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Pathophysiology of Autonomic Dysreflexia

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Pathophysiology of Autonomic Dysreflexia Spinal Cord (1998) 36, 761 ± 770 ã 1998 International Medical Society of Paraplegia All rights reserved 1362 ± 4393/98 $12.00 http://www.stockton-press.co.uk/sc Pathophysiology of autonomic dysre¯exia: long-term treatment with terazosin in adult and paediatric spinal cord injury patients manifesting recurrent dysre¯exic episodes S Vaidyanathan, BM Soni, P Sett, JWH Watt, T Oo and J Bingley Regional Spinal Injuries Centre, District General Hospital, Southport Merseyside PR8 6PN, UK Introduction: Spinal cord injury (SCI) results in disruption of synaptic in¯uences on the sympathetic preganglionic neurones. Remodelling of spinal cord circuits takes place in spinal neurones caudal to cord injury. There is an increased vascular alpha-adrenoceptor responsiveness, and peripheral aerent (bladder) stimulation in SCI subjects induces a marked noradrenaline spillover below the level of spinal lesion. These neurophysiological changes possibly contribute to the development of autonomic dysre¯exia, a condition of sympathetic hyper-excitability that develops after cervical, or upper dorsal cord injury with resultant paroxysmal rise in arterial pressure, and provide the scienti®c basis for the use of terazosin, a once-a-day, selective alpha-one adrenergic blocking drug. Objectives: The use of terazosin, a long-acting, alpha 1-selective blocking agent was investigated in SCI patients who developed recurrent symptoms of autonomic dysre¯exia, eg headache, sweating ¯ushing of the face together with an increase in the arterial pressure. Design: An open, prospective study of the ecacy of terazosin in controlling recurrent autonomic dysre¯exia in traumatic tetraplegic/paraplegic patients manifesting clinical features of dysre¯exia in the absence of an acute precipitating cause such as a blocked catheter. Setting: The initial assessment and treatment were carried out in the Spinal Injuries Centre. Subsequently, the patients were followed-up in the community. They were monitored by telephonic interviews, follow-up visits by the patients to the hospital, and home-visits by the sta of the spinal unit. Subjects: Eighteen adults with tetraplegia (female: 1; male: 17), three children with ventilator- dependent tetraplegia and three adult male patients with paraplegia who exhibited recurrent features of autonomic dysre¯exia in the absence of an acute predisposing factor for dysre¯exia eg performance of an invasive procedure such as cystoscopy, digital evacuation of bowels, or acute urinary retention, were enrolled in this study. Intervention: After discussion with the patients and their carers, terazosin was prescribed with a starting dose of 1 mg in an adult and 0.5 mg in a child administered nocte. The patients were observed for (1) drug-induced hypotension; (2) clinical symptoms due to side eects of terazosin; and (3) continued occurrence of dysre¯exic symptoms. Step-wise increments of the dose of terazosin (1 mg in case of adults, and 0.5 mg in a child) was carried out at intervals of 3 ± 4 days, if a patient continued to develop dysre¯exia but did not manifest any serious side eect. Outcome measures: Complete subsidence of dysre¯exic symptoms, or development of an adverse event necessitating termination of the terazosin therapy was the clinical end point. Results: The dysre¯exic symptoms subsided completely with the terazosin therapy in all the patients. The twenty-one adult patients required a dose varying from 1 ± 10 mg, whereas the paediatric patients required only 1 ± 2 mg of terazosin. The side eects of postural hypotension and drowsiness were transient, and mild. One tetraplegic patient developed persistent dizziness and therefore, the drug therapy was discontinued. Conclusion: In 21 adult and three paediatric spinal cord injury patients manifesting recurrent episodes of autonomic dysre¯exia in the absence of an acute predisposing cause, the use of terazosin, a once-a-day, speci®c alpha-one blocker resulted in complete subsidence of the dysre¯exic symptoms. However, one tetraplegic patient required termination of terazosin therapy because of persistent dizziness. Keywords: terazosin; autonomic dysre¯exia; spinal cord injury; tetraplegia; remodelling of spinal cord circuits Correspondence: S Vaidyanathan Treatment of recurrent autonomic dysreflexia in SCI patients with terazosin S Vaidyanathan et al 762 Introduction These changes may explain why patients do not Autonomic dysre¯exia is an acute syndrome charac- manifest autonomic dysre¯exia immediately after the terised by (1) a sudden increase in blood pressure with spinal cord injury. In chronic spinal cord-injured rats, compensatory bradycardia, (2) headache, and (3) one month after cord transection, there is remodelling profuse sweating and vasodilation with skin ¯ushing of the dendritic arbor of preganglionic neurones and above the level of spinal cord injury. Autonomic the intensity of the reactive gliosis around the dysre¯exia occurs in patients with a spinal cord injury preganglionic neurones was diminished.6 By 30 days above the greater splanchnic out¯ow, usually above T- after complete transection, the atrophy of SPN had 6; however, autonomic dysre¯exia has been reported to been reversed. This recovery of normal morphology in occur with spinal cord injuries at neurological levels as SPN, and reorganization of synaptic inputs to SPN are low as T-8.1 Proprioceptive and noxious stimuli below consistent with the return of large and sustained the level of injury may induce an episode of autonomic excitatory sympathetic responses that cause episodic dysre¯exia, and the acute increase in arterial blood hypertension (autonomic dysre¯exia) after this time pressure may cause seizures, intracerebral haemor- period. In clinical practice also, the episodic hyperten- rhage, or even death.2 Although certain events such sive responses associated with autonomic dysre¯exia as distension of the urinary bladder or bowel, acute undergo a time-dependent increase in magnitude after cystitis, cystoscopy, cystometry, percutaneous nephro- cord injury.7 Moreover, sprouting of the central lithotomy, extracorporeal shock wave lithotripsy and arbour of primary aerent neurones occur by 2 weeks sexual act3 may precipitate autonomic dysre¯exia, after a spinal cord injury in rats.8 This exaggerated dyssynergic voiding and irritation of the trigone by input to spinal interneurones in deeper laminae of the an indwelling urinary catheter are the common causes dorsal horn would also contribute to the development for the occurrence of autonomic dysre¯exia. An of autonomic dysre¯exia. The current concepts on the algorithm has been proposed for the management of neurophysiology of autonomic dysre¯exia in experi- an acute episode of autonomic dysre¯exia after it has mental animals, and in spinal cord injury patients are occurred.4 Sublingual administration of nifedipine, a summarised in Appendix 1. calcium channel blocker, in a dose of ten milligrams These neurophysiological changes constitute the secures rapid control of the sudden increase in blood scienti®c foundation for the pharmacological treat- pressure, and is the standard drug therapy for a spinal ment of recurrent autonomic dysre¯exia with a cord injury patient who has developed the clinical selective alpha-1 adrenergic blocking agent We report features of autonomic dysre¯exia. our clinical experience in 24 spinal cord injury patients Some spinal cord injury patients tend to develop who developed recurrent episodes of autonomic recurrent episodes of autonomic dysre¯exia. In dysre¯exia and were treated with terazosin, a once-a- patients with a predilection for recurrent autonomic day, selective alpha-1 adrenergic blocking drug. dysre¯exia, it is desirable to prevent the occurrence of dysre¯exic episodes. In this subgroup of tetraplegic Patients and methods and paraplegic subjects with a propensity towards recurrent episodes of autonomic dysre¯exia, the Patients with spinal cord injury who are registered with precipitating cause for the occurrence of autonomic the Regional Spinal Injuries Centre, Southport were the dysre¯exia may elude precise identi®cation in some. In source of subjects for this study. Any patient who others, dyssynergic voiding or an indwelling urinary recounted experiencing symptoms of autonomic dysre- catheter may be the underlying reason. But these ¯exia, or who was detected to exhibit recurrent episodes patients may not ®nd it easy to change their life style. of pounding headaches, sweating, or ¯ushing of the face Therefore, elimination of the precipitating cause for accompanied by an acute increase in the arterial blood the occurrence of autonomic dysre¯exia may not be pressure, was investigated further as to the possible feasible. Consequently, these special groups of spinal existence of a predisposing factor for the occurrence of cord injury patients require round the clock protection autonomic dysre¯exia. Whenever an obvious precipitat- against autonomic dysre¯exia on a continual basis. ing factor for the happening of autonomic dysre¯exia Spinal cord injury disrupts control of sympathetic was detected, eg a blocked urinary catheter, appropriate preganglionic neurones (SPN) because bulbospinal treatment was instituted, viz insertion of a new urinary input has been lost, and the remaining regulation is catheter in this patient. If performance of an invasive accomplished by spinal circuits consisting of dorsal procedure was the predisposing factor for the occur- root aerent and spinal interneurones.5 Experimental rence of autonomic dysre¯exia,
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