Anterior Communicating Artery Aneurysm With Refractory Central Vomiting: A Case Report

Endocrine disturbance and vomiting may be provoked by compression of hypothalamus and hypothalamic-pituitary complex by the compression effect; this compression may be due to tumors or rarely aneurysms. This is particularly true for anterior communicating artery (AcomA) because arteries derived from this vessel supply a portion of the hypothalamus (1). It is also known that vomiting can be elicited by stimulation of the supraoptic area of the hypothalamus. We herein report a rare case of anterior communicating aneurysm with refractory vomiting.

A 59-year-old man was admitted to the neurology ward of Firoozgar hospital affiliated to Iran University of Medical Sciences, in November 2013 with a six-month-history of refractory nausea and vomiting. He did not report any other accompanying symptoms during this period. He was a retired man and his past medical and drug history were not significant. He was a smoker but denied use of alcohol or illicit drugs.

His physical and neurological exams were normal. The blood investigations revealed normal hematological, biochemical and hormonal profile. Endoscopy and colonoscopy had been performed before referral to this center; reported to be normal. Abdominopelvic computed tomography (CT) scan with oral and intravenous contrast showed no evidence of abnormality. Unenhanced brain CT scan showed a (12 × 7 mm) hyperdense suprasellar lesion. Brain MRI suggests that the lesion could be an AcomA aneurysm. Digital subtraction angiography (DSA) confirmed the findings of imaging and revealed saccular aneurysm of AcomA. It was decided to treat the aneurysm by the endovascular approach. The aneurysm was completely obliterated by coiling. The operation was successful and interestingly, his symptoms were resolved immediately after the embolization. During the follow up, after six months, he did not experience nausea and vomiting any more.

Twenty-five to thirty-eight percent of all cases of cerebral aneurysms occur in AcomA, making it the most common site among intracranial arteries (2). In the setting of un-ruptured aneurysm, the symptoms arise from either the mass effect of a large aneurysm over the surrounding tissues, or possibly from minimal leakage of blood irritating the meninges (3). Nevertheless, occurrence of large AcomA aneurysms is extremely rare because they are generally susceptible to rupture while they are relatively small (4). Thus, an AcomA aneurysm is expected to cause symptoms due to hemorrhage (mainly subarachnoid hemorrhage) rather than compression effects. According to the literature, an un-ruptured AcomA may present, through its pressure effect, in different ways, with visual disturbance (4-6) being the most common reported presentation, followed by central vomiting, hypopituitarism (7), and cognitive impairment (5). Our patient presented chronic refractory nausea and vomiting without any other accompanying symptom such as headache, which to the best of our knowledge, is a rare presentation of an un-ruptured AcomA and we could not find any other similar report in the literature. Neurons, in the para-ventricular nucleus of the hypothalamus, project to the preganglionic neurons of the sympathetic and parasympathetic divisions in the brainstem and spinal cord. These cells exert hypothalamus control over the visceral motor system and modulate autonomic reflexes such as respiration and vomiting. Compression of these cells by the aneurysm could be responsible for symptoms of intractable nausea and vomiting in our patient (8). In this setting, we expect the occurrence of symptoms after aneurysm treatment.