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LETTER TO EDITOR
Year : 2014  |  Volume : 62  |  Issue : 5  |  Page : 552--554

Co-occurrence of basilar artery and cerebral venous sinus thrombosis in antiphospholipid antibody syndrome

Rohan R Mahale, Anish Mehta, Mahendra Javali, R Srinivasa 
 Department of Neurology, Mathikere Sampangappa Ramaiah Medical College and Hospital, Bangalore, Karnataka, India

Correspondence Address:
Rohan R Mahale
Department of Neurology, Mathikere Sampangappa Ramaiah Medical College and Hospital, Bangalore, Karnataka
India




How to cite this article:
Mahale RR, Mehta A, Javali M, Srinivasa R. Co-occurrence of basilar artery and cerebral venous sinus thrombosis in antiphospholipid antibody syndrome.Neurol India 2014;62:552-554


How to cite this URL:
Mahale RR, Mehta A, Javali M, Srinivasa R. Co-occurrence of basilar artery and cerebral venous sinus thrombosis in antiphospholipid antibody syndrome. Neurol India [serial online] 2014 [cited 2019 Dec 14 ];62:552-554
Available from: http://www.neurologyindia.com/text.asp?2014/62/5/552/144462


Full Text

Sir,

Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by arterial or venous thrombosis, recurrent first-trimester pregnancy loss, and multiple additional clinical manifestations. [1] Literature review failed to reveal any report of co-occurrence of cerebral arterial and venous sinus thrombosis in a patient with APS, hence this report.

A 25-year-old lady presented with holocranial headache, two episodes of generalized tonic-clonic seizures with altered consciousness and one episode of vomiting the previous day. She had a spontaneous abortion at 8 weeks of pregnancy 5 days prior to the occurrence of seizure. She had spontaneous first trimester pregnancy loss 1 year back. Her vitals were normal. Neurologic examination revealed a stuporous lady with eye opening and minimal motor response to deep painful stimulus. Pupils were equal, sluggishly reacting to light, and fundus revealed bilateral papilledema. Doll's eye movement was present. Routine blood tests were normal. Cranial computed tomography (CT) revealed hyperdense left transverse sinus with diffuse cerebral edema. Magnetic resonance imaging (MRI) brain with contrast venography showed lack of contrast filling in left transverse, sigmoid sinus, and internal jugular vein [Figure 1]. Serum homocysteine, protein C, S, and antithrombin III levels were within normal limits. A hypercoagulability clinical evaluation showed significantly elevated antiphospholipid antibodies (aPLas) (immunoglobulin G 26.8 and immunoglobulin M 54.2) and positive lupus-like anticoagulant. Autoantibodies profile was negative. She received anticoagulation with heparin and anti-edema measures (mannitol). There was improvement in her consciousness to a state of drowsiness within 72-96 hours. She was opening eyes to call, but was not following any verbal commands. Eye blinking was present. Vertical vestibulo-ocular reflex (VOR) was preserved but horizontal VOR/doll's eye response was restricted. There was paucity of movement of all the limbs with bilateral extensor plantars. She was in locked-in-state. Repeat MRI brain diffusion-weighted imaging (DWI) sequence showed diffusion restriction in basis pons and left cerebellar hemisphere [Figure 2]. MR angiography (MRA) showed nonvisualization of vertebral arteries and basilar artery with filling of both posterior cerebral arteries from the anterior circulation suggestive of vertebrobasilar artery occlusion/thrombosis [Figure 3]. In view of complete basilar artery occlusion, intra-arterial thrombolysis and stent placement was not contemplated. Anticoagulants and antiplatelets were continued. She succumbed to her neurological illness within 2 weeks due to intercurrent infection.{Figure 1}{Figure 2}{Figure 3}

Neurological manifestations of APS include ischemic stroke, transient ischemic attack, and cerebral venous thrombosis, and seizures, migraine headaches, and cognitive dysfunction are the manifestations of hypercoagulable-induced ischemic infarcts. [2] The mechanisms of thrombosis in APS are many, for example, aPLa interference with endogenous anticoagulant mechanisms, binding and activation of platelets, interaction with endothelial cells and inducing expression of adhesion molecules and tissue factor, and activation of the complement cascade. [3]

Diagnosis of APS is based on clinical criteria of pregnancy morbidity or vascular thromboembolism, and laboratory findings of medium or high titer aPLas that are present on two or more occasions at least after 12 weeks. [3] Our patient satisfied the above criteria, but the aPLa levels could not be estimated after 12 weeks as patient succumbed to the illness. The co-occurrence of basilar artery thrombosis and cerebral venous sinus thrombosis in a patient of APS has not been reported so far.

Survival rates in patients with basilar artery thrombosis undergoing thrombolysis alone range from 30 to 60%. Our patient had complete occlusion of basilar artery with no flow; thrombolysis with stent placement was not contemplated. Shi et al., in their study, successfully placed stent in 90% of the patients with acute basilar artery occlusion who received intraarterial thrombolysis. [4] Stenting in the setting of APL has not been described.

References

1Saad AF, Nickell LT, Heithaus RE, Shamim SA, Opatowsky MJ, Layton KF. Basilar artery thrombosis in the setting of antiphospholipid syndrome. Proc (Bayl Univ Med Cent) 2014;27:210-2.
2Mayer M, Cerovec M, Rados M, Cikes N. Antiphospholipid syndrome and central nervous system. Clin Neurol Neurosurg 2010;112:602-8.
3Pierangeli SS, Chen PP, Raschi E, Scurati S, Grossi C, Borghi MO, et al. Antiphospholipid antibodies and the antiphospholipid syndrome: Pathogenic mechanisms. Semin Thromb Hemost 2008;34:236-50.
4Shi M, Wang S, Zhu H, Feng J, Wu J. Emergent stent placement following intra-arterial thrombolysis for the treatment of acute basilar artery occlusion. J Clin Neurosci 2012;19:152-4.