Transcranial Doppler Ultrasonography during Head-Upright Tilt-Table Testing

Fredman, Carey S.; Biermann, Kurt M.; Patel, Vipool; Uppstrom, Erica L.; Auer, Arthur I.

doi:10.7326/0003-4819-123-11-199512010-00007

Cited by 34 publications

(22 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In accordance with our findings, an exaggerated drop in cerebral blood flow has been reported in patients with panic disorder, similar to that observed in patients with VVS [25,36,37,38]. A predominant vagal activity has also been observed in patients with blood phobia [39].…”

Section: Discussionsupporting

confidence: 79%

Minor Psychiatric Disorders and Syncope: The Role of Psychopathology in the Expression of Vasovagal Reflex

Leftheriotis

Michopoulos²,

Flevari³

et al. 2008

Psychother Psychosom

View full text Add to dashboard Cite

Background: A high prevalence of minor psychiatric disorders (MPDs) has been reported in patients with vasovagal syncope (VVS). However, the relationship between the psychiatric substrate and syncope remains unclear. Methods: In order to test the hypothesis that MPDs may predispose to VVS, we assessed the prevalence of syncope, the response to head-up tilt test (HUTT) and the efficacy of psychiatric drug treatment in reducing syncopal episodes, in patients with recently diagnosed MPDs. The response to HUTT was compared with that in an equal number of matched (a) patients with VVS and (b) healthy controls. Results: A high rate of patients with MPDs (58%) had a positive HUTT. Additionally, 45% had a history of syncope; among them, the rate of positive HUTT was identical to that in the VVS group (83%). Following psychiatric drug treatment, the number of patients with syncope decreased in the MPD group (6/67 from 30/67, p < 0.01). Psychiatric symptoms and quality of life were also improved. The number of syncopal spells decreased equally in the MPD and VVS groups (0.6 ± 0.5 from 2.5 ± 1.4, p < 0.01, and 0.7 ± 0.5 from 2.7 ± 1.3, p < 0.01, respectively). Conclusion: A high proportion of patients with MPDs experience syncope, associated with a high rate of positive HUTT, comparable to that observed in VVS. Psychiatric treatment results in the improvement of syncopal and psychiatric symptoms. These findings suggest involvement of co-occurring MPDs in the pathogenesis of VVS. Therefore, the diagnosis and treatment of MPDs, when present, may be crucial for the effective therapy of vasovagal syndrome.

show abstract

Section: Discussionsupporting

confidence: 79%

Minor Psychiatric Disorders and Syncope: The Role of Psychopathology in the Expression of Vasovagal Reflex

Leftheriotis

Michopoulos²,

Flevari³

et al. 2008

Psychother Psychosom

View full text Add to dashboard Cite

show abstract

“…1 Furthermore, IOI patients have a greater decrease in mean MCA vel than normal control subjects with graded HUT. 11,12 This excessive decrease in mean MCA vel is associated with an excessive increase in regional CVR. 12 In the present study, we observed a similar decrease in mean MCA vel in IOI patients with HUT.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, an excessive decrease in cerebral blood flow velocity with upright posture as well as stable mean arterial pressure (MAP) was reported in a single patient with a history and physical findings suggestive of IOI. 11 Similarly, in a larger group of well-characterized IOI patients, mean middle cerebral blood flow velocity (mean MCA vel ) decreased by 28% with 75°HUT; age-and gender-matched control subjects had only a 10% decrease in mean MCA vel . 12 This substantial decrease in mean MCA vel despite a well-sustained MAP was associated with an increase in regional cerebrovascular resistance (CVR).…”

mentioning

confidence: 93%

Raised Cerebrovascular Resistance in Idiopathic Orthostatic Intolerance

Jordan¹,

Shannon²,

Black³

et al. 1998

Hypertension

View full text Add to dashboard Cite

Abstract-Patients with idiopathic orthostatic intolerance (IOI) exhibit symptoms suggestive of cerebral hypoperfusion and an excessive decrease in cerebral blood flow associated with standing despite sustained systemic blood pressure. In 9 patients (8 women and 1 man aged 22 to 48 years) with IOI, we tested the hypothesis that volume loading (2000 cc normal saline) and ␣-adrenoreceptor agonism improve systemic hemodynamics and cerebral perfusion and that the decrease in cerebral blood flow with head-up tilt (HUT) could be attenuated by ␣-adrenoreceptor blockade with phentolamine. At 5 minutes of HUT, volume loading (Ϫ20Ϯ3.2 bpm) and phenylephrine (Ϫ18Ϯ3.4 bpm) significantly reduced upright heart rate compared with placebo; the effect was diminished at the end of HUT. Phentolamine substantially increased upright heart rate at 5 minutes (20Ϯ3.7 bpm) and at the end of HUT (14Ϯ5 bpm). With placebo, mean cerebral blood flow velocity decreased by 33Ϯ6% at the end of HUT. This decrease in cerebral blood flow with HUT was attenuated by all 3 interventions. We conclude that in patients with IOI, HUT causes a substantial decrease in cerebrovascular blood flow velocity. The decrease in blood flow velocity with HUT can be attenuated with interventions that improve systemic hemodynamics and therefore decrease reflex sympathetic activation. Moreover, ␣-adrenoreceptor blockade also blunts the decrease in cerebral blood flow with HUT but at the price of deteriorated systemic hemodynamics. These observations may suggest that in patients with IOI, excessive sympathetic activity contributes to the paradoxical decrease in cerebral blood flow with upright posture. (Hypertension. 1998;32:699-704.)Key Words: cerebral blood flow Ⅲ receptors, adrenergic Ⅲ phentolamine Ⅲ phenylephrine Ⅲ intolerance, orthostatic Ⅲ tachycardia I diopathic orthostatic intolerance (IOI) is commonly defined as a Ͼ30 bpm increase in heart rate (HR) with standing associated with orthostatic symptoms but without significant orthostatic hypotension.1 The pathophysiology of this disorder, which mainly affects women in the second or third decade of life, is still imperfectly understood.2 It has been suggested that hypovolemia, 3,4 excessive venous pooling in the lower extremities, 5 partial dysautonomia involving the vasculature of the legs, 6-8 or hypersensitivity of ␤-adrenoreceptors 9,10 can contribute to the hemodynamic abnormalities of IOI. The unifying feature of patients with IOI is the presence of symptoms suggestive of cerebral hypoperfusion (eg, presyncope, visual changes, altered mentation) associated with standing despite largely sustained systemic arterial pressure. Recently, an excessive decrease in cerebral blood flow velocity with upright posture as well as stable mean arterial pressure (MAP) was reported in a single patient with a history and physical findings suggestive of IOI.11 Similarly, in a larger group of well-characterized IOI patients, mean middle cerebral blood flow velocity (mean MCA vel ) decreased by 28% with 75°HUT; age-and gender-mat...

show abstract

“…1,4 On the other hand, the concept that impaired local regulation of cerebrovascular tone can also lead to cerebral hypoperfusion with standing is supported by recent findings in patients with orthostatic intolerance. [5][6][7][8] These patients experience typical symptoms of cerebral hypoperfusion when they stand, and these symptoms are associated with excessive reductions in cerebral blood flow velocity despite maintenance of arterial BP. 6 This cerebral vasoconstriction is attenuated either by interventions that blunt sympathetic activation or by ␣-adrenoreceptor blockade.…”

mentioning

confidence: 99%

Interaction of Carbon Dioxide and Sympathetic Nervous System Activity in the Regulation of Cerebral Perfusion in Humans

et al. 2000

View full text Add to dashboard Cite

Abstract-Recent studies suggest that activation of the sympathetic nervous system either directly or indirectly influences cerebrovascular tone in humans even within the autoregulatory range. In 6 healthy subjects (aged 29Ϯ4 years), we used transcranial Doppler sonography to determine cerebral blood flow velocity during sympathetic activation elicited through head-up tilt (HUT) and sympathetic deactivation through ganglionic blockade. PaCO 2 was manipulated through hyperventilation and CO 2 breathing (5%). With subjects in the supine position and during HUT, mean arterial pressure was not influenced by PaCO 2 . During ganglionic blockade, mean arterial pressure decreased markedly with hyperventilation (Ϫ13Ϯ1.9 mm Hg). Manipulation of sympathetic tone elicited only mild changes in cerebral blood flow (64Ϯ5.8 cm/s supine, 58Ϯ4.9 cm/s upright, and 66Ϯ6.2 cm/s during ganglionic blockade; Pϭ0.07 by ANOVA). The slope of the regression between PaCO 2 and mean velocity was 1.6Ϯ0.18 cm/(s ⅐ mm Hg) supine, 1.3Ϯ0.14 cm/(s ⅐ mm Hg) during HUT, and 2.3Ϯ0.36 cm/(s ⅐ mm Hg) during ganglionic blockade (PϽ0.05). Spontaneous PaCO 2 and ventilatory response to hypercapnia were also modulated by the level of sympathetic activity. Changes in sympathetic tone have a limited effect on cerebral blood flow at normal PaCO 2 levels. However, the sympathetic nervous system seems to attenuate the CO 2 -induced increase in cerebral blood flow. This phenomenon may indicate a moderate direct effect of the sympathetic nervous system on the cerebral vasculature. Furthermore, sympathetic activation tends to increase ventilation and thus can indirectly increase cerebrovascular tone. (Hypertension. 2000;36:383-388.)Key Words: carbon dioxide Ⅲ baroreflex Ⅲ receptors, adrenergic Ⅲ phenylephrine Ⅲ sympathetic nervous system T he ability to assume the upright posture depends crucially on sufficient perfusion of the brain. 1,2 Blood flow to the brain can be influenced through adjustments in systemic hemodynamics (ie, perfusion pressure) or through local vascular modulation (ie, cerebral autoregulation). 3 Thus, impaired adjustment of systemic hemodynamics or disordered regulation of cerebrovascular tone could contribute to cerebral hypoperfusion with standing. An example of the former is the profound orthostatic hypotension seen in autonomic failure patients, which leads to cerebral hypoperfusion as the decrease in blood pressure (BP) exceeds the autoregulatory capacity of the brain. 1,4 On the other hand, the concept that impaired local regulation of cerebrovascular tone can also lead to cerebral hypoperfusion with standing is supported by recent findings in patients with orthostatic intolerance. [5][6][7][8] These patients experience typical symptoms of cerebral hypoperfusion when they stand, and these symptoms are associated with excessive reductions in cerebral blood flow velocity despite maintenance of arterial BP. 6 This cerebral vasoconstriction is attenuated either by interventions that blunt sympathetic activation or by ␣-adrenoreceptor blockad...

show abstract

Transcranial Doppler Ultrasonography during Head-Upright Tilt-Table Testing

Cited by 34 publications

References 0 publications

Minor Psychiatric Disorders and Syncope: The Role of Psychopathology in the Expression of Vasovagal Reflex

Minor Psychiatric Disorders and Syncope: The Role of Psychopathology in the Expression of Vasovagal Reflex

Raised Cerebrovascular Resistance in Idiopathic Orthostatic Intolerance

Interaction of Carbon Dioxide and Sympathetic Nervous System Activity in the Regulation of Cerebral Perfusion in Humans

Contact Info

Product

Resources

About