Chronic vagus nerve stimulation for treatment-resistant depression increases regional cerebral blood flow in the dorsolateral prefrontal cortex

Kosel, Markus; Brockmann, Holger; Frick, Caroline; Zobel, Astrid; Schläepfer, Thomas E.

doi:10.1016/j.pscychresns.2010.11.004

Cited by 78 publications

(45 citation statements)

References 32 publications

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“…It is interesting to compare our results with the findings of Kosel et al 17 that regional blood flow (rCBF) after chronic cervical vagal stimulation for adjunctive treatment of depressed patients was increased in the left dorsolateral/ventrolateral prefrontal cortex (Brodmann areas 46 and 47) and decreased in the right posterior cingulate area, the lingual gyrus and the left insula. The similarities concerning locations and differences might be due to the chronic vs. acute stimulation.…”

Section: Eeg Measures During Ec Seriessupporting

confidence: 61%

Effects of Acute Transcutaneous Vagal Stimulation on the EEG Power Maps, EEG Sources Distribution and Steadiness of Quiet and Sensory-conflicted Stance

Dimitrov¹,

Gatev²

2015

Posture, Balance and the Brain

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Transcutaneous vagal stimulation (t-VNS) is a prospective method as a cheap and noninvasive alternative of surgical cervical vagal stimulation widely used for treatment of refractory epilepsy, depression etc. Data on its application in healthy people are scarce. A lot of problems concerning the acting mechanisms and cortical representation are unsolved. We did acute t-VNS and studied the standing balance steadiness, EEG absolute power maps and sources distribution. We found improvement of the steadiness of standing with eyes open (EO), but no changes in the eyes closed (EC) series.In EO Delta and Theta power in the right frontal area increased and Beta and Gamma bands of EEG absolute power in the left and right parieto-occipital areas also increased, which sustained for 20 min after t-VNS. The distribution of maxima of EEG sources revealed by LORETA showed shifts to the right and occipital direction after t-VNS, while 20 min later the maxima were symmetrically located, but the occipital shift was preserved. Pre-treatment sources during EO were in multisensory fields: the inferior parietal lobule, superior temporal gyrus and precuneus, after t-VNS they were in the inferior parietal lobule, middle temporal gyrus, right posterior cingulate, precuneus, cuneus and right lingual gyrus. After 20 min the maxima of EEG sources were in the inferior parietal lobule, superior and middle temporal gyrus and left insula.In EC following t-VNS Delta power first decreased in the right frontal and occipital areas and in the central parietal area, 20 min later it was greater than in pre-treatment series in these areas. The results showed an increase of EEG absolute power in the Beta and Gamma ranges mainly in the occipital area and less expressed in the postero-parietal one. The increase was more expressed for Gamma than Beta band similarly to the EO series. However, this increase in Beta and Gamma EEG power in EC was mainly located in the left side of the cortex. After t-VNS we observed shifts of electrical sources locations to the occipital and top parts of the brain. Unlike, during the EO series we observed shift to the lower frequencies in the absolute power cortical maps. After 20 min a tendency to return to the pre-treatment coordinates occurred, the power, increased immediately after t-VNS, dropped much lower than its initial value. The locations of maxima of electrical sources during EC before t-VNS were in the middle and inferior frontal gyrus, right inferior parietal lobule, cingulate and precuneus. Immediately after t- Bozhidar Dimitrov and Plamen Gatev 46VNS these locations were in the superior temporal gyrus, middle temporal gyrus, precuneus, cuneus and left inferior parietal lobule. After 20 min the locations of the maxima of electrical sources were in the anterior cingulate cortex, medial frontal gyrus, precuneus, cuneus and lingual gyrus.Our results show that cortical processing of the t-VNS information and its effect on standing balance are quite different during standing with EO compared to standing with...

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Section: Eeg Measures During Ec Seriessupporting

confidence: 61%

Effects of Acute Transcutaneous Vagal Stimulation on the EEG Power Maps, EEG Sources Distribution and Steadiness of Quiet and Sensory-conflicted Stance

Dimitrov¹,

Gatev²

2015

Posture, Balance and the Brain

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“…Results of imaging studies in patients with epilepsy or depression who are treated with VNS also show widespread effects on subcortical and cortical regions, with short-term VNS producing increases in blood flow in the hypothalamus, thalamus, and insular cortex but decreases in the hippocampus and posterior cingulate gyrus (Chae et al, 2003). Longterm VNS produced both increased (Kosel et al, 2011) and decreased (Nahas et al, 2007) changes in blood flow in cortical regions although subcortical regions were activated (Henry et al, 2004). Inconsistent results were also obtained in the amygdala (Zobel et al, 2005;Conway et al, 2006).…”

Section: Downloaded Frommentioning

confidence: 77%

Comparison of ΔFosB Immunoreactivity Induced by Vagal Nerve Stimulation with That Caused by Pharmacologically Diverse Antidepressants

Furmaga¹,

Sadhu²,

Frazer³

2012

J Pharmacol Exp Ther

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Vagal nerve stimulation (VNS) has been approved for treatment of refractory depression. However, there have been few, if any, studies directly comparing the effects produced by VNS in animals with those caused by antidepressants, particularly using clinically relevant stimulation parameters in nonanesthetized animals. In this study, ⌬FosB immunohistochemistry was used to evaluate different brain regions activated by long-term administration of VNS. Effects of VNS were compared with those caused by sertraline or desipramine (DMI). Double-labeling of ⌬FosB and serotonin was used to determine whether serotonergic neurons in the dorsal raphe nucleus (DRN) were activated by long-term VNS. VNS significantly increased ⌬FosB staining in the nucleus tractus solitarius (NTS), parabrachial nucleus (PBN), locus ceruleus (LC), and DRN, as well as in many cortical and limbic areas of brain including those involved in mood and cognition. Most, but not all, of these effects were seen also upon long-term treatments of rats with sertraline or DMI. Some areas where VNS increased ⌬FosB (e.g., the NTS, PBN, LC, and peripeduncular nucleus) were not affected significantly by either drug. Sertraline was similar to VNS in causing an increase in the DRN whereas DMI did not. Doublelabeling of the DRN with ⌬FosB and an antibody for serotonin revealed that only a small percentage of ⌬FosB staining in the DRN colocalized with serotonergic neurons. The effects of VNS were somewhat more widespread than those caused by the antidepressants. The increases in ⌬FosB produced by VNS were either equivalent to and/or more robust than those seen with antidepressants.

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“…62 Chronic VNS for treatment of patients with resistant depression also increases regional cerebral blood flow in the dorsolateral prefrontal cortex. 63 It is thought to alter limbic circuitry to reduce epileptogenesis and enhance mood. 60 It is likely that VNS results in increased cerebral blood flow and metabolism in the forebrain, thalamus and reticular formation, 60 which promotes arousal and improved consciousness, 64 thereby improving outcome after TBI resulting in VS or MCS.…”

Section: Altered Neurotransmitter Levels and Cerebral Blood Flowmentioning

confidence: 99%

Vagus nerve stimulation to augment recovery from severe traumatic brain injury impeding consciousness: a prospective pilot clinical trial

Chen

Flanagan

Samadani

2013

Neurological Research

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Objectives-Traumatic brain injury has a high morbidity and mortality in both civilian and military populations. Blast and other mechanisms of traumatic brain injury damage the brain by causing neurons to disconnect and atrophy. Such traumatic axonal injury can lead to persistently vegetative and minimally conscious states, for which limited treatment options exist, including physical, occupational, speech and cognitive therapies.More than 60,000 patients have received vagus nerve stimulation for epilepsy and depression. In addition to decreased seizure frequency and severity, patients report enhanced mood, reduced daytime sleepiness independent of seizure control, increased slow wave sleep, and improved cognition, memory, and quality of life.Early stimulation of the vagus nerve accelerates the rate and extent of behavioral and cognitive recovery after fluid percussion brain injury in rats.Methods-We recently obtained FDA approval for a pilot prospective randomized crossover trial to demonstrate objective improvement in clinical outcome by placement of a vagus nerve stimulator in patients who are recovering from severe traumatic brain injury. Our hypothesis is that stimulation of the vagus nerve results in increased cerebral blood flow and metabolism in the forebrain, thalamus and reticular formation, which promotes arousal and improved consciousness, thereby improving outcome after traumatic brain injury resulting in minimally conscious or persistent vegetative states.Discussion-If this study demonstrates that vagus nerve stimulation can safely and positively impact outcome, then a larger randomized prospective crossover trial will be proposed.

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Chronic vagus nerve stimulation for treatment-resistant depression increases regional cerebral blood flow in the dorsolateral prefrontal cortex

Cited by 78 publications

References 32 publications

Effects of Acute Transcutaneous Vagal Stimulation on the EEG Power Maps, EEG Sources Distribution and Steadiness of Quiet and Sensory-conflicted Stance

Effects of Acute Transcutaneous Vagal Stimulation on the EEG Power Maps, EEG Sources Distribution and Steadiness of Quiet and Sensory-conflicted Stance

Comparison of ΔFosB Immunoreactivity Induced by Vagal Nerve Stimulation with That Caused by Pharmacologically Diverse Antidepressants

Vagus nerve stimulation to augment recovery from severe traumatic brain injury impeding consciousness: a prospective pilot clinical trial

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