Correspondence

Munchausen's Syndrome Presenting as Baroreflex Failure

N Engl J Med 2000; 343:581August 24, 2000

Article

To the Editor:

Baroreflex failure is characterized by episodes of severe hypertension and tachycardia,1 alternating with episodes of normal or even low blood pressure and bradycardia.2 It is often caused by interruption of the baroreflex arch as a result of bilateral damage to the glossopharyngeal and vagus nerves from trauma, radiation, or surgery. Less often, the lesion is in the brain stem,3 and in some cases, the primary cause is not found.

A 68-year-old woman was referred for evaluation of baroreflex failure because of a four-year history of severe episodes of hypertension (systolic blood pressure >200 mm Hg for two to four days) alternating with periods of gradual-onset hypotension (in which the systolic blood pressure dropped below 70 mm Hg over a period of hours), bradycardia (requiring a pacemaker), and extreme sleepiness.

Plasma norepinephrine levels were elevated (900 pg per milliliter) during the hypertensive episodes and inappropriately low (54 pg per milliliter) during the hypotensive episodes, changes consistent with the occurrence of baroreflex failure. However, there was no apparent cause, and baroreflex gain (the magnitude of proportional changes in heart rate per unit change in blood pressure) was only mildly reduced. A suppression test with 0.3 mg of clonidine reduced the blood pressure from 158/99 to 105/62 mm Hg, the heart rate from 93 to 66 beats per minute, and the plasma norepinephrine level from 961 to 93 pg per milliliter, reproducing the conditions recorded during spontaneous episodes.

The alpha₂-antagonist yohimbine, whose effects are the opposite of those of clonidine, reduced the severity and duration of the hypotensive episodes. Plasma samples obtained before and during a hypotensive episode revealed clonidine levels in the high therapeutic range (Figure 1Figure 1Plasma Levels of Clonidine before and during a “Spontaneous” Episode of Hypotension.), indicating that the cause of the episodes was Munchausen's syndrome. The patient denied taking clonidine and refused psychiatric assistance, but the episodes did not recur during nine months of follow-up with strict supervision of the patient by her family and the removal of all medications from the home. The severity of her disorder is underscored by her willingness to undergo invasive diagnostic procedures and treatments (arteriography, Swan–Ganz monitoring, placement of a pacemaker, and possible brain-stem–decompression surgery). The duration of her illness (four years) emphasizes the difficulties in diagnosing this disease and its lack of recognition in the medical community.

Tahir Tellioglu, M.D.
John A. Oates, M.D.
Italo Biaggioni, M.D.
Vanderbilt University, Nashville, TN 37232-2195

3 References

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   Robertson D, Hollister AS, Biaggioni I, Netterville JL, Mosqueda-Garcia R, Robertson RM. The diagnosis and treatment of baroreflex failure. N Engl J Med 1993;329:1449-1455
   Full Text | Web of Science | Medline

2. 2

   Jordan J, Shannon JR, Black BK, et al. Malignant vagotonia due to selective baroreflex failure. Hypertension 1997;30:1072-1077
   Web of Science | Medline

3. 3

   Biaggioni I, Whetsell WO, Jobe J, Nadeau JH. Baroreflex failure in a patient with central nervous system lesions involving the nucleus tractus solitarii. Hypertension 1994;23:491-495
   Web of Science | Medline

Citing Articles (2)

Citing Articles

1. 1

   Jens Jordan. 2012. Baroreflex Failure. , 349-353.
   CrossRef

2. 2

   T Zar, A J Peixoto. (2008) Paroxysmal hypertension due to baroreflex failure. Kidney International 74:1, 126-131
   CrossRef