Cases reported "Hypotension, Orthostatic"

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1/10. Hormonal and cardiovascular reflex assessment in a female patient with pure autonomic failure.

    We report the case of a 72-year-old female with pure autonomic failure, a rare entity, whose diagnosis of autonomic dysfunction was determined with a series of complementary tests. For approximately 2 years, the patient has been experiencing dizziness and a tendency to fall, a significant weight loss, generalized weakness, dysphagia, intestinal constipation, blurred vision, dry mouth, and changes in her voice. She underwent clinical assessment and laboratory tests (biochemical tests, chest X-ray, digestive endoscopy, colonoscopy, chest computed tomography, abdomen and pelvis computed tomography, abdominal ultrasound, and ambulatory blood pressure monitoring). Measurements of catecholamine and plasmatic renin activity were performed at rest and after physical exercise. Finally the patient underwent physiological and pharmacological autonomic tests that better diagnosed dysautonomia.
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2/10. Downbeating nystagmus and postural hypotension due to basilar invagination.

    Downbeating nystagmus is an involuntary vertical rhythmic eye movement with the fast component in the downward direction. The sign indicates a craniocervical disorder. The most common cause is the arnold-chiari malformation, followed by cerebellar degeneration. Basilar invagination is a rare cause of downbeating nystagmus. However, with appropriate treatment its prognosis is good. Here, we report a case of basilar invagination which presented with downbeating nystagmus and postural hypotension. A 31 year-old Thai male patient had a 20 year history of postural hypotension. He had recurrent pneumonia and cough-induced syncope a year before admission. He complained of symptoms of an acute febrile illness and a productive cough. The physical examination showed high grade fever, postural hypotension and medium crepitation in the right upper lobe. The neurological examination showed downbeating nystagmus, atrophy and fasciculation of the right side of the tongue, atrophy of the right sternocleidomastoid muscle, mild weakness of the extremities and generalized hyperreflexia. The cervical spine X-ray revealed upward displacement of the vertebral bodies of C1 and C2, with a mild narrowing of the space between C1 and the occiput. The CT-myelogram and MRI showed upward displacement of C1 with overriding of the dens over the anterior lip of the foramen magnum; this also compressed the medulla. syringomyelia was seen at the C1-C5 level. We report a patient who presented with postural hypotension, recurrent pneumonia and downbeating nystagmus due to basilar invagination. The symptoms were aggravated by cough which caused an increase in intracranial pressure. This resulted from medulla compression in the foramen magnum by the first cervical spine. The treatment of choice was surgical decompression.
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3/10. spinal cord injury medicine. 2. Medical complications after spinal cord injury: Identification and management.

    This is a self-directed learning module that reviews medical complications associated with spinal cord injury (SCI). It is part of a chapter on SCI medicine in the Self-Directed Physiatric Educational Program for practitioners and trainees in physical medicine and rehabilitation. This article includes discussion of common medical complications that impact rehabilitation and long-term follow-up for individuals with SCI. Issues addressed include the rehabilitation approach to SCI individuals with pressure ulcers, unilateral lower-extremity swelling (deep venous thrombosis, heterotopic ossification, fractures), along with the pathophysiology, assessment, and treatment of spasticity, autonomic dysreflexia, orthostatic hypotension, and pain. overall ARTICLE OBJECTIVE: To describe diagnostic and treatment approaches for medical complications common to individuals with SCI.
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4/10. stroke rehabilitation therapy in a patient with a cardiac pacemaker for chronic atrial fibrillation.

    A 65-year-old man was implanted with an artificial pacemaker for chronic bradycardic atrial fibrillation associated with hypertensive heart disease. Five years after the pacemaker implantation, he suffered from a cerebral embolism. Approximately 4.5 months after the ictus, he was transferred to the rehabilitation ward. He had flaccid left hemiplegia and severe disuse syndrome. He could not sit and could tilt his head up for only two minutes because of severe orthostatic hypotension. By modulating the rate-responsive mode of the pacemaker every 2-4 weeks, we were able to rehabilitate the patient. Thus, the patient could sit in a wheelchair for more than three hours. This case emphasizes the importance of examining the mode and function of a previously implanted artificial pacemaker. In accord with varying rehabilitation programs and gradual improvement in a patient's physical activities, periodic modulation of a programmable pacemaker can lead to a better functional outcome during rehabilitation therapy.
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5/10. Aortic stenosis and autonomic dysfunction: co-conspirators in syncope.

    Autonomic dysfunction and aortic stenosis share several clinical characteristics, including, in severe cases, syncope. Both illnesses tend to manifest later in life, and most cases are idiopathic in origin. In a short period of 4 weeks, the authors noted that three patients out of 36 referrals for autonomic dysfunction also had histories of aortic valve replacement due to stenosis. In each case, similar presenting symptoms of fatigue, light-headedness, and syncope were attributed to aortic stenosis without mention of autonomic failure as a possible contributor. The authors propose that patients for whom symptoms of aortic valve stenosis are not relieved by surgical intervention may have concomitant autonomic dysfunction contributing significantly to their symptoms. Furthermore, the two conditions may comprise a dangerous combination, aortic stenosis causing physical obstruction of ventricular outflow, and autonomic dysfunction causing decreased venous return and insufficient cardiac filling. It may be beneficial for patients with aortic stenosis who present with syncope to be considered for possible autonomic dysfunction to address both potential pathophysiologies contributing to the syncope.
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6/10. Orthostatic hypotension following acute intracerebral haemorrhage.

    BACKGROUND: blood pressure regulation may be impaired following acute stroke. Typically, there is overactivity of the sympathetic nervous system and underactivity of the parasympathetic system resulting in transient hypertension. Orthostatic hypotensive responses in acute stroke are less well documented. CASE REPORT: We present a case of severe persistent orthostatic hypotension (OH) following acute intracerebral haemorrhage in a previously fit and well man. Symptomatic OH persisted for 60 days post-stroke. No known causes of OH could be identified. CONCLUSIONS: Such profound and persistent orthostatic hypotension following an acute intracerebral haemorrhage has not previously been documented. The precise cause of this finding in the case described is unknown, but may have been due to impaired higher-level regulation of the autonomic nervous system. A conservative approach with prolonged physical methods proved successful in rehabilitating this patient without the need for pharmacological intervention.
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7/10. Orthostatic blood pressure control in Marfan's syndrome.

    A 33-year old male patient, with Marfan's syndrome, reported symptoms of orthostatic intolerance and fatigue as a longstanding problem. Orthostatic cardiovascular examination showed poor orthostatic tolerance, with a rise in heart rate and a fall in arterial blood pressure and cerebral blood flow velocity. Self-discovered physical counterpressure manoeuvers improved symptoms, related to a substantial increase in arterial pressure and cerebral perfusion. When orthostatic complaint are reported by patients with Marfan's syndrome, physical counterpressure manoeuvers should be advised to reduce symptoms of postural hypotension.
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8/10. A clinical, physiology and pharmacology evaluation of orthostatic hypotension in the elderly.

    Orthostatic hypotension is very common in the elderly. It increases morbidity and is an independant predictor of all cause mortality. It is defined as a fall in systolic blood pressure greater than 20 mm Hg or a fall in diastolic blood pressure greater than 10 mm Hg within 3 minutes of standing. Symptoms include light headedness, weakness, blurred vision, fatigue and lethargy and falls. Most patients have orthostatic hypotension due to non neurogenic causes. Drugs like antihypertensives and tricyclic antidepressants are very common causes of orthostatic hypotension. diagnosis is based on the history and a thorough clinical examination. Based on the history and physical examination, further testing of the heart, kidneys and autonomic nervous system may be required in selected patients. Non pharmacological methods like slow position change, increased fluid and sodium intake, compression stockings and elevation of head of the bed are the key to management of orthostatic hypotension. After these methods, pharmacological treatment with fludrocortisone and midodrine should be tried. Other drugs like desmopresin acetate, xamoterol, erythropoetin and ocreotide can be used as second line agents in selected patients.
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keywords = physical
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9/10. Mental and physical stress as moderators of the postural response in insulin-dependent diabetic patients.

    Two simple stressors, mental arithmetic and isometric handgrip, were studied as moderators of the physiological response to standing in insulin-dependent diabetic patients and in healthy controls. Continuous (beat-to-beat) measures were taken of heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and skin conductance (SC) during postural change under baseline and stressor conditions. Diabetic patients without symptoms of neuropathy and healthy controls showed generally similar responses to postural change and to the stressor conditions. SBP and DBP were more responsive to the mental and physical stressors than were HR or SC, especially after standing. Two diabetic patients with postural hypotension showed significant increases in overall BP levels and less of a fall in BP during postural change under the stressor conditions, despite minimal HR or SC responses. Results indicate that these strategies are effective in increasing BP during postural change in both diabetic and nondiabetic individuals and may be useful in the management of orthostatic hypotension.
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10/10. Physical manoeuvres that reduce postural hypotension in autonomic failure.

    A young female with autonomic failure is described. She successfully reduced the symptoms of orthostatic hypotension by application of physical manoeuvres like leg-crossing, bending forward and placing a foot on a chair. The beneficial effects of these manoeuvres can be explained by a small (10-15 mmHg) increase in mean arterial pressure to a level just sufficient to maintain adequate cerebral blood flow. The underlying common mechanism appears to be an increase of thoracic blood volume by translocation of blood from the vascular beds below the diaphragm to the chest. Instruction in these physical manoeuvres should be part of the management programme to reduce the disabilities arising from postural hypotension in patients with autonomic failure.
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