reduce afferent stimulation are necessary during these procedures.

1a. Botulinum Toxin for the Prevention of AD Resulting from Detrusor-sphincter Dyssynergia

Two pre-post test studies (n=42)31, 32 found that the injection of Botulinum toxin into the detrusor muscle or bladder sphincter is an effective method of treating urinary incontinence secondary to neurogenic detrusor over-activity and bladder sphincter dyssynergia. In these conditions, injections of the Botulinum toxin either allow for increased urinary bladder capacity (i.e., reduced over-activity of the bladder) or facilitate the evacuation of urine (reduced bladder sphincter dyssynergia). The duration of the effect has been reported to be up to 9 months.32 Both studies assessing the use of Botulinum toxin were Level 4 and demonstrated a positive treatment effect. In fact, following Botulinum toxin treatment for AD associated with bladder emptying, AD appeared to disappear completely in 3 individuals with tetraplegia, with no recurrence even after the toxin presumably had lost all effect.32


Based upon the results of 2 pre-post studies,31, 32 there is Level 4 evidence that Botulinum toxin injections into the detrusor muscle may be a safe and effective therapeutic option in SCI patients who perform clean intermittent self-catheterization and have incontinence that is resistant to anticholinergic medication.

1b. Intravesical Capsaicin for the Prevention of AD Resulting from Bladder Sphincter Dyssynergia

One RCT (n=23)33 and one pre-post study (n=7)34 evaluated the effect of capsaicin, an extract from red peppers. Capsaicin exerts a selective action on certain sensory nerves, most notably those involved in reflex contractions of the bladder after SCI. In their pre-post study, Igawa et al. demonstrated that intravesical capsaicin diminishes the number of episodes of AD in patients with SCI during catheterization, suggesting a therapeutic potential of intravesical capsaicin for both AD and detrusor hyperreflexia in SCI patients.34 Giannantoni et al.’s high-quality RCT (PEDro=6) used an analogue of capsaicin (resiniferatoxin RXT) which is more than 1,000 times more potent than capsaicin itself at desensitizing C-fiber bladder afferents, and also identified a reduced number of AD episodes among those receiving active treatment.33 The investigators also found that the intra-vesical administration of resiniferatoxin was superior to that of intravesical capsaicin, in terms of urodynamic results and clinical benefits in SCI patients within 60 days of treatment, and did not cause the inflammatory side effects associated with capsaicin. However, the long-term effects of capsaicin or resiniferatoxin on AD were not evaluated.


Based upon a single pre-post study,34 there is Level 4 evidence that intra-vesical capsaicin may be effective at reducing the frequency of AD in SCI. Based on a single RCT33, there is Level 1 evidence that intravesical resiniferatoxin is effective at reducing the number of episodes of AD in patients with SCI, and that it is more effective than intravesical capsaicin.

1c. Anticholinergics for the Prevention of AD

Anticholinergics are a class of medication that inhibit the binding of the neurotransmitter acetylcholine to its receptors. Acetylcholine is released by the parasympathetic nerve fibers that innervate the urinary bladder and contribute to detrusor contraction and the activation of bladder afferents. These afferent stimuli are responsible for the activation of spinal sympathetic circuits that triggers AD. Therefore, anticholinergic agents might decrease afferent activation, and consequently AD. However, only one study has examined the use of anticholinergic drugs, and it was a cross-sectional observational study (n=48).35 Giannantoni and co-investigators found that the use of anticholinergic drugs was not associated with a reduced incidence of AD, unless it resulted in detrusor areflexia.35


Based upon Level 5 evidence from a single cross-sectional correlational study,35 anticholinergics are not associated with a reduced incidence of AD episodes.

1d. Sacral Denervation

When post-SCI detrusor hyperreflexia does not respond to conservative treatment, and patients are not eligible for ventral sacral root stimulation for electrically-induced micturition, sacral bladder denervation may be considered a stand-alone procedure to treat urinary incontinence and AD. Two Level 4 studies (n=19)36, 37 on sacral denervation have generated conflicting results. Hohenfellner et al. concluded that sacral bladder denervation is a valuable treatment option, based upon their study in which the procedure eliminated detrusor hyperreflexia and AD in all 9 subjects.37 However, Schurch et al. found that complete bladder deafferentation did not abolish AD during bladder urodynamic investigations.36


Based upon two Level 4 studies,36, 37 it can be said that there is conflicting evidence regarding the effectiveness of sacral deafferentation in the prevention of AD.

1e. Bladder and Urethral Sphincter Surgery

The association between episodes of AD and the presence of detrusor sphincter dyssynergia, and high intravesical and urethral pressure has led to the development of surgical procedures to alleviate voiding dysfunction and, consequently, AD in patients with SCI. Two surgical studies38, 39 included indicators of AD (e.g., blood pressure changes). Although the older study, by Barton et al.,38 demonstrated a reduced incidence of AD post external sphincterotomy, such procedures now are rarely performed, because they are associated with significant risks, including hemorrhage and erectile dysfunction,71 and the need for repeat procedures.72 Thus, alternatives have been investigated, such as urethral stents and Botulinum toxin (Botox) injections.71 Augmentation enterocystoplasty has demonstrated long-term success, based upon urodynamic evaluations, and has been found to reduce the symptoms of AD.39 Enterocystoplasty with a Mitrofanoff Procedure has become a more frequent choice of bladder augmentation in individuals with SCI, due to more favorable long-term outcomes.


Based upon three pre-post/case series,38, 39 there is Level 4 evidence that urinary bladder surgical augmentation may result in a decrease in intravesical and urethral pressure, and may diminish or resolve episodes of AD. Enterocystoplasty may result in better long-term viability, relative to sphincterotomy.

2. Prevention of AD during Anorectal Procedures

Pain or irritation within the colorectal area is the second most common cause of AD. Constipation, hemorrhoids, and anal fissures frequently are observed in patients with SCI and contribute to episodes of AD.2, 62, 73, 74 Furthermore, bowel routines in SCI individuals frequently involve digital stimulation that can trigger AD. Rectosigmoid distension and anal manipulation are common iatrogenic triggers of AD in this population.40 In two small RCTs (n=70),40, 41 topical and local anesthesia of the anorectal area were compared with respect to the prevention of AD during anorectal procedures. Investigators demonstrated that anoscopy, which involves stretching of the anal sphincters, was a more potent stimulus for AD than flexible sigmoidoscopy, which involves gaseous distention of the rectosigmoid. Anal sphincter stretch and rectosigmoid distention, rather than mucosal stimulation, are likely nociceptive triggers for procedure-associated AD.41 In one randomized, double-blind, placebo-controlled trial, AD was not abolished during anorectal procedures by applying topical lidocaine in the rectum.41 However, in a later RCT, the same investigators demonstrated that intersphincteric anal block with lidocaine was effective at limiting anorectal procedure-associated AD.40 Both anoscopy and flexible sigmoidoscopy cause significant blood pressure elevation.


There is Level 1 evidence (from one RCT)40 that intersphincteric anal block with lidocaine limits the AD response in susceptible patients undergoing anorectal procedures. There is also Level 1 evidence (from one RCT)41 that topical lidocaine does not limit or prevent AD in susceptible patients during anorectal procedures.

3. Prevention of AD during Pregnancy and Labour

Based upon North American statistics, women represent a third of the SCI population.75 In the United states, approximately 3,000 women of childbearing age are affected by SCI each year.42 The ability of women to have children is not usually affected, once their menstrual cycle resumes.76 There are increasing numbers of women with SCI who become pregnant and have healthy babies.42 However, women with SCI are at high risk of developing uncontrolled AD during labor and delivery.77, 78

Recognition and prevention of this life-threatening emergency is critical for the management of labor in women with SCI.79 In women with SCI, the onset of AD during labour is intermittently timed with uterine contractions. In the majority of women with SCI above T10, the uterine contractions may present only as abdominal discomfort, an increase in spasticity and AD.43 The results of numerous observational studies and case reports, as well as expert opinions recommend adequate anesthesia in women with SCI during labour and delivery, despite their apparent lack of sensation. However, only four studies (n=54)4245 with observational evidence have recorded management specific to AD during labour. Epidural anesthesia has been reported to be the best choice for the control of AD. The American College of Obstetrics and Gynecology emphasized that it is important that obstetricians caring for these patients are aware of the specific problems related to SCI.80


With vaginal delivery or when cesarean delivery or instrumental delivery is indicated, adequate anesthesia (spinal or epidural if possible) is needed. There is Level 4 evidence (from a single case series42 and 2 observational studies)43, 44 that epidural anesthesia is preferred and may be effective for most patients with AD during labor and delivery.

4. Prevention of AD during General Surgery

AD may be precipitated by a host of somatic and visceral noxious or non-noxious stimuli below the level of injury. Therefore, a variety of interventions have been used to decrease afferent information to the spinal cord, including peripheral anesthetic blocks, epidural anesthesia, general anesthesia, and even dorsal rhizotomy.38, 40, 41, 79, 81 Despite the partial or total loss of sensation below the level of injury, it is important to recognize that surgical procedures or manipulations can initiate episodes of AD. Anesthesiologists and surgeons undertaking surgery on SCI patients must be aware of the interactions of the anesthetic and its effects on AD, and how to prevent or manage AD during these procedures. Two observational studies46, 47 have revealed that AD is a common complication during general surgery in individuals with SCI. Up to 90 % of individuals with SCI undergoing surgery with topical anesthesia or no anesthesia develop AD. Moreover, the results of both studies suggest that patients at risk for AD can be protected, either by general or spinal anesthesia.


There is Level 5 evidence (from 2 observational studies)46, 47 that indicate that patients at risk for AD may be protected against developing intra-operative hypertension by either general or spinal anesthesia. Anesthesiologists and surgeons dealing with SCI patients must know how to recognize AD syndrome, how to prevent its occurrence, and how to manage it once it occurs.

5. Prevention of AD during FES Exercise

FES is a commonly-used modality during the rehabilitation of individuals with SCI.82, 83 Unfortunately, similar to any non-noxious or noxious stimuli below the level of injury, FES can result in significant afferent stimulation, thereby precipitating the development of AD.48, 84 One RCT (n=7)48 evaluated the effect of a topical anaesthetic versus a placebo cream applied to the skin over the quadriceps muscle one hour prior to FES, on two different days. Cardiovascular and AD responses during FES were unaffected by the use of topical anaesthetic cream on the skin at the stimulation site. The authors suggested that mechanisms other than skin nociception contribute to FES-induced AD.


There is Level 1 evidence (from one RCT)48 that there is no beneficial effect of topical anesthetic in the prevention of AD during FES.

B. Management of Acute AD

Despite appropriate preventative strategies, AD is a common condition among individuals with SCI. As we acknowledged previously, even with a significant increase in arterial blood pressure, episodes of AD may be asymptomatic, especially in individuals with cervical or high thoracic injuries.5, 6, 85 As recommended in the Guidelines of the Consortium for Spinal Cord Medicine for the management of AD, non-pharmacological measures must be employed initially; if they fail, and systolic blood pressure continues to be at or above 150 mmHg in an adult, 140 mmHg in an adolescent, 130 mmHg in a child 6–12 years old, or 120 mmHg in a child under 5 years old, some type of pharmacological agent should be initiated.86

1. Non-pharmacological Management of AD

The initial management of an episode of AD involves placing the patient in an upright position to take advantage of any orthostatic reduction in blood pressure.86 Having said this, no studies have evaluated the effect of the sitting-up position on blood pressure during episodes of AD. Nonetheless, significant decreases in resting blood pressure have been demonstrated when individuals with SCI are moved from a flat supine position to being tilted or sat up.8789 It is thought that an upright posture induces pooling of blood in the abdominal and lower extremity vessels, due to the loss of peripheral vasoconstriction that follows SCI, thereby causing a reduction in arterial blood pressure. The next step in managing acute AD must be to loosen any tight clothing and/or constrictive devices.86 This procedure allows for further blood pooling in vessels beds below the level of injury, and removes possible triggers for peripheral sensory stimulation. It is critical that blood pressure is checked at least every 5 minutes throughout the episode of AD, until the individual is stable.86 It then is necessary to search for and eliminate the precipitating stimulus which, in 85% of cases, is related either to bladder distention or bowel impaction.2, 3 The use of antihypertensive drugs should be considered a last resort, but may be necessary if systolic blood pressure remains 150 mmHg or greater following the steps outlined above.86 The goals of such an intervention are to alleviate symptoms and to avoid the complications associated with uncontrolled hypertension.710


There is Level 5 evidence based upon physiological studies and clinical consensus86 for the non-pharmacological management of episodes of AD. Identifying the possible trigger and decreasing afferent stimulation to the spinal cord appear to comprise the most effective non-pharmaceutical therapeutic strategy in clinical practice.

2. Pharmacological Management of AD

Episodes of AD in individuals with SCI can vary in severity. In some patients and in some instances, they are asymptomatic. In many other instances, they can be managed by the individual, once he or she becomes familiar with his/her own triggers and symptoms.5 However, in some individuals and instances, it is difficult or seemingly impossible to identify what has triggered the acute elevation in blood pressure, and immediate pharmaceutical medical attention is required.17 Antihypertensive drugs with a rapid onset and short duration of action should be used in the management of acute episodes90 The Consortium for Spinal Cord Medicine recommends that, if non-pharmacological measures (moving the patient to an upright posture, loosening clothes, reducing irritation to the bladder and bowel, etc.) fail and arterial blood pressure is 150 mmHg or greater, then pharmacological management should be initiated.86 However, the Consortium does not preferentially identify any particular medication for acute AD management.86 Numerous pharmacological agents (e.g., nifedipine, nitrates, captopril, terzaosin, prazosin, phenoxybenamine, Prostaglandin E2, and sildanefil) have been proposed for the management of AD episodes.86, 90, 91 The majority of the recommendations are based upon experience with and studies on the clinical management of hypertensive crises in able-bodied populations. The characteristics and outcomes of studies assessing pharmacological interventions for the management of AD are presented in Table 3.

Table 3
Pharmacological management of AD

2a. Nifedipine (Adalat, Procardia)

Nifedipine is a Calcium-channel blocker that selectively inhibits calcium ion influx across the cell membrane of cardiac muscle and vascular smooth muscle, without changing serum calcium concentrations. Nifedipine causes decreased peripheral vascular resistance and a modest fall in systolic and diastolic pressure (5–10 mm Hg systolic), though the drop in blood pressure sometimes can be more dramatic. The drug generally is given for an acute episode of AD using the ‘bite and swallow’ method, in a dose of 10 mg. Five studies (n=59)4953 have evaluated nifedipine, including two Level 2 controlled, but non-randomized trials49, 50 and three Level 4 studies.5153 Four of these five studies demonstrated a reduction or alleviation of AD with nifedipine.49, 5153 Nifedipine was successfully tested in one non-RCT involving SCI individuals undergoing electroejaculation.49 In this study, Steinberger and co-investigators49 reported that sublingual nifedipine decreased peak systolic, diastolic and mean blood pressure. Furthermore, Braddom and Rocco surveyed 86 physicians with an average of 16.8 years experience managing SCI patients with AD,92 and found that the pharmacologic treatment of AD varied greatly from physician to physician; however, antihypertensive medications were the most frequently used medications. Nifedipine was used preferentially by 48% of physicians for minor AD cases, and by 58% of physicians for severe symptomatic AD. Even though nifedipine has been the most commonly-used agent in the management of AD in individuals with SCI,51, 53, 54, 92 its use has declined recently, Because of concern over the potential for adverse events.93, 94 There have been no reported serious adverse events from the use of nifedipine in the treatment of AD,90 albeit, sample size has been small in all the studies. However, a review of nifedipine in the management of hypertensive emergencies not specific to SCI identifies serious adverse effects, like stroke, acute myocardial infarction, numerous instances of severe hypotension, and death.95 Due to several reports of serious adverse reactions occurring after the administration of immediate-release nifedipine, the Joint National Committee on Detection, Evaluation and Treatment of High Blood Pressure has discouraged the use of this drug.96


There is Level 2 evidence (from 2 prospective, controlled trials)49, 50 that nifedipine is useful to prevent dangerous blood pressure reactions; e.g. during cystoscopy and other diagnostic or therapeutic procedures in SCI patients with AD. However, there is clinical consensus that the potential exists for serious adverse events with this drug, based upon what has been reported in other, non-SCI populations.

2b. Nitrates (Nitroglycerine, Depo-Nit, Nitrostat, Nitrol, Nitro-Bid)

Nitrates have been used for acute episodes of AD because they cause relaxation of vascular smooth muscle, producing vasodilator effects on peripheral arteries and veins. Dilation of post-capillary vessels, including large veins, promotes peripheral pooling of blood and decreases venous return to the heart, thereby reducing left ventricular end-diastolic pressure (preload). Arteriolar relaxation reduces systemic vascular resistance and arterial pressure (after-load). Before nitrates (e.g., nitroglycerin, isosorbide dinitrate, or sodium nitroprusside) are administered, a person with a SCI presenting with acute AD should be questioned regarding their use of sildenafil, however. If this agent has been used within the last 24 hours, it is recommended that an alternative, short-acting, rapid-onset non-nitrate antihypertensive agent be used. Nitrates are the second most commonly used agents after nifedipine in the management of AD in individuals with SCI86, 92 Having said this, with the exception of a single case report involving the intravenous administration of nitroprusside,45 no studies, and only expert opinions86 support the use of nitrates in patients with SCI.


There is Level 5 evidence (clinical consensus),86, 92 but no clinical studies which support the use of nitrates in the acute management of AD post SCI

2c. Captopril

Captopril is a specific competitive inhibitor of angiotensin I-converting enzyme (ACE). During an acute episode of AD, 25 mg captopril often is administered sublingually. In one pre-post study (n=26),54 captopril was safe and effective for AD management in 4 out of 5 episodes. This prospective, open-labeled study and numerous expert opinions suggest the use of the captopril as a primary medication in the management of AD86, 93, 94


There is Level 4 evidence (from one pre-post study)54 that captopril may be beneficial in the acute management of AD in SCI patients.

2d. Terazosin

Terazosin is a long-acting, alpha-1 adrenoceptor selective blocking agent. Selective alpha-1 blockade has been suggested as an appropriate pharmacological choice in the management of AD, because of its added effect at the bladder level, which includes inhibition of the urinary sphincter and relaxation of the smooth muscles of blood vessels. Regular doses of Terazosin over weeks or months have been evaluated in three Level 4 studies (n=57),5557 and appear to be effective in preventing AD without producing erectile dysfunction. In these studies, patients reported moderate to excellent improvement57 or even complete termination of their dysreflexic symptoms55 over the 3-month period of Terazosin administration.


There is Level 4 evidence (from 3 pre-post studies)5557 that the regular use of Terazosin may have positive effects, in terms of alleviating incontinence and preventing episodes of AD.

2e. Prazosin (Minipress)

Prazosin is a postsynaptic alpha-1 adrenoceptor blocker, which lowers blood pressure by relaxing blood vessels. It has a minimal effect on cardiac function, due to its alpha-1 receptor selectivity. The recommended starting dose in adults is 0.5 or 1 milligram (mg) 2–3 times daily. In a small (n=15),58 but high-quality RCT, Prazosin twice daily was well tolerated and did not excessively lower baseline blood pressure; AD episodes also were less severe and shorter in duration over a 2-week period.


There is Level 1 evidence (from one RCT)58 that Prazosin is superior to placebo in the prophylactic management of AD.

2f. Phenoxybenzamine hydrochloride (Dibenzyline)

Phenoxybenzamine (trade name = Dibenzyline) is a long-acting, adrenergic, alpha-receptor blocking agent that can increase blood flow to skin, mucosa, and abdominal viscera, and can lower both supine and erect blood pressures. The initial dose is 10 mg of phenoxybenzamine hydrochloride bid, with incremental increases daily, usually up to 20–40 mg 2–3 times per day.


Study results are conflicting with respect to using phenoxybenzamine for AD in SCI patients, with no effect on AD occurrence or severity in one study50 and a positive treatment effect in the other.59

2g. Prostaglandin E2

Prostaglandins comprise a group of hormone-like substances that participate in a wide range of bodily functions, such as the contraction and relaxation of smooth muscle, the dilation and constriction of blood vessels, and control of blood pressure. Frankel and Mathias60 studied five SCI subjects, among whom, 3 underwent electrical ejaculation both with and without Prostaglandin E2, and found that the level of BP recorded during electrical ejaculation decreased with the drug.


There is Level 2 evidence from a very small prospective controlled study60 that the level of BP recorded during electrical ejaculation is substantially reduced with Prostaglandin E2.

2h. Sildanefil (Viagra)

Sildanefil is an inhibitor of phosphodiesterase type 5 (PDE5). It causes increased levels of cGMP in the corpus cavernosum, as well as smooth muscle relaxation and increased inflow of blood to the corpus cavernosum. At recommended doses, Sildenafil does not have these effects in the absence of sexual stimulation. The recommended dose is 50 mg taken, as needed, approximately 1 hour before sexual activity; but may be taken anywhere from 4 hours to 0.5 hour before-hand. The drug is known to potentiate the hypotensive effects of nitrates and, therefore, nitrates in any form are contraindicated with sildanefil use, and vice versa. The effect of sildenafil on AD has been recorded in one RCT (n=13).61 Although sildenafil decreased resting BP, there was no effect on the magnitude of AD resulting from vibrostimulation in men with SCI.


Based on a single RCT,61 there is Level 2 evidence that sildaenafil citrate has no effect on changes in BP during episodes of AD initiated by vibrostimulation in men with SCI.

2i. Other Pharmacological Agents Tested for the Management of AD

The use of other pharmacological agents for the management of AD in individuals with SCI has been reported in the literature (e.g., expert opinion, case reports), but the evidence is insufficient to warrant their recommendation. These drugs include phenazopyridine for AD associated with cystitis;97 magnesium sulfate for AD associated with labour98 or life-threatening AD in intensive care;99 and diazoxide (Hyperstat)100 for acute AD episodes. In addition, there have been reports on the use of beta blockers,101 mecamylamine (Inversine)92 and hydralzine (Apresoline)100 for the general management of AD symptoms in individuals with SCI.


The objective of this review was to evaluate the latest evidence from clinical literature on present strategies in the management and prevention of AD, as well as present latest basic science and clinical data on mechanisms and pathophysiology of this condition. The very small number of RCTs (n=6)33, 40, 41, 48, 58, 61 demonstrates the difficulty of applying this type of review to assessing AD. In many instances (e.g., acute life-threatening episodes of AD), it would be unethical to have a ‘no treatment’ control group, when a well-established protocol for the management of AD has been proposed by the Consortium for Spinal Cord Medicine,86 based upon physiological evidence and clinical consensus. Education on the causes of AD, appropriate bladder and bowel routines, and pressure sore prevention, appear to be the most effective measures for prevention of AD in individuals with SCI. However, for each individual, the identification and elimination of specific triggers for AD also should be employed to manage and prevent this condition.2, 3, 90 Based upon the physiological mechanisms of AD, it is assumed that a multi-modal protocol to reduce triggers of AD would be most effective and there is a need to formally evaluate a combined approach. The most effective approach to AD seems to be preventing it.92 This includes careful evaluation of individuals with SCI and early recognition of possible triggers that could result in AD. Improved clinician awareness of AD and greater attention to eliminating noxious stimuli in individuals with SCI is a priority. Clinicians, family members, and caregivers should be aware that increased afferent stimulation (e.g., via surgery, invasive investigational procedures, and labour) in persons with SCI will increase their risk for AD; and that a variety of procedures can be used to prevent AD episodes.

When conservative management of AD with an established bladder program is not sufficient, detrusor hyperreflexia can be treated pharmacologically and in more difficult cases, with surgery. However, note that all the pharmacological interventions (except for intra-vesical resiniferatoxin) and surgical interventions were lacking in controlled trials. The lack of controlled trials (even those involving other deemed therapeutic interventions) seriously undermines the strength of this evidence. On the positive side, several of these studies have established effects over long periods (e.g., the positive effect of botulinum toxin on detrusor hyperreflexia over nine months, and the positive effect of augmentation enterocystoplasy on detrusor hyperreflexia over one year).

We emphazis that AD is often not recognized outside of specialized SCI rehabilitation facilities. Despite appropriate medical care and advances in our understanding of the possible pathophysiology of AD, the majority of individuals susceptible to AD (those with cervical and high thoracic SCI) experience numerous episodes of AD during their acute and sub-acute rehabilitation period.14, 15 Unfortunately, the level of awareness of AD among family physicians, and medical personal in ER or ambulance services appears to be low, especially as it pertains to SCI patients (unpublished observations). This reinforces the need to educate and empower individuals with SCI and their families, so that they can direct their own treatment. This reinforces the need to educate and empower individuals with SCI and their families, so that they can direct their own treatment. Furthermore, all individuals with SCI should carry a Medical Emergency Card for Autonomic Dysreflexia.86 This card provides a short description of AD as a medical emergency, and gives brief details on its causes, presentation and management. The ultimate goal in the management of AD in individuals with SCI is protecting them from its development and ensuring appropriate and timely intervention. However when non-pharmacological measures fail and systolic blood pressure remains elevated, pharmacological agents should be initiated. Nifedipine, nitrates, and captopril are the most commonly used and recommended agents for the management of acute AD episodes,86, 90, 92 and are supported by Level 2, 5 and 4 evidence, respectively. To date, no RCTs have been conducted to determine which of these agents is best, however.

In some instances, individuals with SCI should be supplied with short-acting antihypertensive agents, like nifedipine or nitrates, which they can take themselves, prior to seeking medical attention. However, if their symptoms continue and/or their blood pressure does not stabilize, they must proceed or be brought to the nearest emergency department for further management.


There was a severe lack of controlled trials in the management and prevention of AD. A variety of options are available to prevent AD (e.g., surgical, pharmacological), but only intersphincteric anal block with lidocaine when undergoing anorectal procedures had evidence using a control group (Level 1). The identification and elimination of specific triggers for AD (e.g., distended bladder) are considered the first line of treatment based on physiological rationale and expert consensus, but there are virtually no controlled trials which evaluate these effects. When non-pharmacological actions fail in an acute episode, pharmacological agents are required and nifedipine, nitrates, and captopril are the most commonly used and recommended agents. However, only nifedipine is supported by controlled trials (Level 2). RCTs to determine which of these agents or combinations of therapies are effective are severely needed.


We would like to acknowledge the support we have received from the Rick Hansen Man in Motion Foundation and the Ontario Neurotrauma Foundation. In addition, career scientist awards were provided from the Michael Smith Foundation for Health Research and from the Canadian Institutes of Health Research (to JE and DW).

This research was supported by Canadian Institute for Health Research (grant no. MSH-63617)


Reprints available from the author.


1. Mathias CJ, Frankel HL. Cardiovascular control in spinal man. Annu Rev Physiol. 1988;50:577–92. [PubMed]
2. Teasell RW, Arnold JM, Krassioukov A, Delaney GA. Cardiovascular consequences of loss of supraspinal control of the sympathetic nervous system after spinal cord injury. Arch Phys Med Rehabil. 2000;81:506–16. [PubMed]
3. Mathias CJ, Bannister R. Autonomic disturbances in spinal cord lesions. In: Mathias CJ, editor. Autonomic failure: a textbook of clinical disorders of the autonomic nervous system. Oxford University Press; Oxford: 2002. pp. 839–81.
4. Claydon VE, Elliott SL, Sheel AW, Krassioukov A. Cardiovascular responses to vibrostimulation for sperm retrieval in men with spinal cord injury. J Spinal Cord Med. 2006;29:207–16. [PMC free article] [PubMed]
5. Linsenmeyer TA, Campagnolo DI, Chou IH. Silent autonomic dysreflexia during voiding in men with spinal cord injuries. J Urol. 1996;155:519–22. [PubMed]
6. Ekland M, Krassioukov A, McBride KE, Elliott SL. Incidence of autonomic dysreflexia and silent autonomic dysreflexia in men with SCI undergoing sperm retrieval: Implications for clinical practice. J Spinal Cord Med. 2007;30:43–50. [PMC free article] [PubMed]
7. Yarkony GM, Katz RT, Wu YC. Seizures secondary to autonomic dysreflexia. Arch Phys Med Rehabil. 1986;67:834–35. [PubMed]
8. Pine ZM, Miller SD, Alonso JA. Atrial fibrillation associated with autonomic dysreflexia. Am J Phys Med Rehabil. 1991;70:271–73. [PubMed]
9. Eltorai I, Kim R, Vulpe M, Kasravi H, Ho W. Fatal cerebral hemorrhage due to autonomic dysreflexia in a tetraplegic patient: case report and review. Paraplegia. 1992;30:355–60. [PubMed]
10. Valles M, Benito J, Portell E, Vidal J. Cerebral hemorrhage due to autonomic dysreflexia in a spinal cord injury patient. Spinal Cord. 2005;43:738–40. [PubMed]
11. Dolinak D, Balraj E. Autonomic dysreflexia and sudden death in people with traumatic spinal cord injury. Am J Forensic Med Pathol. 2007;28:95–8. [PubMed]
12. Mathias CJ, Frankel HL. The cardiovascular system in tetraplegia and paraplegia. In: Frankel HL, editor. Handbook of Clinical Neurology. Elsevier Science; New York: 1992. pp. 435–56.
13. Curt A, Nitsche B, Rodic B, Schurch B, Dietz V. Assessment of autonomic dysreflexia in patients with spinal cord injury. J Neurol Neurosurg Psychiatry. 1997;62:473–77. [PMC free article] [PubMed]
14. Krassioukov AV, Furlan JC, Fehlings MG. Autonomic dysreflexia in acute spinal cord injury: an under-recognized clinical entity. J Neurotrauma. 2003;20:707–16. [PubMed]
15. Silver JR. Early autonomic dysreflexia. Spinal Cord. 2000;38:229–33. [PubMed]
16. Krassioukov A, Claydon VE. The clinical problems in cardiovascular control following spinal cord injury: an overview. Prog Brain Res. 2006;152:223–29. [PubMed]
17. Elliott S, Krassioukov A. Malignant autonomic dysreflexia in spinal cord injured men. Spinal Cord. 2006;44:386–92. [PubMed]
18. Ramer LM, Ramer MS, Steeves JD, Krassioukov AV. Sympaththetic-sensory coupling in the peripheral nervous system may contribute to autonomic dysreflexia following spinal cord injury. J Spinal Cord Med. 2007;30:177.
19. Krenz NR, Meakin SO, Krassioukov AV, Weaver LC. Neutralizing intraspinal nerve growth factor blocks autonomic dysreflexia caused by spinal cord injury. J Neurosci. 1999;19:7405–14. [PubMed]
20. Krassioukov AV, Johns DG, Schramm LP. Sensitivity of sympathetically correlated spinal interneurons, renal sympathetic nerve activity, and arterial pressure to somatic and visceral stimuli after chronic spinal injury. J Neurotrauma. 2002;19:1521–29. [PubMed]
21. Furlan JC, Fehlings MG, Shannon P, Norenberg MD, Krassioukov AV. Descending vasomotor pathways in humans: correlation between axonal preservation and cardiovascular dysfunction after spinal cord injury. J Neurotrauma. 2003;20:1351–63. [PubMed]
22. Rabchevsky AG. Segmental organization of spinal reflexes mediating autonomic dysreflexia after spinal cord injury. Prog Brain Res. 2006;152:265–74. [PMC free article] [PubMed]
23. Ackery AD, Norenberg MD, Krassioukov A. Calcitonin gene-related peptide immunoreactivity in chronic human spinal cord injury. Spinal Cord. 2007;45:678–86. [PubMed]
24. Krassioukov AV, Bunge RP, Pucket WR, Bygrave MA. The changes in human spinal sympathetic preganglionic neurons after spinal cord injury. Spinal Cord. 1999;37:6–13. [PubMed]
25. Krassioukov AV, Weaver LC. Morphological changes in sympathetic preganglionic neurons after spinal cord injury in rats. Neuroscience. 1996;70:211–25. [PubMed]
26. Arnold JM, Feng QP, Delaney GA, Teasell RW. Autonomic dysreflexia in tetraplegic patients: evidence for alpha-adrenoceptor hyper-responsiveness. Clin Auton Res. 1995;5:267–70. [PubMed]
27. McLachlan EM. Diversity of sympathetic vasoconstrictor pathways and their plasticity after spinal cord injury. Clin Auton Res. 2007;17:6–12. [PMC free article] [PubMed]
28. Moseley AM, Herbert RD, Sherrington C, Maher CG. Evidence for physiotherapy practice: a survey of the Physiotherapy Evidence Database (PEDro) Aust J Physiother. 2002;48:43–9. [PubMed]
29. Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Aubut JA, Abramson C, Hsieh JTC, Connolly S, Konnyu K. Spinal Cord Injury Rehabilitation Evidence: Method of the SCIRE Systematic Review. Top Spinal Cord Inj Rehabil. 2007;13:1–10. [PMC free article] [PubMed]
30. Sackett DL, Strauss SE, Richardson WS, Rosenberg W, Haynes RB. Evidence-based medicine: how to practice and teach EBM. Edinburgh: Churchill Livingstone; 2000.
31. Dykstra DD, Sidi AA, Scott AB, Pagel JM, Goldish GD. Effects of botulinum A toxin on detrusor-sphincter dyssynergia in spinal cord injury patients. J Urol. 1988;139:919–22. [PubMed]
32. Schurch B, Stohrer M, Kramer G, Schmid DM, Gaul G, Hauri D. Botulinum-A toxin for treating detrusor hyperreflexia in spinal cord injured patients: a new alternative to anticholinergic drugs? Preliminary results. J Urol. 2000;164:692–7. [PubMed]
33. Giannantoni A, Di Stasi SM, Stephen RL, Navarra P, Scivoletto G, Mearini E, Porena M. Intravesical capsaicin versus resiniferatoxin in patients with detrusor hyperreflexia: a prospective randomized study. J Urol. 2002;167:1710–4. [PubMed]
34. Igawa Y, Satoh T, Mizusawa H, Seki S, Kato H, Ishizuka O, Nishizawa O. The role of capsaicin-sensitive afferents in autonomic dysreflexia in patients with spinal cord injury. BJU Int. 2003;91:637–41. [PubMed]
35. Giannantoni A, Di Stasi SM, Scivoletto G, Mollo A, Silecchia A, Fuoco U, Vespasiani G. Autonomic dysreflexia during urodynamics. Spinal Cord. 1998;36:756–60. [PubMed]
36. Schurch B, Knapp PA, Jeanmonod D, Rodic B, Rossier AB. Does sacral posterior rhizotomy suppress autonomic hyper-reflexia in patients with spinal cord injury? Br J Urol. 1998;81:73–82. [PubMed]
37. Hohenfellner M, Pannek J, Botel U, Dahms S, Pfitzenmaier J, Fichtner J, Hutschenreiter G, Thuroff JW. Sacral bladder denervation for treatment of detrusor hyperreflexia and autonomic dysreflexia. Urology. 2001;58:28–32. [PubMed]
38. Barton CH, Khonsari F, Vaziri ND, Byrne C, Gordon S, Friis R. The effect of modified transurethral sphincterotomy on autonomic dysreflexia. J Urol. 1986;135:83–85. [PubMed]
39. Sidi AA, Becher EF, Reddy PK, Dykstra DD. Augmentation enterocystoplasty for the management of voiding dysfunction in spinal cord injury patients. J Urol. 1990;143:83–85. [PubMed]
40. Cosman BC, Vu TT. Lidocaine anal block limits autonomic dysreflexia during anorectal procedures in spinal cord injury: a randomized, double-blind, placebo-controlled trial. Dis Colon Rectum. 2005;48:1556–61. [PubMed]
41. Cosman BC, Vu TT, Plowman BK. Topical lidocaine does not limit autonomic dysreflexia during anorectal procedures in spinal cord injury: a prospective, double-blind study. Int J Colorectal Dis. 2002;17:104–8. [PubMed]
42. Cross LL, Meythaler JM, Tuel SM, Cross AL. Pregnancy, labor and delivery post spinal cord injury. Paraplegia. 1992;30:890–902. [PubMed]
43. Hughes SJ, Short DJ, Usherwood MM, Tebbutt H. Management of the pregnant woman with spinal cord injuries. Br J Obstet Gynaecol. 1991;98:513–18. [PubMed]
44. Cross LL, Meythaler JM, Tuel SM, Cross AL. Pregnancy following spinal cord injury. West J Med. 1991;154:607–11. [PMC free article] [PubMed]
45. Ravindran RS, Cummins DF, Smith IE. Experience with the use of nitroprusside and subsequent epidural analgesia in a pregnant quadriplegic patient. Anesth Analg. 1981;60:61–63. [PubMed]
46. Lambert DH, Deane RS, Mazuzan JE., Jr Anesthesia and the control of blood pressure in patients with spinal cord injury. Anesth Analg. 1982;61:344–48. [PubMed]
47. Eltorai IM, Wong DH, Lacerna M, Comarr AE, Montroy R. Surgical aspects of autonomic dysreflexia. J Spinal Cord Med. 1997;20:361–64. [PubMed]
48. Matthews JM, Wheeler GD, Burnham RS, Malone LA, Steadward RD. The effects of surface anaesthesia on the autonomic dysreflexia response during functional electrical stimulation. Spinal Cord. 1997;35:647–51. [PubMed]
49. Steinberger RE, Ohl DA, Bennett CJ, McCabe M, Wang SC. Nifedipine pretreatment for autonomic dysreflexia during electroejaculation. Urology. 1990;36:228–31. [PubMed]
50. Lindan R, Leffler EJ, Kedia KR. A comparison of the efficacy of an alpha-I-adrenergic blocker in the slow calcium channel blocker in the control of autonomic dysreflexia. Paraplegia. 1985;23:34–8. [PubMed]
51. Thyberg M, Ertzgaard P, Gylling M, Granerus G. Effect of nifedipine on cystometry-induced elevation of blood pressure in patients with a reflex urinary bladder after a high level spinal cord injury. Paraplegia. 1994;32:308–13. [PubMed]
52. Kabalin JN, Lennon S, Gill HS, Wolfe V, Perkash I. Incidence and management of autonomic dysreflexia and other intraoperative problems encountered in spinal cord injury patients undergoing extracorporeal shock wave lithotripsy without anesthesia on a second generation lithotriptor. J Urol. 1993;149:1064–67. [PubMed]
53. Dykstra DD, Sidi AA, Anderson LC. The effect of nifedipine on cystoscopy-induced autonomic hyperreflexia in patients with high spinal cord injuries. J Urol. 1987;138:1155–57. [PubMed]
54. Esmail Z, Shalansky KF, Sunderji R, Anton H, Chambers K, Fish W. Evaluation of captopril for the management of hypertension in autonomic dysreflexia: a pilot study. Arch Phys Med Rehabil. 2002;83:604–8. [PubMed]
55. Vaidyanathan S, Soni BM, Sett P, Watt JW, Oo T, Bingley J. Pathophysiology of autonomic dysreflexia: long-term treatment with terazosin in adult and paediatric spinal cord injury patients manifesting recurrent dysreflexic episodes. Spinal Cord. 1998;36:761–70. [PubMed]
56. Swierzewski SJ, 3rd, Gormley EA, Belville WD, Sweetser PM, Wan J, McGuire EJ. The effect of terazosin on bladder function in the spinal cord injured patient. J Urol. 1994;151:951–54. [PubMed]
57. Chancellor MB, Erhard MJ, Hirsch IH, Stass WE., Jr Prospective evaluation of terazosin for the treatment of autonomic dysreflexia. J Urol. 1994;151:111–13. [PubMed]
58. Krum H, Louis WJ, Brown DJ, Howes LG. A study of the alpha-1 adrenoceptor blocker prazosin in the prophylactic management of autonomic dysreflexia in high spinal cord injury patients. Clin Auton Res. 1992;2:83–8. [PubMed]
59. McGuire J, Wagner FM, Weiss RM. Treatment of autonomic dysreflexia with phenoxybenzamine. J Urol. 1976;115:53–5. [PubMed]
60. Frankel HL, Mathias CJ. Severe hypertension in patients with high spinal cord lesions undergoing electro-ejaculation--management with prostaglandin E2. Paraplegia. 1980;18:293–99. [PubMed]
61. Sheel AW, Krassioukov AV, Inglis JT, Elliott SL. Autonomic dysreflexia during sperm retrieval in spinal cord injury: influence of lesion level and sildenafil citrate. J Appl Physiol. 2005;99:53–8. [PubMed]
62. McGuire TJ, Kumar VN. Autonomic dysreflexia in the spinal cord-injured. What the physician should know about this medical emergency. Postgrad Med. 1986;80:81–4. 89. [PubMed]
63. Waites KB, Canupp KC, DeVivo MJ. Epidemiology and risk factors for urinary tract infection following spinal cord injury. Arch Phys Med Rehabil. 1993;74:691–95. [PubMed]
64. Vaidyanathan S, Soni BM, Dundas S, Krishnan KR. Urethral cytology in spinal cord injury patients performing intermittent catheterisation. Paraplegia. 1994;32:493–500. [PubMed]
65. Vaidyanathan S, Singh G, Soni BM, Hughes PL, Mansour P, Oo T, Bingley J, Sett P. Do spinal cord injury patients always get the best treatment for neuropathic bladder after discharge from regional spinal injuries centre? Spinal Cord. 2004;42:438–42. [PubMed]
66. Consortium for Spinal Cord Medicine. Paralyzed Veterans of America; 2006. Bladder management for adults with spinal cord Injury: A clinical Practice guideline for health-care providers. [PMC free article] [PubMed]
67. Waites KB, Canupp KC, DeVivo MJ. Eradication of urinary tract infection following spinal cord injury. Paraplegia. 1993;31:645–52. [PubMed]
68. DeVivo MJ, Krause JS, Lammertse DP. Recent trends in mortality and causes of death among persons with spinal cord injury. Arch Phys Med Rehabil. 1999;80:1411–19. [PubMed]
69. Snow JC, Sideropoulos HP, Kripke BJ, Freed MM, Shah NK, Schlesinger RM. Autonomic hyperreflexia during cystoscopy in patients with high spinal cord injuries. Paraplegia. 1978;15:327–32. [PubMed]
70. Chancellor MB, Rivas DA, Erhard MJ, Hirsch IH, Bagley DH. Flexible cystoscopy during urodynamic evaluation of spinal cord-injured patients. J Endourol. 1993;7:531–35. [PubMed]
71. Ahmed HU, Shergill IS, Arya M, Shah PJ. Management of detrusor-external sphincter dyssynergia. Nat Clin Pract Urol. 2006;3:368–80. [PubMed]
72. Secrest CL, Madjar S, Sharma AK, Covington-Nichols C. Urethral reconstruction in spinal cord injury patients. J Urol. 2003;170:1217–21. discussion 1221. [PubMed]
73. Hawkins RL, Jr, Bailey HR, Donnovan WH. Autonomic dysreflexia resulting from prolapsed hemorrhoids. Report of a case. Dis Colon Rectum. 1994;37:492–3. [PubMed]
74. Teichman JM, Barber DB, Rogenes VJ, Harris JM. Malone antegrade continence enemas for autonomic dysreflexia secondary to neurogenic bowel. J Spinal Cord Med. 1998;21:245–7. [PubMed]
75. Ackery A, Tator C, Krassioukov A. A global perspective on spinal cord injury epidemiology. J Neurotrauma. 2004;21:1355–70. [PubMed]
76. Jackson AB, Wadley V. A multicenter study of women’s self-reported reproductive health after spinal cord injury. Arch Phys Med Rehabil. 1999;80:1420–8. [PubMed]
77. Sipski ML. The impact of spinal cord injury on female sexuality, menstruation and pregnancy: a review of the literature. J Am Paraplegia Soc. 1991;14:122–6. [PubMed]
78. Sipski ML, Arenas A. Female sexual function after spinal cord injury. Prog Brain Res. 2006;152:441–7. [PubMed]
79. McGregor JA, Meeuwsen J. Autonomic hyperreflexia: a mortal danger for spinal cord-damaged women in labor. Am J Obstet Gynecol. 1985;15:330–3. [PubMed]
80. American College of Obstetrics and Gynecology. ACOG committee opinion. Obstetric management of patients with spinal cord injuries. Number 275, September 2002. Committee on Obstetric Practice. American College of Obstetrics and Gynecology. Int J Gynaecol Obstet. 2002;79:189–91. [PubMed]
81. Kutzenberger J, Domurath B, Sauerwein D. Spastic bladder and spinal cord injury: seventeen years of experience with sacral deafferentation and implantation of an anterior root stimulator. Artif Organs. 2005;29:239–41. [PubMed]
82. Sampson EE, Burnham RS, Andrews BJ. Functional electrical stimulation effect on orthostatic hypotension after spinal cord injury. Arch Phys Med Rehabil. 2000;81:139–43. [PubMed]
83. Wood DE, Dunkerley AL, Tromans AM. Results from bone mineral density scans in twenty-two complete lesion paraplegics. Spinal Cord. 2001;39:145–8. [PubMed]
84. Ashley EA, Laskin JJ, Olenik LM, Burnham R, Steadward RD, Cumming DC, Wheeler GD. Evidence of autonomic dysreflexia during functional electrical stimulation in individuals with spinal cord injuries. Paraplegia. 1993;3:593–605. [PubMed]
85. McGillivray CF, Krassioukov A, Hitzing SL, Tonack M, Craven C, Greene C. Autonomic Dysreflexia – Evaluating Knowledge among individuals with SCI and Health Practitioners. Journal of Spinal Cord Medicine. 2006;29:331.
86. Consortium for Spinal Cord Medicine. Paralyzed Veterans of America; 2001. Acute management of autonomic dysreflexia: Individuals with spinal cord injury presenting to health-care facilities. [PubMed]
87. Claydon VE, Krassioukov AV. Orthostatic hypotension and autonomic pathways after spinal cord injury. J Neurotrauma. 2006;23:1713–25. [PubMed]
88. Krassioukov AV, Harkema SJ. Effect of harness application and postural changes on cardiovascular parameters of individuals with spinal cord injury. Spinal Cord. 2006;44:780–6. [PubMed]
89. Sidorov EV, Townson AF, Dvorak MF, Kwon BK, Steeves J, Krassioukov A. Orthostatic hypotension in the first month following acute spinal cord injury. Spinal Cord. 2008;46:65–9. [PubMed]
90. Blackmer J. Rehabilitation medicine: 1. Autonomic dysreflexia. CMAJ. 2003;169:931–35. [PMC free article] [PubMed]
91. Naftchi NE, Richardson JS. Autonomic dysreflexia: pharmacological management of hypertensive crises in spinal cord injured patients. J Spinal Cord Med. 1997;20:355–60. [PubMed]
92. Braddom RL, Rocco JF. Autonomic dysreflexia. A survey of current treatment. Am J Phys Med Rehabil. 1991;70:234–41. [PubMed]
93. Frost F. Antihypertensive therapy, nifedipine, and autonomic dysreflexia. Arch Phys Med Rehabil. 2002;83:1325–6. author reply 1326. [PubMed]
94. Anton HA, Townson A. Drug therapy for autonomic dysreflexia. CMAJ. 2004;170:1210. [PMC free article] [PubMed]
95. Grossman E, Messerli FH, Grodzicki T, Kowey P. Should a moratorium be placed on sublingual nifedipine capsules given for hypertensive emergencies and pseudoemergencies? JAMA. 1996;276:1328–31. [PubMed]
96. The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure. Arch Intern Med. 1997;157:2413–46. [PubMed]
97. Paola FA, Sales D, Garcia-Zozaya I. Phenazopyridine in the management of autonomic dysreflexia associated with urinary tract infection. J Spinal Cord Med. 2003;26:409–11. [PubMed]
98. Maehama T, Izena H, Kanazawa K. Management of autonomic hyperreflexia with magnesium sulfate during labor in a woman with spinal cord injury. Am J Obstet Gynecol. 2000;183:492–3. [PubMed]
99. Jones NA, Jones SD. Management of life-threatening autonomic hyper-reflexia using magnesium sulphate in a patient with a high spinal cord injury in the intensive care unit. Br J Anaesth. 2002;88:434–38. [PubMed]
100. Erickson RP. Autonomic hyperreflexia: pathophysiology and medical management. Arch Phys Med Rehabil. 1980;61:431–40. [PubMed]
101. Pasquina PF, Houston RM, Belandres PV. Beta blockade in the treatment of autonomic dysreflexia: a case report and review. Arch Phys Med Rehabil. 1998;79:582–84. [PubMed]