Abstract:Acute oculomotor nerve palsies with pupillary involvement warrant thorough investigation. When routine work-up fails to elucidate an etiology, extracranial carotid pathology should be considered.
“…Further, magnetic resonance imaging findings postoperatively did not demonstrate any midbrain stroke to explain the patient's examination findings [Figure 4b and c ]. Finally, the clinical course after discovery of the pupil is certainly compatible with previous reports of ICA dissection-associated third nerve palsy[ 8 ] or ischemic injury from perforator loss in the recanalized PCA. Our hypothesis, therefore, is that the most likely cause of third nerve palsy in this case was the recanalization of the fetal PCA.…”
Section: Discussionsupporting
confidence: 87%
“…[ 6 10 ] In a recent case report and review, Nizam et al . [ 8 ] summarized 16 cases of partial or complete third nerve involvement, along with other symptoms, in the setting of carotid artery dissection that have been reported in the literature. Interestingly, a fetal PCA variant would allow for additional proximal involvement of the nerve as well.…”
Section: Discussionmentioning
confidence: 99%
“…Interestingly, a fetal PCA variant would allow for additional proximal involvement of the nerve as well. Consequently, it has been suggested previously that the presence of fetal PCA anatomy increases the likelihood of third nerve ischemia during dissection,[ 8 ] and such palsies have been reported in other cases. [ 3 5 ]…”
Background:Common causes of oculomotor nerve palsy are diabetes, aneurysmal compression, and uncal herniation. A lesser-known cause of third nerve dysfunction is ischemia, often due to carotid artery dissection.Case Description:An 80-year-old man presented with an acute ischemic stroke with a National Institutes of Health Stroke Scale score of >20 from a high cervical internal carotid artery (ICA) dissection and a tandem ICA terminus embolic occlusion with extension of clot into the adjacent fetal posterior cerebral artery (PCA). We used a stentriever to perform selective PCA thrombectomy, with immediate postthrombectomy development of ipsilateral anisocoria. The anisocoria progressed into complete oculomotor nerve palsy over 8 h after the procedure.Conclusions:The clinical course described in this case is consistent with injury to the third nerve due to mechanical injury or occlusion of perforator supply to the nerve during thrombectomy. Oculomotor nerve palsy is a rare but known complication after ischemia; however, to our knowledge, this is the first case after thrombectomy for a PCA embolus.
“…Further, magnetic resonance imaging findings postoperatively did not demonstrate any midbrain stroke to explain the patient's examination findings [Figure 4b and c ]. Finally, the clinical course after discovery of the pupil is certainly compatible with previous reports of ICA dissection-associated third nerve palsy[ 8 ] or ischemic injury from perforator loss in the recanalized PCA. Our hypothesis, therefore, is that the most likely cause of third nerve palsy in this case was the recanalization of the fetal PCA.…”
Section: Discussionsupporting
confidence: 87%
“…[ 6 10 ] In a recent case report and review, Nizam et al . [ 8 ] summarized 16 cases of partial or complete third nerve involvement, along with other symptoms, in the setting of carotid artery dissection that have been reported in the literature. Interestingly, a fetal PCA variant would allow for additional proximal involvement of the nerve as well.…”
Section: Discussionmentioning
confidence: 99%
“…Interestingly, a fetal PCA variant would allow for additional proximal involvement of the nerve as well. Consequently, it has been suggested previously that the presence of fetal PCA anatomy increases the likelihood of third nerve ischemia during dissection,[ 8 ] and such palsies have been reported in other cases. [ 3 5 ]…”
Background:Common causes of oculomotor nerve palsy are diabetes, aneurysmal compression, and uncal herniation. A lesser-known cause of third nerve dysfunction is ischemia, often due to carotid artery dissection.Case Description:An 80-year-old man presented with an acute ischemic stroke with a National Institutes of Health Stroke Scale score of >20 from a high cervical internal carotid artery (ICA) dissection and a tandem ICA terminus embolic occlusion with extension of clot into the adjacent fetal posterior cerebral artery (PCA). We used a stentriever to perform selective PCA thrombectomy, with immediate postthrombectomy development of ipsilateral anisocoria. The anisocoria progressed into complete oculomotor nerve palsy over 8 h after the procedure.Conclusions:The clinical course described in this case is consistent with injury to the third nerve due to mechanical injury or occlusion of perforator supply to the nerve during thrombectomy. Oculomotor nerve palsy is a rare but known complication after ischemia; however, to our knowledge, this is the first case after thrombectomy for a PCA embolus.
“…Campos et al 6 described a case of a 50-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. Nizam et al 7 described a case of a 24-year-old man presenting a right hemianopsia, hemiparesis and hemihypestaesia 2 days after the onset of a right complete oculomotor nerve palsy, with MRI evidence of a dissection involving extracranial left ICAD and an acute infarct in left middle cerebral artery. …”
A 58-year-old man reported sudden-onset binocular double vision that appeared 3 days earlier. He denied history of headache/cervical pain or trauma. 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. 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. A year later he was asymptomatic and CT angiography confirmed ICA recanalisation.
“…The spectrums of clinical presentations of ICA dissection included facial pain, neck pain, and concurrent HS in 4 patients; facial pain, HS, and contralateral sensorimotor deficit in 6; headache and contralateral sensorimotor deficit in 2; and contralateral sensorimotor deficit with or without speech impairment in 10. 93 Nizam et al 94 reported a left, pupil-involving oculomotor palsy as a rare presenting sign of left ICA dissection.…”
This annual review provides a brief update on a number of neuroophthalmic conditions that might be of interest to the practicing clinical ophthalmologist.
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