Abstract
We report two cases of lower cranial nerve palsies (XII in case 1, IX–X–XII in case 2) associated with abnormalities of the internal carotid artery at the base of the skull. In case 1 a limited dissection of the carotid wall produced both paresis of the hypoglossal nerve and Horners syndrome by compression of the nerve trunk against the base of the skull and stretching of the periarterial sympathetic fibres respectively. In case 2 we speculate that a narrow angled kinking of the internal carotid artery may have damaged cranial nerves IX, X and XII by interfering with the blood supply to the nerve trunks. In both cases the outcome was favorable with almost complete regression of the initial symptoms. We conclude that the association between lower cranial nerve disturbances and internal carotid artery abnormalities is probably more common than was thought. We suggest that the pathogenesis of the damage to the cranial nerves may differ from one case to the next.
Riassunto
Gli Autori riportano due casi di paralisi dei nervi cranici bulbari (XII nel caso 1, IX–X–XII nel caso 2) causate da anomalie dell'arteria carotide interna alla base cranica.
Nel caso 1 la paresi del XII nervo cranico, associato con sindrome di Claude Bernard Horner ipsilaterale, è state determinata da un anuerisma dissecante della carotide con conseguente compressione del tronco nervoso contro la base cranica e stiramento delle fibre simpatiche periarteriose. Nel caso 2 viene ipotizzato che la lesione del IX, X e XII nervo cranico sia stata di origine ischemica per la presenza di un'ansa ad angolo acuto dell'arteria carotide interna.
In entrambi i casi il decorso è stato favorevole, con regressione pressochè completa dei sintomi iniziali. L'associazione fra anomalie della carotide interna e disturbi dei nervi cranici bulbari è probabilmente più frequente di quanto si ritenesse in precedenza e la patogenesi della lesione nervosa può essere variabile da caso a caso.
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Anzola, G.P., Gualandi, G.F., Orlandini, A. et al. Lower cranial nerve palsy produced by internal carotid artery dilatation. Report of two cases. Ital J Neuro Sci 8, 375–379 (1987). https://doi.org/10.1007/BF02335742
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DOI: https://doi.org/10.1007/BF02335742