Acute Hydrocephalus and Stroke in a 20 Year‐Old Man

Abstract

A 20 year-old male complaining of headache, photophobia and altered mental status arrived to the ER from another hospital. His symptoms began a few months earlier with diarrhea and vomiting, daily fever up to 39°C, and weight loss. At that time, the neurological examination showed a Glasgow Coma Scale (GCS) score of 8 points and nuchal rigidity. A brain CT scan was normal, and ceftriaxone 2 gr per day, vancomycin 2 gr every 12 hours, ampicillin 2 gr every 4 hours, clarithromycin 500 mg every 12 hours, and acyclovir 800 mg every 5 hours were started. Because there was no improvement, two days later he was transferred to our hospital. At entry the heart rate was 53 beats per minute, breathing rate was 18 per minute with Cheyne-Stokes respiration, blood pressure was 100/60 mmHg, and temperature was 38°C. The GCS score was of 6 points: 2 points for the ocular response, 1 point for the verbal response and 3 points for the motor the response. His head and gaze were persistently deviated to the right. He had bilateral papilledema, and his pupils were asymmetric, with the right pupil size of 2 mm and the left of 5 mm. Strength was abated, but when pain was elicited he acquired a posture of decerebration. The Hoffman and Babinski signs were produced on the right side. He had involuntary myoclonic jerks in the upper and lower extremities that lasted more than 5 minutes. Nuchal rigidity was present. He was intubated and put on mechanical ventilation. Dexamethasone was administrated for cerebral edema, levetiracetam and propofol for persistent epileptic seizures. Amphotericin B was added and the antibiotics were continued. Two days later mannitol, meropenem, rifampicin, pyrazinamide and ethambutol were included, however, the patient continued to be hypothermic and had severe slow heart rate and hypotension. He died 9 days later. LABORATORY AND NEUROIMAGECBC showed a total blood count of 7000 cells/mm 3 (neutrophils of 87%, lymphocytes of 7.95% and monocytes of 4.8%), hemoglobin of 15.4 gr/dL and platelets of 124,000 cells/mm 3 . Serum glucose was 101 mg/dL, creatinine was 0.9 mg/L and sodium was 134 mg/ dL. The rest of the laboratory studies including liver function tests were normal. An ELISA for HIV was negative.A brain MRI showed enlargement of the ventricles with transependymal migration of CSF surrounding the ventricles symptomatic of acute hydrocephalus, effacement of sulci due to cerebral edema, bilateral extensive hyperintense images in the basal ganglia and surrounding parenchyma in the DWI suggesting ischemic lesions in both territories of the middle cerebral artery (MCA) (Figure 1a, 1b), and generalized dense leptomeningeal enhancement and arachnoiditis in the post-contrast T1-weighted images. An angioMRI showed a severely injured left MCA (Figure 1c).A lumbar puncture was performed with an opening pressure of 22 cmH20, and the CSF showed a pH of 7.47, glucose of 52 mm/ dL, proteins of 111 mg/dL, and WBC of 32cells/mm 3 . Adenosine deaminase enzyme (ADA) in CSF was 9 UI. CSF PCR for M. tuberculosis, CMV, VSH and V...

Successful Intravenous Thrombolysis in Ischemic Stroke Caused by Tuberculous Meningitis: A Case Report

“…Cerebral infarction is a predictor of poor outcomes (3), and the mortality rate of TBM patients with stroke may be three times that of patients without infarction (4). The extension of the inflammatory exudate along the perforating blood vessels into the brain substance causes vascular damage, which may lead to spasm or thrombosis of the vessels, with resulting ischemia or infarction (5). Most cerebral infarctions associated with TBM are multiple, and up to 75% of them are located in the basal ganglia, anteromedial thalamus, anterior limb, and genu of the internal capsule (6)(7)(8).…”