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IntruductionOrthostatic hypotension (OH) is one of the complications in patients with spinal cord injury (SCI) particularly in the acute stage. Impairment in the autonomic nervous system, usually in patients with cervical and high thoracic SCI, causes OH that is defined as decrease in systolic blood pressure of at least 20 mm Hg or diastolic blood pressure of at least 10 mm Hg upon changing body position from supine to upright posture. It results from an inefficient response to postural changes in blood pressure. OH may be symptomatic or asymptomatic. Symptoms of OH include dizziness, light-headedness, fainting, blurred vision, muscle weakness, fatigue, nausea, palpitations, and headache (1-4).Non-pharmacological interventions that have been used are salt and fluid regulation, pressure to the abdominal region, upper body exercise, functional electrical stimulation (FES) applied to the legs, compression bandages and/or pressure stockings and tilt training program (3,5). Pharmacological treatment includes agents acting on blood vessels, on blood volume or on other pressor mechanisms. The medications used are fludrocortisone, pyridostigmine, ergotamine, ephedrine, desmopressin, erythropoietin and midodrine (3,4,6).We experienced two cases of tetraplegia having OH treated with midodrine that did not respond to conventional nonpharmacological interventions. Both of the patients were women. One of them was 33-year-old with C4 tetraplegia AIS-A and the other was 19-year-old with C5 tetraplegia AIS-A. The subjects were in acute stage of SCI that were in the first 3 months postinjury. They continued to have OH during transfer to wheelchair or tilt table exercises despite use of antiembolic compression bandage, abdominal binder, and progressive exercises with tilt table. Five mg/d midodrine in two divided doses was started. Improvement in symptoms was observed in both of the patients after 20 days, thus, the dosage was decreased to 2.5 mg/d in two divided doses. One month later, patients' tolerated tilt angle was 90 degrees, so midodrine was stopped in both of the patients. Midodrine was not continued in one of the patients. In the other patient, midodrine 2.5 mg/d was started again one week later because OH continued occasionally. Autonomic dysreflexia (AD) was not observed. No side effects were observed.The predisposition to OH following SCI is not fully understood, but it is thought to be multifactorial (3). Following SCI, the low level of efferent sympathetic activity and the loss of reflex vasoconstriction are among the major causes of OH. OH is more common in tetraplegia than in paraplegia. OH persisting during the first month following SCI was reported to occur in 74% of cervical and in 20% of upper thoracic motor complete SCI patients (7). Both of our two patients had complete tetraplegia. We...