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Supplemental Material for Top 10 global educational topics in stroke: A survey by the World Stroke Organization by Monica Saini, Sarah Belson, Carmen Lahiff-Jenkins and Peter Sandercock in International Journal of Stroke

Background and Aims:Background : Haemorrhage in bacterial meningitis is < 3% . Meningitis presenting as subarachnoid haemorrhage (SAH) is rare. Meningitis due to Streptococcus (S) dysgalactiae is rare [< 10 cases reported].Aim: To describe first case of S. dysgalactiae meningitis presenting as SAH.Methods:Case DescriptionResults:62 year gentleman with history of heroin dependence was admitted to psychiatric institute for detoxification, developed progressive drowsiness (2 days ) and was referred to our institute. CT brain showed a left sulcal SAH [also noted on subsequent MRI ; Fig 1]. Neurological review was sought. Examination revealed febrile, drowsy patient, signs of meningeal irritation, absence of focal motor/ sensory/ cerebellar signs. Laboratory investigations : neutrophilic leukocytosis and elevated C- reactive protein. Given the history of substance use, possibility of secondary vasculitis and reversible cerebral vasoconstriction syndrome considered. CT angiogram was normal. In view of fever/ elevated inflammatory markers, cerebrospinal fluid evaluation done ( 540 leucocytes ; 65% neutrophils; protein 12.6 g/L; glucose 0.1 mmol/L). Blood and CSF cultures positive for Strep, dysgalactiae. Intravenous ceftriaxone 2 gm BD started. Repeat brain imaging (day 5) for persistent drowsiness showed (Fig 1) evidence of ventriculitis, left temporal l hematoma, bilateral infarcts (perforating arteries) . Antibiotic was changed to Meropenem, and continued for 2 weeks. Echocardiogram normal. Slow recovery to independent ambulation noted over several weeks.Conclusions:This is the first reported case of Strep dysgalactiae meningitis presenting as spontaneous SAH. Mechanism is likely to be either endothelial dysfunction, cerebral disseminated intravascular coagulation and/ or secondary vasculitis.

Embolic Sulcal Artery Stroke : Report of Two CasesSaini M 11 Department of Neurology , Changi General Hospital, SingaporeObjective :To describe two rare cases of Embolic, Sulcal Artery Infarcts.Background:Spinal cord infarction accounts for < 2 % of all strokes.Majority of spinal infarcts occur in the setting of aortic surgery ormanipulation, involve the Anterior Spinal Artery territory, andpresent as an anterior cord syndrome.Sulcal Arteries arise from the anterior spinal artery, and tend toalternate in their distribution to the left or right side of the spinalcord. Sulcal Artery infarcts are rare, and have previously beenreported predominantly in relation to vertebral artery dissection.Here, two cases of embolic Sulcal Artery infarcts ,presenting as Brown-Su00e9quard Syndrome, are described.ResultsCase 1:A 64 year old gentleman, with history of hypertension,hyperlipidemia and ischemic heart disease was admitted forrecurrent hemoptysis. Bronchial artery embolization ( BAE) wasperformed via femoral approach; bronchial arteries ( 1 right ; 2left) and hypertrophic right 3rd intercostal artery were embolizedwith glue. Acute onset of right lower limb numbness, followed byprogressive (over several hours) weakness and urinaryretention, were noted immediately post-procedure.Clinical examination was significant for findings of Brown-Su00e9quard syndrome (BSS) , with a sensory level at T4-5 andpower grade 0-2 in right lower limb. Magnetic resonance imagingof the spine ( 48 Hours) showed T2 hyperintensities in thethoracic spine, largest of which was at T3-4 level (right hemicord;Figure 1a and b). Diagnosis of BSS secondary to embolic sulcalartery infarct , as a complication of BAE, was made. Patient wasmanaged conservatively.Case 2:A 74 year old gentleman, with history of hypertension,hyperlipidemia, diabetes, and ischemic heart disease wasadmitted with sudden onset lower sternal pain, tingling in rightchest and abdomen, followed by numbness and weakness of theright lower limb.Clinical examination was significant for BSS ( power grade 2 inright lower limb). MRI spine showed a short segment T2hyperintensity at T4-5 region ( Figure 2a and b).CT Aortogram showed chronic dissection flap at the middescending thoracic aorta, with complete thrombosis of the falselumen. Diagnosis of sulcal artery infarct , secondary to embolus[of aortic origin] was made. Patient was managedconservatively.Clinical Course : Clinical improvement to independentambulation was noted in both cases, over a follow-up period of4-5 months.CONCLUSIONSThough rare, Brown-Su00e9quard syndrome may occur as aconsequence of spinal Sulcal Artery infarcts. Prognosis of sulcalartery infarcts may be better as compared to anterior spinalartery infarcts.References:1. Sandson TA, Friedman JH. Spinal cord infarction. Report of 8 cases andreview of the literature. Medicine (Baltimore) 1989;68:282-292.2. Li Y, Jenny D, Bemporad JA, Liew CJ, Castaldo J. Sulcal arterysyndrome after vertebral artery dissection. J Stroke Cerebrovasc Dis. 2010Jul-Aug;19(4):333-5

Background and Aims:Background :Developmental venous anomalies (DVA )are brain vascular malformations - autopsy incidence ~ 2.6%; magnetic resonance imaging (MRI) detection rate 0.48u20130.7%. Symptomatic DVAs are rare; < 35 patients with spontaneous DVA thrombosis (DVAT) have been reported till date, several of whom had associated parenchymal hemorrhage. Aim: To describe a rare case of symptomatic, spontaneous DVAT managed with anticoagulation.Methods: Case descriptionResults:35 year male presented with one day of left upper limb (LUL) weakness, headache. Neurological exam showed LUL monoparesis. Brain Imaging in Emergency department showed right, partially thrombosed (saccular component) frontal DVA with drainage into deep ependymal vein and superior sagittal sinus (Fig 1; Left panel). No associated bleed or venous infarct noted. Therapeutic dose Clexane was initiated. He had 3 episodes generalized seizures; subsequent MRI showed thrombosis progression and localized FLAIR hyperintensity surrounding the thrombosed DVA (Fig; Middle Panel). Epilim was given , Laboratory tests for inherited and acquired procoagulant states were negative; Clexane was continued. 4Vessel angiogram, 6 weeks later, showed partial recanalization only. Neurosurgeons opined conservative management. Clexane was continued. Evaluation at 12 weeks showed no focal deficits. There were no hemorrhagic complications. Switch to oral anticoagulation was planned but patient was subsequently lost to follow-up.Conclusions:Symptomatic, spontaneous DVAT is very rare. There are no guidelines regarding management. DVA resection is avoided so as to prevent catastrophic venous infarction. Anticoagulation appears safe, but duration is debatable in absence of known procoagulant states.