British Journal of Radiology (2005) 78, 659-661
© 2005 British Institute of Radiology
doi: 10.1259/bjr/57426025
Internal carotid artery dissection presenting with ipsilateral tenth and twelfth nerve palsies and apparent mass lesion on MRI
J Knibb, MA, MRCP
R Lenthall, MRCP, MSc, FRCR
and
N Bajaj, MA, MRCP, PhD
Queen's Medical Centre, Derby Road, Nottingham NG7 2UH, UK
Correspondence: J Knibb, University Department of Neurology, R3 Neurosciences, Box 83, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK
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Abstract
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We report the case of a 47-year-old man who presented with a few months' history of right-sided headache and dysphagia, with ipsilateral tenth and twelfth cranial nerve palsies on examination. The initial MRI showed an enhancing mass lesion in relation to the right carotid sheath and jugular foramen, and was reported as a possible paraganglioma. Subsequent angiography performed to assess tumour vascularity demonstrated a dissection involving a tonsillar loop of the right internal carotid artery (ICA). Imaging findings at MRI and angiography and the presentations and mechanisms of ICA dissection are briefly discussed.
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Case report
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A 47-year-old man presented to his general practitioner complaining of a right-sided temporal headache. He had a past medical history of migraine, hypothyroidism, asthma, eczema and purpuric dermatosis. His headache radiated to the occiput and neck, and had been present continuously since waking a few days previously. Over the next 2 weeks he experienced a gradual onset of dysphagia for solids and slurring of speech, and noticed a change in the appearance of his tongue. He was taking sumatriptan and thyroxine, but no other prescribed medications.
The patient was referred urgently to the neurology department, where examination revealed tongue deviation to the right, accompanied by very marked wasting of the right side of the tongue. Arrangements were made for further investigation, but 3 days later he returned with worsening of his symptoms including dysphonia, uvular deviation to the left, and failure of right palate elevation. Examination of the remaining cranial nerves and peripheral nervous system was unremarkable, and there were no vascular bruits. No significant abnormality was identified on routine laboratory investigations, including electrolytes, calcium, full blood count, thyroid function tests, erythrocyte sedimentation rate, angiotensin-converting enzyme, auto-antibody and vasculitic screening. Alkaline phosphatase and gamma-glutamyl transferase levels were mildly elevated, although a subsequent ultrasound scan of the liver and abdomen showed no abnormality. Examination of the cerebrospinal fluid (CSF) showed a glucose level of 4.0 mM (blood glucose 5.8 mM), a protein level of 0.26 g l–1 and no cells.
An MRI scan of the brain was reported to show an enhancing lesion in relation to the right carotid sheath and jugular foramen, surrounding the vessels within the carotid space (Figure 1a, b
).
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Figure 1. (a) Axial T1 weighted image showing a rounded soft tissue lesion at the skull base with well defined low signal components. The tonsillar loop was not appreciated at this stage. (b) Axial T1 weighted image following contrast showing enhancement of the soft tissue "tumour" encasing the carotid.
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On T1 weighted axial images the lesion was well defined and of intermediate signal, containing low signal components interpreted as flow voids. On the short tau inversion recovery (STIR) images the lesion returned high signal and also contained equivalent low signal components consistent with flow voids. The post contrast T1 weighted images showed intense enhancement of the soft tissue lesion. These findings were interpreted as a vascular mass encasing the carotid artery.
On this basis, a paraganglioma was suggested. A carotid angiogram was requested for further evaluation of tumour vascularity prior to consideration of surgery. This failed to confirm the suspicion of a paraganglioma, but instead showed a dissection of the right internal carotid artery proximal to a tonsillar loop (Figure 2).
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Figure 2. Cerebral angiogram: common carotid run showing a dissection of the internal carotid artery extending into a tonsillar loop.
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It was felt that these findings were sufficient to explain the clinical presentation and MRI appearances, and no further diagnostic investigations were performed. At this stage the headache had resolved, and the tongue wasting and dysphagia had begun to improve. He was prescribed aspirin and discharged. He made a satisfactory recovery on subsequent outpatient assessment, and repeat MRI showed resolution of the dissection with no new collection of thrombus.
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Discussion
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Internal carotid artery dissection (ICAD) is an important cause of stroke in young people. It may occur following local trauma, or may be spontaneous. The cardinal features of ICAD are, ipsilaterally: unilateral headache, facial pain and/or neck pain; Horner's syndrome; cerebral and/or retinal ischaemia, which may be transient or persistent; and a cervical bruit, which may be audible to the patient as pulsatile tinnitus. Spontaneous ICAD usually occurs unilaterally, but may occasionally occur synchronously in both carotid arteries [1], and bilateral dissection of both carotid and vertebral arteries has been reported [2]. Cerebral ischaemia is due either to embolism from thrombosis at the site of dissection, or to local internal carotid occlusion by such a thrombus. For this reason, anticoagulation is widely used in treatment of acute spontaneous ICAD, and haemorrhagic complications from this seem to be rare [3]. However, no randomized controlled trial of anticoagulation in ICAD has been performed [4].
Cranial nerve palsies are well recognized as a feature of ICAD, and have been observed to occur in some 10% to 20% of cases [3, 5–7]. The lower cranial nerves (IX to XII) are most often affected, although involvement of the trigeminal and facial nerves, and more rarely of the oculomotor, trochlear and abducens nerves, has been reported. The hypoglossal nerve is almost always involved when other lower cranial nerves are affected. The eponyms of Collet [8] and Sicard [9] are applied to these cases of lower cranial nerve palsy when there is no accompanying oculosympathetic palsy, although the Collet–Sicard syndrome is not confined to this aetiology and has also been reported in association with true aneurysms [10], venous thromboses [11], tumours [12] and fractures [13] in relation to the jugular foramen.
The mechanism by which ICAD affects cranial nerves is disputed. The most likely explanation in most cases is that the dissecting vessel dilates, causing pressure effects on adjoining structures. Alternatively the mechanism may be ischaemic. The lower cranial nerves are supplied by the neuromeningeal trunk, a branch of the ascending pharyngeal artery. The ascending pharyngeal artery originates from the external carotid artery [7]. Occasionally, however, it arises from the internal carotid, and in these cases it may be affected by ICAD.
Perhaps the most salient aspect of the present case is the unusual appearance of the dissection on MRI. The combination of vessel tortuosity due to a tonsillar loop and enhancing mural thrombus resulted in an appearance suggestive of a vascular tumour encasing the carotid. The lesion returned intermediate T1 and high T2 signal and appearances were suggestive of tumour or inflammatory tissue rather than intramural blood products. However, the MRI was performed over 3 weeks after the initial presentation and the typical signal characteristics of blood products were not apparent. Rather, the appearances represented an inflammatory response associated with arterial wall repair.
As a jugular paraganglioma was suspected in this case, catheter angiography was performed to demonstrate tumour vascularization. In retrospect, contrast enhanced MR angiography could have provided further useful information, although debate might have arisen as to whether segmental calibre changes were related to dissection or arterial wall invasion by a mass.
This is the first report of a case of spontaneous ICAD in which the delayed and atypical clinical presentation was associated with MRI appearances that suggested a mass lesion encasing the carotid at the skull base. The atypical presentation of ICAD in this case, with gradual onset of lower cranial nerve palsies and only mild headache, led to significant delay in making the correct diagnosis. Also, assuming that the event of dissection can be timed roughly to the onset of headache, the development of tongue wasting was remarkably rapid, reaching an advanced stage after only a week.
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Footnotes
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Full informed consent to the publication of this report has been obtained from the patient. 
Received for publication September 27, 2004.
Revision received February 15, 2005.
Accepted for publication March 3, 2005.
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References
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