Cerebral vasodilation and vasoconstriction associated with acute anxiety

Mathew, Roy J.; Wilson, William H.; Humphreys, Diane F.; Lowe, Joe V.; Wiethe, Kathryn E.

doi:10.1016/s0006-3223(96)00178-3

Cited by 15 publications

(9 citation statements)

References 65 publications

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“…On the other hand, none of the subjects who did not have a PA showed any MFV modification while performing the challenge. Some studies reported that severe anxiety decreases CBF [51, 52]. The observation that this kind of response is specific for acute anxiety and not for PD is confirmed by the fact that in our study no difference in MFV modifications was found when comparing PD subjects with controls.…”

Section: Resultssupporting

confidence: 87%

Brain Circulation during Panic Attack: A Transcranial Doppler Study with Clomipramine Challenge

et al. 2014

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Introduction. Cerebral blood flow has been well studied in patients with panic disorder, but only few studies analyzed the mechanisms underlying the onset of a panic attack. The aim of the present study was to monitor the cerebral hemodynamics modifications during a panic attack. Materials and Methods. 10 panic disorder patients with recent onset, fully drug naïve, were compared to 13 patients with panic disorder with a previous history of treatment and to 14 controls. A continuous bilateral monitoring of mean flow velocities in right and left middle cerebral arteries was performed by transcranial Doppler. Clomipramine was chosen as challenge. Results. Eight out of 10 patients drug naïve and 6 control subjects out of 13 had a full blown panic attack during the test, whereas none of the patients with a history of treatment panicked. The occurrence of a panic attack was accompanied by a rapid decrease of flow velocities in both right and left middle cerebral arteries. Discussion. The bilateral acute decrease of mean flow velocity during a panic attack suggests the vasoconstriction of the microcirculation of deep brain structures perfused by middle cerebral arteries and involved in the so-called “fear circuitry,” thus suggesting that cerebral homeostatic dysfunctions seem to have a key role in the onset of a panic attack.

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Section: Resultssupporting

confidence: 87%

Brain Circulation during Panic Attack: A Transcranial Doppler Study with Clomipramine Challenge

et al. 2014

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“…in BHDs) resulted from increases in both blood velocity and the CSA. In addition, it has been shown that sympathetic activation limits hypercapnic cerebral vasodilatation in animals (Mathew et al 1997). Thus, as NDs did not present any significant HR variation during SA, this might explain the lack of a significant increase in their CBF.…”

Section: Discussionmentioning

confidence: 83%

“…Activation of trigeminal afferents (Goadsby et al 1997), sciatic nerve stimulation, nociceptive or somatosensory stimuli (Ibayashi et al 1991), mental activity (Kim & Ugurbil 1997), anxiety (Mathew & Wilson 1988) and stress (Bryan 1990) can increase CBF. In addition, it has been shown that sympathetic activation limits hypercapnic cerebral vasodilatation in animals (Mathew et al 1997). As the HR decrease is a good index of the parasympathetic/sympathetic activity ratio, the BHDs' bradycardia during SA ()22%) would partly explain their CBF increase in spite of a less marked hypercapnia compared with NDs.…”

Section: Discussionmentioning

confidence: 99%

Circulatory effects of apnoea in elite breath‐hold divers

et al. 2009

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“…Vasoconstriction also can be triggered in the periphery by the induction of anxiety, such as in fingers preceding an anticipated personal speech to confederates (Vassend and Knardahl, 2005). These processes may support increased mean cerebral blood flow (vasodilation) during anxiety (Mathew et al, 1997). On the other hand, cognitive stressors (e.g., repeating digits backwards during exercise in Roth et al, 1990) have been documented to dampen vasodilative effects.…”

Section: Discussionmentioning

confidence: 99%