A case of meningococcal meningitis with multiple cerebellar microbleeds detected by susceptibility-weighted imaging
BACKGROUND There is a widely held belief that cerebral infarction after bacterial meningitis is always caused by vasculitis; however, evidence is weak. We hypothesized that diffuse cerebral intravascular coagulation is an additional explanation of cerebral infarction in patients with pneumococcal meningitis. METHODS Sixteen brains of adults who died from pneumococcal meningitis were investigated. Clinical data were collected, and brain sections were scored for signs of inflammation and activation of coagulation. Patients with and without cerebral infarction on autopsy were compared. RESULTS In total, 38% of patients had focal neurological deficits. Patients died at a median of 7 days (range, 0-32 days) after admission. On autopsy, the nine patients (56%) with cerebral infarctions more often had arterial thrombosis (p = 0.04) than patients without infarction. Patients with infarction tended to have more inflammatory infiltrations of brain parenchyma, microvascular proliferation, small vessel vasculitis/endarteritis obliterans, blood clotting/vessel clogging, and venous thrombosis. None of the patients had large vessel vasculitis. Five patients had cerebral infarctions without vasculitis or endarteritis obliterans. Although four patients with cerebral infarctions had small vessel vasculitis or endarteritis obliterans, areas of infarction could not be localized to the blood flow distribution of these vessels. Blood clotting/vessel clogging was seen in all four patients with vasculitis or endarteritis obliterans, but this was also observed in 10 patients without vasculitis or endarteritis obliterans. None of the patients developed disseminated intravascular coagulation. CONCLUSIONS Our results suggest that diffuse cerebral intravascular coagulation is an additional explanation of cerebral infarction complicating pneumococcal meningitis.