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DOI 10.1016/s0140-6736(97)11343-5

Медицинская библиотека · Lancet (London, England) · 1998

Decrease of blood pressure by ventrolateral medullary decompression in essential hypertension.

Geiger H, Naraghi R, Schobel H P, Frank H, Sterzel R B, Fahlbusch R

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Аннотация

BACKGROUND

About 20% of adults worldwide will develop hypertension. Studies and clinical observations suggest an association between hypertension and pulsatile compression of the ventrolateral medulla oblongata by a looping artery. We investigated whether neurosurgical microvascular decompression substantially decreases blood pressure long-term in patients with severe essential hypertension.

METHODS

We included eight patients who had received three or more antihypertensive drugs without adequate control of blood pressure, intolerable side-effects, or both. All patients underwent microvascular decompression at the root-entry zone of cranial nerves IX and X after neurovascular compression of the ventrolateral medulla oblongata was seen on magnetic-resonance angiography.

FINDINGS: 3 months after surgery, blood pressure and antihypertensive regimens had decreased substantially in three patients. Four patients who were followed up for more than 1 year became normotensive, but their antihypertensive regimens remained the same as those at 3 months. One patient did not improve. No complications associated with decompression occurred. One patient experienced a transient vocal-cord paresis after the laryngeal part of the vagus nerve was manoeuvered during surgery.

INTERPRETATION: We showed a direct causal relation between raised blood pressure and irritation of cranial nerves IX and X. A subgroup of patients with essential hypertension may exist who have secondary forms of hypertension related to neurovascular compression at the ventrolateral medulla and who may be successfully treated with decompression.

Для цитирования: Geiger H, Naraghi R, Schobel H P, Frank H, Sterzel R B, Fahlbusch R. Decrease of blood pressure by ventrolateral medullary decompression in essential hypertension.. Lancet (London, England). 1998. DOI: 10.1016/s0140-6736(97)11343-5.

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