Deep-Brain Stimulation May Relieve Refractory Hypertension

Susan Jeffrey

February 09, 2011

February 9, 2011 — An observation made in a patient with refractory chronic pain has suggested a new potential treatment for refractory hypertension: deep-brain stimulation (DBS).

Researchers are reporting the case of a man who was being treated for post-stroke left-sided chronic pain syndrome by using deep-brain stimulation of the ventrolateral periaqueductal gray/periventricular gray (PAG/PVG).

Although the DBS did not provide lasting pain relief, it did decrease his blood pressure (BP), which had previously ranged above levels considered hypertensive despite treatment with 4 antihypertensive medications.

Switching the stimulator off resulted in an increase in BP, while turning it back on reduced BP again, report the investigators.

"PAG/PVG stimulation can produce a large, sustained lowering of blood pressure in a patient with refractory hypertension, which seems to be efficacious, because all antihypertensive medication could be withdrawn," the authors concluded.

Their report was published in the January 25 issue of Neurology.

Effect Independent of Pain

The patient was a 55-year-old man who developed a left-sided central pain syndrome that had been refractory to treatment for about 3 years, first author Nikunj K. Patel, MBBS, MD, from Frenchay Hospital in Bristol, the United Kingdom, told Medscape Medical News. "Central pain syndromes are some of the most challenging to treat, and this led to my implanting a deep brain–stimulating electrode to try and find a path for pain resolution," he said.

The stroke had resulted from uncontrolled hypertension, and the patient's blood pressure was still not controlled, he noted. "He required 4 antihypertensives and was still achieving varying degrees of control, so intermittently he was still found to be systolically hypertensive."

A previous report by researchers at Oxford University had suggested that similar stimulation ventrolateral to the PAG in rats acutely reduced blood pressure, while stimulation dorsal to the PAG would acutely increase it (Carrive P, Bandler R. Brain Res. 1991;541:206-215).

"Knowing that the optimal pain target is also ventral to the aqueduct in the PAG, I was interested to identify whether there would be a blood pressure response from the onset. So it wasn’t necessarily something I wasn't looking for; however, no one's ever documented a chronic reduction in any individual," Dr. Patel said.

The pain reduction response was good for about 4 months but then the pain returned, not uncommon for central pain syndromes treated surgically, he said. "But what has been striking throughout is that the blood pressure was and has remained controlled with the stimulation to the point we were able to take him off all his medications," Dr. Patel added.

BP reached a trough of 80/53 mm Hg immediately after surgery that had prompted withdrawal of medications; at 8 weeks, BP averaged 110/65 mm Hg. It finally reached 124/76 mm Hg at 12 weeks, when a combination of perindopril and indapamide was reinstituted because of the patient's stroke history. However, at 27 weeks, the medications were again withdrawn.

At that point, the researchers measured BP while DBS was turned off over 24 hours. It rose by 18/5 mm Hg. When they turned the stimulator on again, the patient's BP dropped by 33/13 mm Hg, an effect that was repeatable.

Unfortunately, Dr. Patel noted, "we haven't been able to recapture the control for his pain, so I guess in one way we've been able to qualify that his reduction in blood pressure is not related to a reduction in his pain. Someone might argue that it's an alleviation of his stress helping his blood pressure to be controlled, whereas we haven't identified that in any shape. His pain remains as severe, if not more severe, than before."

The proposed mechanism is unclear, he said, but they are working to pursue this in animal models.

"I certainly feel that this paves the way to us identifying the mechanism for neurogenic hypertension — or essential hypertension — where we don't know the causes," he said. "As we know, it's one of the biggest, if not the biggest, cause of morbidity in modern society in causing vascular disease and complications such as stroke, chronic heart failure, and renal disease."

Although noninvasive methods of treatment for refractory hypertension would be preferable, the dangers posed by uncontrolled high blood pressure mean that DBS might represent a possible treatment avenue in some cases, Dr. Patel suggested. Other invasive treatments that are now being investigated for refractory hypertension include renal nerve denervation, carotid sinus stimulation, and vagal nerve stimulation. "The first 2 have some quite interesting results, and the renal nerve denervation especially has been quite profound in reducing hypertension in the majority of cases that have been treated."

Although DBS carries a risk for complications, they are relatively infrequent, on the order of 1% to 2%. "We don't belittle it, but in someone with repeated stroke or at risk for repeated stroke, it may be justified."

Dr. Patel has received speaker honoraria from Boston Scientific and Medtronic, Inc. Disclosures for coauthors appear in the paper.

Neurology. 2011;76:405-407.

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