Lower cranial nerve palsies in various combinations involving the hypoglossal, glossopharyngeal, vagal, and the accessory nerves occur in internal carotid artery (ICA) dissection.1-8 17 The hypoglossal nerve (cn-XII) is most often affected. It is suggested that the close proximity of these nerves to the cervical ICA may subject them to mechanical injury either by the expansion of the dissected artery or by aneurysm formation.1 3 9 10 Dissection of the ICA may cause transient or permanent disruption of the blood supply to these cranial nerves.6 11 Therefore, cranial nerve injuries may result from “mechanical, embolic, or haemodynamic” processes caused by ICA dissection.6 This hypothesis is supported by anatomical and clinical findings.2 6 12Each half of the genioglossus muscle that protrudes the tongue is innervated by contralateral corticobulbar (crossed) fibres whereas all other intrinsic and extrinsic tongue muscles that move the tongue within the mouth in all directions have bilateral cortical innervation.13 14 Unilateral cortical lesion in the topography representing the tongue may therefore cause contralateral genioglossus muscle weakness, resulting in deviation of the protruded tongue away from the side of the cortical lesion. By contrast, cn-XII injury causes ipsilateral genioglossus muscle weakness; hence the protruded tongue deviates to the side of the injured nerve.

When clinical history is unrevealing and lower cranial nerves are involved, diagnosing ICA dissection becomes challenging. We present a patient with complete tongue paralysis that resulted from a frontal lobe stroke and a cn-XII injury, both caused by an ipsilateral ICA dissection. In the absence of binuclear cn-XII lesion or a pseudobulbar syndrome, localisation of the lesions responsible for the complete tongue paralysis can be difficult. This patient illustrates that in the presence of bilateral acute tongue paralysis …