1/32. Cerebrovascular and cardiovascular responses associated with orthostatic intolerance and tachycardia.Idiopathic orthostatic intolerance syndrome is characterized by postural symptoms of cerebral hypoperfusion without arterial hypotension. Abnormal baroreceptor responses with deranged cerebral autoregulation leading to cerebral vasoconstriction have been proposed as a causative mechanism. The authors report the cerebrovascular and cardiovascular responses in a patient who recovered from orthostatic intolerance and tachycardia. Changes in the orthostatic responses of mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and transcranial Doppler middle cerebral artery (MCA) mean blood flow velocity (Vmean) were assessed at admission and again 6 months after recovery. Normal cardiovascular responses to forced breathing and to standing indicated intact overall baroreflex integrity with normal baroreflex sensitivity (10.2 msec.mm Hg(-1)). After the patient stood for 8 minutes, presyncopal symptoms developed, with unchanged MAP but increased HR ( 41 beats/min) and reduced stroke volume (SV) (-69%), CO (-50%), and MCA Vmean (-46%; 57 to 31 cm. s(-1)). After a reconditioning program and recovery, the patient was reexamined. The supine MCA Vmean was larger (79 cm. s(-1)), as were MAP (76 versus 70 mm Hg) and CO ( 15%). The orthostatic HR increase was smaller ( 5 beats/min), as was the reduction in SV (-44%) and CO (-30%), with an increase in MAP to 93 mm Hg. The orthostatic reduction in MCA Vmean was smaller (-13 versus -26 cm.s(-1)) and standing cerebrovascular resistance decreased (1.41 versus 2.39 mm Hg.cm. s(-1)). In this patient who had intact baroreflex control and no postural decrease in blood pressure, the reduction in MCA Vmean, concomitant with a large decrease in CO, seemed reversible. The result suggests that a symptomatic reduction in cerebrovascular conductance during standing is to be interpreted as being an adaptive response to a critically limited systemic blood flow, rather than to derangement of cerebral autoregulation.- - - - - - - - - - ranking = 1keywords = cerebral (Clic here for more details about this article) |
2/32. Autoregulatory cerebral vasodilation occurs during orthostatic hypotension in patients with primary autonomic failure.It is unclear whether patients with autonomic failure autoregulate cerebral blood flow during hypotension. The objective in this study was to examine cerebral autoregulatory capacity in patients with autonomic failure by studying changes in middle cerebral artery blood flow velocity using transcranial Doppler ultrasonography before, during, and after tilt-induced hypotension. Nine patients with primary autonomic failure were evaluated. Mean arterial pressure and middle cerebral artery blood flow velocity were simultaneously recorded while the patients were in the supine position, during 60 degrees head-up tilt, and after they were returned to the horizontal position. The results were as follows: during tilt-induced hypotension, mean arterial pressure decreased significantly more than middle cerebral artery mean blood flow velocity (58% versus 36%, p <0.0002). After return to the horizontal position, mean arterial pressure returned to baseline, and middle cerebral artery blood flow velocity transiently increased above pretilt value (p <0.02). It is concluded that cerebral autoregulatory vasodilation occurs in patients with autonomic failure. This was demonstrated by a more pronounced decline in mean arterial pressure than in middle cerebral artery blood flow velocity during hypotension and by a transient increase in middle cerebral artery blood flow velocity (ie, hyperemic response) after blood pressure was restored.- - - - - - - - - - ranking = 2.6keywords = cerebral (Clic here for more details about this article) |
3/32. Provoking vasodepressor syncope with head-up tilt-table testing.head-up tilt testing has proven effective in identifying individuals prone to vasodepressor syncope (VDS). VDS refers to the transient loss of consciousness/cerebral anoxia seen with hypotension produced by autonomic imbalance. In this case, the hypotension is the result of parasympathetic domination. Most episodes appear to be triggered by reduced venous return which stimulates the cardiac mechanoreceptors in the inferior-posterior left ventricle. Once activated, these receptors send out afferent signals along the unmyelinated C of the vagus nerve and cause vasodilation. Once venous return is restored, the usual sympathetic compensations (increased heart rate/force of contraction and vasoconstriction) overcome the parasympathetic domination. A tilt-study allows one to passively tilt the patient up to 40-80 degrees and abruptly reduce venous return in a controlled environment. One can then determine which mechanism will dominate--the usual sympathetic vasoconstriction or the parasympathetic reflex (Bezold-Jarisch)--by frequent observations of blood pressure and ECG. bradycardia/ventricular standstill may also occur during parasympathetic domination. Once susceptibility to vasodepressor syncope is identified by a tilt study, medications to expand the blood volume and/or minimize venous pooling are often needed. Other drugs to block the parasympathetic pathway and/or the effects of excessive catecholamine levels may also be ordered. Dual chamber pacing may be required for malignant episodes of bradycardia or ventricular standstill.- - - - - - - - - - ranking = 0.2keywords = cerebral (Clic here for more details about this article) |
4/32. 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.- - - - - - - - - - ranking = 0.2keywords = cerebral (Clic here for more details about this article) |
5/32. case reports and review of postural orthostatic tachycardia syndrome (POTS).postural orthostatic tachycardia syndrome (POTS) is a type of orthostatic intolerance that is characterized by excessive tachycardia and decreased cerebral blood flow in the upright position. This can result in significant symptoms of dizziness and light-headedness that can eventually lead to syncope. In this review, we describe two patients with POTS that varied in their degree of symptoms and treatment. One patient was able to be treated as an outpatient, while the other required hospitalization and extensive medical therapy. We would like to emphasize with this review that POTS is probably more common than it is diagnosed and is often confused with other conditions, such as chronic fatigue syndrome or functional syncope. It is important to make the correct diagnosis in order to allow appropriate treatment and to improve the quality of life for these patients.- - - - - - - - - - ranking = 0.2keywords = cerebral (Clic here for more details about this article) |
6/32. association between cardiac denervation and parkinsonism caused by alpha-synuclein gene triplication.Parkinson's disease patients frequently have symptoms and signs of autonomic nervous dysfunction that are the source of considerable disability. Recent studies have revealed that most patients with Parkinson's disease, and all with Parkinson's disease-associated orthostatic hypotension, have a loss of cardiac sympathetic innervation. Familial Parkinson's disease, caused by mutation of the gene encoding alpha-synuclein, also features orthostatic hypotension, sympathetic neurocirculatory failure and cardiac sympathetic denervation. We have recently described a whole-gene triplication of alpha-synuclein causing Lewy body parkinsonism in a large, well characterized family called the 'iowa kindred'. Here we report the results of cardiac PET scanning using the sympathoneural imaging agent, 6-[18F]fluorodopamine in affected and unaffected members of this kindred. Four family members were studied, two with parkinsonism, one clinically normal and one with benign essential tremor alone. Both affected members had obvious loss of cardiac sympathetic innervation; the unaffected member had normal innervation, as did the member with isolated essential tremor. The results indicate that, in this family, where disease is caused by overexpression of normal alpha-synuclein, cardiac sympathetic denervation cosegregates with parkinsonism. Post-mortem studies have demonstrated synuclein-positive Lewy body formation in the brains of individuals with parkinsonism who were also in the family described here and who also carry this triplication. These results indicate that both parkinsonism and cardiac sympathetic denervation can result from an excess of normal synuclein.- - - - - - - - - - ranking = 0.0025822231610642keywords = brain (Clic here for more details about this article) |
7/32. 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.- - - - - - - - - - ranking = 1.2keywords = cerebral (Clic here for more details about this article) |
8/32. 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.- - - - - - - - - - ranking = 0.4keywords = cerebral (Clic here for more details about this article) |
9/32. Thyrocervical trunk-external carotid artery bypass for positional cerebral ischemia due to common carotid artery occlusion. Report of three cases.Medically refractory positional cerebral ischemia and concomitant orthostatic hypotension associated with chronic common carotid artery (CCA) occlusion are rare. The authors detail their experience with three cases treated exclusively by an extracranial bypass in which the thyrocervical trunk was used as the donor vessel. Postoperatively grafts were patent and symptoms resolved in all three patients, although orthostatic hypotension remained. Postural cerebral ischemia due to CCA occlusion can be treated by extracranial bypass surgery. The thyrocervical trunk is a suitable donor for reconstruction of the external carotid artery in these cases.- - - - - - - - - - ranking = 1.2keywords = cerebral (Clic here for more details about this article) |
10/32. Focal cerebral ischaemia induced by postural change.Three middle-aged men with risk factors for vascular disease developed brief, stereotyped hemi-sensory symptoms on sitting or standing. These symptoms occurred in the absence of postural hypotension. On clinical criteria, these episodes were indicative of small vessel (perforator) ischaemia, rather than large vessel disease. This was supported by the absence of any stenosis on duplex scanning of the neck vessels. Two of the patients progressed to develop a fixed deficit. In all 3 patients the outcome was benign, with minimal residual disability.- - - - - - - - - - ranking = 119.1050285889keywords = cerebral ischaemia, ischaemia, cerebral (Clic here for more details about this article) |
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