Local embolism from vertebral artery occlusion

M S Pessin, N Daneault, E S Kwan, M A Eisengart, L R Caplan
1988 Stroke  
Basilar artery territory stroke may result from embolism arising from the site of vertebral artery occlusion. This stroke mechanism (local embolism) has been well documented in the middle cerebral artery territory from extracranial internal carotid artery disease but not fully appreciated in the vertebral basilar circulation. We report two patients whose clinical presentation indicated major basilar artery territory infarction documented by angiography to be the result of vertebral artery
more » ... tebral artery occlusion and artery-to-artery embolism. Vertebral artery occlusion has often been associated with a benign course, but under certain circumstances embolism to the basilar artery may complicate the outcome. {Stroke 1988;19:112-115) A rtery-to-artery embolism, so-called local embo-/ \ lism, 1 refers to dislodgement and distal mi-J. \ * gration of material from an athero-occlusive plaque or thrombus. In the carotid circulation, local embolism is the major mechanism for middle cerebral artery (MCA) territory stroke as a result of extracranial internal carotid artery disease. 2 " 4 This mechanism is not as well recognized in the vertebral basilar system although Fisher and Kames 1 called attention to it more than 20 years ago. Recognition that specific large artery occlusion may cause distal embolization may help in planning initial therapy, perhaps in the form of short-term anticoagulation, in an effort to avoid this unwanted complication of local embolism. We report two patients widi vertebral artery (VA) occlusion and distal embolism to the basilar artery. Case Reports Patient 1. A 34-year-old man noted the onset of a persistent nonthrobbing headache localized to the left posterior neck area 4 days prior to admission. On the evening before admission, while watching television, he developed a transient, prickly sensation in his right arm and leg. A few hours later, while in bed, his left arm and leg became weak and his vision was fuzzy. There was no history of trauma, transient ischemic attacks (TIAs), or medical conditions. He was a smoker and admitted to regular beer drinking. On admission evaluation, the general physical and neurovascular examinations were normal. On neurologic examination, he was alert with normal speech and mental status. Cranial nerves were normal except for definite upbearing nystagmus present in the neutral position, accentuated with upgaze. Horizontal nystagmus was also present, most prominent with left lateral gaze. Left comeal sensation was diminished compared From the with the right, but sensations on his face were intact. There was a left hemiparesis involving his arm more than his leg with sparing of his face. Deep tendon reflexes were brisker on the left side. Primary and cortical sensations were normal. Routine laboratory data included normal hemoglobin, hematocrit, white blood cells, platelet count, prothrombin time, partial thromboplastin times, sedimentation rate, and glucose. An electrocardiogram (ECG) and echocardiogram were both normal. Computed tomography (CT scan) on admission was normal, but a repeat CT scan several days later showed a right pontine infarction. Angiography within 24 hours of admission revealed an occlusion of the left VA at the C2 level and an intraluminal filling defect (embolus) in the distal basilar artery and proximal superior cerebellar artery (Figure 1) . The patient was anticoagulated with heparin and then warfarin. His neurologic status gradually improved, and the left posterior head and neck pain disappeared in 3 weeks. He was reevaluated 6 months later, at which time he had only mild impairment of fine and rapid alternating movements in his left limbs and increased deep tendon reflexes on his left side. His gait showed spasticity and slight foot slapping on the left. Repeat angiography showed an unchanged left VA occlusion, but the distal basilar artery was now normal (Figure 2) . Patient 2. A 62-year-old man awakened one night to go to the bathroom; his wife heard an unusual sound and found him leaning on the sink, poorly responsive. The emergency medical technicians found him lethargic and unresponsive to verbal commands. Purposeful movements of his left hand were noted. His medical history was unremarkable; there was no history of TIAs. On admission, he was comatose. Blood pressure ranged from 158/87 to 230/120 mm Hg, and pulse was regular at 85 beats/min. Respirations were spontaneous and regular. His general physical and neurovascular examinations were normal. On neurologic examination, spontaneous decerebrate posturing of his left extremities was present. His right eye deviated to the right, his left eye rested down and in. Pupils were by guest on July 14, 2015 http://stroke.ahajournals.org/ Downloaded from
doi:10.1161/01.str.19.1.112 pmid:3336891 fatcat:4iyrxembpjegfkh3w2g75z6dr4