DISSEMINATED TUBERCULOSIS PRESENTING AS ISOLATED APHASIA: A NOVEL PRESENTATION

Abstract

INTRODUCTION: Disseminated tuberculosis (TB) results from the hematogenous spread of tubercle bacilli throughout the body. Clinical manifestations are non-specific and typical chest radiographic findings may not be seen until late in the course of the disease (1). Although presenting symptoms can vary, we are not aware of prior cases in North America presenting with isolated aphasia. CASE PRESENTATION: A 67 year old man of Chinese descent, born in Canada, presented with a one day history of progressive aphasia. The remainder of the physical and neurological exam was normal. Past medical history was significant for hypertension, previous myocardial infarctionm, and type II diabetes mellitus. Initial computed tomography (CT) of the head revealed no causative lesions; subsequent CT-angiography (CTA) revealed that the left middle cerebral artery (MCA) was irregular throughout its course, while the extracranial circulation was normal. However, upper lobe lung nodules and mediastinal lymphadenopathy were seen on thoracic cuts of the CTA. The pulmonary service was consulted to facilitate a diagnosis. A dedicated high resolution CT of the chest was obtained which confirmed a miliary pattern of nodules with a right upper lobe spiculated mass. A chest radiograph obtained at the same time was normal with no visible nodules or lymphadenopathy.The patient was a life-long non-smoker, with no prior pulmonary history or known TB contacts. He denied fevers, chills, or night sweats, but did confirm a 10lb weight loss in the past month following the death of his mother. He also disclosed an intermittent chronic cough and 2-3 episodes of small volume hemoptysis in the past month. Initial investigations included three acid fast bacilli (AFB) positive sputum and a negative HIV test. A clinical diagnosis of disseminated TB was made, and the patient was started on traditional 4 drug therapy. Subsequent cultures confirmed Mycobacterium tuberculosis that was sensitive to all anti-TB medications. A magnetic resonance image (MRI) of the brain ultimately revealed a left temporal ischemic stroke as the culprit for his aphasia. The left MCA irregularity suggested that TB vasculopathy was the most likely cause for his stroke. There were also several gadolinium enhancing nodules within the brain. A lumbar puncture revealed elevated protein and mild lymphocytosis, but negative AFB smears and culture. Follow up MRI demonstrated that the vascular irregularities and enhancing cerebral nodules were almost completely resolved after a full course of anti-TB therapy. Cardiac echocardiogram, 24 hour Holter study and carotid Doppler study did not reveal any other possible causes for his stroke. The final clinical diagnosis was felt to be an ischemic stroke secondary to disseminated TB vasculopathy. DISCUSSIONS: This case represents many unique and illustrative aspects. Firstly, a review of the literature did not reveal any cases of disseminated TB presenting with isolated aphasia. While cerebral infarcts have been previously described, they have been seen in association with TB meningitis in pediatric populations and immunocomprised adults (2). Therefore, this is the first reported case of TB vasculopathy causing a cerebral infarct in an immunocompitent North American born adult. CONCLUSION: We present a novel case of TB vasculopathy, secondary to disseminated TB, presenting as isolated aphasia.