Hypoglossal nerve palsy after extensive vomiting

Abstract

C. Dissection of the left internal carotid artery. Dissection of the internal carotid artery (ICAD; Fig. 1) is not only widely accepted as an important component of stroke aetiology, it is also well recognised as a focal cause of lower cranial nerve palsy.[1]Mokri B. Silbert P.L. Schievink W.I. et al.Cranial nerve palsy in spontaneous dissection of the extracranial internal carotid artery.Neurology. 1996; 46: 356-359Crossref PubMed Scopus (241) Google Scholar In the present patient, a duplex ultrasound revealed a left, submandibular ICAD originating 3 cm distal to the ICA bifurcation. In parallel, a high-grade, long-distance stenosis was confirmed by a time-of-flight magnetic resonance angiogram. Axial T2-weighted MRI showed a crescent-like, hyperintense signal corresponding to an intramural haematoma. In addition, an asymptomatic dissecting vertebral artery (VA) aneurysm on the right V2-segment was detected. This additional finding was not surprising, since simultaneous dissection of more than one extracranial artery is reported in up to 28% of patients.[1]Mokri B. Silbert P.L. Schievink W.I. et al.Cranial nerve palsy in spontaneous dissection of the extracranial internal carotid artery.Neurology. 1996; 46: 356-359Crossref PubMed Scopus (241) Google Scholar There was no evidence of either brainstem or supratentorial infarction on MRI. The pathogenesis of extracranial ICAD[1]Mokri B. Silbert P.L. Schievink W.I. et al.Cranial nerve palsy in spontaneous dissection of the extracranial internal carotid artery.Neurology. 1996; 46: 356-359Crossref PubMed Scopus (241) Google Scholar includes trivial precipitating events such as coughing and sneezing. We speculate that abrupt and extensive rotation of the head and neck during retching and vomiting caused the ICA and VA to suddenly become either stretched or compressed, ultimately leading to intimal tearing and subsequent dissection. In clinical practice, ipsilateral Horner’s syndrome and neck/head pain are recognised as the most common local manifestations of extracranial ICAD. However, cranial nerve palsy also develops in up to 12% of patients with extracranial ICAD, and in almost half of these patients, the hypoglossal nerve is involved either alone or combined with other lower cranial nerve palsies.[1]Mokri B. Silbert P.L. Schievink W.I. et al.Cranial nerve palsy in spontaneous dissection of the extracranial internal carotid artery.Neurology. 1996; 46: 356-359Crossref PubMed Scopus (241) Google Scholar The anatomical course of the distal hypoglossal nerve in the dorsolateral parapharyngeal space is close to the ICA; therefore, direct compression of the hypoglossal nerve by the expanding intramural haematoma of an extracranial ICAD may manifest clinically as an isolated unilateral hypoglossal nerve palsy.[1]Mokri B. Silbert P.L. Schievink W.I. et al.Cranial nerve palsy in spontaneous dissection of the extracranial internal carotid artery.Neurology. 1996; 46: 356-359Crossref PubMed Scopus (241) Google Scholar Haemodynamic or even embolic (as for anomalous vessels derived from the ICA) disturbances to the nutrient arteries supplying the cranial nerves can lead to segmental ischemia of the hypoglossal nerve itself.[1]Mokri B. Silbert P.L. Schievink W.I. et al.Cranial nerve palsy in spontaneous dissection of the extracranial internal carotid artery.Neurology. 1996; 46: 356-359Crossref PubMed Scopus (241) Google Scholar Early diagnosis of ICAD is therefore essential to ensure successful antiplatelet or anticoagulation treatment, since about three-quarters of patients with ICAD eventually develop thromboembolic cerebral ischemia.[2]Baumgartner R.W. Bogousslavsky J. Clinical manifestations of carotid dissection.Front Neurol Neurosci. 2005; 20: 70-76Crossref PubMed Scopus (66) Google Scholar The authors thank Dr. Sandra Dieni for reading the manuscript. Hypoglossal nerve palsy after extensive vomitingJournal of Clinical NeuroscienceVol. 19Issue 5PreviewA previously healthy, 44-year-old woman suffered five to six attacks of retching and extensive vomiting over a period of 30 hours. Metoclopramide (10 mg) was administered intravenously on the emergency ward for antiemetic treatment. Within a few hours the patient experienced a left-sided deviation of the tongue, accompanied by slightly slurred speech, difficulty with food transfer, and left-sided headache and neck pain. Subsequent neurological examination revealed a unilateral left hypoglossal nerve palsy (Fig. Full-Text PDF