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Thread: Terazocin, an alpha-1 adrenergic receptor blocker, suppresses autonomic dysreflexia

  1. #1

    Terazocin, an alpha-1 adrenergic receptor blocker, suppresses autonomic dysreflexia

    This is an older paper reporting that terazocin (an alpha-1 adrenergic receptor blocker) in doses of 1-10 mg per day for adults and 1-2 mg for children, completely blocked autonomic dysreflexia in patients. Only one of 24 patients had to stop the drug because of side-effects of dizziness; otherwise the drug appears to be well-tolerated.

    • Vaidyanathan S, Soni BM, Sett P, Watt JW, Oo T and Bingley J (1998). Pathophysiology of autonomic dysreflexia: long-term treatment with terazosin in adult and paediatric spinal cord injury patients manifesting recurrent dysreflexic episodes. Spinal Cord. 36 (11): 761-70. Summary: INTRODUCTION: Spinal cord injury (SCI) results in disruption of synaptic influences 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 afferent (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 dysreflexia, 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 scientific 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 dysreflexia, eg headache, sweating flushing of the face together with an increase in the arterial pressure. DESIGN: An open, prospective study of the efficacy of terazosin in controlling recurrent autonomic dysreflexia in traumatic tetraplegic/paraplegic patients manifesting clinical features of dysreflexia 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 staff 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 dysreflexia in the absence of an acute predisposing factor for dysreflexia 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 effects of terazosin; and (3) continued occurrence of dysreflexic 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 dysreflexia but did not manifest any serious side effect. OUTCOME MEASURES: Complete subsidence of dysreflexic symptoms, or development of an adverse event necessitating termination of the terazosin therapy was the clinical end point. RESULTS: The dysreflexic 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 effects 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 dysreflexia in the absence of an acute predisposing cause, the use of terazosin, a once-a-day, specific alpha-one blocker resulted in complete subsidence of the dysreflexic symptoms. However, one tetraplegic patient required termination of terazosin therapy because of persistent dizziness. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&li st_uids=9848483> Regional Spinal Injuries Centre, District General Hospital, Southport Merseyside, UK.

  2. #2

    Is this a blood pressure med?

    What would the brand name of this med be?

    Thanks

    //

  3. #3
    Linda,

    It is available, I believe as a generic but is also called Hytrin capsules.

    http://www.rxlist.com/cgi/generic/teraz.htm

    It is made by Geneva Company and it is on contract to the VA
    http://dscp305.dscp.dla.mil/dmmonlin.../terazosin.asp

    It is used to treat hypertension and therefore lowers blood pressure. It also is used to treat benign prostatic hyperplasia.

    I was struck by the positive results in this trial and it is cheap. At $37.53 for ninety 10 mg capsules, it is costs less than 40 cents a day.

    http://www.drugstore.com/pharmacy/pr...401&trx=1Z5006

    wise.

  4. #4
    Senior Member Jeff's Avatar
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    Hmmmm....

    Maybe I'll get a few and try my FertiCare, again. Sounds promising.

    ~See you at the SCIWire-used-to-be-paralyzed Reunion ~

  5. #5
    Wise,

    Question re - 'recurrent episodes of AD in the absence of an acute precipitating cause' - can a person get AD without there being a cause in the body for it?

    Also, re the Hytrin - Matt is on Hytrin to help suppress bladder sphincter spasms - 5 mg. 2X a day - and still gets AD - although when he gets AD, there IS an acute precipitating cause! I'm confused! Jackie

  6. #6
    Jackie, you are right. This treatment is effective only in those patients without an acute precipitating cause. The autonomic system cannot be completely suppressed with a once a day alpha-1 receptor blocker. Other treatments have to be used, including calcium channel blockers, beta blockers, and combined alpha and beta blockers.

    Jeff, it would be good to keep the above in mind. This does not prevent AD resulting from acute precipitating causes.

    Wise.

  7. #7

    AD management

    Anyone with SCI above T7 should also be sure that this hypertension is not due to autonomic dysreflexia, which can have many causes. Masking hypertension due to AD may eliminate the benefits of AD, which is to tell you that your body is in pain and something is seriously wrong. The cause of the AD should still be explored vigorously. Although there is some mention in the literature of AD with no cause, in my experience if you search long enough, a cause is almost always identified. Masking this could cause you to become seriously ill or worse due to the proximate cause of the AD.

    (KLD)

  8. #8

    Thank You

    Thanks for the info. Definitely seems like it might help me. I'm going to forward info to my doctor and see if it would be for me. My AD affects the heart rhythm and I am concerned that these episodes will cause CHF. I have been chemically converted. The cardio told me the meds would be ineffective because it is the autonomic nervous system not some other type of physical abnormality.

    //

  9. #9
    Senior Member Jeff's Avatar
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    Thanks for warning me

    Guess I'll hold off....

    ~See you at the SCIWire-used-to-be-paralyzed Reunion ~

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