Posterior stroke (PS) together with upper limb ischemia is an infrequently associated clinical presenta tion caused by embolism, aortic dissection, vascular trauma, thoracic outlet syndrome, coagulation disorders and, less commonly, subclavian artery thrombosis.

A 59-year-old male patient, former smoker (40 pack/year), hypertensive and dyslipidemic, presented with a 2-week gait disorder and referred a left upper limb hypotension record. Upon consultation with his occupational physician, expressive aphasia, right temporal hemianopsia and gait instability determined the decision to hospitalize him. The electrocardiogram confirmed sinus rhythm, and the echocardiogram evidenced preserved left ventricular systolic function, without shunt or intraluminal thrombi. Neck vessels Doppler ultrasound showed subintimal carotid plaques, without significant hemodynamic findings, and very low flow velocity in the left vertebral artery. Brain computed tomography (CT) revealed hypodense frontoparietal white matter areas in both hemispheres. Brain magnetic resonance angiography showed acute left temporo-occipital ischemic lesion in the left posterior cerebral artery territory, with absence of flow in the intracranial segment of the vertebral artery (Figure 1).

Fig. 1 Brain magnetic resonance angiography: acute left temporo-occipital ischemic lesion with absence of flow in the in tracranial segment of the vertebral artery 

On the second day the patient referred left upper limb paresthesia, and lower temperature was detected with absence of humeral, radial, and ulnar pulses.

Left upper limb arterial echo-Doppler revealed very low velocity monophasic flow, and high resistance in the humeral, radial and ulnar arteries, with subclavian artery thrombosis. Neck vessels and aortic arch computed tomography angiography ruled out aortic dissection and thoracic outlet syndrome and showed complete left subclavian artery thrombosis from its origin, and part extending as intraaortic thrombus, and altered homolateral vertebral artery staining in the intraosseous and intracranial segments (Figure 2A). Thorax, abdomen, and pelvis CT scan revealed bilateral pulmonary emphysema. Laboratory results were: platelets 373 000 ml/mm³, normal D-dimer and IgG and IgM antiphospholipid antibodies, negative lupus inhibitor, normal homocysteine, negative anti-beta 2 antibodies and IgG and IgM glycoproteins, protein C 108% and free protein S 66%. Electrocardiographic 24-hour Holter monitoring indicated predominant sinus rhythm, without ventricular or supraventricular extrasystoles. Control brain magnetic resonance imaging (MRI) performed on the 4th day did not evidence hemorrhagic temporo-occipital lesion transformation.

Endovascular or surgical treatment for complete left subclavian artery thrombosis with intrathoracic extension associated with posterior ischemic stroke was discarded due to high risk of systemic embolic complications, and anticoagulation by continuous pump sodium-heparin infusion was decided, under strict neurological control and subsequent rotation to oral acenocoumarol. The patient was discharged on the 10th day with no neurological or upper limb ischemic complications. At 1-year oral anticoagulation was suspended due to recurrent episodes of hematuria and hematemesis, and the patient continued with oral clopidogrel and cilostazol. The last control computed tomography angiography at 3 years evidenced par tial recanalization of the subclavian thrombosis, with complete disappearance of the intraaortic thrombus in the subclavian ostium. (Figure 2B)

Fig. 2 A. Neck vessels and aortic arch computed tomography angiography: complete left subclavian artery thrombosis from its origin, with part of intraaortic thrombus. B. Control computed tomography angiography at 3 years: partial recanalization of subclavian thrombosis, with complete disappearance of the intraaortic thrombus in the subclavian ostium 

The patient is currently asymptomatic, with humeral pulse recovery. Studies for thrombophilia were repeated with negative results.

Almost 20-25% of strokes occur in the posterior circulatory system (posterior cerebral, basilar and vertebral arteries) and can compromise the brainstem, cerebellum, thalamus and/or temporo-occipital region. Caplan et al. described embolism as the most frequent mechanism of posterior stroke (40-54%), mainly of cardiac origin (24% of cases), while arterio-arterial embolism was reported only in 14% of cases. ¹ Other mechanisms are atherosclerotic lesions of the great arteries, small vessel occlusion, and rare causes such as coagulation disorders or carotid atheroembolism associated with the fetal origin of the posterior cerebral artery. Due to the wide cerebral area irrigated by the vertebrobasilar arterial system, ischemic strokes in this territory exhibit with various signs and symptoms. The most frequent signs are gait ataxia, unilateral limb weakness, dysarthria, nystagmus, and visual field defects, while reported symptoms are usually vertigo, dizziness, nausea and vomiting, headache, and consciousness disorders.

Subclavian artery thrombosis occurs due to vascular wall intimal injury. Atherosclerosis is its most frequent etiology, and is more commonly located in the right carotid-subclavian and left subclavian-vertebral areas, so these regions are usually involved in occlusive thrombosis. Subclavian atherosclerosis risk factors are hypertension, smoking, diabetes, obesity, and dyslipidemia. ² Subclavian artery thrombosis presents in less than 1% of the population and is generally asymptomatic, resulting in an underdiagnosed disease. Left subclavian thrombosis is four time more common that its right counterpart. ²

The emergence of ischemic symptoms as a result of decreased arterial flow due to subclavian artery thrombosis is conditioned to the presence or not of collateral circulation, and the most usual clinical manifestations include upper limb intermittent claudication and paresthesia. Subclavian artery thrombosis complications are upper limb, mainly digital, ischemic gangrene, acute ischemia of the limb artery and rarely, posterior ischemic stroke. The pathogenesis of these infarctions in the vertebrobasilar territory is due to arterio-arterial embolism or the “retrograde” propagation to the vertebral artery from a homolateral subclavian artery thrombosis. ^3,4

Other causes of subclavian artery thrombosis associated with posterior stroke are hypercoagulability states (S-protein deficit, essential thrombocytopenia, etc.), aortic dissection, arterial trauma, cardiac embolism, and thoracic outlet syndrome with arterial involvement (arterial TOS). The latter is characterized by a subclavian artery disease due to compression by osseous anomalies as a cervical rib, with intimal lesion with or without post-stenotic dilation and thrombus formation prone to distal embolization, generating severe complications such as upper limb arterial ischemia and less frequently a posterior ischemic stroke. ^3-6

Castillo Costa et al. reported a case of posterior stroke with upper limb ischemia due to thrombosis of a structurally healthy aorta with systemic embolism. ⁷

Computed tomography angiography of the aortic arch and the compromised upper limb allows confirming the diagnosis of subclavian artery thrombosis as possible embolic source in patients with posterior stroke, as well as identifying some of its causes (atherosclerosis, arterial TOS, dissection, trauma, etc.).

Treatment of subclavian artery thrombosis complicated with a posterior stroke will depend on the degree of upper limb ischemia and the vascular disease that originated it. In general, endovascular or surgical therapeutic interventions (embolectomy or decompression treatment with arterial TOS revascularization) are only indicated in patients presenting threatened upper limb, due to the risk of systemic embolization during the intervention. ^3,4 Anticoagulant treatment through initial intravenous infusion of sodium heparin and subsequent oral anticoagulation is an effective therapy described for patients with subclavian artery thrombosis and posterior stroke coursing with compensated upper limb ischemia, to avoid arterial thrombosis and its progression. ^2,5,6

In conclusion, posterior ischemic stroke is an infrequent complication of subclavian artery thrombosis, that should be suspected in patients with vertebrobasilar infarctions and absence of homolateral upper limb arterial pulse. Computed tomography angiography can confirm its diagnosis.