Deep brain stimulation relieves refractory hypertension

Patel, Nikunj K.; Javed, Shazia; Khan, Sadaquate; Papouchado, M; Malizia, AL; Pickering, Anthony E.; Paton, Julian F. R.

doi:10.1212/wnl.0b013e3182088108

Cited by 57 publications

(44 citation statements)

References 9 publications

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“…She traveled to Bristol, UK, and was evaluated for a deep-brain stimulator to lower her blood pressure. 19 The Bristol group was initially very hesitant about implanting such a device into our patient, although we understand that the investigators are reconsidering that decision.…”

Section: The Casementioning

confidence: 99%

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Truly Refractory Hypertension

et al. 2013

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Section: The Casementioning

confidence: 99%

“…Patel et al described a 55-year-old man who had developed a stroke. 19 In the peristroke period, refractory hypertension developed. Deep-brain stimulation of the ventrolateral periaqueductal gray/periventricular gray was performed, as a treatment for a refractory pain syndrome.…”

Section: Commentmentioning

confidence: 99%

Truly Refractory Hypertension

et al. 2013

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“…14 Intriguingly, deep brain stimulation of the ventrolateral periaqueductal grey matter area has also been shown to effectively reduce blood pressure in refractory hypertension. 109,110 Animal studies have identified the ventrolateral periaqueductal grey as a depressor area and shown that its stimulation elicits hypotension with peripheral vasodilatation, indicative of sympathetic withdrawal. 111 Owing to its analgesic effects, this region is clinically targeted with chronic electrical stimulation in patients with chronic pain, however long-term blood pressure lowering can be independent of pain.…”

Section: Drug-resistant Hypertension-how To Treat?mentioning

confidence: 99%

“…111 Owing to its analgesic effects, this region is clinically targeted with chronic electrical stimulation in patients with chronic pain, however long-term blood pressure lowering can be independent of pain. 110 Notably, in one particular patient, the normalisation of blood pressure with deep brain stimulation meant that all prescribed antihypertensive medications could be withdrawn and when the stimulator was turned off after 3 years, blood pressure remained low, suggesting that a central resetting of blood pressure control had occurred. 110 New horizons in central regulation of SNA in hypertension…”

Section: Drug-resistant Hypertension-how To Treat?mentioning

confidence: 99%

“…110 Notably, in one particular patient, the normalisation of blood pressure with deep brain stimulation meant that all prescribed antihypertensive medications could be withdrawn and when the stimulator was turned off after 3 years, blood pressure remained low, suggesting that a central resetting of blood pressure control had occurred. 110 New horizons in central regulation of SNA in hypertension…”

Section: Drug-resistant Hypertension-how To Treat?mentioning

confidence: 99%

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The sympathetic nervous system and blood pressure in humans: implications for hypertension

2011

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A neurogenic component to primary hypertension (hypertension) is now well established. Along with raised vasomotor tone and increased cardiac output, the chronic activation of the sympathetic nervous system in hypertension has a diverse range of pathophysiological consequences independent of any increase in blood pressure. This review provides a perspective on the actions and interactions of angiotensin II, inflammation and vascular dysfunction/brain hypoperfusion in the pathogenesis and progression of neurogenic hypertension. The optimisation of current treatment strategies and the exciting recent developments in the therapeutic targeting of the sympathetic nervous system to control hypertension (for example, catheter-based renal denervation and carotid baroreceptor stimulation) will be outlined. Keywords: sympathetic nerve activity; neurogenic hypertension; immune-to-brain signalling The sympathetic renaissancePrimary (or essential) hypertension (termed hypertension from here on) accounts for the vast majority of hypertensive cases (B95%).1 Although the aetiology of this condition is incompletely understood, it appears that along with genetic factors, several environmental and behavioural 'hypertensiogenic' factors have been identified, such as obesity, insulin resistance, high-salt intake, low physical activity levels and stress.1 Given the elevated risk of stroke, renal failure, myocardial infarction and coronary heart disease in those afflicted with high blood pressure, the elucidation of the key pathogenic features and optimisation of effective therapeutic strategies are critical.The most common form of hypertension is neurogenic hypertension, defined as high blood pressure with sympathetic overdrive, loss of parasympathetically mediated cardiac variability and excessive angiotensin II (Ang II) activity.2 The importance of the sympathetic nervous system in the short-term regulation of blood pressure via the modulation of peripheral vascular tone and cardiac output is well established, while the role of the sympathetic nerve activity (SNA) in long-term blood pressure control is more controversial. [3][4][5] Although the concept of a potential neurogenic component to hypertension is not new, 4 it has perhaps received less attention than the renin-angiotensin system (RAS), which has been a prominent therapeutic and research target in hypertension over the past few decades. Nevertheless, the activation of the sympathetic nervous system and the RAS in hypertension appears inextricably, and reciprocally, linked. Evidence from studies in both patients and animal models of hypertension strongly implicate the chronic sympathetic neural activation in the aetiology and progression of hypertension (Figure 1). 2,[6][7][8][9] The use of regional surgical sympathectomy to treat hypertension over 50 years ago before the availability of antihypertensive medications that lower sympathetic activity provides an early indication of the clinical appreciation for a significant neurogenic component to hypertension.10 Recent clini...

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Cortical Structures Associated With Human Blood Pressure Control

et al. 2018

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IMPORTANCE A better understanding of the role of cortical structures in blood pressure control may help us understand cardiovascular collapse that may lead to sudden unexpected death in epilepsy (SUDEP).OBJECTIVE To identify cortical control sites for human blood pressure regulation. DESIGN, SETTING, AND PARTICIPANTSPatients with intractable epilepsy undergoing intracranial electrode implantation as a prelude to epilepsy surgery in the Epilepsy Monitoring Unit at University Hospitals Cleveland Medical Center were potential candidates for this study. Inclusion criteria were patients 18 years or older who had electrodes implanted in one or more of the regions of interest and in whom deep brain electrical stimulation was indicated for mapping of ictal onset or eloquent cortex as a part of the presurgical evaluation. Twelve consecutive patients were included in this prospective case series from June 1, 2015, to February 28, 2017. MAIN OUTCOMES AND MEASURESChanges in continuous, noninvasive, beat-by-beat blood pressure parameter responses from amygdala, hippocampal, insular, orbitofrontal, temporal, cingulate, and subcallosal stimulation. Electrocardiogram, arterial oxygen saturation, end-tidal carbon dioxide, nasal airflow, and abdominal and thoracic plethysmography were monitored. RESULTS Among 12 patients (7 female; mean [SD] age, 44.25 [12.55] years), 9 electrodes (7 left and 2 right) all in Brodmann area 25 (subcallosal neocortex) in 4 patients produced striking systolic hypotensive changes. Well-maintained diastolic arterial blood pressure and narrowed pulse pressure indicated stimulation-induced reduction in sympathetic drive and consequent probable reduction in cardiac output rather than bradycardia or peripheral vasodilation-induced hypotension. Frequency-domain analysis of heart rate and blood pressure variability showed a mixed picture. No other stimulated structure produced significant blood pressure changes.CONCLUSIONS AND RELEVANCE These findings suggest that Brodmann area 25 has a role in lowering systolic blood pressure in humans. It is a potential symptomatogenic zone for peri-ictal hypotension in patients with epilepsy.

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Deep brain stimulation relieves refractory hypertension

Cited by 57 publications

References 9 publications

Truly Refractory Hypertension

Truly Refractory Hypertension

The sympathetic nervous system and blood pressure in humans: implications for hypertension

Cortical Structures Associated With Human Blood Pressure Control

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