Pair Of Terrifying But Yet Progressive Crizotinib Helpful Hints

10 11 We believe our case to be unique in that we identify the minor trauma associated with upper respiratory tract infection as the likely cause of the dissection in this patient given his 10-day history of common cold symptoms preceding the onset of neurological symptoms and the absence of major traumatic injury. Two possible mechanisms of cranial nerve involvement in carotid dissection have been described.12 The mechanical compromise resulting from dissection can impede blood flow through the nutrient vessels supplying the cranial nerves. Although anatomical variations are possible, the site of the dissection determines which nutrient vessels are haemodynamically compromised. Given that the external carotid artery supplies the lower cranial nerves through the ascending pharyngeal system we deem this an unlikely mechanism as the dissection in our patient occurred in the internal rather than the external carotid artery. Alternatively, intramural haematoma can cause the artery to expand and directly compress the cranial nerves (IX, X, XI, XII) running through the upper carotid sheath. Although we cannot definitively rule out ischaemic damage to the cranial nerves, this is the more likely mechanism given the dissection of the internal carotid and the accompanying lower cranial nerve palsies that our patient demonstrates: Glossopharyngeal (IX): reported difficulty swallowing and loss of taste sensation. Vagus (X): left vocal cord palsy observed on flexible laryngoscopy. Spinal accessory (XI): atrophy of trapezius established on examination at monthly follow-up. Hypoglossal (XII): ipsilateral tongue paresis. The common site of c-Met inhibitor convergence of all the lower cranial nerves is the retrostyloid section of the parapharyngeal space. The posterior boundary of this space is the fascia of the carotid sheath, hence explaining how an intramural haematoma of the carotid artery can directly compress the lower cranial nerves to manifest clinically as multiple palsies. Interestingly, our patient does not demonstrate any signs of Horner's syndrome which could also be expected as sympathetic fibres also pass through the parapharyngeal space. Such sparing of the sympathetic plexus provides further argument for the classification of this case as CSS. However, we do exercise a degree of caution in definitively describing this as a case of CSS given that the patient was found to have an intact bilateral gag reflex. The vagus nerve palsy could also account for the patients reported difficulty in swallowing. Despite this we feel that the combination of difficulty in swallowing and the altered sense of taste are suggestive enough of glossopharyngeal nerve palsy for the classification of CSS to be given serious consideration.