It’s All in Your Head: An Unusual Cause of Secondary Hypertension

Case Presentation:

A 42 year old male with a history of uncontrolled hypertension

presented with acute onset of transient left sided weakness, numbness, vertigo and ataxia lasting about an hour. The patient had carried a diagnosis of hypertension since the age of 18, and, despite compliance with five antihypertensive agents as an outpatient, he continued to have baseline systolic blood pressures in the 200s. . He also has history of hyperlipidemia, diabetes and a prior stroke with residual effect of memory impairment. His home medications included hydrochlorothiazide, atenolol, clonidine, quinapril and norvasc.

On presentation to the emergency room his systolic blood pressure was 250mmHg. Physical exam was non focal. He had no nystagmus. He was admitted to hospitalist service to rule out stroke. CT scan of head showed old small remote infarcts involving the right cerebellum and left thalamus but no acute intracranial process. MRI of the head showed prior infarcts in left thalamus/ posterior right cerebellum but no acute infarctions. MRI also reported indentation of the left ventrolateral medulla due to tortuosity of the distal left vertebral artery.

During the hospital course he had malignant hypertension. He had negative work up for secondary hypertension. His urine drug screen was negative for cocaine. Plasma renin, aldosterone and free metanephrine levels were within normal limits. Renal Duplex was also performed to rule out renal artery stenosis. Thyroid stimulating harmone level was normal and overnight continous pulsoximetry did not show any hypoxia. He transiently required nicardipine infusion while oral medications were titrated. He was eventually discharged home on multiple oral anti‐hypertensives and was referred to a neurosurgeon at a tertiary center for potential surgical decompression.

Discussion:

The rostral ventrolateral medulla (RVLM), a major center of the sympathetic nervous system, helps regulate the cardiovascular system. Studies have shown that electrical or chemical stimulation of the RVLM causes an increase in blood pressure and chemical inhibition of the RVLM causes a decrease in blood pressure.There have been several case reports suggesting pulsatile compression of the left ventrolateral medulla ablongata can cause arterial hypertension. In 80% of the angiograms of the hypertensive patients, an artery crossed the left root entry zone of the 9^th and 10^thcranial nerves. MR imaging was used to study this relation in a Japanese study, in which 29 out of 32 patients with essential hypertension showed neurovascular compression. It was also noted that left sided compression was more common.

In a small German study, neurosurgical microvascular decompression at this root‐entry zone showed clinical improvement in seven of the eight patients included.

Conclusions:

A subgroup of patients with essential hypertension may exist who have secondary forms of hypertension related to neurovascular compression at the ventrolateral medulla. In those patients in whom this is discovered, and whose hypertension is poorly controlled on medications, neurosurgical decompression might be a therapeutic option.