I read with great interest the prospective evaluation by Venkatesan, et al1 of autonomic nerve function in adult patients with cyclic vomiting syndrome (CVS). The authors identified both vasomotor and sudomotor dysfunction, with preservation of parasympathetic activity in their patient cohort. How these deficits may be reconciled with the clinical features is an unanswered and intriguing question. One basic point to consider is that the symptoms of nausea and vomiting may theoretically arise as part of the physiologic spectrum in response to sympathetic vascular insufficiency.
Nausea and vomiting are symptoms which commonly occur in the setting of orthostatic intolerance, and often are ameliorated by treatment of the underlying insufficiency.2 Interestingly, the very act of emesis often leads to a subjective sense of relief, along with a state of increased alertness. Ferrier, in 1878, speculated that ‘the violent compression and concussion of the abdominal walls in the act of vomiting serve to propel the blood onwards, and thus raise the blood pressure.’3 This observation has been substantiated by contemporary knowledge of the splanchnic circulation to be a venous capacitance bed, which holds up to 30% of the blood volume. The mobilization of this pool by sympathetic venoconstriction is thought to play an important role in systemic blood pressure regulation.
During vomiting, two patterns of blood pressure changes are observed.4 First, a rapid, projectile type, with minimal prodromata, accompanied with a sharp drop in blood pressure, and marked slowing of the heart rate is seen. A vagal etiology has been implicated in this situation, as hypotension can be protected against by administration of atropine. A second type of vomiting consists of a slow, labored course with prolonged violent retching, correlating with spikes in blood pressure. These blood pressure fluctuations can be suppressed by curare administration, pointing to a dependency on skeletal muscle contraction. Further, the neuroendocrinologic correlates of nausea and vomiting have been emphasized as part of an adaptive stress response by Gupta,5 as arginine-vasopressin (AVP) release is known to participate in vasomotor activity, fluid retention, antinociception, and behavioral control.
The pathophysiology of CVS remains incompletely understood, and the data provided by Venkatesan, et al1 represent an important clue in deciphering this enigmatic condition. Nausea and vomiting in CVS may be a manifestation of an adaptive physiologic response to sympathetic insufficiency, or to other yet unidentified pathophysiological stressors.