A 19-year-old male presented to the emergency department at 10:42 a.m.,42 min after the sudden onset of slurred speech with weakness of his right upper and lower extremities. He reported no headache, dizziness, nausea, vomiting, fever, or convulsions. He denied any significant medical history, drug abuse, or high-risk sexual behaviors. He had no history of migraines, trauma, insect bites, exposure to chemicals, or use of medications. Apart from cigarette smoking for 1 year, he denied other risk factors for stroke. There was no history of early cardiovascular disease in the family.
On physical examination, the patient’s vital signs were normal. His weight was 65 kg (69 kg, 3 weeks ago), body mass index (BMI) 21.47 kg/m2. His chest examination was clear, and no additional murmurs were detected upon cardiac examinations. The liver, spleen and cervical lymph nodes were not enlarged; no skin or mucosal lesions were seen.He was alert and oriented to person, place, and time. The pupils were equal and reactive to light and accommodation. He had mild right hemiplegia with strength of 4:5 in the right upper and lower extremities; slight dysarthria and right lower facial paresis were also noted. The neurologic examination was otherwise unremarkable. The National Institutes of Health Stroke Scale (NIHSS) score was 3.
Rapid blood glucose was in the normal range (6.3 mmol/L). Complete blood count results showed white blood cell (WBC) count 3.0 × 109/L, hemoglobin 11.9 g/dL, and platelets 273 × 1012/L. Stroke was first considered. As he was then in the 4.5-h time window for IV-rtPA, an urgent brain CT with computed tomography angiography (CTA) of intra–extracranial vessels and whole-brain computed tomography perfusion (CTP) imaging were performed in the emergency department. The nonenhanced CT (NECT) scan (Fig. 1a) and CTA (Fig. 1b) were normal. CTP showed hypoperfusion in the left hemisphere with prolonged mean transit time (MTT) and time-to-peak (TTP), slightly increased cerebral blood volume (CBV), and relatively preserved cerebral blood flow (CBF) (Fig. 1c-f). A diagnosis of acute ischemic stroke was made. After excluding absolute contraindications for intravenous thrombolysis, 58.5 mg (0.9 mg/kg) rtPA was given at 12:30 a.m., immediately after the patient signed the informed consent. After 1 h of rtPA, his symptoms were alleviated, and the NIHSS score was decreased to 1, with slight asymmetry of the nasolabial sulcus. The patient was then admitted to the department of neurology for further investigations and treatment. Within 60 min after admission, the clinical neurological examination had completely normalized.
On the next day, the patient had no complaints of discomfort. The NIHSS score was 0. Cerebral magnetic resonance imaging (MRI) was performed, and no acute lesion was seen in the diffusion-weighted image (DWI) sequences (Fig. 1g). Doppler ultrasonography of carotidal and intracranial arteries showed no abnormality. Electrocardiogram, electroencephalogram (EEG) and chest CT scan were all normal. Echocardiography showed that the left and right heart chambers were within normal size and function(left ventricle ejection fraction 70%). His laboratory tests showed WBC count 2.2 × 109/L, hemoglobin 10.4 g/dL, platelets 210 × 1012/L, ESR 18 mm/h (normal 0–15.0), CRP 0.66 mg/L (normal 0–8.0), homocystein 10.4 umol/L (normal < 15.0), and mild impairment of liver function (ALT 132 U/L (normal 5–40), AST 106 U/L (normal 8–40), GGT 257 U/L (normal 11–50), ALP 127 U/L (normal 40–150)). Serologies showed the following: rapid plasma reagin, negative; antinuclear antibody and antineutrophil cytoplasmic antibody, negative; complement level including C3, C4 levels, normal; anticardiolipin immunoglobulin G(ACL-IgG), ACL-IgM, and ACL-IgA antibody levels, normal; β2 glycoprotein I immunoglobulin G (β2-GP1- IgG) and β2-GP1- IgM antibody levels, normal; high β2-GP I-IgA antibody level, 67.16 units/mL (normal 0–18). HIV enzyme-linked immunosorbent assay and Western blot confirmed HIV infection with CD4 cell count of 7 cells/uL; the CD4:CD8 T cell ratio was 0.04 (7/173). Hepatitis B virus surface antigen and hepatitis C antibody were unremarkable.
On the third day of admission, the patient received a lumbar puncture with pressure of 140 mmH2O. Cerebrospinal fluid (CSF) studies showed normal-range white cell and red cell counts but a high protein level at 1185 mg/L. The CSF glucose and chloride were in the normal range. CSF viral PCRs (including herpes simplex virus, varicella zoster, Epstein Barr, cytomegalovirus and JC virus), cryptococcal antigen, and bacterial and fungal cultures were all negative. CSF syphilis TRUST and TPPA tests were also negative. There was no meninges or brain parenchymal enhancement on his brain contrast-enhanced MRI (Fig. 1h).
The patient was diagnosed with aborted stroke and HIV infection. Oral aspirin 100 mg and atorvastatin calcium 20 mg daily were given. For further treatment, the patient was transferred to the HIV/AIDS ward on the fourth day of admission. On follow up 2 months later, he reported no similar symptoms.
