A 30-year-old Filipino female admitted to our hospital with a 1-week history of fever and cough. The patient has diabetes mellitus 1 year ago, but she was not receiving any medication. Other medical histories were unremarkable. On examination, the patient looked well, not dyspneic. Her blood pressure was 110/70 mmHg, pulse rate 90 beats/min, respiratory rate 20 cycles/min and temperature 37°C. Chest examination revealed bronchial breathing with crackles, mainly on the right lung. The rest of the clinical examination otherwise was normal.\nBlood investigations revealed a hemoglobin level of 13.8 g/dL, a total leukocyte count of 12,900/mm3(91.7% neutrophils, 1.7% lymphocytes) and an adequate number of platelets. Erythrocyte sedimentation rate was 53 mm/hour. Blood chemistry, liver profile and coagulation studies were within normal limits. Chest X-ray showed widespread bilateral consolidation with cavity formation, suggesting active tuberculosis infection, whereas sputum was positive for acid fast bacilli (AFB). Human immunodeficiency virus enzyme-linked immunosorbent was negative.\nOn the 3rd day of hospitalization, four-drug antituberculous treatment was started. To control her blood sugar, the patient was kept on sliding scale insulin.\nTwo weeks after starting antituberculous treatment, the patient developed two episodes of loss of consciousness, which were unwitnessed. The exact duration was unknown, but when awakened, the patient complained of severe headache and backache. Neurological examination was unremarkable.\nECG and blood chemistry (including blood sugar), complete blood count (CBC) and liver profile were normal. Lumber puncture was carried out to rule out tuberculous meningitis. Cerebrospinal fluid (CSF) was clear with an opening pressure of 40 mm H2O, and analysis of CSF revealed the following values: WBC count of 5 cells/mm3(100% lymphocytes); glucose level 3.8 mmol/L; and protein level 0.78 g/L. Gram and Zeihl-Neelsen stains were negative. Echocardiography and holter monitoring also were normal, whereas urgent brain computed tomography (CT) showed multiple infarctions without abnormal dural enhancement [Figures and ]. Screening for thrombophilia and vasculitis was carried out. Anti-thrombin III, activated protein C resistance, factor V Leiden, protein C, protein S, clotting time, prothrombin time, activated partial thromboplastin time, fibrinogen, anticardiolipin antibody, lupus anticoagulant screen, homocystine, antinuclear antibody (ANA), C3, C4, C-reactive protein (CRP) and anti-neutrophil cytoplasmic antibodies (ANCAs), all these tests were within normal limits. The electroencephalogram (EEG) showed epileptic discharges. Magnetic resonance imaging (MRI) showed infarction at the head of the left caudate nucleus, the antero-lateral aspect of putamen and intervening internal capsule [], whereas magnetic resonance (MR) angiography showed a picture consistent with moyamoya. Brain CT angiography was performed and it showed the same pictures [].\nThe patient was diagnosed with pulmonary tuberculosis-associated moyamoya syndrome. On the following days, she was discharged on antituberculous, antiepileptic (Leveteracetam) and oral hypoglycemic (Gliclazide) medications. After 6 weeks, CSF culture failed to grow Mycobacterium tuberculosis. One year later, the patient was seen in the clinic; she was well and seizure-free.
A 13-month-old Syrian baby boy born to a non-consanguineous couple was admitted to our hospital with complaints of sudden onset focal tonic-clonic seizure, mainly on the right side, for further evaluation and management. The seizure attack lasted approximately a few minutes. The second attack was associated with loss of consciousness and uprolling of the eyes. There was a history of sudden falls during playing. However, there was no history of fever, head trauma, headache, vomiting, or ear discharge. He had normal growth parameters. there was no significant family history of early stroke, ischemic heart disease, or autoimmune disease. His past medical history was significant for right arm weakness one month before his presentation and resolved without treatment. Upon presentation, he was vitally normal except for HR of 128, and RR of 28.\nA head CT revealed nonspecific hypodensity, bilateral periventricular white matter, and the left parietofrontal subcortical area requiring further workup.\nAn MRI (Figure ) revealed acute infarction involving the left frontal lobe cortical and subcortical region and multiple bilateral periventricular white matter changes likely due to leu-co-encephalopathy/chronic ischemic. MRA (Figure ) showed attenuated and irregular distal intracranial ICAs at the cavernous and supraclinoid segments and bilateral stenosis seen at both MCAs, almost occluded on the right side, and are surrounded by extensive lenticulostriate collaterals.\nEncephalo-duro-arterio-synangiosis (EDAS) surgery was performed due to failure of the first attempt of cerebral angiography. The baby was discharged home in a stable condition on Tegretol and aspirin for follow-up in the clinic and revascularization surgery on the right side was scheduled three months after the first one.\nThree weeks later, the child presented with lethargy, weakness in his left arm, and vomiting. Upon admission, he was afebrile, maintaining room air. Physical examination findings were normal apart from bilateral chest rhonchi, and weakness of the left upper and lower limbs. Hematologists recommended starting the patient on clexane and continuing with aspirin.\nConventional cerebral angiography (Figure ) was performed post left EDAS surgery and demonstrated bilateral ICAs stenosis seen at the carotid terminus with multiple collateral formation compatible with the history of MMD. There is evidence of right MCA M2 segment thrombosis compatible with MRI finding of acute infarction, left distal MCA branches thrombosis, and posterior circulation collateral formation synangiosis to the anterior circulation. Neurologists were consulted, and right-side revascularization was scheduled.\nA post-operative MRI brain (Figure ) was performed because the patient still had upper and lower left side weakness, and it revealed a large right parietal-temporal-occipital area cortical and sub-cortical area of restricted diffusion consistent with acute infarct. The previously seen large right cerebral diffusion restriction now shows residual small areas of cortical and adjacent subcortical spaces.\nThe clinical and radiological findings were suggestive of a progressive vascular occlusive disease that could be seen in MMD. Several investigations including factor V, factor VII, antithrombin activity, protein C, protein S, and EEG were carried to rule out associated medical conditions. The patient was discharged in a stable condition with residual left side weakness. Therefore, an appointment with physiotherapy was reserved.