Age and Ageing Advance Access originally published online on June 12, 2008
Age and Ageing 2008 37(5):602-604; doi:10.1093/ageing/afn105
Case Reports |
Vagolysis
Canterbury District Health Board, Christchurch, New Zealand
Address correspondence to: C. D. Hutchinson. Tel: 0064 3 3640640; Fax: 0064 3 364 1025. Email: Christopher.Hutchinson{at}cdhb.govt.nz
Abstract
We describe the case of a 75-year-old man presenting with labile hypertension and symptomatic postural hypotension 13 months following radiotherapy for squamous cell carcinoma of his external auditory canal. Magnetic resonance image (MRI) scan demonstrated scarring and a probable recurrence of his tumour. He underwent autonomic testing, including muscle sympathetic nerve activity (MSNA), heart rate (HR) and blood pressure (BP) responses to a variety of stimuli. Results were consistent with baroreflex failure. Urinary catecholamine levels were within the high normal range. We postulate that baroreflex failure was caused by vagal and glossopharyngeal nerve damage secondary to radiotherapy and tumour recurrence. This diagnosis is rare, but should be considered with pure autonomic failure and phaeochromocytoma in the presence of labile hypertension, especially in patients with a history of radiotherapy to the neck and high-normal catecholamine levels.
Keywords: baroreflex failure, sympathetic nervous system, labile hypertension, elderly
In March 2001, a 75-year-old man was admitted after collapsing in the shower, following 1 week of postural symptoms and progressive right facial weakness. Thirteen months previously he underwent radical excision of a T4 N0 M0 squamous cell carcinoma of the right external auditory canal followed by local radiotherapy (110 Gy) to the neck. He had been smoking for 50 years, had peripheral vascular disease and a 15-year history of previously well-controlled hypertension. His only medication was Labetalol 100 mg bd. On examination, there was right lower motor neurone facial weakness and a 3 x 3 cm woody mass under the right mandible. His supine blood pressure (BP) was labile, ranging from 70/40 to 240/120 mmHg with postural falls of up to 58 mmHg systolic. Labetalol was stopped and it became clear that he could not tolerate any form of anti-hypertensive medication because of postural hypotension. Following surgical review and magnetic resonance imaging (MRI) (Figure 1A), a recurrence of tumour was diagnosed. One week later, he developed dysphagia and right vocal chord paralysis.
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Labile hypertension may be caused by phaeochromocytoma, renal artery stenosis, autonomic failure and raised intra-cranial pressure, but when associated with impaired vagomotor function is suggestive of baroreflex failure. We therefore measured sympathetic and heart rate (HR) responses to standard autonomic stimuli. We monitored continuous BP, HR and efferent muscle sympathetic nerve activity (MSNA) from the right leg using microneurography [1]. MSNA mediates vasoconstriction and is recorded as a series of positive bursts quantified by measuring total burst area per minute. MSNA bursts are normally baroreflex-modulated, gated to heart rhythm and inversely related to mean BP (MBP) [2]. At rest, supine MBP was 130 mmHg, HR was relatively fixed at 81 bpm and MSNA at 11 units/min. During a 2-min handgrip, MBP and MSNA increased to 174 mmHg and 15.6 units/min, respectively. Responses to Valsalva are shown with those of a normal subject of similar age (Figure 1 C and D). Despite the rapid increase in BP to 170 mmHg during phase IV, there was no slowing of HR (94 bpm) or decrease in MSNA (10 units/min). Therefore, although handgrip responses were normal, there was loss of baroreflex modulation of MSNA and HR in response to BP during Valsalva. Urinary catecholamine levels were in the high normal range and renal artery stenosis was excluded by magnetic resonance angiography. His dysphagia necessitated gastrostomy tube feeding and he was discharged of all anti-hypertensive medication in May 2001. His condition continued to deteriorate and he died 2 weeks later following a myocardial infarction.
Sympathetic output from the brainstem is normally inhibited by baroreceptor afferents terminating in the medulla on the nucleus tractus solitarius (NTS, Figure 1B). The same afferents stimulate the cardiac vagal nuclei, the dominant modulators of HR. Any process which interrupts these pathways will cause increased MSNA and HR. In the absence of baroreflex buffering, the brainstem becomes more susceptible to stimulation from the higher centres (via central pathways) resulting in surges of MSNA and labile hypertension [3]. In our patient, damage to vagal cardiac efferents protected the patient from excessive central stimulation, resulting in a relatively fixed HR [4]. Baroreflex failure usually requires bilateral dysfunction of vagus and glossopharyngeal nerves, as there is major redundancy of baro-afferent input [5]. Following radiotherapy, damage to the cranial nerves occurs in the neck as they course to the mediastinum, whereas the efferent sympathetic interneurones are relatively protected in the cervical spinal cord. Baroreflex failure is relatively rare, but well documented following neck radiotherapy and carotid body tumour resection [3]. Diagnosis is based on normal or exaggerated MSNA and HR responses to central stimuli (e.g. handgrip exercise) with impaired baroreflex responses. When postural hypotension is present, this condition must be differentiated from pure autonomic failure (where MSNA levels are decreased and unresponsive) and multiple system atrophy. Phaeochromocytoma should be considered but is less likely in the patient with neck pathology, vagal dysfunction and only moderately raised catecholamine levels.
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References
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[Abstract/Free Full Text]
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