A 15 year-old male, with no medical history, presented with febrile coma. Cerebral CT scan was normal and cerebrospinal fluid (CSF) analysis showed lymphocytic pleocytosis (160cells/mm3), protein concentration up to 0.97g/l, glucose at 1.6mmol/l (CSF/blood glucose < 0.5) and hyponatremia in serum analysis. The patient was treated by intravenous steroids for three days and antituberculous drugs. Fifteen days later; the patient developed agitated confusion with left hemiparesis and was referred to our department for further investigation and care. Neurological examination revealed fluctuant altered consciousness, left hemiparesis, axial twisting movements on the left upper limb with severe dystonia. Brain MRI found bilateral anterior and medial thalami ischemic lesions extended to internal globus pallidus and subthalamic nucleus with hypothalamic enhancement (Figure 1 and Figure 2). CSF analysis showed 36 cells/mm3 (92% lymphocytes), protein at 1.19g/l, glucose 2mmol/l. Mycobacterium tuberculosis Culture in CSF and 3 sputum examinations were negative. Plasma Angiotensin I-converting enzyme was normal. Thoracic CT scan showed bilateral asymmetric mediastinal lymphadenopathy with hypodense centers evoking caseous necrosis. Bronchoscopy with bronchial biopsies revealed no specific bronchial mucosal inflammation. Bronchoalveolar lavage showed polynucleosis. The diagnosis of bilatreal thalamic infarct complicating TME was made. Antituberculous drugs were maintained and oral corticosteroids administered with symptomatic treatment based on trihexyphenidyle, diazepam, botulinum toxine and fluoxetine. The outcome was favorable concerning hemiparesis, mutism and movement disorders but the patient was disabled by left segmental dystonia and showed some behavioral disorders that resolved with haloperidol. Three months later, cerebral MRI showed nearly complete resolution of signal abnormalities but neuropsychological assessment revealed thalamic dementia.