1/116. Postural hypotension in idiopathic Parkinson's disease. Etiopathology.Postural changes in blood pressure were recorded in all 391 patients suffering from Parkinson's syndrome over a period of six years. Intraarterial blood pressure studies were carried out in those with significant postural hypotension. Histological examination of the entire central nervous system and the sympathetic ganglia was performed in six patients suffering from idiopathic Parksinson's disease. Five of the six patients had lewy bodies in the sympathetic ganglia. Loss of nerve cells was noted in the sympathetic ganglia in those patients that demonstrated postural hypotension. The severity of the lesions in the ganglia correlated with the severity of postural hypotension in idiopathic Parkinson's disease, One case of shy-drager syndrome was similarly studied to demonstrate the differences in spinal cord and sympathetic ganglia lesions in the two conditions.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
2/116. Supine hypotensive syndrome caused by intra-abdominal mass: a case report.An obese woman who presented with 3 separate intra-abdominal masses developed a supine hypotensive syndrome following induction of general anesthesia. The hypotension was corrected by positioning the patient in a left lateral tilt and by releasing intra-abdominal pressure. Following decompression of the vena cava, arterial and central venous pressure rose and remained at a high level. urine output was poor until IV furosemide was administered.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
3/116. The use of oral vasopressors in the management of autonomic dysfunction and orthostatic hypotension.OBJECTIVE: To describe a patient with hypotension secondary to autonomic dysfunction who was successfully treated with oral vasopressors. CASE SUMMARY: A 76-year-old African-American man with a history of cerebrovascular accident with right hemiparesis 30 years prior to admission was admitted from another hospital four days after a new posterior inferior cerebellar artery occlusion and poor distal flow as manifested by weakness and hypotension. This was treated with intravenous fluids and dopamine. The dopamine was weaned and changed to phenylephrine to maintain systolic blood pressure >80 mm Hg. fludrocortisone 0.3 mg orally once daily was initiated; pressure support garments were used for the management of orthostatic hypotension. ephedrine 25 mg po tid was added and titrated up to 50 mg p.o. tid. yohimbine 5.4 mg po every eight hours was added due to continued dependence on phenylephrine to maintain adequate blood pressure. yohimbine was titrated up to 10.8 mg p.o. tid in an unsuccessful effort to wean the patient from phenylephrine. fludrocortisone was decreased to 0.1 mg po tid and the phenylephrine was tapered off. The patient developed a pan-sensitive escherichia coli urinary tract infection that was treated with oral trimethoprim/sulfamethoxazole. Over the subsequent days, an 80% left subclavian stenosis was detected; yohimbine and pressure support garments were discontinued. Subsequently, oral ephedrine was tapered off over two days, and fludrocortisone was tapered to 0.1 mg p.o. bid. The patient was transferred in a stable normotensive condition to an inpatient rehabilitation unit. The fludrocortisone was later discontinued with no further hypotension or orthostatic symptoms. DISCUSSION: In this case, orthostatic hypotension associated with autonomic dysfunction was successfully managed with a combination of intravenous vasopressors and hydration, pressure support garments, oral mineralocorticoids, and oral vasopressors. Oral vasopressors and mineralocorticoids are effective treatment options in the management of the vasopressor-dependent patient. In our patient the adverse effects were tolerable. After continued therapy, the oral vasopressors were withdrawn without a return of orthostatic symptoms. CONCLUSIONS: Orthostatic hypotension due to autonomic dysfunction may be successfully managed with combination oral therapy after initial treatment with intravenous vasopressors as evidenced by the absence of orthostasis.- - - - - - - - - - ranking = 2.5keywords = pressure (Clic here for more details about this article) |
4/116. Interaction of genetic predisposition and environmental factors in the pathogenesis of idiopathic orthostatic intolerance.BACKGROUND: The hemodynamic and autonomic abnormalities in idiopathic orthostatic intolerance (IOI) have been studied extensively. However, the mechanisms underlying these abnormalities are not understood. If genetic predisposition were important in the pathogenesis of IOI, monozygotic twins of patients with IOI should have similar hemodynamic and autonomic abnormalities. methods: We studied two patients with IOI and their identical twins. Both siblings in the first twin pair had orthostatic symptoms, significant orthostatic tachycardia, increased plasma norepinephrine levels with standing, and a greater than normal decrease in systolic blood pressure with trimethaphan infusion. RESULTS: Both siblings had a normal response of plasma renin activity to upright posture. In the second twin pair, only one sibling had symptoms of orthostatic intolerance, an orthostatic tachycardia, and raised plasma catecholamines with standing. The affected sibling had inappropriately low plasma renin activity with standing and was 8-fold more sensitive to the pressor effect of phenylephrine than the unaffected sibling. CONCLUSIONS: We conclude that in some patients, IOI seems to be strongly influenced by genetic factors. In others, however, IOI may be mainly caused by nongenetic factors. These findings suggest that IOI is heterogenous, and that both genetic and environmental factors contribute individually or collectively to create the IOI phenotype.- - - - - - - - - - ranking = 0.5keywords = pressure (Clic here for more details about this article) |
5/116. Successful treatment of severe orthostatic hypotension with cardiac tachypacing in dual chamber pacemakers.Orthostatic hypotension is an evolving and disabling disease usually observed in elderly patients with dramatic consequences on morbidity, mortality, and impairing the quality of life. We studied the effects of the pacing rate and AV interval on the blood pressure drop in the upright position in two patients with previously implanted pacemakers for sinus node dysfunction. Although the AV interval did not affect the blood pressure drop in the upright position, tachypacing at 100 paces/min improved it dramatically and prevented syncope. Cardiac tachypacing is a useful therapeutic option in severe refractory orthostatic hypotensive patients, especially those with chronotropic incompetence.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
6/116. Clinico-pathological features of postural hypotension in diabetic autonomic neuropathy.We report the clinico-pathological features and management of a 49-year-old male with a 30-year history of Type 1 diabetes mellitus who had nephropathy (proteinuria 1.81 g/24 h, creatinine 136 micromol/l), proliferative retinopathy and severe somatic and autonomic neuropathy. A sural nerve biopsy demonstrated marked myelinated fibre loss with unmyelinated fibre degeneration and regeneration combined with extensive endoneurial microangiopathy. The management of the patient's blood pressure problems (supine hypertension) and symptomatic postural hypotension is discussed.- - - - - - - - - - ranking = 0.5keywords = pressure (Clic here for more details about this article) |
7/116. 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.- - - - - - - - - - ranking = 0.5keywords = pressure (Clic here for more details about this article) |
8/116. Endogenous circulating sympatholytic factor in orthostatic intolerance.Sympathotonic orthostatic hypotension (SOH) is an idiopathic syndrome characterized by tachycardia, hypotension, elevated plasma norepinephrine, and symptoms of orthostatic intolerance provoked by assumption of an upright posture. We studied a woman with severe progressive SOH with blood pressure unresponsive to the pressor effects of alpha(1)-adrenergic receptor (AR) agonists. We tested the hypothesis that a circulating factor in this patient interferes with vascular adrenergic neurotransmission. Preincubation of porcine pulmonary artery vessel rings with patient plasma produced a dose-dependent inhibition of vasoconstriction to phenylephrine in vitro, abolished vasoconstriction to direct electrical stimulation, and had no effect on nonadrenergic vasoconstrictive stimuli (endothelin-1), PGF-2alpha (or KCl). Preincubation of vessels with control plasma was devoid of these effects. SOH plasma inhibited the binding of an alpha(1)-selective antagonist radioligand ([(125)I]HEAT) to membrane fractions derived from porcine pulmonary artery vessel rings, rat liver, and cell lines selectively overexpressing human ARs of the alpha(1B) subtype but not other AR subtypes (alpha(1A) and alpha(1D)). We conclude that a factor in SOH plasma can selectively and irreversibly inhibit adrenergic ligand binding to alpha(1B) ARs. We propose that this factor contributes to a novel pathogenesis for SOH in this patient. This patient's syndrome represents a new disease entity, and her plasma may provide a unique tool for probing the selective functions of alpha(1)-ARs.- - - - - - - - - - ranking = 0.5keywords = pressure (Clic here for more details about this article) |
9/116. Hypotensive akathisia: autonomic failure associated with leg fidgeting while sitting.The author describes a distinct clinical syndrome in six patients with autonomic failure who manifested habitual, voluntary, transiently suppressible, yet irresistible leg movements occurring only in the sitting position. Keeping the legs still brought on vague symptoms of fatigue, lightheadedness, or apprehension. Repetitive leg crossing, muscle tensing, foot twirling or wiggling, or heel or toe floor tapping while sitting may have compensated for orthostatic hypotension and raised systolic blood pressure by a mean of 28 mm Hg and diastolic pressure by a mean of 11 mm Hg.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
10/116. 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.- - - - - - - - - - ranking = 0.5keywords = pressure (Clic here for more details about this article) |
| | Next -> |