He had a medical history of well-controlled diabetes, hypertension and dyslipidaemia. Neurological examination revealed a left-sided ptosis and binocular horizontal diplopia in dextroversion without apparent extraocular-muscle paresis or pupillary involvement, cranial nerve affecting carotid blood pressure.
Other cranial nerves were spared as well as motor, sensory and coordination systems. There were no signs of ocular erythema, proptosis or palpable orbital mass.
Brain MR angiography revealed a crescent-shaped mural hyperintensity in left internal carotid artery ICA at skull base, extending to intrapetrous segment, with reduced calibre and flow, suggesting a left ICA dissection. The patient was started on antiaggregation therapy. ICAD pathophysiology lies in a compromise of structural integrity of the arterial wall through the formation of an intimal tear, resulting in stenosis, occlusion, intraluminal thrombus or extravascular haemorrhage.
Most cases comprise extracranial arteries but, rarely, intracranial arteries are affected. However, most patients do not show the complete triad and may exhibit less common manifestations such as cranial nerve palsies. Nevertheless, the mechanism underlying these cranial neuropathies is still not fully understood. Direct compression by an enlarged dissected vessel is proposed to be responsible for lower cranial nerve palsies.
We present a case report on ICAD presented as III nerve palsy to emphasise the importance of considering a cervicocerebral dissection in less typical clinical presentations. He denied headache, cervical pain and trauma history. He had medical history of well-controlled diabetes, hypertension and dyslipidaemia.
Family medical history was irrelevant for stroke or connective tissue disorders. General physical examination was normal. He showed no signs of ocular erythema, proptosis or palpable orbital mass. On neurological examination he was alert, oriented, with no evidence of higher function abnormalities.
The patient presented isocoric and normally reactive pupils, partial left ptosis and, although with no obvious limitation in eye movements, the patient consistently mentioned binocular horizontal diplopia in dextroversion. There was no evidence of abnormalities involving other cranial pairs, muscle tonus and strength, osteotendinous reflexes, cutaneoplantar reflexes, sensation, coordination and gait.
Brain MRI angiography revealed a crescent-shaped mural hyperintensity in left ICA at skull base that extends to the intrapetrous segment with reduced calibre and flow, acquiring his normal pattern in the intracavernous portion suggesting a left ICAD.
Brain MRI did not show evidence of parenchymal signal abnormalities figures 1 and 2. MR angiography showing irregularities in left internal carotid artery lumen. Fat-suppressed T1-weighted MRI showing a crescent-shaped haematoma within the wall of the left internal carotid artery, adjacent to the eccentric lumen. Addressing a sudden-onset persistent horizontal diplopia with clinical signs of incomplete pupil-sparing oculomotor nerve palsy partial left ptosis and diplopia maximal at dextroversionthe main differential diagnosis includes stroke and ischaemic oculomotor mononeuropathy.
The sudden onset and presence of vascular risk factors arterial hypertension, diabetes and dyslipidaemia favours an ischaemic aetiology.
An infarct involving oculomotor nucleus is rare and clinically different from III cranial nerve palsy. Paired oculomotor nuclear complexes are located in dorsal midbrain at superior colliculus level.
An infarct involving the caudal subnucleus located in midline may result in bilateral ptosis as this nucleus provides innervation for bilateral levator palpebrae superioris. As already described, our patient had a unilateral ptosis that did not support this hypothesis.
Regarding the hypothesis of an ischaemic mononeuropathy, it is well known that oculomotor is the most frequent cranial nerve palsy associated with diabetes, affecting predominantly older patients with long-term diabetes.
The clinical presentation has a sudden onset, usually spares pupillary involvement and can be accompanied with retro-orbital pain. Addressing a cervicocerebral artery dissection, cranial nerve affecting carotid blood pressure, the current accepted therapy remains antithrombotic medication anticoagulation or antiaggregation and there is cranial nerve affecting carotid blood pressure consistent medical evidence to guide therapy.
Brain CT confirmed ICA recanalisation and cervical doppler ultrasonography showed normal morphological and haemodynamic features. The patient reported a horizontal binocular diplopia maximal when looking to the right, which, in association with left ptosis, is consistent with a left oculomotor nerve palsy.
Although we were not able to observe any limitation in ocular movements, this does not exclude III nerve palsy. It has been reported that some ICAD cases are actually asymptomatic.
We do not support the hypothesis that a left oculomotor nerve palsy and a left intrapetrous ICAD are simply a manifestation of two different conditions an ischaemic mononeuropathy and an asymptomatic ICAD. Moreover, cranial nerve affecting carotid blood pressure, the patient denied ocular pain that often accompanies an ischaemic neuropathy. Anatomically, the distal part of the III nerve is supplied by the inferior cavernous cranial nerve affecting carotid blood pressure and cranial nerve affecting carotid blood pressure arteries, both branches from the intracavernous segment of ICA.
ICAD presented with oculomotor nerve palsy is rare and there are few cases described in the literature. There are also reports of cases involving extracranial ICA segment. Campos et al 6 described a case of a year-old man who began having an occipital headache and developed diplopia days later, with objective impairment in right eye adduction and upward gaze and slight pupillary dilation with MR angiography evidence of a dissection of right extracranial ICA.
Considering the small group of patients presenting cranial nerve palsies in the setting of an ICAD, oculomotor nerve involvement is extremely rare.
The hypothesis of a cervicocerebral dissection should be considered when addressing a young patient with cranial nerve palsy. Contributors TS and PB cranial nerve affecting carotid blood pressure the article.
HM corrected and revised it. GO was responsible for the selection and review of imaging components. Provenance and peer review Not commissioned; externally peer reviewed. The full text of Images in Search this site Advanced search. BMJ Case Reports ; doi: Isolated oculomotor nerve palsy: Previous Section Next Section. In a new window Download as PowerPoint Slide. Although rare, cranial nerve palsies can be the only manifestation of an ICAD.
Bogousslavsky JPierre P, cranial nerve affecting carotid blood pressure. Ischemic stroke in patients under 45 years. Neurol Clin ; Cerebrovascular dissections—a review part I: Neurosurgery ; Cranial nerve palsy in spontaneous dissection of the extracranial internal carotid artery. Neurology ; Upper cranial nerve palsy resulting from spontaneous carotid dissection. J Neurol ; Dissection of the intracranial internal carotid artery producing isolated oculomotor nerve palsy with sparing of pupil.
Acta Neurol Scand ; Isolated oculomotor nerve palsy in spontaneous internal carotid artery dissection: Arq Neuropsiquiatr ; Internal carotid artery dissection heralded by an oculomotor nerve palsy: Neurologist ; Services Email this link to a friend Alert me when this article is cited Alert me if a correction is posted Alert me when eletters are published Article Usage Statistics Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Add article to my folders Download to citation manager Request permissions Add to portfolio.
Responses Submit a response No responses published. Google Scholar Articles by Santos, T. Articles by Barros, P. Search for related content.
Related Content Images in Blog Most Read Top Rated. Online submission site Instructions for authors Become a fellow: Become a fellow Help: Subscribe here Activate your subscription. Remember me Remember me. Forgot your sign in details? Login via your home organisation.
Recommend to your Institution.