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 53-year-old Arab woman living in Saudi Arabia presented to the emergency department with an acute onset of unsteadiness, a tendency to fall forward present for one week, and slurred speech present for one day. She had a negative history of loss of consciousness, abnormal movement, weakness, numbness, and vertigo. She had a history of chronic headaches. She has diabetes and suffered a stroke two years ago. She had one abortion and twelve successful pregnancies; the last two were C-section. She had no history of sickle-cell disease or other chronic diseases. Her neurological assessment was normal with no focal signs. Other examinations were unremarkable. A head computed tomography (CT) scan and a magnetic resonance imaging (MRI) of her brain (Figure ) upon presentation revealed acute corpus callosum hemorrhage.\nHer brain CT venogram was normal. Other diagnostic studies were normal. A cerebral angiogram (Figures -) showed severe narrowing or occlusion of both distal internal carotid arteries (ICA) with multiple intracranial collaterals, including the choroidal arteries and the posterior pericallosal artery as well as the lenticulostriate arteries; this was a classical presentation of the moyamoya pattern.