Background: Thalamic blood supply consists of four major vascular territories. Out of them paramedian arteries supply ipsilateral paramedian thalami and occasionally rostral mid brain. Rarely both paramedian arteries arise from a common trunk that arise from P1 segment of one sided posterior cerebral artery (PCA). This is usually due to hypoplastic or absent other P1 and this common trunk is termed Artery of Percheron (AOP). Its prevalence is in the range of 7-11% among the general population and AOP infarcts account in an average of 0.4-0.5% of ischemic strokes. Clinical presentation of AOP infarction is characterized by impaired arousal and memory, language impairment and vertical gaze palsy. It also can present with cerebellar signs, hemi paresis and hemi sensory loss. We herein present a case of AOP infarction presenting as transient loss of consciousness and nuclear third nerve palsy. Case presentation: A 51 year old previously healthy male, was brought to us, with a Glasgow coma scale (GCS) of 7/15. GCS improved to 11/15 by the next day, however he had a persisting expressive aphasia. Right sided nuclear third nerve palsy was apparent with the improvement of GCS. He did not have pyramidal or cerebellar signs. Thrombolysis was not offered as the therapeutic window was exceeded by the time of diagnosis. Diagnosis was made using magnetic resonance imaging (MRI) that was done after the initial normal non-contrast computer tomography (NCCT) brain. He was enrolled in stroke rehabilitation. Aspirin and atorvastatin was started for the secondary prevention of stroke. He achieved independency of advanced daily living by 1 month, however could not achieve full recovery to be employed as a taxi driver. Conclusions: Because of the rarity and varied clinical presentation with altered levels of consciousness, AOP infarcts are easily overlooked as a stroke leading to delayed diagnosis. Timely diagnosis can prevent unnecessary investigations and the patient will be benefitted by early revascularization. As it is seldom reported, case reports remain a valuable source of improving awareness among physicians about this clinical entity.

Background: Dengue fever is a hemorrhagic fever caused by flaviviruses. Hemorrhagic manifestations are well known to be associated with dengue fever, though the thrombotic events are only seldom reported. Underlying pathophysiology of thrombotic events is multifactorial and the management is challenging due to associated thrombocytopenia and bleeding tendency. We report a case of dengue shock syndrome with severe thrombocytopenia complicated by ilio-femoral deep vein thrombosis. Case presentation: A 16 year old boy presented with dengue fever. He had dengue shock syndrome after entering the critical phase on the fifth day of the illness. With the recovery from the critical phase he developed deep vein thrombosis involving right external iliac, common femoral and superficial femoral veins. There were no provocative factors other than dengue fever itself. His platelet count was 12,000/μl at the time of diagnosis with deep vein thrombosis. Anticoagulation was started with intravenous unfractionated heparin 500 IU/hour while closely being observed for bleeding complications. 1000 IU/hour dose was commenced with the recovery of the platelet count above 50,000/μl. Thrombophilia screening was negative and he was discharged on warfarin. Venous duplex done after 6 weeks showed normal lower limb venous flow and warfarin was omitted after three months. Conclusions: With dengue fever, complications like deep vein thrombosis can be easily missed given its rarity and that the major concern is on hemorrhagic complications. Management is challenging due to associated thrombocytopenia and hemorrhagic complications.

Miller Fisher syndrome (MFS) is an immune mediated neuropathy commonly triggered by an infection. It is considered as a variant of Guillain-Barre syndrome. Although bilateral ophthalmoplegia is the commonest ocular involvement in MFS, there are reported cases of unilateral ophthalmoplegia. MFS has a benign course and treatment is not required in majority of cases unless there is a lifethreatening complication.We report an unusual case of MFS, presented with isolated right sided oculomotor nerve palsy with pupillary involvement, ataxia and areflexia. Patient was treated with intravenous immunoglobulin (IVIG) achieving a remarkable recovery by five days of treatment. We believe this is a treatment effect rather than the natural course of her illness. Although it is rare, MFS should be included in the differential diagnosis of unilateral 3 rd nerve palsy with pupillary involvement, especially when associated with ataxia or areflexia. Having a low threshold to initiate IVIG in MFS may accelerate the recovery with a positive impact on patient's functional status.